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Sepsis other diagnostic studies

Jason Le — Sat, 26 Sep 2026 09:43:37 GMT

← Older revision		Revision as of 09:43, 26 September 2026
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	{{Sepsis}}		{{Sepsis}}
	{{CMG}}; '''Associate Editor(s)-In-Chief:''' [[Priyamvada Singh\|Priyamvada Singh, M.B.B.S.]] [mailto:psingh@perfuse.org]		{{CMG}}; '''Associate Editor(s)-In-Chief:''' [[Priyamvada Singh\|Priyamvada Singh, M.B.B.S.]] [mailto:psingh@perfuse.org] {{JL}}

	{{SK}} sepsis syndrome; septic shock; septicemia		{{SK}} sepsis syndrome; septic shock; septicemia

	==~~Overview~~==		==Other Diagnostic Studies==
	~~There~~ are no ~~other imaging findings~~ for sepsis.
			No single test diagnoses [[sepsis]]. Other diagnostic studies include microbiological cultures, culture-independent pathogen detection, host-response sepsis-likelihood assays, rapid host biomarkers, and advanced hemodynamic monitoring. Routine chemistries, lactate, CBC, and coagulation studies belong in [[Sepsis laboratory findings\|Laboratory findings]]; SOFA/qSOFA belongs in [[Sepsis classification\|Classification]]; echocardiography and fluid-responsiveness testing belong in the echocardiography/ultrasound microchapter.<ref name="ssc2026">{{cite journal \|author=Prescott HC, Antonelli M, Alhazzani W, et al. \|title=Surviving Sepsis Campaign: International Guidelines for Management of Sepsis and Septic Shock 2026 \|journal=Critical Care Medicine \|year=2026 \|volume=54 \|issue=4 \|pages=725-812 \|doi=10.1097/CCM.0000000000007075}}</ref>

			===Cultures===

			A pathogen is identified in approximately 60–70% of patients with sepsis, whereas blood cultures are positive in only approximately 10–20%. The 2026 Surviving Sepsis Campaign (SSC) strongly recommends collecting blood cultures as soon as possible and ideally before antimicrobial therapy, without delaying antimicrobials in unstable patients.<ref name="ssc2026" />

			Blood-culture yield depends on pretest probability, the number of culture sets, blood volume, use of anaerobic bottles, and prior antimicrobial exposure. Approximately 10 mL of blood per bottle is used for adult blood cultures. The yield is higher in septic shock, with bacteremia detected in at least 50% of patients in some high-risk populations. Blood-culture positivity decreased from 31.4% to 19.4% when cultures were obtained at a median of 70 minutes after antimicrobial administration.<ref name="ssc2026" />

			Two-site sampling is traditional; one study cited by the SSC reported sensitivity increasing from 91.5% with one site to 99.3% with two sites. However, 2025 German national guidance favors single-site sampling, reflecting ongoing practice variation.<ref name="ssc2026" />

			Repeat blood cultures should be obtained to document clearance in patients with [[Staphylococcus aureus]] bacteremia, [[Staphylococcus lugdunensis]] bacteremia, or [[Candida]] bloodstream infection.<ref name="ssc2026" />

			===Culture-independent pathogen detection===

			The 2026 SSC conditionally recommends rapid molecular or syndromic pathogen-detection tests in selected patients rather than routinely in all patients with sepsis. When used in isolation, rapid diagnostic testing has shown little or no mortality benefit (RR 1.03; 95% CI 0.78–1.13); clinical benefit is more apparent when rapid diagnostics are paired with an effective antimicrobial-stewardship strategy.<ref name="ssc2026" /><ref name="rhee2026">{{cite journal \|author=Rhee C, Masur H, Klompas M, et al. \|title=IDSA/ACEP/ASM/PIDS/SCCM/SHEA/SHM/SIDP Multisociety Position Paper: Hospital Strategies to Improve Sepsis Outcomes \|journal=Clinical Infectious Diseases \|year=2026 \|pmid=42640090}}</ref><ref name="peri2024">{{cite journal \|author=Peri AM, Chatfield MD, Ling W, et al. \|title=Rapid Diagnostic Tests and Antimicrobial Stewardship Programs for the Management of Bloodstream Infection: What Is Their Relative Contribution to Improving Clinical Outcomes? A Systematic Review and Network Meta-Analysis \|journal=Clinical Infectious Diseases \|year=2024 \|volume=79 \|issue=2 \|pages=502-515 \|doi=10.1093/cid/ciae234 \|pmid=38676943}}</ref>

			Metagenomic next-generation sequencing (mNGS), including microbial cell-free DNA sequencing, can identify pathogens at substantially higher rates than conventional culture in selected patients with sepsis. Across published cohorts, pathogen positivity has been approximately 3–4 times higher than with culture. Interpretation remains limited by cost, turnaround time, detection of organisms of uncertain clinical significance, and lack of standardized interpretation; results require clinical correlation.<ref name="chien2022">{{cite journal \|author=Chien JY, Yu CJ, Hsueh PR. \|title=Utility of Metagenomic Next-Generation Sequencing for Etiological Diagnosis of Patients With Sepsis in Intensive Care Units \|journal=Microbiology Spectrum \|year=2022 \|volume=10 \|issue=4 \|pages=e0074622 \|doi=10.1128/spectrum.00746-22 \|pmid=35861525}}</ref><ref name="wu2023">{{cite journal \|author=Wu C, Yu X, Gai W, et al. \|title=Diagnostic Value of Plasma and Blood Cells Metagenomic Next-Generation Sequencing in Patients With Sepsis \|journal=Biochemical and Biophysical Research Communications \|year=2023 \|volume=683 \|pages=149079 \|doi=10.1016/j.bbrc.2023.10.011 \|pmid=37871447}}</ref><ref name="brown2026">{{cite journal \|author=Brown JR, Chiu CY, López-Labrador FX, de Vries JJC. \|title=The Impact of Clinical Metagenomic Testing on Patient Management: Facts Versus Fantasy \|journal=The Lancet Infectious Diseases \|year=2026 \|volume=26 \|issue=9 \|pages=e342-e354 \|doi=10.1016/S1473-3099(26)00106-4 \|pmid=42030968}}</ref><ref name="zhang2024">{{cite journal \|author=Zhang D, Li X, Wang Y, Zhao Y, Zhang H. \|title=The Clinical Importance of Metagenomic Next-Generation Sequencing in Detecting Disease-Causing Microorganisms in Cases of Sepsis Acquired in the Community or Hospital Setting \|journal=Frontiers in Microbiology \|year=2024 \|volume=15 \|pages=1384166 \|doi=10.3389/fmicb.2024.1384166 \|pmid=38686114}}</ref>

			Rapid direct-from-blood nucleic-acid amplification tests, including T2Bacteria and T2Candida, can provide pathogen detection within hours but should be used concurrently with blood cultures because cultures provide broader organism coverage and antimicrobial susceptibility information.<ref name="fevericu">{{cite journal \|author=O'Grady NP, Alexander E, Alhazzani W, et al. \|title=Society of Critical Care Medicine and the Infectious Diseases Society of America Guidelines for Evaluating New Fever in Adult Patients in the ICU \|journal=Critical Care Medicine \|year=2023 \|volume=51 \|issue=11 \|pages=1570-1586 \|doi=10.1097/CCM.0000000000006022}}</ref>

			===Host-response sepsis-likelihood assays===

			FDA-cleared host-response assays include monocyte distribution width (MDW), IntelliSep, SeptiCyte Rapid/TriVerity, Sepsis ImmunoScore, and pancreatic stone protein (PSP). These assays provide a graded probability of sepsis rather than a binary diagnostic result. The 2026 SSC did not recommend any specific host-response assay because of cost and insufficient outcome data. Their incremental diagnostic value is limited when the pretest probability of sepsis is already very high.<ref name="ssc2026" />

			MDW is reported as part of an activated CBC with differential when the assay is available.<ref name="ssc2026" />

			===Rapid host biomarkers===

			[[Procalcitonin]], C-reactive protein (CRP), and presepsin are adjunctive biomarkers rather than stand-alone rule-in tests for sepsis. Their principal practical value is as part of an overall clinical assessment, including support for antimicrobial de-escalation when interpreted with the clinical course and other microbiological data.<ref name="fevericu" />

	==~~Other Diagnostic Studies~~==		Procalcitonin can increase in severe viral illness. CRP responses may be blunted by neutropenia, immunosuppression, or nonsteroidal anti-inflammatory drug exposure; these limitations should be considered when interpreting results.<ref name="fevericu" />
	~~There are no other imaging findings~~ for sepsis.
			===Advanced hemodynamic monitoring===

			Advanced hemodynamic monitoring may be considered when noninvasive assessment is insufficient in refractory shock. Transpulmonary thermodilution and pulmonary artery catheterization can characterize cardiac output and its determinants in selected patients. The pulmonary artery catheter has a narrower role, particularly in patients with [[right ventricular failure]] or [[pulmonary hypertension]].<ref name="ssc2026" />

			The 2026 SSC found insufficient evidence to recommend for or against minimally invasive or noninvasive cardiac-output monitoring. These techniques should therefore be selected according to the clinical question, available expertise, and patient physiology rather than used routinely in all patients with sepsis.<ref name="ssc2026" />

	==References==		==References==
	{{~~reflist~~\|2}}		{{Reflist\|2}}

	{{WH}}		{{WH}}
	{{WS}}		{{WS}}

	~~[[Category:Needs content]]~~
	[[Category:Intensive care medicine]]		[[Category:Intensive care medicine]]
	~~[[Category:Causes of death]]~~
	[[Category:Emergency medicine]]		[[Category:Emergency medicine]]
	[[Category:Disease]]		[[Category:Disease]]
	~~[[Category:Emergency mdicine]]~~
	[[Category:Up-To-Date]]		[[Category:Up-To-Date]]
	[[Category:Infectious disease]]		[[Category:Infectious disease]]

Sepsis other imaging findings

Jason Le — Sat, 26 Sep 2026 09:12:40 GMT

← Older revision		Revision as of 09:12, 26 September 2026
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	{{Sepsis}}		{{Sepsis}}
	{{CMG}}; '''Associate Editor(s)-In-Chief:''' [[Priyamvada Singh\|Priyamvada Singh, M.B.B.S.]] [mailto:psingh@perfuse.org]		{{CMG}}; '''Associate Editor(s)-In-Chief:''' [[Priyamvada Singh\|Priyamvada Singh, M.B.B.S.]] [mailto:psingh@perfuse.org] {{JL}}

	{{SK}} sepsis syndrome; septic shock; septicemia		{{SK}} sepsis syndrome; septic shock; septicemia

	==~~Overview==~~		==Sepsis other imaging findings==
	~~There are no~~ other imaging findings ~~for sepsis.~~

	==~~Other~~ Imaging ~~Findings~~==		===Overview===
	~~There are~~ no ~~other~~ imaging findings for ~~sepsis~~.		No imaging finding establishes the diagnosis of [[sepsis]] itself. Imaging in sepsis serves to identify the infectious source, characterize organ dysfunction, and detect complications amenable to source control. This microchapter focuses on the cross-modality source-identification strategy and imaging applications not primarily covered by dedicated chest radiograph, CT, MRI, and echocardiography/ultrasound microchapters, particularly nuclear/molecular imaging, image-guided source control, and characteristic cross-sectional complications.<ref name="acr2024">{{cite journal \|author=Brixey AG, Fung A, De Leon AD, et al. \|title=ACR Appropriateness Criteria® Sepsis \|journal=Journal of the American College of Radiology \|year=2024 \|volume=21 \|issue=6S \|pages=S292-S309 \|doi=10.1016/j.jacr.2024.02.029}}</ref><ref name="yealy2021">{{cite journal \|author=Yealy DM, Mohr NM, Shapiro NI, et al. \|title=Early Care of Adults With Suspected Sepsis in The Emergency Department and Out-of-Hospital Environment: A Consensus-Based Task Force Report \|journal=Annals of Emergency Medicine \|year=2021 \|volume=78 \|issue=1 \|pages=1-19 \|doi=10.1016/j.annemergmed.2021.02.006}}</ref>

			===Multimodality source identification===
			When no infectious source is clinically apparent, obtain a [[chest radiograph]] and evaluate for urinary infection, followed by targeted imaging based on the clinical assessment. Contrast-enhanced CT of the chest, abdomen, and pelvis is a high-yield conventional cross-sectional study when a source remains unclear; in an emergency department cohort, a septic focus was identified in approximately 76.5% of CT examinations, including chest/pneumonia (38.6%), abdomen (22.0%), and pelvis/genitourinary tract (20.5%), with a positive predictive value of approximately 82%. The negative predictive value was low (approximately 22%), so a negative CT does not exclude an infectious source.<ref name="acr2024" />

			Targeted CT is preferred over untargeted whole-body scanning and should be selected according to the suspected source and clinical findings. Intravenous contrast improves detection and characterization of abdominal infectious sources; noncontrast CT may be used when intravenous contrast is contraindicated.<ref name="acr2024" /><ref name="yealy2021" />

			Detailed modality-specific findings are addressed in the dedicated chest radiograph, CT, MRI, and echocardiography/ultrasound microchapters.

			===Nuclear and molecular imaging===
			For an occult infectious source or fever of unknown origin after an unrevealing or inconclusive conventional evaluation, [[18F-FDG PET/CT]] is the principal molecular imaging modality. Reported pooled diagnostic performance is approximately 84.4% sensitivity and 61.8% specificity, with higher sensitivity than radiolabeled leukocyte scintigraphy and gallium-67 scintigraphy in this setting.<ref name="rijsewijk2023">{{cite journal \|author=van Rijsewijk ND, IJpma FFA, Wouthuyzen-Bakker M, Glaudemans AWJM. \|title=Molecular Imaging of Fever of Unknown Origin: An Update \|journal=Seminars in Nuclear Medicine \|year=2023 \|volume=53 \|issue=1 \|pages=4-17 \|pmid=35902280 \|doi=10.1053/j.semnuclmed.2022.07.002}}</ref><ref name="eanm2024">{{cite journal \|author=Hess S, Noriega-Álvarez E, Leccisotti L, et al. \|title=EANM consensus document on the use of [18F]FDG PET/CT in fever and inflammation of unknown origin \|journal=European Journal of Nuclear Medicine and Molecular Imaging \|year=2024 \|volume=51 \|issue=9 \|pages=2597-2613 \|doi=10.1007/s00259-024-06732-8}}</ref>

			For suspected [[cardiovascular infection]] or endovascular infection, [[18F-FDG PET/CT]] is an important primary molecular imaging modality. Radiolabeled-leukocyte SPECT/CT has higher specificity but lower sensitivity in selected cardiovascular infections and has limited utility for gram-negative or fungal infection.<ref name="asnc2024">{{cite journal \|author=Bourque JM, Birgersdotter-Green U, Bravo PE, et al. \|title=18F-FDG PET/CT and Radiolabeled Leukocyte SPECT/CT Imaging for the Evaluation of Cardiovascular Infection in the Multimodality Context: ASNC Imaging Indications (ASNC I2) Series Expert Consensus Recommendations From ASNC, AATS, ACC, AHA, ASE, EANM, HRS, IDSA, SCCT, SNMMI, and STS \|journal=JACC: Cardiovascular Imaging \|year=2024 \|volume=17 \|issue=6 \|pages=669-701 \|pmid=38466252 \|doi=10.1016/j.jcmg.2024.01.004}}</ref>

			===Image-guided source control===
			The [[Surviving Sepsis Campaign]] 2026 guideline conditionally recommends early source control, typically within approximately 6 hours, when a source requiring source control is identified. Evidence certainty is very low; pooled evidence cited by the guideline showed lower mortality with early source control (RR 0.70; 95% CI 0.51-0.95).<ref name="ssc2026">{{cite journal \|author=Prescott HC, Antonelli M, Alhazzani W, et al. \|title=Surviving Sepsis Campaign: International Guidelines for Management of Sepsis and Septic Shock 2026 \|journal=Critical Care Medicine \|year=2026 \|volume=54 \|issue=4 \|pages=725-812 \|doi=10.1097/CCM.0000000000007075}}</ref>

			When anatomically feasible, ultrasound- or CT-guided percutaneous catheter drainage provides a minimally invasive method of source control for accessible infected collections. Surgical source control is used when percutaneous drainage is not feasible, inadequate, or otherwise inappropriate.<ref name="ssc2026" />

			===Imaging of characteristic complications===
			'''Bilateral adrenal hemorrhage/Waterhouse-Friderichsen syndrome:''' CT may demonstrate bilateral hyperattenuating adrenal enlargement, approximately 50-90 HU, with associated periadrenal stranding. Extensive bilateral adrenal hemorrhage can cause acute adrenal insufficiency and should be recognized as a potentially life-threatening complication.<ref name="adrenal2019">{{cite journal \|author=Alshahrani MA, Bin Saeedan M, Alkhunaizan T, Aljohani IM, Azzumeea FM. \|title=Bilateral adrenal abnormalities: imaging review of different entities \|journal=Abdominal Radiology \|year=2019 \|volume=44 \|issue=1 \|pages=154-179 \|doi=10.1007/s00261-018-1670-5}}</ref>

			'''Non-occlusive mesenteric ischemia:''' CT angiography may demonstrate reduced or absent bowel-wall enhancement. Increased unenhanced bowel-wall attenuation is also among the more specific CT findings. This complication should be considered in septic patients with clinical features suggesting intestinal ischemia despite the absence of an arterial occlusion.<ref name="mesenteric2022">{{cite journal \|author=Pinto A, Lanzetta MM, Addeo G, et al. \|title=Errors in MDCT diagnosis of acute mesenteric ischemia \|journal=Abdominal Radiology \|year=2022 \|volume=47 \|issue=5 \|pages=1699-1713 \|doi=10.1007/s00261-020-02732-y}}</ref>

	==References==		==References==
	{{~~reflist~~\|2}}		{{Reflist\|2}}

	{{WH}}		{{WH}}
	{{WS}}		{{WS}}

	~~[[Category:Needs content]]~~
	[[Category:Intensive care medicine]]		[[Category:Intensive care medicine]]
	~~[[Category:Causes of death]]~~
	[[Category:Emergency medicine]]		[[Category:Emergency medicine]]
	~~[[Category:Disease]]~~
	~~[[Category:Emergency mdicine]]~~
	~~[[Category:Up-To-Date]]~~
	[[Category:Infectious disease]]		[[Category:Infectious disease]]
			[[Category:Radiology]]

Sepsis echocardiography or ultrasound

Jason Le — Fri, 25 Sep 2026 20:13:31 GMT

Show changes

Sepsis MRI

Jason Le — Fri, 25 Sep 2026 07:07:45 GMT

@@ Line 5: / Line 5: @@
 |}
 {{Sepsis}}
-{{CMG}};  '''Associate Editor(s)-In-Chief:''' [[Priyamvada Singh|Priyamvada Singh, M.B.B.S.]] [mailto:psingh@perfuse.org]
+{{CMG}};  '''Associate Editor(s)-In-Chief:''' [[Priyamvada Singh|Priyamvada Singh, M.B.B.S.]] [mailto:psingh@perfuse.org] {{JL}}
 {{SK}} sepsis syndrome; septic shock; septicemia
-==Overview==
+==Sepsis MRI==
-There are no specific MRI findings associated with sepsis but may show the features consistent with the primary source of [[infection]].
+Magnetic resonance imaging (MRI) has '''no imaging pattern specific for [[sepsis]]''' and is not a first-line or screening study for the undifferentiated septic patient. The 2024 [[American College of Radiology]] (ACR) Appropriateness Criteria for Sepsis state that there are no data supporting MRI as an initial or next-line study for undifferentiated sepsis, because most septic patients are too unstable for a relatively long acquisition when faster [[CT]] and ultrasound are available. MRI's value is targeted: characterizing a specific, clinically suspected deep source such as musculoskeletal infection, spinal epidural abscess/discitis, perianal or pelvic abscess, or selected hepatobiliary processes, and evaluating suspected sepsis-associated encephalopathy.<ref name="Brixey2024">{{cite journal |author=Brixey AG, Fung A, De Leon AD, et al. |title=ACR Appropriateness Criteria® Sepsis |journal=Journal of the American College of Radiology |year=2024 |volume=21 |issue=6S |pages=S292-S309 |doi=10.1016/j.jacr.2024.02.029}}</ref>
-==MRI==
+===Targeted indications===
-There are no specific MRI findings associated with sepsis but may show the features consistent with the primary source of [[infection]].
+* '''Musculoskeletal infection:''' MRI is the study of choice for suspected [[osteomyelitis]], [[septic arthritis]], and deep soft-tissue infection after initial radiographs. A normal MRI can effectively exclude active osteomyelitis, and contrast is useful for characterizing associated soft-tissue infection, abscess, fistula, and vascular complications.<ref name="Pierce2022">{{cite journal |author=Expert Panel on Musculoskeletal Imaging, Pierce JL, Perry MT, et al. |title=ACR Appropriateness Criteria® Suspected Osteomyelitis, Septic Arthritis, or Soft Tissue Infection (Excluding Spine and Diabetic Foot): 2022 Update |journal=Journal of the American College of Radiology |year=2022 |volume=19 |issue=11S |pages=S473-S487 |doi=10.1016/j.jacr.2022.09.013}}</ref>
 ==References==
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 {{WikiDoc Sources}}
 [[Category:Intensive care medicine]]
 [[Category:Emergency medicine]]
 [[Category:Disease]]
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 [[Category:Infectious disease]]

Sepsis CT

Jason Le — Fri, 25 Sep 2026 06:41:29 GMT

@@ Line 5: / Line 5: @@
 |}
 {{Sepsis}}
-{{CMG}};  '''Associate Editor(s)-In-Chief:''' [[Priyamvada Singh|Priyamvada Singh, M.B.B.S.]] [mailto:psingh@perfuse.org]
+{{CMG}};  '''Associate Editor(s)-In-Chief:''' [[Priyamvada Singh|Priyamvada Singh, M.B.B.S.]] [mailto:psingh@perfuse.org] {{JL}}
 {{SK}} sepsis syndrome; septic shock; septicemia
-==Overview==
+==Sepsis CT==
-There are no specific CT findings associated with sepsis but may show the features consistent with the primary source of [[infection]].
+Computed tomography (CT) has '''no imaging pattern specific for [[sepsis]]'''. Its principal role is to identify an anatomic source of infection when no source is clinically apparent or when first-line evaluation is normal or equivocal, characterize complications of a suspected source, and facilitate '''source control''' through image-guided drainage or surgical planning.<ref name="Brixey2024">{{cite journal |author=Brixey AG, Fung A, De Leon AD, et al. |title=ACR Appropriateness Criteria® Sepsis |journal=Journal of the American College of Radiology |year=2024 |volume=21 |issue=6S |pages=S292-S309 |doi=10.1016/j.jacr.2024.02.029}}</ref> Septic foci are most commonly identified in the chest, abdomen, and pelvis.<ref name="Brixey2024" />
-==CT==
+The 2024 [[American College of Radiology]] Appropriateness Criteria support '''contrast-enhanced CT (CECT)''' of the relevant body region when the source is undifferentiated or initial evaluation is nondiagnostic. In patients without localizing features, CT of the chest, abdomen, and pelvis with intravenous contrast is an appropriate strategy.<ref name="Brixey2024" />
-There are no specific CT findings associated with sepsis but may show the features consistent with the primary source of [[infection]].
 ==References==
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 [[Category:Intensive care medicine]]
 [[Category:Emergency medicine]]
 [[Category:Disease]]
-[[Category:Emergency mdicine]]
+[[Category:Infectious disease]]
 [[Category:Up-To-Date]]

Sepsis chest x ray

Jason Le — Thu, 24 Sep 2026 23:32:13 GMT

Show changes

Sepsis electrocardiogram

Jason Le — Thu, 24 Sep 2026 22:18:30 GMT

@@ Line 5: / Line 5: @@
 |}
 {{Sepsis}}
-{{CMG}};  '''Associate Editor(s)-In-Chief:''' [[Priyamvada Singh|Priyamvada Singh, M.B.B.S.]] [mailto:psingh@perfuse.org]
+{{CMG}};  '''Associate Editor(s)-In-Chief:''' [[Priyamvada Singh|Priyamvada Singh, M.B.B.S.]] [mailto:psingh@perfuse.org] {{JL}}
 {{SK}} sepsis syndrome; septic shock; septicemia
-==Electrocardiogram==
+==Sepsis electrocardiogram==
-On ECG, sepsis is characterized by decreased [[QRS complex|QRS]] amplitudes, increased [[QRS duration]] with or without [[bundle branch block]]. These findings are due to altered cardiac excitability.<ref name="pmid12145473">{{cite journal |vauthors=Rich MM, McGarvey ML, Teener JW, Frame LH |title=ECG changes during septic shock |journal=Cardiology |volume=97 |issue=4 |pages=187–96 |year=2002 |pmid=12145473 |doi= |url=}}</ref>
 ==References==
 {{Reflist|2}}
-{{WikiDoc Help Menu}}
+[[Category:Medicine]]
 [[Category:Emergency medicine]]
-[[Category:Disease]]
+[[Category:Infectious disease]]
-[[Category:Emergency mdicine]]
+[[Category:Cardiology]]
 [[Category:Up-To-Date]]

User:Hasnain Ali

Hasnain Ali — Thu, 24 Sep 2026 22:09:03 GMT

Clinical Experience

← Older revision		Revision as of 22:09, 24 September 2026
(One intermediate revision by the same user not shown)
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	==Clinical Experience==		==Clinical Experience==
	*'''Liaquat University of Medical & Health Sciences, Jamshoro, Pakistan (~~Jan~~/2026 - Current)'''
	'''Position:''' Resident Physician~~<br>~~'''Supervisor Attending:''' Dr. Muhammad Aslam, MBBS, FCPS, FRCP (UK)		* '''Liaquat University of Medical & Health Sciences, Jamshoro, Pakistan (01/2026 - Current)'''

			'''Position:''' Resident Physician

			'''Supervisor Attending:''' Dr. Muhammad Aslam, MBBS, FCPS, FRCP (UK)

			* '''Brown University Health (06/2026 - 06/2022)'''

			'''Position:''' Medical Observer

			'''Supervisor Attending:''' Dr. Farukhuddin MD.

			* '''inova loudoun hospital (07/2026 - 07/2022)'''

			'''Position:''' Medical Observer

			'''Supervisor Attending:''' Dr. Rauf Chaudhry, MD.

			* '''Liaquat University Civil Hospital, Hyderabad/Jamshoro Pakistan (05/2023 - 12/2025)'''

			'''Position:''' Medical Officer with Dept. of Neurology and General Medicine

			'''Supervisor Attending:''' Prof. Dr. Manzoor Ali Lakhair, MBBS, FCPS.; Dr. Muhammad Aslam Rind, MBBS, FCPS, FRCP.

	* '''Carondelet St. Joseph’s Hospital, Tucson, AZ (06/2025 - 06/2025)'''		* '''Carondelet St. Joseph’s Hospital, Tucson, AZ (06/2025 - 06/2025)'''

	'''Position:''' Observer~~<br>~~'''Supervisor Attending:''' Dr. Fahad J. Laghari, MD.		'''Position:''' Observer

			'''Supervisor Attending:''' Dr. Fahad J. Laghari, MD.

	* '''Charleston Area Medical Center, Charleston, WV (05/2025 - 05/2025)'''		* '''Charleston Area Medical Center, Charleston, WV (05/2025 - 05/2025)'''

	'''Position:''' Observer~~<br>~~'''Supervisor Attending:''' Dr. Suzanne Crandall, DO, AOA.		'''Position:''' Observer
	*'''Boston Medical Center-South, Brockton, MA (04/2025 - 04/2025)'''
	'''Position:''' Observer~~<br>~~'''Supervisor Attending:''' Dr. Terri Spenser, MD ~~; Dr. David Miller MD.~~		'''Supervisor Attending:''' Dr. Suzanne Crandall, DO, AOA.
	*'''Liaquat University Civil Hospital, Hyderabad/Jamshoro Pakistan (May/2023 - December 2025)'''
	~~'''Position:''' Medical Officer with Dept. of Neurology<br>'''Supervisor Attending:''' Prof. Dr. Manzoor Ali Lakhair, MBBS, FCPS. ; Dr. Abdul Hafeez Bughio, MBBS, FCPS~~.		* '''Boston Medical Center-South, Brockton, MA (04/2025 - 04/2025)'''
	*'''Liaquat University Civil Hospital, Hyderabad/Jamshoro Pakistan (Jan/2022 - July/2022)'''
	~~'''Position:''' Intern/House officer<br>'''Supervisor Attending:''' Multiple~~		'''Position:''' Observer
	*'''Dr. Ruth. K. M. Pfau Civil hospital Karachi, Pakistan (July/2021 - Jan/2022)'''
	~~'''Position:''' Intern/House officer<br>'''Supervisor Attending:''' Multiple~~		'''Supervisor Attending:''' Dr. Terri Spenser, MD.

	==Contributions at WikiDoc==		==Contributions at WikiDoc==

NUZOLVENCE- zoliflodacin for suspension

Anum Ijaz — Thu, 24 Sep 2026 20:00:51 GMT

← Older revision		Revision as of 20:00, 24 September 2026
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	* The chemical name of zoliflodacin is (2R,4S,4aS)-11-Fluoro-1,2,4,4a-tetrahydro-2,4-dimethyl-8-[(4S)-4-methyl-2-oxo-3-oxazolidinyl]spiro[isoxazolo[4,5-g][1,4]oxazino[4,3-a]quinoline-5(6H),5'(2'H)-pyrimidine]-2',4',6'(1'H,3'H)-trione.		* The chemical name of zoliflodacin is (2R,4S,4aS)-11-Fluoro-1,2,4,4a-tetrahydro-2,4-dimethyl-8-[(4S)-4-methyl-2-oxo-3-oxazolidinyl]spiro[isoxazolo[4,5-g][1,4]oxazino[4,3-a]quinoline-5(6H),5'(2'H)-pyrimidine]-2',4',6'(1'H,3'H)-trione.

	~~Add~~ structure image		[[File:Zoliflodacin structure image.jpeg]]

	* Its molecular formula is C22H22FN5O7 and molecular mass is 487.4 g/mol.		* Its molecular formula is C22H22FN5O7 and molecular mass is 487.4 g/mol.
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	\|storage=* NUZOLVENCE should be stored in the original packaging at room temperature 20 °C to 25 °C (68 °F to 77 °F); excursions permitted to 15 °C to 30 °C (59 °F to 86 °F). [See USP Controlled Room Temperature].		\|storage=* NUZOLVENCE should be stored in the original packaging at room temperature 20 °C to 25 °C (68 °F to 77 °F); excursions permitted to 15 °C to 30 °C (59 °F to 86 °F). [See USP Controlled Room Temperature].
	* Do not freeze.		* Do not freeze.
	\|packLabel=~~Add Display Panel~~		\|packLabel=[[File:Zoliflodacin PD suspension.jpeg\|400px\|thumb\|right\|PRINCIPAL DISPLAY PANEL - 3 g Packet Carton]]
	\|fdaPatientInfo=Advise the patient to read the FDA-approved labeling (Medication Guide and Instructions for Use).		\|fdaPatientInfo=Advise the patient to read the FDA-approved labeling (Medication Guide and Instructions for Use).

LEROCHOL- lerodalcibep-liga injection, solution

Anum Ijaz — Thu, 24 Sep 2026 19:40:22 GMT

VOYXACT- sibeprenlimab injection

Anum Ijaz — Thu, 24 Sep 2026 19:35:12 GMT

← Older revision		Revision as of 19:35, 24 September 2026
Line 181:		Line 181:
	* The observed geometric mean percent change from baseline over time for uPCR from spot first morning void samples is shown in Figure 2.		* The observed geometric mean percent change from baseline over time for uPCR from spot first morning void samples is shown in Figure 2.

	~~'''Figure~~ 1: Estimated Percent Change Compared to Baseline in uPCR-24h at Month 9 in Patients with IgAN in the VISIONARY Study~~'''~~		[[File:Voyxact Fir. 1.jpeg\|400px\|thumb\|right\|Estimated Percent Change Compared to Baseline in uPCR-24h at Month 9 in Patients with IgAN in the VISIONARY Study]]

	<table class="wikitable">		<table class="wikitable">
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	<sup>*</sup> 96.5% CI corresponds to the two-sided significance level of 0.035 for the interim analysis (IA).		<sup>*</sup> 96.5% CI corresponds to the two-sided significance level of 0.035 for the interim analysis (IA).

	~~Add Figure~~ 2. Percent Change Compared to Baseline in Spot uPCR Over Time in Patients with IgAN in the VISIONARY Study~~'''~~		[[File:Voyxact Fig. 2.jpeg\|400px\|thumb\|right\|Percent Change Compared to Baseline in Spot uPCR Over Time in Patients with IgAN in the VISIONARY Study]]

	CI = Confidence Interval		CI = Confidence Interval
Line 219:		Line 219:
	* Once VOYXACT prefilled syringe has reached room temperature, do not return it to the refrigerator.		* Once VOYXACT prefilled syringe has reached room temperature, do not return it to the refrigerator.
	* Do not use VOYXACT if it has been at room temperature for 7 days or longer.		* Do not use VOYXACT if it has been at room temperature for 7 days or longer.
	\|packLabel=~~Add Display Panel~~		\|packLabel= [[File:Voyxact.jpeg\|400px\|thumb\|right\|PRINCIPAL DISPLAY PANEL - 200 mg/mL Syringe Carton]]
	\|fdaPatientInfo=Advise the patient and/or caregiver to read the FDA-approved patient labeling (Patient Information and Instructions for Use).		\|fdaPatientInfo=Advise the patient and/or caregiver to read the FDA-approved patient labeling (Patient Information and Instructions for Use).

HYRNUO- sevabertinib tablet, film coated

Anum Ijaz — Thu, 24 Sep 2026 19:30:11 GMT

← Older revision		Revision as of 19:30, 24 September 2026
Line 359:		Line 359:
	* The chemical name of the drug substance is 3-(3-chloro-2-methoxyanilino)-2-{3-[(2S)-1,4-dioxan-2-ylmethoxy]pyridin-4-yl}-1,5,6,7-tetrahydro-4H-pyrrolo[3,2-c]pyridin-4-one hydrate.		* The chemical name of the drug substance is 3-(3-chloro-2-methoxyanilino)-2-{3-[(2S)-1,4-dioxan-2-ylmethoxy]pyridin-4-yl}-1,5,6,7-tetrahydro-4H-pyrrolo[3,2-c]pyridin-4-one hydrate.

	~~Add~~ structure ~~image~~		[[File:Hyrnuo structure.jpeg]]

	* The molecular formula is C24H25ClN4O5 (anhydrate) and the molecular weight is 484.93 g/mol (anhydrate).		* The molecular formula is C24H25ClN4O5 (anhydrate) and the molecular weight is 484.93 g/mol (anhydrate).
Line 487:		Line 487:
	* NDC 50419-397-01		* NDC 50419-397-01
	\|storage=Store at 20°C to 25°C (68°F to 77°F); excursions permitted between 15°C to 30°C (59°F to 86°F) [see USP Controlled Room Temperature].		\|storage=Store at 20°C to 25°C (68°F to 77°F); excursions permitted between 15°C to 30°C (59°F to 86°F) [see USP Controlled Room Temperature].
	\|packLabel=~~Add Display Panel~~		\|packLabel=[[File:PD Hyrnuo.jpeg\|400px\|thumb\|right\|PRINCIPAL DISPLAY PANEL - 10 mg Tablet Bottle Label]]
	\|fdaPatientInfo=Advise the patient to read the FDA-approved patient labeling (Patient Information).		\|fdaPatientInfo=Advise the patient to read the FDA-approved patient labeling (Patient Information).

Sepsis laboratory findings

Jason Le — Thu, 24 Sep 2026 18:50:05 GMT

Show changes

Intervention in Small Vessels

Anum Ijaz — Thu, 24 Sep 2026 16:43:18 GMT

@@ Line 75: / Line 75: @@
 * In [[acute coronary syndrome]] treated with drug-coated balloons alone, stepwise de-escalation (aspirin plus [[ticagrelor]] for one month, [[ticagrelor]] monotherapy to six months, then aspirin monotherapy) is non-inferior to 12 months of [[dual antiplatelet therapy]] for net adverse clinical events and reduces major bleeding; this evidence comes from a predominantly East Asian population and was not restricted to small vessels.<ref name="doi101136bmj2024082945">{{cite journal |author=Gao C, Zhu B, Ouyang F, Wen S, Xu Y, Jia W, et al. |title=Stepwise dual antiplatelet therapy de-escalation in patients after drug coated balloon angioplasty (REC-CAGEFREE II): multicentre, randomised, open label, assessor blind, non-inferiority trial |journal=[[BMJ]] |volume=388 |pages=e082945 |year=2025 |doi=10.1136/bmj-2024-082945 |url=https://doi.org/10.1136/bmj-2024-082945 |accessdate=2026-09-23}}</ref>
-====Summary of Steps for Management====
+====Management Algorithm====
-:'''Step 1: Confirm that the target vessel is small'''
+The algorithm below summarizes the management steps supported by the evidence cited in this chapter.<ref name="doi101016jjscai2022100403"/><ref name="doi101016jjacc202510027"/><ref name="doi101001jama20241361"/><ref name="doi101093eurheartjehae177"/><ref name="doi101016jjacc202507049"/><ref name="doi104244eijd1801056"/><ref name="doi101016S0140673618317197"/><ref name="doi101016S0140673620321735"/><ref name="pmid39981922"/><ref name="doi101016jjcin202309026"/><ref name="pmid32473887"/>
 ==Complications==
 * Bailout [[stent]] implantation after drug-coated balloon treatment of small vessels is needed in roughly 5% to 20% of lesions, most often for a flow-limiting [[dissection]] or an inadequate residual lumen.<ref name="pmid30522667"/><ref name="pmid23158530"/>

Intervention in Small Vessels

Anum Ijaz — Thu, 24 Sep 2026 14:25:05 GMT

Created page with "__NOTOC__ {{Percutaneous Coronary Intervention}} {{CMG}}; {{AIJ}} ==Overview== Small vessel coronary artery disease is one of the most frequent lesion subsets encountered during percutaneous coronary intervention, and it is more common in women, in patients with diabetes mellitus or chronic kidney disease, in distal coronary segments and in bifurcation lesions. There is no single accepted definition; randomized trials have used reference vessel diameter..."

New page

__NOTOC__
{{Percutaneous Coronary Intervention}}
{{CMG}}; {{AIJ}}

==Overview==
Small vessel coronary artery disease is one of the most frequent lesion subsets encountered during [[percutaneous coronary intervention]], and it is more common in women, in patients with [[diabetes mellitus]] or [[chronic kidney disease]], in distal coronary segments and in [[bifurcation lesions]]. There is no single accepted definition; randomized trials have used reference vessel diameter thresholds between 2.5 mm and 3.0 mm, and a standardized cut-off below 2.5 mm, measured preferably by intracoronary imaging, has been proposed. Angiography frequently underestimates the true diameter of these vessels, so intravascular imaging is useful to confirm that a vessel is genuinely small before a treatment strategy is chosen.

Small vessels carry a higher risk of [[restenosis]] and target lesion failure after [[stent]] implantation than larger vessels. New-generation [[drug-eluting stent]]s remain the default treatment, and thinner stent struts are associated with fewer repeat revascularizations. A drug-coated balloon strategy, which leaves no permanent metallic scaffold and permits a shorter course of [[dual antiplatelet therapy]], is the best-supported alternative in de novo small vessel disease: paclitaxel-coated balloons, used after adequate lesion preparation, have produced clinical outcomes comparable to second-generation drug-eluting stents up to three years. The benefit does not extend to vessels of 3.0 mm or larger and is not a class effect across devices: sirolimus-coated balloon performance depends on the coating formulation, and no sirolimus-coated balloon has yet been shown to match drug-eluting stents specifically in small vessels. Diabetes mellitus and high bleeding risk are the settings in which avoiding further metal and shortening dual antiplatelet therapy are most appealing, although the supporting data come from subgroup analyses.

Because small vessels are prone to restenosis, in-stent restenosis is the second major small vessel indication for a drug-coated balloon, which treats the lesion without adding a further layer of metal. A paclitaxel-coated balloon is superior to uncoated balloon angioplasty for in-stent restenosis, with a consistent effect in small vessels, and received US Food and Drug Administration approval for this indication in 2024; the 2024 ESC guidelines, however, recommend a drug-eluting stent over a drug-coated balloon for restenosis within a drug-eluting stent. Intravascular imaging is useful beyond sizing: guidance of drug-coated balloon angioplasty improves the angiographic result, and imaging guidance is recommended for anatomically complex lesions. No ACC/AHA/SCAI or ESC guideline currently carries a recommendation specific to small vessel intervention.

==Definition==
* There is no universally accepted definition of small vessel [[coronary artery disease]]; randomized trials have used reference vessel diameter thresholds of less than 2.5 mm, 2.75 mm or less, and less than 3.0 mm, which limits comparison between studies.<ref name="doi101016jjscai2022100403">{{cite journal |author=Sanz-Sánchez J, Chiarito M, Gill GS, van der Heijden LC, Piña Y, Cortese B, et al. |title=Small Vessel Coronary Artery Disease: Rationale for Standardized Definition and Critical Appraisal of the Literature |journal=[[Journal of the Society for Cardiovascular Angiography & Interventions]] |volume=1 |issue=5 |pages=100403 |year=2022 |doi=10.1016/j.jscai.2022.100403 |url=https://doi.org/10.1016/j.jscai.2022.100403 |accessdate=2026-09-23}}</ref>
* A standardized cut-off of a reference vessel diameter below 2.5 mm has been proposed, measured preferably by intracoronary imaging, with [[quantitative coronary angiography]] or visual estimation used only when imaging is not available.<ref name="doi101016jjscai2022100403"/>
* Consensus documents on drug-coated balloons apply the small vessel evidence to vessels of 2.75 mm or less, or less than 3.0 mm,<ref name="pmid32473887">{{cite journal |author=Jeger RV, Eccleshall S, Wan Ahmad WA, Ge J, Poerner TC, Shin ES, et al. |title=Drug-Coated Balloons for Coronary Artery Disease: Third Report of the International DCB Consensus Group |journal=[[JACC: Cardiovascular Interventions]] |volume=13 |issue=12 |pages=1391–1402 |year=2020 |pmid=32473887 |doi=10.1016/j.jcin.2020.02.043 |url=https://doi.org/10.1016/j.jcin.2020.02.043 |accessdate=2026-09-23}}</ref> or to a reference diameter below 2.75 mm.<ref name="doi101016jjacc202507049">{{cite journal |author=Fezzi S, Serruys PW, Cortese B, Scheller B, Alfonso F, Jeger R, et al. |title=Indications for Use of Drug-Coated Balloons in Coronary Intervention: Academic Research Consortium Position Statement |journal=[[Journal of the American College of Cardiology]] |volume=86 |issue=15 |pages=1170–1202 |year=2025 |doi=10.1016/j.jacc.2025.07.049 |url=https://doi.org/10.1016/j.jacc.2025.07.049 |accessdate=2026-09-23}}</ref>

==Epidemiology and Demographics==
* Small vessel disease is present in roughly 30% to 67% of patients undergoing [[percutaneous coronary intervention]], the range reflecting the different definitions in use.<ref name="doi101016jjscai2022100403"/>
* It is more common in women and in patients with [[diabetes mellitus]] or [[chronic kidney disease]], and it clusters in distal coronary segments and in the side branches of [[bifurcation lesions]].<ref name="doi101016jjscai2022100403"/>

==Prognosis==
* [[Stent]] implantation in small vessels carries a higher risk of target lesion failure and other adverse cardiovascular events than stenting of larger vessels.<ref name="doi101016jjscai2022100403"/><ref name="doi101001jamacardio20191776">{{cite journal |author=Buiten RA, Ploumen EH, Zocca P, Doggen CJM, van der Heijden LC, Kok MM, et al. |title=Outcomes in Patients Treated With Thin-Strut, Very Thin-Strut, or Ultrathin-Strut Drug-Eluting Stents in Small Coronary Vessels |journal=[[JAMA Cardiology]] |volume=4 |issue=7 |pages=659 |year=2019 |doi=10.1001/jamacardio.2019.1776 |url=https://doi.org/10.1001/jamacardio.2019.1776 |accessdate=2026-09-23}}</ref>
* New-generation [[drug-eluting stent]]s have substantially reduced [[restenosis]] in small vessels compared with earlier devices, but small vessel disease remains an unmet clinical need.<ref name="doi101016jjscai2022100403"/>

==Lesion Assessment==
* Coronary [[angiography]] frequently underestimates the true diameter of a vessel that appears small, and positive and negative [[vascular remodeling|remodeling]] are common in small vessels, making the angiographic lumen particularly misleading.<ref name="doi101016jjscai2022100403"/>
* [[Intravascular ultrasound]] and [[optical coherence tomography]] define the true lumen shape and size better than angiography and should be used, where available, to confirm vessel size before a small vessel strategy is chosen.<ref name="doi101016jjscai2022100403"/>
* Intracoronary imaging guidance by [[intravascular ultrasound]] or [[optical coherence tomography]] is recommended for [[percutaneous coronary intervention]] of anatomically complex lesions, in particular the left main stem, true [[bifurcation lesions|bifurcations]] and long lesions, settings in which small vessels are frequently involved.<ref name="doi101093eurheartjehae177">{{cite journal |author=Vrints C, Andreotti F, Koskinas KC, Rossello X, Adamo M, Ainslie J, et al. |title=2024 ESC Guidelines for the management of chronic coronary syndromes |journal=[[European Heart Journal]] |volume=45 |issue=36 |pages=3415–3537 |year=2024 |doi=10.1093/eurheartj/ehae177 |url=https://doi.org/10.1093/eurheartj/ehae177 |accessdate=2026-09-24}}</ref><ref name="doi101016jjscai2022100403"/>
* Imaging also guides the intervention itself: [[intravascular ultrasound]]-guided drug-coated balloon angioplasty produces less late lumen loss and a larger minimal lumen diameter than angiography-guided treatment of de novo lesions in vessels of 2.0 mm to 4.0 mm, although a reduction in clinical events has not been shown.<ref name="pmid38842991">{{cite journal |author=Gao XF, Ge Z, Kong XQ, Chen X, Han L, Qian XS, et al. |title=Intravascular Ultrasound vs Angiography-Guided Drug-Coated Balloon Angioplasty: The ULTIMATE III Trial |journal=[[JACC: Cardiovascular Interventions]] |volume=17 |issue=13 |pages=1519–1528 |year=2024 |pmid=38842991 |doi=10.1016/j.jcin.2024.04.014 |url=https://doi.org/10.1016/j.jcin.2024.04.014 |accessdate=2026-09-24}}</ref>
* Few patients in the randomized comparisons of drug-coated balloons and [[drug-eluting stent]]s in small vessels underwent physiological or intravascular imaging guidance, so whether imaging improves the clinical outcome of a drug-coated balloon strategy specifically in small vessels has not been established.<ref name="pmid40036794">{{cite journal |author=Lalani C, Secemsky EA, Yeh RW |title=Drug-coated balloons in small vessel de novo coronary artery disease: better than DES? |journal=[[European Heart Journal]] |volume=46 |issue=17 |pages=1600–1602 |year=2025 |pmid=40036794 |doi=10.1093/eurheartj/ehaf083 |url=https://doi.org/10.1093/eurheartj/ehaf083 |accessdate=2026-09-23}}</ref>

==Treatment==
===Drug-Eluting Stents===
* New-generation [[drug-eluting stent]]s perform well in small vessel disease and remain the default treatment.<ref name="doi101016jjscai2022100403"/>
* Thinner stent struts are associated with lower rates of angiographic [[restenosis]] and clinically driven revascularization in small vessels.<ref name="doi101016jjscai2022100403"/>
* In small vessels, ultrathin-strut [[sirolimus]]-eluting stents reduce repeat [[target lesion revascularization]] compared with previous-generation thin-strut [[zotarolimus]]-eluting stents, without a difference in cardiac death, target vessel [[myocardial infarction]] or [[stent thrombosis]].<ref name="doi101001jamacardio20191776"/>
* The evidence is not uniform: a thin composite-wire-strut [[zotarolimus]]-eluting stent and an ultrathin-strut [[sirolimus]]-eluting stent have produced similar target vessel failure and [[target lesion revascularization]] in small vessels.<ref name="doi101016jjcin202001230">{{cite journal |author=Buiten RA, Ploumen EH, Zocca P, Doggen CJM, Jessurun GAJ, Schotborgh CE, et al. |title=Thin Composite-Wire-Strut Zotarolimus-Eluting Stents Versus Ultrathin-Strut Sirolimus-Eluting Stents in BIONYX at 2 Years |journal=[[JACC: Cardiovascular Interventions]] |volume=13 |issue=9 |pages=1100–1109 |year=2020 |doi=10.1016/j.jcin.2020.01.230 |url=https://doi.org/10.1016/j.jcin.2020.01.230 |accessdate=2026-09-23}}</ref>
* [[Drug-eluting stent]] platforms of 2.0 mm and 2.25 mm diameter are available and are associated with low rates of [[target lesion revascularization]] in vessels of 2.25 mm or less.<ref name="doi101016jjscai2022100403"/>

===Drug-Coated Balloon and Hybrid Strategies===
* A drug-coated balloon strategy leaves no permanent metallic scaffold in the vessel and allows a shorter course of [[dual antiplatelet therapy]], both of particular relevance in small vessels.<ref name="doi101016jjscai2022100403"/>
* De novo small vessel disease is the de novo indication with the strongest randomized support for drug-coated balloons, which are non-inferior to second-generation [[drug-eluting stent]]s in vessels of 2.75 mm or less or less than 3.0 mm.<ref name="pmid32473887"/>
* After successful predilatation, a paclitaxel-coated balloon is non-inferior to a second-generation [[drug-eluting stent]] for the composite of cardiac death, non-fatal [[myocardial infarction]] and [[target vessel revascularization]] at one year in vessels of less than 3.0 mm.<ref name="doi101016S0140673618317197">{{cite journal |author=Jeger RV, Farah A, Ohlow MA, Mangner N, Möbius-Winkler S, Leibundgut G, et al. |title=Drug-coated balloons for small coronary artery disease (BASKET-SMALL 2): an open-label randomised non-inferiority trial |journal=[[The Lancet]] |volume=392 |issue=10150 |pages=849–856 |year=2018 |doi=10.1016/S0140-6736(18)31719-7 |url=https://doi.org/10.1016/S0140-6736(18)31719-7 |accessdate=2026-09-23}}</ref>
* This equivalence is maintained to three years, with similar rates of cardiac death, [[myocardial infarction]], [[target vessel revascularization]] and all-cause death.<ref name="doi101016S0140673620321735">{{cite journal |author=Jeger RV, Farah A, Ohlow MA, Mangner N, Möbius-Winkler S, Weilenmann D, et al. |title=Long-term efficacy and safety of drug-coated balloons versus drug-eluting stents for small coronary artery disease (BASKET-SMALL 2): 3-year follow-up of a randomised, non-inferiority trial |journal=[[The Lancet]] |volume=396 |issue=10261 |pages=1504–1510 |year=2020 |doi=10.1016/S0140-6736(20)32173-5 |url=https://doi.org/10.1016/S0140-6736(20)32173-5 |accessdate=2026-09-23}}</ref>
* Paclitaxel-coated balloons produce less angiographic late lumen loss than [[everolimus]]-eluting stents in vessels of 2.75 mm or less,<ref name="pmid33248978">{{cite journal |author=Cortese B, Di Palma G, Guimaraes MG, Piraino D, Silva Orrego P, Buccheri D, et al. |title=Drug-Coated Balloon Versus Drug-Eluting Stent for Small Coronary Vessel Disease: PICCOLETO II Randomized Clinical Trial |journal=[[JACC: Cardiovascular Interventions]] |volume=13 |issue=24 |pages=2840–2849 |year=2020 |pmid=33248978 |doi=10.1016/j.jcin.2020.08.035 |url=https://doi.org/10.1016/j.jcin.2020.08.035 |accessdate=2026-09-23}}</ref> and in one trial this was accompanied by fewer major adverse cardiac events and vessel thromboses at three years.<ref name="doi101016jjcin202302011">{{cite journal |author=Cortese B, Testa G, Rivero F, Erriquez A, Alfonso F |title=Long-Term Outcome of Drug-Coated Balloon vs Drug-Eluting Stent for Small Coronary Vessels: PICCOLETO-II 3-Year Follow-Up |journal=[[JACC: Cardiovascular Interventions]] |volume=16 |issue=9 |pages=1054–1061 |year=2023 |doi=10.1016/j.jcin.2023.02.011 |url=https://doi.org/10.1016/j.jcin.2023.02.011 |accessdate=2026-09-23}}</ref>
* Paclitaxel-coated balloons also produce less late lumen loss than [[paclitaxel]]-eluting stents in vessels below 2.8 mm,<ref name="pmid23158530">{{cite journal |author=Latib A, Colombo A, Castriota F, Micari A, Cremonesi A, De Felice F, et al. |title=A Randomized Multicenter Study Comparing a Paclitaxel Drug-Eluting Balloon With a Paclitaxel-Eluting Stent in Small Coronary Vessels: The BELLO (Balloon Elution and Late Loss Optimization) Study |journal=[[Journal of the American College of Cardiology]] |volume=60 |issue=24 |pages=2473–2480 |year=2012 |pmid=23158530 |doi=10.1016/j.jacc.2012.09.020 |url=https://doi.org/10.1016/j.jacc.2012.09.020 |accessdate=2026-09-23}}</ref> and are angiographically non-inferior to [[zotarolimus]]-eluting stents in vessels of 2.25 mm to 2.75 mm, with comparable one-year target lesion failure.<ref name="pmid30522667">{{cite journal |author=Tang Y, Qiao S, Su X, Chen Y, Jin Z, Chen H, et al. |title=Drug-Coated Balloon Versus Drug-Eluting Stent for Small-Vessel Disease: The RESTORE SVD China Randomized Trial |journal=[[JACC: Cardiovascular Interventions]] |volume=11 |issue=23 |pages=2381–2392 |year=2018 |pmid=30522667 |doi=10.1016/j.jcin.2018.09.009 |url=https://doi.org/10.1016/j.jcin.2018.09.009 |accessdate=2026-09-23}}</ref>
* Pooled patient-level data suggest fewer major adverse cardiac events with paclitaxel-coated balloons than with [[drug-eluting stent]]s at three years, driven by less [[myocardial infarction]] and [[target vessel revascularization]]. This signal is not robust across analytic methods, target lesion failure does not differ, and no advantage is seen when the comparison is limited to second-generation [[drug-eluting stent]]s, so a drug-coated balloon should be regarded as an alternative to, not an improvement on, a contemporary [[drug-eluting stent]].<ref name="pmid39981922">{{cite journal |author=Fezzi S, Giacoppo D, Fahrni G, Latib A, Alfonso F, Colombo A, et al. |title=Individual patient data meta-analysis of paclitaxel-coated balloons vs. drug-eluting stents for small-vessel coronary artery disease: the ANDROMEDA study |journal=[[European Heart Journal]] |volume=46 |issue=17 |pages=1586–1599 |year=2025 |pmid=39981922 |doi=10.1093/eurheartj/ehaf002 |url=https://doi.org/10.1093/eurheartj/ehaf002 |accessdate=2026-09-23}}</ref>
* [[Diabetes mellitus]] is common among patients with small vessel disease; in a prespecified diabetic subgroup, drug-coated balloons produced major adverse cardiac event rates similar to [[drug-eluting stent]]s with less [[target vessel revascularization]] at three years, but this is supported only by subgroup data and should not be regarded as established.<ref name="doi101016jjcin202106025">{{cite journal |author=Wöhrle J, Scheller B, Seeger J, Farah A, Ohlow MA, Mangner N, et al. |title=Impact of Diabetes on Outcome With Drug-Coated Balloons Versus Drug-Eluting Stents: The BASKET-SMALL 2 Trial |journal=[[JACC: Cardiovascular Interventions]] |volume=14 |issue=16 |pages=1789–1798 |year=2021 |doi=10.1016/j.jcin.2021.06.025 |url=https://doi.org/10.1016/j.jcin.2021.06.025 |accessdate=2026-09-24}}</ref><ref name="doi101016jjscai2022100403"/>
* The evidence is not uniformly positive. In a large trial of unselected non-complex de novo lesions, paclitaxel-coated balloon angioplasty with rescue stenting failed to show non-inferiority to intended [[drug-eluting stent]] implantation; the excess in device-oriented events was concentrated in vessels of 3.0 mm or larger and was much smaller in vessels below 3.0 mm.<ref name="pmid39236727">{{cite journal |author=Gao C, He X, Ouyang F, Zhang Z, Shen G, Wu M, et al. |title=Drug-coated balloon angioplasty with rescue stenting versus intended stenting for the treatment of patients with de novo coronary artery lesions (REC-CAGEFREE I): an open-label, randomised, non-inferiority trial |journal=[[The Lancet]] |volume=404 |issue=10457 |pages=1040–1050 |year=2024 |pmid=39236727 |doi=10.1016/S0140-6736(24)01594-0 |url=https://doi.org/10.1016/S0140-6736(24)01594-0 |accessdate=2026-09-23}}</ref>
* The excess [[target lesion revascularization]] with drug-coated balloons in that population persisted to three years without a difference in cardiac death or target vessel [[myocardial infarction]]; a [[drug-eluting stent]] should be preferred in de novo vessels of 3.0 mm or larger.<ref name="doi101016jjacc202510027">{{cite journal |author=Tao L, He X, Shen G, Wu M, He Y, Ma L, et al. |title=Drug-Coated Balloon Angioplasty vs Up-Front Stenting for De Novo CAD: 3-Year Follow-Up of REC-CAGEFREE I Trial |journal=[[Journal of the American College of Cardiology]] |volume=87 |issue=3 |pages=312–329 |year=2026 |doi=10.1016/j.jacc.2025.10.027 |url=https://doi.org/10.1016/j.jacc.2025.10.027 |accessdate=2026-09-23}}</ref>
* There is no class effect among drug-coated balloons: balloon design, drug dose, coating formulation and release kinetics all influence results, so outcomes from one device should not be extrapolated to another.<ref name="pmid32473887"/>
* The performance of [[sirolimus]]-coated balloons depends on the coating formulation. In de novo small vessels, one sirolimus-coated balloon produced greater late lumen loss and more [[restenosis]] than a paclitaxel-coated balloon,<ref name="doi101016jjcin202309026">{{cite journal |author=Ninomiya K, Serruys PW, Colombo A, Reimers B, Basavarajaiah S, Sharif F, et al. |title=A Prospective Randomized Trial Comparing Sirolimus-Coated Balloon With Paclitaxel-Coated Balloon in De Novo Small Vessels |journal=[[JACC: Cardiovascular Interventions]] |volume=16 |issue=23 |pages=2884–2896 |year=2023 |doi=10.1016/j.jcin.2023.09.026 |url=https://doi.org/10.1016/j.jcin.2023.09.026 |accessdate=2026-09-23}}</ref> whereas a crystalline sirolimus coating was angiographically non-inferior to a paclitaxel-coated balloon in de novo vessels of 2.5 mm or larger.<ref name="doi104244eijd2300868">{{cite journal |author=Scheller B, Mangner N, Jeger RV, Afan S, Mahfoud F, Woitek FJ, et al. |title=A randomised trial of sirolimus- versus paclitaxel-coated balloons for de novo coronary lesions |journal=[[EuroIntervention]] |volume=20 |issue=21 |pages=e1322–e1329 |year=2024 |doi=10.4244/EIJ-D-23-00868 |url=https://doi.org/10.4244/EIJ-D-23-00868 |accessdate=2026-09-24}}</ref>
* In de novo lesions of 2.0 mm to 5.0 mm, a strategy of a [[sirolimus]]-eluting balloon with provisional stenting is non-inferior to systematic [[drug-eluting stent]] implantation for one-year target vessel failure, at the cost of more clinically driven [[target vessel revascularization]], and non-inferiority was not confirmed in the per-protocol analysis.<ref name="doi101161circulationaha126079033">{{cite journal |author=Spaulding C, Krackhardt F, Bogaerts K, Abdelaal E, Alfonso F, Briguori C, et al. |title=Sirolimus-Eluting Balloon With Provisional Stenting Versus Systematic Drug-Eluting Stent Implantation to Treat De Novo Coronary Lesions: A Randomized, Open-Label, Noninferiority Trial |journal=[[Circulation]] |volume=154 |issue=3 |pages=185–197 |year=2026 |doi=10.1161/CIRCULATIONAHA.126.079033 |url=https://doi.org/10.1161/CIRCULATIONAHA.126.079033 |accessdate=2026-09-24}}</ref>
* Equivalence of any [[sirolimus]]-coated balloon to a [[drug-eluting stent]] specifically in small vessel disease has not been established.<ref name="pmid40036794"/><ref name="doi101161circulationaha126079033"/>

====Lesion Preparation and Drug-Coated Balloon Technique====
* Lesion preparation is required before drug-coated balloon treatment.<ref name="pmid32473887"/>
* Predilatation should use a semi-compliant balloon at a 1:1 balloon-to-vessel ratio, adding cutting or scoring balloons for resistant lesions.<ref name="doi101016jjacc202507049"/>
* Coronary lithotripsy balloons are available only in diameters of 2.5 mm to 4.0 mm, which limits their use in the smallest calcified vessels; atherectomy is an alternative when a lithotripsy catheter cannot cross the lesion.<ref name="doi104244eijd1801056">{{cite journal |author=Sorini Dini C, Tomberli B, Mattesini A, Ristalli F, Valente S, Stolcova M, et al. |title=Intravascular lithotripsy for calcific coronary and peripheral artery stenoses |journal=[[EuroIntervention]] |volume=15 |issue=8 |pages=714–721 |year=2019 |doi=10.4244/EIJ-D-18-01056 |url=https://doi.org/10.4244/EIJ-D-18-01056 |accessdate=2026-09-24}}</ref>
* A drug-coated balloon should be applied only when predilatation leaves a residual stenosis of 30% or less and any [[dissection]] is non-flow-limiting with [[TIMI grade flow|TIMI 3 flow]].<ref name="doi101016jjacc202507049"/><ref name="doi101016S0140673618317197"/>
* A [[fractional flow reserve]] above 0.80 may help confirm that a residual [[dissection]] is acceptable.<ref name="pmid32473887"/>
* The drug-coated balloon should extend at least 2 mm proximal and distal to the prepared segment, the manufacturer's maximum transit time and minimum inflation time should be observed, and the same balloon should generally not be reinserted.<ref name="pmid32473887"/>
* Lesions that do not meet these criteria after preparation should be treated with a [[drug-eluting stent]].<ref name="doi101016S0140673618317197"/><ref name="pmid39236727"/>

===In-Stent Restenosis in Small Vessels===
* Small vessels carry a higher risk of [[restenosis]] after stenting, and a drug-coated balloon allows [[in-stent restenosis]] to be treated without implanting a further layer of metal inside the failed [[stent]].<ref name="doi101016jjscai2022100403"/><ref name="doi101161circulationaha108839282">{{cite journal |author=Unverdorben M, Vallbracht C, Cremers B, Heuer H, Hengstenberg C, Maikowski C, et al. |title=Paclitaxel-Coated Balloon Catheter Versus Paclitaxel-Coated Stent for the Treatment of Coronary In-Stent Restenosis |journal=[[Circulation]] |volume=119 |issue=23 |pages=2986–2994 |year=2009 |doi=10.1161/CIRCULATIONAHA.108.839282 |url=https://doi.org/10.1161/CIRCULATIONAHA.108.839282 |accessdate=2026-09-24}}</ref>
* Drug-coated balloons are an established treatment for restenosis of both bare-metal and drug-eluting stents.<ref name="pmid32473887"/>
* A paclitaxel-coated balloon reduces target lesion failure, [[target lesion revascularization]] and target vessel [[myocardial infarction]] compared with uncoated balloon angioplasty for [[in-stent restenosis]] in vessels of 2.0 mm to 4.0 mm,<ref name="doi101001jama20241361">{{cite journal |author=Yeh RW, Shlofmitz R, Moses J, Bachinsky W, Dohad S, Rudick S, et al. |title=Paclitaxel-Coated Balloon vs Uncoated Balloon for Coronary In-Stent Restenosis: The AGENT IDE Randomized Clinical Trial |journal=[[JAMA]] |volume=331 |issue=12 |pages=1015 |year=2024 |doi=10.1001/jama.2024.1361 |url=https://doi.org/10.1001/jama.2024.1361 |accessdate=2026-09-24}}</ref> and the benefit is consistent in vessels of 2.75 mm or less, with no interaction by vessel size.<ref name="pmid41297981">{{cite journal |author=Wen J, Dohad S, Shlofmitz R, Moses J, Bachinsky W, Rudick S, et al. |title=Paclitaxel-Coated Balloon for the Treatment of Small Vessel In-Stent Restenosis: A Subgroup Analysis of the AGENT IDE Randomized Trial |journal=[[JACC: Cardiovascular Interventions]] |volume=18 |issue=22 |pages=2701–2710 |year=2025 |pmid=41297981 |doi=10.1016/j.jcin.2025.09.032 |url=https://doi.org/10.1016/j.jcin.2025.09.032 |accessdate=2026-09-24}}</ref>
* This paclitaxel-coated balloon was approved by the US [[Food and Drug Administration]] in 2024 for coronary [[in-stent restenosis]].<ref name="fdaP230035">{{cite web |title=AGENT Paclitaxel-Coated Balloon Catheter – P230035 |publisher=U.S. Food and Drug Administration |url=https://www.fda.gov/medical-devices/recently-approved-devices/agent-paclitaxel-coated-balloon-catheter-p230035 |accessdate=2026-09-24}}</ref>
* The evidence is not uniformly positive. European guidance previously gave drug-coated balloons the highest class of recommendation for [[in-stent restenosis]], but the 2024 ESC guidelines recommend a [[drug-eluting stent]] over a drug-coated balloon for restenosis within a [[drug-eluting stent]]; the trial supporting US approval compared the balloon with uncoated balloon angioplasty, not with a [[drug-eluting stent]].<ref name="doi101093eurheartjehae177"/><ref name="pmid40036794"/><ref name="doi101001jama20241361"/>

===Adjunctive Antiplatelet Therapy===
* After drug-coated balloon-only treatment of a de novo lesion in [[chronic coronary syndrome]], four weeks of [[dual antiplatelet therapy]] is recommended by consensus, which makes the strategy attractive in patients at high bleeding risk; this duration rests on expert opinion rather than randomized evidence.<ref name="pmid32473887"/><ref name="doi101093eurheartjehaf029">{{cite journal |author=Fezzi S, Scheller B, Cortese B, Alfonso F, Jeger R, Colombo A, et al. |title=Definitions and standardized endpoints for the use of drug-coated balloon in coronary artery disease: consensus document of the Drug Coated Balloon Academic Research Consortium |journal=[[European Heart Journal]] |volume=46 |issue=26 |pages=2498–2519 |year=2025 |doi=10.1093/eurheartj/ehaf029 |url=https://doi.org/10.1093/eurheartj/ehaf029 |accessdate=2026-09-24}}</ref>
* In small vessels, drug-coated balloons are as effective as [[drug-eluting stent]]s regardless of bleeding risk, but a reduction in major bleeding has not been shown in patients at high bleeding risk, and the overall trend towards less major bleeding did not reach significance.<ref name="pmid35411792">{{cite journal |author=Scheller B, Rissanen TT, Farah A, Ohlow MA, Mangner N, Wöhrle J, et al. |title=Drug-Coated Balloon for Small Coronary Artery Disease in Patients With and Without High-Bleeding Risk in the BASKET-SMALL 2 Trial |journal=[[Circulation: Cardiovascular Interventions]] |volume=15 |issue=4 |year=2022 |pmid=35411792 |doi=10.1161/CIRCINTERVENTIONS.121.011569 |url=https://doi.org/10.1161/CIRCINTERVENTIONS.121.011569 |accessdate=2026-09-24}}</ref><ref name="doi101016S0140673620321735"/>
* In [[acute coronary syndrome]] treated with drug-coated balloons alone, stepwise de-escalation (aspirin plus [[ticagrelor]] for one month, [[ticagrelor]] monotherapy to six months, then aspirin monotherapy) is non-inferior to 12 months of [[dual antiplatelet therapy]] for net adverse clinical events and reduces major bleeding; this evidence comes from a predominantly East Asian population and was not restricted to small vessels.<ref name="doi101136bmj2024082945">{{cite journal |author=Gao C, Zhu B, Ouyang F, Wen S, Xu Y, Jia W, et al. |title=Stepwise dual antiplatelet therapy de-escalation in patients after drug coated balloon angioplasty (REC-CAGEFREE II): multicentre, randomised, open label, assessor blind, non-inferiority trial |journal=[[BMJ]] |volume=388 |pages=e082945 |year=2025 |doi=10.1136/bmj-2024-082945 |url=https://doi.org/10.1136/bmj-2024-082945 |accessdate=2026-09-23}}</ref>

====Summary of Steps for Management====
:'''Step 1: Confirm that the target vessel is small'''
::* Measure the reference diameter, preferably with [[intravascular ultrasound]] or [[optical coherence tomography]], because angiography tends to underestimate it<ref name="doi101016jjscai2022100403"/>
::* True reference diameter 3.0 mm or larger → treat as a standard-size vessel with a [[drug-eluting stent]]<ref name="doi101016jjacc202510027"/>
::* Reference diameter below 3.0 mm → proceed to Step 2
::* Restenosis within a previously implanted [[stent]] → paclitaxel-coated balloon or repeat [[drug-eluting stent]] (see In-Stent Restenosis in Small Vessels)<ref name="doi101001jama20241361"/><ref name="doi101093eurheartjehae177"/>

:'''Step 2: Prepare the lesion'''
::* Semi-compliant balloon at a 1:1 ratio; cutting or scoring balloon for resistant lesions<ref name="doi101016jjacc202507049"/>
::* Severe calcification in a vessel below 2.5 mm, or a lesion a lithotripsy catheter cannot cross → consider atherectomy<ref name="doi104244eijd1801056"/>

:'''Step 3: Assess the result of lesion preparation'''
::* Residual stenosis 30% or less, no flow-limiting [[dissection]], [[TIMI grade flow|TIMI 3 flow]] → a drug-coated balloon-only strategy may be chosen as an alternative to a [[drug-eluting stent]], using a paclitaxel-coated device with randomized small vessel data<ref name="doi101016S0140673620321735"/><ref name="pmid39981922"/><ref name="doi101016jjcin202309026"/>
::* Criteria not met → implant a new-generation thin-strut [[drug-eluting stent]]<ref name="doi101016S0140673618317197"/><ref name="doi101016jjscai2022100403"/>

:'''Step 4: After drug-coated balloon application'''
::* Residual stenosis above 30% or a flow-limiting [[dissection]] → bailout [[drug-eluting stent]]<ref name="doi101016jjacc202507049"/>
::* Non-flow-limiting [[dissection]] with [[TIMI grade flow|TIMI 3 flow]] and an acceptable residual lumen → finish the procedure without a [[stent]]<ref name="doi101016jjacc202507049"/>

:'''Step 5: Antiplatelet therapy after drug-coated balloon-only treatment'''
::* Four weeks of [[dual antiplatelet therapy]] for a de novo lesion, as recommended by consensus<ref name="pmid32473887"/>

==Complications==
* Bailout [[stent]] implantation after drug-coated balloon treatment of small vessels is needed in roughly 5% to 20% of lesions, most often for a flow-limiting [[dissection]] or an inadequate residual lumen.<ref name="pmid30522667"/><ref name="pmid23158530"/>
* Thrombotic events are uncommon after either strategy. The absence of a permanent scaffold was associated with fewer vessel thromboses in one trial, but a consistent reduction in [[stent thrombosis]] or vessel thrombosis has not been shown.<ref name="doi101016jjcin202302011"/><ref name="doi101016S0140673620321735"/>
* [[Restenosis]] requiring repeat [[target lesion revascularization]] is more frequent with drug-coated balloons than with [[drug-eluting stent]]s in vessels of 3.0 mm or larger.<ref name="doi101016jjacc202510027"/>
* Observational registry data have associated drug-coated balloon treatment with a higher risk of [[restenosis]] than [[drug-eluting stent]] implantation, in contrast to the randomized small vessel trials; this signal is supported only by observational data and should not be regarded as established.<ref name="doi101016jjscai2022100403"/>

==References==
{{reflist|2}}
{{WH}}
{{WS}}
[[Category:Disease]]
[[Category:Cardiology]]

[[Category:Up-To-Date]]
[[Category:Up-To-Date cardiology]]

Template;IE

Ibrahim Elkhayat — Wed, 23 Sep 2026 19:43:45 GMT

Created page with "Ibrahim Elkhayat, M.B.B.Ch.[mailto:Ibrahimelkhayat98@gmail.com]"

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[[User:Ibrahim Elkhayat|Ibrahim Elkhayat, M.B.B.Ch.]][mailto:Ibrahimelkhayat98@gmail.com]

User:Fahad Hasan

Fahad Hasan — Wed, 23 Sep 2026 17:23:56 GMT

Current Position

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	==Current Position==		==Current Position==
	~~WikiDoc Scholar~~, [[Main Page\|wikidoc.org]]		Associate Editor, [[Main Page\|wikidoc.org]]

	== About ==		== About ==

Dyspepsia overview

Fahad Hasan — Wed, 23 Sep 2026 17:16:46 GMT

Epidemiology and Demographics

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	==Epidemiology and Demographics==		==Epidemiology and Demographics==
	Global pooled prevalence estimates vary substantially by definition: uninvestigated dyspepsia affects approximately 20.8% of the general population ~~(95% CI 17.8–23.9%)~~, while Rome-criteria-defined functional dyspepsia has a global pooled prevalence of 8.4% ~~(95% CI 7.4–9.5%)~~, and in the most recent Rome Foundation internet-based epidemiology study, 7.2% (range 2.2%–12.3% across countries). Prevalence is consistently higher in women than in men across all diagnostic criteria and is higher in developing countries than in developed countries. The global prevalence of functional dyspepsia has declined gradually over the past three decades, from 12.4% in studies conducted during 1990–2002 to 7.3% in studies conducted during 2013–2020, and it decreases with advancing age, findings that contrast with the age-related increase seen with ''[[H. pylori]]'' infection.		Global pooled prevalence estimates vary substantially by definition: uninvestigated dyspepsia affects approximately 20.8% of the general population, while Rome-criteria-defined functional dyspepsia has a global pooled prevalence of 8.4%, and in the most recent Rome Foundation internet-based epidemiology study, 7.2% (range 2.2%–12.3% across countries). Prevalence is consistently higher in women than in men across all diagnostic criteria and is higher in developing countries than in developed countries. The global prevalence of functional dyspepsia has declined gradually over the past three decades, from 12.4% in studies conducted during 1990–2002 to 7.3% in studies conducted during 2013–2020, and it decreases with advancing age, findings that contrast with the age-related increase seen with ''[[H. pylori]]'' infection.

	==Risk Factors==		==Risk Factors==
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	===Laboratory Findings===		===Laboratory Findings===
	There is no ~~specific~~ diagnostic laboratory test for dyspepsia ~~but in~~ the ~~patient with the history of~~ dyspepsia, ~~the laboratory test is used~~ to ~~rule out~~ [[~~bleeding~~]] and to ~~document the status of~~ eradication ~~therapy~~ and to ~~test refractory~~ [[~~ulcers~~]]		There is no diagnostic laboratory test for [[dyspepsia]] itself. Laboratory evaluation serves three purposes: to detect [[anemia]] or other findings that redirect the diagnosis away from [[functional dyspepsia]] (FD), to establish ''[[Helicobacter pylori]]'' status for a test-and-treat strategy and to confirm eradication, and, in selected patients, to investigate uncommon organic causes such as [[Zollinger-Ellison syndrome]] (ZES).<ref name="Sayuk2020" /><ref name="Tornblom2026" /> Current guidance favors a targeted approach; reflexive laboratory panels are low-yield, costly, and may reinforce illness behavior.<ref name="Sayuk2020" /><ref name="Tornblom2026" />

	~~===Imaging Findings===~~
	~~===Esophagogastroduodenoscopy===~~
	People without risk factors for serious causes of dyspepsia usually do not need investigation beyond an office-based clinical examination. However, people over the age of 55 years and those with alarm features are usually investigated by esophagogastroduodenoscopy (~~EGD or OGD in Britain~~). ~~In this painless investigation the esophagus, stomach, and duodenum~~ are ~~examined through an endoscope passed down through the mouth. This will rule out peptic ulcer disease~~, ~~medication-related ulceration~~, ~~malignancy~~ and ~~other rarer causes~~.

	~~===Other Diagnostic Studies=~~==
	~~There are no other diagnostic studies associated with dyspepsia.~~

	==Treatment==		==Treatment==

Dyspepsia laboratory findings

Fahad Hasan — Wed, 23 Sep 2026 17:14:38 GMT

Show changes

Dyspepsia overview

Fahad Hasan — Wed, 23 Sep 2026 17:09:50 GMT

History and Symptoms

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	===History and Symptoms===		===History and Symptoms===
	The history ~~and~~ symptoms ~~of dyspepsia~~ are ~~as follows: pain or a burning feeling in the upper portion of the [[stomach]], [[nausea]], bloating, sometimes uncontrollable [[burping]], [[~~heartburn~~]], fever, metallic taste, rumbling in the stomach, sense of fullness after eating, feeling as though something is lodged in the esophagus, pain~~ and ~~discomfort at the [[Xiphoid process\|xiphoid]] region~~, ~~sudden [[chills]], comparable to those felt during fevers~~		The history in dyspepsia has three purposes: (1) confirm that symptoms are epigastric-predominant rather than heartburn-predominant; (2) screen for alarm features and age/risk factors that direct endoscopy; and (3) identify culprit medications and ''H. pylori'' risk. Symptom pattern alone discriminates poorly between functional and organic causes and should not be used to make an etiologic diagnosis.<ref name="Ford2020" /><ref name="Sayuk2020">Sayuk, Gyawali. ''Drugs''. 2020.</ref>

	===Physical Examination===		===Physical Examination===
	~~Patients with dyspepsia may appear pale. Some patients may appear~~ [[~~Fatigue\|fatigued~~]] ~~and in distress,~~ is ~~associated with [[abdominal pain]]. Vital signs generally appear to be~~ normal~~. When associated with [[gastrointestinal bleed]]~~, ~~vital signs include [[Tachycardia\|tachycardia]]. [[Pallor]] may observed in patients presenting with [[melena]]~~ and [[~~hematemesis~~]]~~. On examination of the~~ [[~~eyes~~]], [[~~conjunctival~~]] ~~[[pallor]] may be observed~~. ~~[[Halitosis]] may be observed in case of chronic gastritis~~. ~~Chest~~ tenderness ~~may be present on palpation in case of~~ ''~~[[Helicobacter pylori]]~~'' ~~infection associated gastritis~~. ~~Epigastric~~ [[~~tenderness~~]] ~~may be present. Gastritis associated with~~ [[~~Gastric ulcer\|gastric ulcers~~]] ~~may result in [[~~blood loss]] and ~~the~~ [[~~stool test~~]] ~~may be guaiac~~-~~positive~~.		The physical examination in [[dyspepsia]] is usually normal, and no examination finding reliably distinguishes [[functional dyspepsia]] (FD) from organic causes such as [[peptic ulcer disease]], [[gastroesophageal reflux disease]], or upper gastrointestinal malignancy.<ref name="Ford2020">Ford et al. ''Lancet''. 2020.</ref><ref name="Enck2017">Enck et al. ''Nature Reviews Disease Primers''. 2017.</ref> Mild epigastric tenderness is the most common finding but is nonspecific.<ref name="Vakil2024">Vakil. ''JAMA''. 2024.</ref> The examination has two main purposes: to detect findings that fall outside the FD spectrum (a palpable mass, lymphadenopathy, organomegaly, [[jaundice]], an [[acute abdomen]], or signs of gastrointestinal blood loss), which redirect the diagnostic pathway, and to elicit [[Carnett's sign]], which distinguishes chronic abdominal-wall pain from visceral pain and can spare unnecessary gastrointestinal testing.<ref name="Ford2020" /><ref name="Enck2017" />

	===Laboratory Findings===		===Laboratory Findings===

Dyspepsia physical examination

Fahad Hasan — Wed, 23 Sep 2026 16:59:11 GMT

Show changes

Dyspepsia history and symptoms

Fahad Hasan — Wed, 23 Sep 2026 16:45:09 GMT

Show changes

Dyspepsia overview

Fahad Hasan — Wed, 23 Sep 2026 16:34:14 GMT

← Older revision		Revision as of 16:34, 23 September 2026
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	==Risk Factors==		==Risk Factors==
	~~The secondary prevention strategies~~ for ~~gastritis following ''~~[[H. pylori]]'' infection ~~to prevent recurrence~~ of [[peptic ulcer disease]] and [[~~gastric cancer~~]] ~~include the use of~~ [[~~antibiotics~~]] ~~to prevent recurrence of~~ [[~~infection~~]] and ~~the post~~-~~treatment confirmation~~ of ''[[H. pylori]]~~'' eradication after treatment using diagnostic tests~~.		[[Risk factors]] for the development of dyspepsia are multifactorial and include [[Helicobacter pylori]] [[infection]], chronic use of [[Non-steroidal anti-inflammatory drug\|NSAIDs]], [[family history]] of [[peptic ulcer disease]], prior acute [[gastroenteritis]] (post-infectious dyspepsia), [[emotional stress]] and [[psychological]] [[comorbidity]] (particularly [[anxiety]] and [[depression]]), [[female sex]], [[tobacco]] smoking, and dietary factors including increased intake of high-fiber, high-fat, and greasy foods and overconsumption of [[caffeine]].<ref name="pmid27147122">{{cite journal \|vauthors=Stanghellini V, Chan FK, Hasler WL, Malagelada JR, Suzuki H, Tack J, Talley NJ \|title=Gastroduodenal Disorders \|journal=Gastroenterology \|volume=150 \|issue=6 \|pages=1380–1392 \|date=2016 \|pmid=27147122 \|doi=10.1053/j.gastro.2016.02.011 \|url=}}</ref><ref name="pmid25147201">{{cite journal \|vauthors=Ford AC, Marwaha A, Sood R, Moayyedi P \|title=Global prevalence of, and risk factors for, uninvestigated dyspepsia: a meta-analysis \|journal=Gut \|volume=64 \|issue=7 \|pages=1049–1057 \|date=2015 \|pmid=25147201 \|doi=10.1136/gutjnl-2014-307843 \|url=}}</ref> A large meta-analysis of population-based studies found that the prevalence of uninvestigated dyspepsia was significantly higher among women, smokers, NSAID users, and individuals who were H. pylori-positive.<ref name="pmid25147201" /> A single Mendelian randomization study provides emerging, genetically-supported evidence for [[depression]] and [[gastroesophageal reflux disease]] as risk factors for [[functional dyspepsia]]; this inference rests on genetic-instrument assumptions and requires replication.<ref name="pmid38718064">{{cite journal \|vauthors=Xu W, Zhu Y, Ma Z, Fu Z, Chen R, Zhang X \|title=The associations between functional dyspepsia and potential risk factors: A comprehensive Mendelian randomization study \|journal=PLoS One \|volume=19 \|issue=5 \|pages=e0302809 \|date=2024 \|pmid=38718064 \|doi=10.1371/journal.pone.0302809 \|url=}}</ref> The relationship with [[body mass index]] is bidirectional: higher BMI is the more consistent independent predictor of incident functional dyspepsia in longitudinal and large global data, while underweight/leanness is associated with functional dyspepsia in several Asian and primary-care cohorts, and a U-shaped relationship confined to women has been described. Alcohol consumption is a less consistent association. Age ≥60 years is the dominant risk marker for underlying organic or malignant disease and, per the 2017 ACG/CAG guideline, warrants [[upper gastrointestinal endoscopy\|upper endoscopy]]; [[alarm features]] (unintentional [[weight loss]], [[gastrointestinal bleeding]], [[dysphagia]], persistent vomiting, family history of upper GI malignancy) raise concern but do not by themselves mandate endoscopy in patients under 60.<ref name="pmid28631728">{{cite journal \|vauthors=Moayyedi PM, Lacy BE, Andrews CN, Enns RA, Howden CW, Vakil N \|title=ACG and CAG Clinical Guideline: Management of Dyspepsia \|journal=Am J Gastroenterol \|volume=112 \|issue=7 \|pages=988–1013 \|date=2017 \|pmid=28631728 \|doi=10.1038/ajg.2017.154 \|url=}}</ref>

	==Screening==		==Screening==
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	==Treatment==		==Treatment==
	===Medical Therapy===		===Medical Therapy===
	~~Functional~~ and ~~undifferentiated dyspepsia have similar treatments~~. ~~Decisions around the use of drug therapy are difficult because trials included heartburn in the definition of~~ dyspepsia~~. This led~~ to ~~the results favoring~~ [[proton pump ~~inhibitors~~]] (~~PPIs~~), ~~which are questionably effective~~ for the ~~treatment~~ of ~~heartburn~~.		Medical therapy for [[dyspepsia]] is stepwise, empiric, and symptom-directed. The same treatment sequence applies to uninvestigated dyspepsia and to [[functional dyspepsia]] (FD) once organic disease has been excluded: ''[[Helicobacter pylori]]'' test-and-treat, then a time-limited [[proton pump inhibitor]] (PPI) trial, then a central neuromodulator, then a prokinetic, with psychological therapy for non-responders. ''H. pylori'' eradication and empiric PPI therapy both carry strong ACG/CAG recommendations; eradication is the only therapy that is potentially disease-modifying, since sustained benefit reclassifies the patient as having ''H. pylori''-associated dyspepsia. Effect sizes across all effective therapies are modest.<ref name="pmid28631728">{{cite journal \|vauthors=Moayyedi PM, Lacy BE, Andrews CN, Enns RA, Howden CW, Vakil N \|title=ACG and CAG Clinical Guideline: Management of Dyspepsia \|journal=Am J Gastroenterol \|volume=112 \|issue=7 \|pages=988–1013 \|date=2017 \|pmid=28631728 \|doi=10.1038/ajg.2017.154}}</ref><ref name="rome2026">{{cite journal \|vauthors=Törnblom H, Carbone F, Hasler WL, ((et al)) \|title=Gastroduodenal Disorders \|journal=Gastroenterology \|volume=170 \|issue=6 \|pages=1240–1260 \|date=2026 \|pmid=41713705 \|doi=10.1053/j.gastro.2026.01.038}}</ref>

	===Surgery===		===Surgery===
	~~Surgical intervention~~ is ~~not recommended~~ for the management of dyspepsia		Surgery has a limited, narrowly defined role in dyspepsia and is directed almost exclusively at complications of organic disease — principally [[peptic ulcer disease]] (PUD) complicated by perforation, refractory haemorrhage, or [[gastric outlet obstruction]], rather than at [[functional dyspepsia]] (FD) itself.<ref name="Almadi2024">Almadi MA, Lu Y, Alali AA, Barkun AN. Peptic Ulcer Disease. Lancet. 2024;404(10447):68-81. doi:10.1016/S0140-6736(24)00155-7.</ref> Contemporary guidelines, including the British Society of Gastroenterology (BSG) 2022 guideline, explicitly recommend '''against surgery for refractory FD''' given the absence of high-quality evidence of benefit and the recognised risk of iatrogenic harm.<ref name="BSG2022">Black CJ, Paine PA, Agrawal A, Aziz I, Eugenicos MP, Houghton LA, Hungin P, Overshott R, Vasant DH, Rudd S, Winning RC, Corsetti M, Ford AC. British Society of Gastroenterology guidelines on the management of functional dyspepsia. Gut. 2022;71(9):1697-1723. doi:10.1136/gutjnl-2022-327737.</ref><ref name="PasrichaTalley2026">Pasricha PJ, Talley NJ. Functional Dyspepsia. N Engl J Med. 2026;394(2):166-176. doi:10.1056/NEJMcp2501860.</ref> The marked decline in elective peptic ulcer surgery over recent decades reflects the success of [[Helicobacter pylori\|H. pylori]] eradication and [[proton pump inhibitor]] therapy.<ref name="Almadi2024" /><ref name="Lagoo2014">Lagoo J, Pappas TN, Perez A. A Relic or Still Relevant: The Narrowing Role for Vagotomy in the Treatment of Peptic Ulcer Disease. Am J Surg. 2014;207(1):120-126. doi:10.1016/j.amjsurg.2013.02.012.</ref> Procedural interventions such as gastric peroral endoscopic myotomy (G-POEM) and gastric electrical stimulation (GES) are established only in the context of scintigraphically confirmed [[gastroparesis]], not FD per se.<ref name="Camilleri2026">Camilleri M. Gastroparesis. JAMA. 2026. doi:10.1001/jama.2026.12181.</ref>

	==Prevention==		==Prevention==
	===Primary prevention===		===Primary prevention===
	~~Effective measures for the primary~~ prevention of dyspepsia ~~include avoiding long-term or extended use~~ of ~~medications such as~~ [[~~NSAIDs~~]], ~~abstinence from alcohol,~~ [[~~smoking cessation~~]], ~~coffee or acidic beverages, spicy foods~~ and ~~avoiding stress~~. ~~Inculcating healthy eating habits~~, ~~exercising regularly and maintaining healthy body weight may help in avoiding~~ dyspepsia. ~~Effective measures~~ for ~~primary prevention~~ of ~~the~~ ''[[H. pylori]]~~'' infection include hand washing (antibacterial soaps~~)~~, avoid contaminated food and water, maintain proper~~ [[~~hygiene~~]] (~~hand sanitizers~~, ~~antiseptic washes)~~ and ~~avoid close contact~~ with ~~infected family members ( e~~.g., ~~kissing~~, ~~sharing eating utensils~~ and ~~drinking glasses)~~.		Primary prevention of [[dyspepsia]] targets three modifiable domains: eradication of ''[[Helicobacter pylori]]'', prevention of [[Nonsteroidal anti-inflammatory drug\|NSAID]]- and [[aspirin]]-related mucosal injury, and lifestyle modification.<ref name="ford2020">{{cite journal \|author=Ford AC, Mahadeva S, Carbone MF, Lacy BE, Talley NJ \|title=Functional dyspepsia \|journal=Lancet \|year=2020 \|volume=396 \|issue=10263 \|pages=1689–1702 \|doi=10.1016/S0140-6736(20)30469-4}}</ref><ref name="ford2022">{{cite journal \|author=Ford AC, Tsipotis E, Yuan Y, Leontiadis GI, Moayyedi P \|title=Efficacy of eradication therapy for functional dyspepsia: updated systematic review and meta-analysis \|journal=Gut \|year=2022 \|doi=10.1136/gutjnl-2021-326583}}</ref><ref name="almadi2024">{{cite journal \|author=Almadi MA, Lu Y, Alali AA, Barkun AN \|title=Peptic ulcer disease \|journal=Lancet \|year=2024 \|volume=404 \|issue=10447 \|pages=68–81 \|doi=10.1016/S0140-6736(24)00155-7}}</ref> Prevention of organic dyspepsia ([[peptic ulcer disease]], ''H. pylori''-associated dyspepsia, [[gastric cancer]]) is supported by stronger evidence than prevention of [[functional dyspepsia]] (FD), for which the benefit of lifestyle and dietary measures remains disputed.<ref name="ford2020" /><ref name="pasricha2026">{{cite journal \|author=Pasricha PJ, Talley NJ \|title=Functional dyspepsia \|journal=N Engl J Med \|year=2026 \|volume=394 \|issue=2 \|pages=166–176 \|doi=10.1056/NEJMcp2501860}}</ref> ''H. pylori'' eradication is the only intervention with disease-modifying potential across PUD, gastric cancer, and dyspepsia.<ref name="mulder2026">{{cite journal \|author=Mülder DT, O'Mahony JF, Kapteijn N, et al \|title=The disease burden of Helicobacter pylori beyond gastric cancer: quantifying the forgotten potential benefits of mass eradication \|journal=Gastroenterology \|year=2026 \|volume=170 \|issue=2 \|pages=344–352 \|doi=10.1053/j.gastro.2025.08.015}}</ref><ref name="ford2025">{{cite journal \|author=Ford AC, Yuan Y, Park JY, Forman D, Moayyedi P \|title=Eradication therapy to prevent gastric cancer in Helicobacter pylori-positive individuals: systematic review and meta-analysis of randomized controlled trials and observational studies \|journal=Gastroenterology \|year=2025 \|volume=169 \|issue=2 \|pages=261–276 \|doi=10.1053/j.gastro.2024.12.033}}</ref>

	===Secondary prevention===		===Secondary prevention===
	~~The secondary~~ prevention ~~strategies for dyspepsia following ''~~[[~~H. pylori~~]]~~'' infection~~ to prevent recurrence of [[~~peptic ulcer disease~~]] ~~and~~ [[~~gastric cancer~~]] ~~include the use of~~ [[~~antibiotics~~]] ~~to prevent recurrence of~~ [[~~infection~~]] and ~~the post~~-~~treatment confirmation~~ of ''[[H. pylori]]'' eradication ~~after treatment using diagnostic tests.~~		Secondary prevention of [[dyspepsia]] aims to prevent symptom relapse and recurrence of the underlying lesion in patients who have already been diagnosed and treated. This includes treated uninvestigated dyspepsia, treated [[functional dyspepsia]] (FD), treated ''[[Helicobacter pylori]]''-associated dyspepsia, and healed [[peptic ulcer disease]] (PUD). [[Functional dyspepsia\|FD]] is a disorder of gut–brain interaction with a chronic, relapsing–remitting course.<ref name="sayuk2020">{{cite journal \|author=Sayuk GS, Gyawali CP \|title=Functional Dyspepsia: Diagnostic and Therapeutic Approaches \|journal=Drugs \|year=2020 \|volume=80 \|issue=13 \|pages=1319–1336 \|doi=10.1007/s40265-020-01362-4}}</ref><ref name="moayyedi2017">{{cite journal \|author=Moayyedi P, Lacy BE, Andrews CN, et al. \|title=ACG and CAG Clinical Guideline: Management of Dyspepsia \|journal=Am J Gastroenterol \|year=2017 \|volume=112 \|issue=7 \|pages=988–1013 \|doi=10.1038/ajg.2017.154}}</ref> The main secondary prevention measures are:
			* Confirmed and sustained ''H. pylori'' eradication
			* The lowest effective acid suppression, with periodic [[deprescribing]]
			* Removal or mitigation of [[NSAID]] exposure
			* Psychological therapy and central neuromodulators for relapsing FD

	==References==		==References==
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	~~[[Category:Needs overview]]~~
	~~[[Category:Needs content]]~~
	[[Category:Gastroenterology]]		[[Category:Gastroenterology]]
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Dyspepsia risk factors

Fahad Hasan — Wed, 23 Sep 2026 16:29:27 GMT

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Dyspepsia overview

Fahad Hasan — Wed, 23 Sep 2026 16:10:42 GMT

Epidemiology and Demographics

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	==Causes==		==Causes==
	~~Life threatening~~ causes of dyspepsia ~~include~~ [[~~coronary disease~~]] ~~and [[ischemic bowel~~ disease]]. ~~Other common causes~~ of dyspepsia ~~include~~ [[gastroesophageal reflux]], [[~~gastritis~~]], [[~~lactose intolerance~~]]~~, and~~ [[~~peptic ulcer~~]].		Its causes are divided into two groups:<ref name="Stanghellini2016">{{cite journal \|vauthors=Stanghellini V, Chan FK, Hasler WL, Malagelada JR, Suzuki H, Tack J, Talley NJ \|title=Gastroduodenal Disorders \|journal=Gastroenterology \|volume=150 \|issue=6 \|pages=1380–1392 \|year=2016 \|pmid=27147122 \|doi=10.1053/j.gastro.2016.02.011}}</ref>
			* '''Organic (secondary) dyspepsia''': a structural, systemic, metabolic, infectious, or drug-related cause is identified, and symptoms resolve when it is treated.
			* '''[[Functional dyspepsia]] (FD)''': no explanatory disease is found on evaluation.
			Approximately 80% of patients with dyspepsia have no structural explanation and are classified as FD.<ref name="Ford2020">{{cite journal \|vauthors=Ford AC, Mahadeva S, Carbone MF, Lacy BE, Talley NJ \|title=Functional dyspepsia \|journal=Lancet \|volume=396 \|issue=10263 \|pages=1689–1702 \|year=2020 \|pmid=33049222 \|doi=10.1016/S0140-6736(20)30469-4}}</ref><ref name="Wauters2021">{{cite journal \|vauthors=Wauters L, Dickman R, Drug V, et al. \|title=United European Gastroenterology (UEG) and European Society for Neurogastroenterology and Motility (ESNM) consensus on functional dyspepsia \|journal=Neurogastroenterol Motil \|volume=33 \|issue=9 \|pages=e14238 \|year=2021 \|doi=10.1111/nmo.14238}}</ref> History and examination cannot reliably distinguish organic from functional dyspepsia, and no accurate biomarker exists.<ref name="Ford2020" /><ref name="Wauters2021" /> The most common organic contributors are [[gastroesophageal reflux disease]], [[peptic ulcer disease]], and [[NSAID]]/[[aspirin]] use. [[Myocardial ischemia]] is the key extra-luminal cause that must not be missed.

	==Differentiating dyspepsia from Other Diseases==		==Differentiating dyspepsia from Other Diseases==
	~~Dyspepsia must be differentiated~~ from ~~other diseases that presents with epigastric pain such~~ as [[~~Gastritis~~\|~~gastritis~~,]] [[~~Gastroesophageal reflux~~ disease\|~~gastroesophageal reflux disease~~, ~~acute pancreatitis~~, ~~primary biliary cirrhosis~~, ~~cholelithiasis~~, ~~gastric outlet syndrome~~, ~~myocardial infarction~~, ~~pleural empyema]]~~<~~nowiki~~/>~~e [[appendicitis]]~~		Symptoms cannot reliably separate organic from functional dyspepsia, and no single history finding, examination finding, or biomarker distinguishes them. The differential diagnosis is therefore approached in three steps: exclude a limited set of organic mimics, keep myocardial ischemia in mind as the can't-miss extra-luminal cause, and then apply Rome IV criteria to diagnose [[functional dyspepsia]] (FD).<ref name="Ford2020">{{cite journal \|author=Ford AC, Mahadeva S, Carbone MF, Lacy BE, Talley NJ \|title=Functional dyspepsia \|journal=Lancet \|volume=396 \|issue=10263 \|pages=1689–1702 \|year=2020 \|pmid=33049222 \|doi=10.1016/S0140-6736(20)30469-4}}</ref> About 80% of patients with dyspepsia have no clinically significant finding at endoscopy. Fewer than 10% have [[peptic ulcer disease\|peptic ulcer]], and fewer than 0.5% have gastro-esophageal malignancy, so the pretest probability strongly favors FD.<ref name="Nasseri2023">{{cite journal \|author=Nasseri-Moghaddam S, Mousavian AH, Kasaeian A, et al. \|title=What is the prevalence of clinically significant endoscopic findings in subjects with dyspepsia? Updated systematic review and meta-analysis \|journal=Clin Gastroenterol Hepatol \|volume=21 \|issue=7 \|pages=1739–1749.e2 \|year=2023 \|doi=10.1016/j.cgh.2022.05.041}}</ref> FD must then be distinguished from other disorders of gut–brain interaction (DGBI) and from the chronic nausea and vomiting disorders it overlaps with.<ref name="Pasricha2026">{{cite journal \|author=Pasricha PJ, Talley NJ \|title=Functional dyspepsia \|journal=N Engl J Med \|volume=394 \|issue=2 \|pages=166–176 \|year=2026 \|doi=10.1056/NEJMcp2501860}}</ref>

	==Epidemiology and Demographics==		==Epidemiology and Demographics==
	The [[incidence]] of new cases of ''[[H. pylori]]'' infection each year ranges from 3,000 to 10,000 per 100,000 individuals in developing countries. It has been observed that with advancing age, the [[incidence]] of ''[[H. pylori]]'' infection increases. In united states, 20~~% of adolescents are infected with [[H~~. ~~pylori]] when compared to 90~~% ~~by 5 years~~ of ~~age in~~ the ~~developing countries. In United States, [[H~~. ~~pylori\|''H~~. ~~pylori'']] infection associated gastritis is more common in African Americans (54~~%), ~~Hispanics~~ (52%), and the ~~elderly compared to Whites~~ (21%). ~~In acute gastritis, females are usually more affected~~ than men~~. In ''[[H. pylori]]'' infection associated gastritis, males are more commonly affected~~ than ~~females~~. The ~~[[incidence]] rates~~ of ~~''[[H~~. ~~pylori]]'' infection are high~~ in ~~Japan, Columbia~~, ~~Costa Rica~~ and ~~China~~, ~~and comparatively low in~~ the ~~United States.~~ [[H. pylori]] infection ~~is common in Southern and Eastern Europe, Mexico, South America, Africa, most Asian countries, and aboriginal people in North America~~.		Global pooled prevalence estimates vary substantially by definition: uninvestigated dyspepsia affects approximately 20.8% of the general population (95% CI 17.8–23.9%), while Rome-criteria-defined functional dyspepsia has a global pooled prevalence of 8.4% (95% CI 7.4–9.5%), and in the most recent Rome Foundation internet-based epidemiology study, 7.2% (range 2.2%–12.3% across countries). Prevalence is consistently higher in women than in men across all diagnostic criteria and is higher in developing countries than in developed countries. The global prevalence of functional dyspepsia has declined gradually over the past three decades, from 12.4% in studies conducted during 1990–2002 to 7.3% in studies conducted during 2013–2020, and it decreases with advancing age, findings that contrast with the age-related increase seen with ''[[H. pylori]]'' infection.

	==Risk Factors==		==Risk Factors==

Dyspepsia differential diagnosis

Fahad Hasan — Wed, 23 Sep 2026 16:07:11 GMT

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Dyspepsia causes

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Dyspepsia overview

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	{{Dyspepsia}}		{{Dyspepsia}}

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	==Pathophysiology==		==Pathophysiology==
	~~The~~ symptoms of ~~functional dyspepsia are directly caused by two major pathophysiological~~ abnormalities ~~abnormal gastric motility~~ and ~~visceral hypersensitivity~~.These mechanisms occur in patients who have acquired excessive responsiveness to stress as a result of the environment during early life, genetic abnormalities, residual inflammation after gastrointestinal infections, or other causes~~, with the~~ process modified by factors including psychophysiological abnormalities, abnormal secretion of gastric acid, Helicobacter pylori infection, diet, and lifestyle.		Functional dyspepsia is heterogeneous, with symptoms associated with several overlapping mechanisms: impaired [[gastric accommodation]] (~40%), [[visceral]] hypersensitivity to gastric distention (~40%), and mild [[delayed gastric emptying]] (~30%); approximately 30% of patients have none of these, and these abnormalities correlate poorly with symptoms and occur in asymptomatic controls. Increasing evidence implicates low-grade [[duodenal]] microinflammation (modestly increased [[eosinophil]]s and [[mast cell]]s with impaired barrier function) driving an aberrant type 2 helper T (Th2) immune response in a subgroup.<ref name="pmid33049222">{{cite journal \|vauthors=Ford AC, Mahadeva S, Carbone MF, Lacy BE, Talley NJ \|title=Functional dyspepsia \|journal=Lancet \|volume=396 \|issue=10263 \|pages=1689–1702 \|year=2020 \|pmid=33049222 \|doi=10.1016/S0140-6736(20)30469-4 \|url=}}</ref><ref name="pmid41Tornblom" /> These [[Mechanism of action\|mechanisms]] occur in patients who have acquired excessive responsiveness to stress as a result of the environment during early life, [[genetic]] abnormalities, [[residual]] [[inflammation]] after [[gastrointestinal]] [[Infection\|infections]], or other causes. The process may be modified by factors including psychophysiological abnormalities, [[abnormal]] secretion of [[gastric acid]], [[Helicobacter pylori infection]], impaired duodenal [[mucosal barrier]] integrity, diet, and lifestyle.

	==Causes==		==Causes==

Dyspepsia pathophysiology

Fahad Hasan — Wed, 23 Sep 2026 15:32:42 GMT

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	==Overview==		==Overview==
	[[Functional dyspepsia]] is now classified as a [[disorder of gut-brain interaction]], affecting approximately 7% of the community, and is diagnosed by the presence of one or more of bothersome [[epigastric pain]], epigastric burning, early satiation, and/or postprandial fullness, present for the last 3 months with symptom onset at least 6 months before diagnosis, in the absence of an identifiable [[Organic disease\|organic]] cause on evaluation including upper endoscopy.<ref name="pmid35798375">{{cite journal \|vauthors=Black CJ, Paine PA, Agrawal A, Alqahtani A, Anand B, Byrne P, Clark CE, Corr A, Doherty G, Excell L, Ford AC, Kemp K, Nwokolo C, Owen L, Paranandi B, Ritchie N, Robertson E, Whorwell P, Wright S, Hasan B \|title=British Society of Gastroenterology guidelines on the management of functional dyspepsia \|journal=Gut \|volume=71 \|issue=9 \|pages=1697–1723 \|year=2022 \|pmid=35798375 \|doi=10.1136/gutjnl-2022-327737 \|url=}}</ref> Functional dyspepsia is heterogeneous, with symptoms associated with ~~— rather than directly explained by —~~ several overlapping mechanisms: impaired [[gastric accommodation]] (~40%), [[visceral]] hypersensitivity to gastric distention (~40%), and mild [[delayed gastric emptying]] (~30%); approximately 30% of patients have none of these, and these abnormalities correlate poorly with symptoms and occur in asymptomatic controls. Increasing evidence implicates low-grade [[duodenal]] microinflammation (modestly increased [[eosinophil]]s and [[mast cell]]s with impaired barrier function) driving an aberrant type 2 helper T (Th2) immune response in a subgroup.<ref name="pmid33049222">{{cite journal \|vauthors=Ford AC, Mahadeva S, Carbone MF, Lacy BE, Talley NJ \|title=Functional dyspepsia \|journal=Lancet \|volume=396 \|issue=10263 \|pages=1689–1702 \|year=2020 \|pmid=33049222 \|doi=10.1016/S0140-6736(20)30469-4 \|url=}}</ref><ref name="pmid41Tornblom" /> These [[Mechanism of action\|mechanisms]] occur in patients who have acquired excessive responsiveness to stress as a result of the environment during early life, [[genetic]] abnormalities, [[residual]] [[inflammation]] after [[gastrointestinal]] [[Infection\|infections]], or other causes. The process may be modified by factors including psychophysiological abnormalities, [[abnormal]] secretion of [[gastric acid]], [[Helicobacter pylori infection]], impaired duodenal [[mucosal barrier]] integrity, diet, and lifestyle.		[[Functional dyspepsia]] is now classified as a [[disorder of gut-brain interaction]], affecting approximately 7% of the community, and is diagnosed by the presence of one or more of bothersome [[epigastric pain]], epigastric burning, early satiation, and/or postprandial fullness, present for the last 3 months with symptom onset at least 6 months before diagnosis, in the absence of an identifiable [[Organic disease\|organic]] cause on evaluation including upper endoscopy.<ref name="pmid35798375">{{cite journal \|vauthors=Black CJ, Paine PA, Agrawal A, Alqahtani A, Anand B, Byrne P, Clark CE, Corr A, Doherty G, Excell L, Ford AC, Kemp K, Nwokolo C, Owen L, Paranandi B, Ritchie N, Robertson E, Whorwell P, Wright S, Hasan B \|title=British Society of Gastroenterology guidelines on the management of functional dyspepsia \|journal=Gut \|volume=71 \|issue=9 \|pages=1697–1723 \|year=2022 \|pmid=35798375 \|doi=10.1136/gutjnl-2022-327737 \|url=}}</ref> Functional dyspepsia is heterogeneous, with symptoms associated with several overlapping mechanisms: impaired [[gastric accommodation]] (~40%), [[visceral]] hypersensitivity to gastric distention (~40%), and mild [[delayed gastric emptying]] (~30%); approximately 30% of patients have none of these, and these abnormalities correlate poorly with symptoms and occur in asymptomatic controls. Increasing evidence implicates low-grade [[duodenal]] microinflammation (modestly increased [[eosinophil]]s and [[mast cell]]s with impaired barrier function) driving an aberrant type 2 helper T (Th2) immune response in a subgroup.<ref name="pmid33049222">{{cite journal \|vauthors=Ford AC, Mahadeva S, Carbone MF, Lacy BE, Talley NJ \|title=Functional dyspepsia \|journal=Lancet \|volume=396 \|issue=10263 \|pages=1689–1702 \|year=2020 \|pmid=33049222 \|doi=10.1016/S0140-6736(20)30469-4 \|url=}}</ref><ref name="pmid41Tornblom" /> These [[Mechanism of action\|mechanisms]] occur in patients who have acquired excessive responsiveness to stress as a result of the environment during early life, [[genetic]] abnormalities, [[residual]] [[inflammation]] after [[gastrointestinal]] [[Infection\|infections]], or other causes. The process may be modified by factors including psychophysiological abnormalities, [[abnormal]] secretion of [[gastric acid]], [[Helicobacter pylori infection]], impaired duodenal [[mucosal barrier]] integrity, diet, and lifestyle.
	==Pathophysiology==		==Pathophysiology==
	The pathophysiology of dyspepsia is as follows:<ref name="pmid26535514">{{cite journal \|vauthors=Talley NJ, Ford AC \|title=Functional Dyspepsia \|journal=N. Engl. J. Med. \|volume=373 \|issue=19 \|pages=1853–63 \|year=2015 \|pmid=26535514 \|doi=10.1056/NEJMra1501505 \|url=}}</ref><ref name="pmid26901578">{{cite journal \|vauthors=Napthali K, Koloski N, Walker MM, Talley NJ \|title=Women and functional dyspepsia \|journal=Womens Health (Lond) \|volume=12 \|issue=2 \|pages=241–50 \|year=2016 \|pmid=26901578 \|pmc=5375052 \|doi=10.2217/whe.15.88 \|url=}}</ref><ref name="pmid27048251">{{cite journal \|vauthors=Talley NJ \|title=Functional dyspepsia: new insights into pathogenesis and therapy \|journal=Korean J. Intern. Med. \|volume=31 \|issue=3 \|pages=444–56 \|year=2016 \|pmid=27048251 \|pmc=4855108 \|doi=10.3904/kjim.2016.091 \|url=}}</ref><ref name="pmid24716560">{{cite journal \|vauthors=Ganesh M, Nurko S \|title=Functional dyspepsia in children \|journal=Pediatr Ann \|volume=43 \|issue=4 \|pages=e101–5 \|year=2014 \|pmid=24716560 \|doi=10.3928/00904481-20140325-12 \|url=}}</ref><ref name="pmid21443707">{{cite journal \|vauthors=Fock KM \|title=Functional dyspepsia, H. pylori and post infectious FD \|journal=J. Gastroenterol. Hepatol. \|volume=26 Suppl 3 \|issue= \|pages=39–41 \|year=2011 \|pmid=21443707 \|doi=10.1111/j.1440-1746.2011.06649.x \|url=}}</ref><ref name="pmid22327302">{{cite journal \|vauthors=Oustamanolakis P, Tack J \|title=Dyspepsia: organic versus functional \|journal=J. Clin. Gastroenterol. \|volume=46 \|issue=3 \|pages=175–90 \|year=2012 \|pmid=22327302 \|doi=10.1097/MCG.0b013e318241b335 \|url=}}</ref><ref name="pmid19663903">{{cite journal \|vauthors=Kindt S, Dubois D, Van Oudenhove L, Caenepeel P, Arts J, Bisschops R, Tack J \|title=Relationship between symptom pattern, assessed by the PAGI-SYM questionnaire, and gastric sensorimotor dysfunction in functional dyspepsia \|journal=Neurogastroenterol. Motil. \|volume=21 \|issue=11 \|pages=1183–e105 \|year=2009 \|pmid=19663903 \|doi=10.1111/j.1365-2982.2009.01374.x \|url=}}</ref><ref name="pmid35798375" /><ref name="pmid33049222" />		The pathophysiology of dyspepsia is as follows:<ref name="pmid26535514">{{cite journal \|vauthors=Talley NJ, Ford AC \|title=Functional Dyspepsia \|journal=N. Engl. J. Med. \|volume=373 \|issue=19 \|pages=1853–63 \|year=2015 \|pmid=26535514 \|doi=10.1056/NEJMra1501505 \|url=}}</ref><ref name="pmid26901578">{{cite journal \|vauthors=Napthali K, Koloski N, Walker MM, Talley NJ \|title=Women and functional dyspepsia \|journal=Womens Health (Lond) \|volume=12 \|issue=2 \|pages=241–50 \|year=2016 \|pmid=26901578 \|pmc=5375052 \|doi=10.2217/whe.15.88 \|url=}}</ref><ref name="pmid27048251">{{cite journal \|vauthors=Talley NJ \|title=Functional dyspepsia: new insights into pathogenesis and therapy \|journal=Korean J. Intern. Med. \|volume=31 \|issue=3 \|pages=444–56 \|year=2016 \|pmid=27048251 \|pmc=4855108 \|doi=10.3904/kjim.2016.091 \|url=}}</ref><ref name="pmid24716560">{{cite journal \|vauthors=Ganesh M, Nurko S \|title=Functional dyspepsia in children \|journal=Pediatr Ann \|volume=43 \|issue=4 \|pages=e101–5 \|year=2014 \|pmid=24716560 \|doi=10.3928/00904481-20140325-12 \|url=}}</ref><ref name="pmid21443707">{{cite journal \|vauthors=Fock KM \|title=Functional dyspepsia, H. pylori and post infectious FD \|journal=J. Gastroenterol. Hepatol. \|volume=26 Suppl 3 \|issue= \|pages=39–41 \|year=2011 \|pmid=21443707 \|doi=10.1111/j.1440-1746.2011.06649.x \|url=}}</ref><ref name="pmid22327302">{{cite journal \|vauthors=Oustamanolakis P, Tack J \|title=Dyspepsia: organic versus functional \|journal=J. Clin. Gastroenterol. \|volume=46 \|issue=3 \|pages=175–90 \|year=2012 \|pmid=22327302 \|doi=10.1097/MCG.0b013e318241b335 \|url=}}</ref><ref name="pmid19663903">{{cite journal \|vauthors=Kindt S, Dubois D, Van Oudenhove L, Caenepeel P, Arts J, Bisschops R, Tack J \|title=Relationship between symptom pattern, assessed by the PAGI-SYM questionnaire, and gastric sensorimotor dysfunction in functional dyspepsia \|journal=Neurogastroenterol. Motil. \|volume=21 \|issue=11 \|pages=1183–e105 \|year=2009 \|pmid=19663903 \|doi=10.1111/j.1365-2982.2009.01374.x \|url=}}</ref><ref name="pmid35798375" /><ref name="pmid33049222" />

Dyspepsia overview

Fahad Hasan — Wed, 23 Sep 2026 15:31:29 GMT

Classification

← Older revision		Revision as of 15:31, 23 September 2026
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	==Classification==		==Classification==
	~~Dyspepsia is broadly classified into two major types:~~ ulcer ~~and~~ non-ulcer dyspepsia. ~~The latter~~ is ~~also known~~ as functional dyspepsia.		Contemporary classification has moved away from the older dichotomy of "ulcer" versus "non-ulcer" dyspepsia. Patients are now categorized along a three-tier framework: '''uninvestigated dyspepsia''' (symptoms present but no diagnostic workup yet performed), '''organic (secondary) dyspepsia''' (an identifiable structural, [[Helicobacter pylori infection\|H. pylori]]-related, metabolic, or [[Drug\|drug-induced]] cause is found), and '''functional dyspepsia (FD)''' (no explanatory organic disease is found on evaluation, including a normal upper [[endoscopy]]). Functional dyspepsia, as redefined by the [[Rome IV criteria]], is further split into '''postprandial distress syndrome (PDS)''' and '''epigastric pain syndrome (EPS)''', which frequently overlap.<ref name="pmid27147122">{{cite journal \|vauthors=Stanghellini V, Chan FK, Hasler WL, Malagelada JR, Suzuki H, Tack J, Talley NJ \|title=Gastroduodenal Disorders \|journal=Gastroenterology \|volume=150 \|issue=6 \|pages=1380–1392 \|date=2016 \|pmid=27147122 \|doi=10.1053/j.gastro.2016.02.011 \|url=}}</ref> More than 70% of patients with uninvestigated dyspepsia ultimately meet criteria for functional dyspepsia rather than organic disease.<ref name="pmid22591037">{{cite journal \|vauthors=Lacy BE, Talley NJ, Locke GR, Bouras EP, DiBaise JK, El-Serag HB, Vela MF, Camilleri M, Freeman J, Khicha M, Fernandez y Fernandez M \|title=Review article: current treatment options and management of functional dyspepsia \|journal=Aliment Pharmacol Ther \|volume=36 \|issue=1 \|pages=3–15 \|date=2012 \|pmid=22591037 \|doi=10.1111/j.1365-2036.2012.05128.x \|url=}}</ref>

	==Pathophysiology==		==Pathophysiology==

Dyspepsia

Fahad Hasan — Wed, 23 Sep 2026 15:28:34 GMT

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	* [[Indigestion]]		* [[Indigestion]]
	* [[Functional bowel disorder]]		* [[Functional bowel disorder]]
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	{{~~Gastroenterology~~}}
	~~[[de:Verdauungsstörung]]~~
	[[es:Dispepsia]]		[[es:Dispepsia]]
	[[fr:Dyspepsie]]		[[fr:Dyspepsie]]
	~~[[it:Dispepsia]]~~
	~~[[nl:Dyspepsie]]~~
	[[pl:Dyspepsja]]		[[pl:Dyspepsja]]
	[[pt:Dispepsia]]		[[pt:Dispepsia]]
	[[ru:Диспепсия]]		[[ru:Диспепсия]]
	~~[[sv:Dyspepsi]]~~
	[[tr:Dispepsi]]		[[tr:Dispepsi]]

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	[[Category:Gastroenterology]]		[[Category:Gastroenterology]]

Dyspepsia pathophysiology

Fahad Hasan — Wed, 23 Sep 2026 14:51:50 GMT

Show changes

Peptic ulcer

Fahad Hasan — Wed, 23 Sep 2026 13:09:24 GMT

← Older revision		Revision as of 13:09, 23 September 2026
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	{{Peptic ulcer}}		{{Peptic ulcer}}

	{{CMG}} ; {{AE}} {{MKK}}		{{CMG}} ; {{AE}}; {{FAHA}} {{MKK}}

	{{SK}} Gastroduodenal ulcers; Peptic ulceration; gastric ulcer; duodenal ulcer.		{{SK}} Gastroduodenal ulcers; Peptic ulceration; gastric ulcer; duodenal ulcer.

Pancreatic cancer

Fahad Hasan — Wed, 23 Sep 2026 13:09:00 GMT

← Older revision		Revision as of 13:09, 23 September 2026
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	{{Pancreatic cancer}}		{{Pancreatic cancer}}
	'''For patient information click [[{{PAGENAME}} (patient information)\|here]]'''		'''For patient information click [[{{PAGENAME}} (patient information)\|here]]'''
	{{CMG}}; {{AE}} {{Cherry}} {{ARK}}		{{CMG}}; {{AE}} {{Cherry}} {{ARK}} {{FAHA}}

	{{SK}} Carcinoma of pancreas		{{SK}} Carcinoma of pancreas

Helicobacter pylori infection

Fahad Hasan — Wed, 23 Sep 2026 13:08:19 GMT

← Older revision		Revision as of 13:08, 23 September 2026
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	__NOTOC__		__NOTOC__
	{{Helicobacter pylori infection}}		{{Helicobacter pylori infection}}
	{{CMG}}; {{AE}}{{YK}}		{{CMG}}; {{AE}}; {{FAHA}} {{YK}}

	== [[Helicobacter pylori infection overview\|Overview]] ==		== [[Helicobacter pylori infection overview\|Overview]] ==

Hemorrhoids

Fahad Hasan — Wed, 23 Sep 2026 13:07:52 GMT

← Older revision		Revision as of 13:07, 23 September 2026
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	'''For patient information click [[{{PAGENAME}} (patient information)\|here]]'''		'''For patient information click [[{{PAGENAME}} (patient information)\|here]]'''

	{{CMG}} {{AE}} {{FAHA}} [[User: Mohammed Sbeih\|Mohammed A. Sbeih, M.D.]]~~; {{AY}}~~		{{CMG}} {{AE}} {{FAHA}; {{AY}}; [[User: Mohammed Sbeih\|Mohammed A. Sbeih, M.D.]]

	{{SK}} Piles, Hemorrhoid		{{SK}} Piles, Hemorrhoid

← Older revision		Revision as of 19:40, 24 September 2026
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	LDL-C, Total Cholesterol, non-HDL-C and ApoB at Week 52 were missing for 7.5% and 10.4% of patients assigned to placebo and LEROCHOL, respectively. Multiple imputation washout model was implemented for imputing missing values at Week 52. Least-squares mean from an Analysis of Covariance (ANCOVA) model including treatment as a factor and baseline value as a covariate, assuming unequal variances between groups. p-value <0.001 for superiority, controlled for Type I error rate. Not controlled for Type I error rate.		LDL-C, Total Cholesterol, non-HDL-C and ApoB at Week 52 were missing for 7.5% and 10.4% of patients assigned to placebo and LEROCHOL, respectively. Multiple imputation washout model was implemented for imputing missing values at Week 52. Least-squares mean from an Analysis of Covariance (ANCOVA) model including treatment as a factor and baseline value as a covariate, assuming unequal variances between groups. p-value <0.001 for superiority, controlled for Type I error rate. Not controlled for Type I error rate.

	~~'''Figure~~ 1: Mean Percent Change from Baseline in LDL-C Over 52 Weeks in Patients with Hypercholesterolemia and ASCVD or Increased Risk for ASCVD Events on Maximally Tolerated Statin Therapy (Trial 1)~~'''~~		[[File:Lerochol Fig. 1.jpeg\|400px\|thumb\|right\|Mean Percent Change from Baseline in LDL-C Over 52 Weeks in Patients with Hypercholesterolemia and ASCVD or Increased Risk for ASCVD Events on Maximally Tolerated Statin Therapy (Trial 1)]]

	* The primary efficacy outcome measure in Trial 2 was the percent change in LDL-C from baseline compared to placebo to Week 52.		* The primary efficacy outcome measure in Trial 2 was the percent change in LDL-C from baseline compared to placebo to Week 52.
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	LDL-C and non-HDL-C at Week 52 were missing for 10.7% and 11.2% of patients assigned to placebo and LEROCHOL, respectively. Total Cholesterol and ApoB at Week 52 were missing for 10.4% and 11.2% of patients assigned to placebo and LEROCHOL, respectively. Multiple imputation washout model was implemented for imputing missing values at Week 52. Least-squares mean from an Analysis of Covariance (ANCOVA) model including treatment and CVD status as factors and baseline value as a covariate, assuming unequal variances between groups. p-value <0.001 for superiority, controlled for Type I error rate. Not controlled for Type I error rate.		LDL-C and non-HDL-C at Week 52 were missing for 10.7% and 11.2% of patients assigned to placebo and LEROCHOL, respectively. Total Cholesterol and ApoB at Week 52 were missing for 10.4% and 11.2% of patients assigned to placebo and LEROCHOL, respectively. Multiple imputation washout model was implemented for imputing missing values at Week 52. Least-squares mean from an Analysis of Covariance (ANCOVA) model including treatment and CVD status as factors and baseline value as a covariate, assuming unequal variances between groups. p-value <0.001 for superiority, controlled for Type I error rate. Not controlled for Type I error rate.

	~~'''Figure~~ 2: Mean Percent Change from Baseline in LDL-C Over 52 Weeks in Patients with Hypercholesterolemia and ASCVD or Increased Risk for ASCVD Events on Maximally Tolerated Statin Therapy (Trial 2)~~'''~~		[[File:Lerochol Fig. 2.jpeg\|400px\|thumb\|right\|Mean Percent Change from Baseline in LDL-C Over 52 Weeks in Patients with Hypercholesterolemia and ASCVD or Increased Risk for ASCVD Events on Maximally Tolerated Statin Therapy (Trial 2)]]

	===Heterozygous Familial Hypercholesterolemia in Adults===		===Heterozygous Familial Hypercholesterolemia in Adults===
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	LDL-C, Total Cholesterol and non-HDL-C at Week 24 were missing for 3.1% and 2.8% of patients assigned to placebo and LEROCHOL, respectively. ApoB at Week 24 was missing for 3.1% and 3.1% of patients assigned to placebo and LEROCHOL, respectively. Multiple imputation washout model was implemented for imputing missing values at Week 24. Least-squares mean from an Analysis of Covariance (ANCOVA) model including treatment and CVD status as factors and baseline value as a covariate, assuming unequal variances between groups. p-value <0.001 for superiority, controlled for Type I error rate. Not controlled for Type I error rate.		LDL-C, Total Cholesterol and non-HDL-C at Week 24 were missing for 3.1% and 2.8% of patients assigned to placebo and LEROCHOL, respectively. ApoB at Week 24 was missing for 3.1% and 3.1% of patients assigned to placebo and LEROCHOL, respectively. Multiple imputation washout model was implemented for imputing missing values at Week 24. Least-squares mean from an Analysis of Covariance (ANCOVA) model including treatment and CVD status as factors and baseline value as a covariate, assuming unequal variances between groups. p-value <0.001 for superiority, controlled for Type I error rate. Not controlled for Type I error rate.

	~~'''Figure 3: Mean Percent Change from Baseline in LDL-C Over 24 Weeks in Patients with HeFH on Maximally Tolerated Statin Therapy (Trial 3)'''~~
	\|howSupplied=* LEROCHOL (lerodalcibep-liga) injection 300 mg/1.2 mL (250 mg/mL) is supplied as a single-dose prefilled syringe for subcutaneous injection and is a clear to slightly opalescent, brownish-yellow to amber, sterile, preservative-free solution.		\|howSupplied=* LEROCHOL (lerodalcibep-liga) injection 300 mg/1.2 mL (250 mg/mL) is supplied as a single-dose prefilled syringe for subcutaneous injection and is a clear to slightly opalescent, brownish-yellow to amber, sterile, preservative-free solution.
	* LEROCHOL is supplied in cartons containing one single-dose prefilled syringe (NDC 84685-300-01).		* LEROCHOL is supplied in cartons containing one single-dose prefilled syringe (NDC 84685-300-01).
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	* If needed, LEROCHOL may be kept at room temperature up to 25°C (77°F) in the original carton and must be used within 3 months of being removed from the refrigerator.		* If needed, LEROCHOL may be kept at room temperature up to 25°C (77°F) in the original carton and must be used within 3 months of being removed from the refrigerator.
	* If not used within 3 months, discard LEROCHOL.		* If not used within 3 months, discard LEROCHOL.
	\|packLabel=~~Add Display Panel~~		\|packLabel=[[File:LEROCHOL PD 1.jpeg\|400px\|thumb\|right\|PRINCIPAL DISPLAY PANEL]]
	\|fdaPatientInfo=* Advise the patient and/or caregiver to read the FDA-Approved Patient Labeling (Patient Information and Instructions for Use).		\|fdaPatientInfo=* Advise the patient and/or caregiver to read the FDA-Approved Patient Labeling (Patient Information and Instructions for Use).
	* Provide guidance to patients and caregivers on proper subcutaneous injection technique and how to use the prefilled syringe correctly.		* Provide guidance to patients and caregivers on proper subcutaneous injection technique and how to use the prefilled syringe correctly.