Acute pancreatitis natural history, complications and prognosis

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]Associate Editor(s)-in-Chief: Monish Thuvooru Muthu Kalyanaraman, M.B.B.S[2]

Natural History, Complications, and Prognosis

Overview

This section covers the clinical course of acute pancreatitis (AP) stratified by severity, the two-phase mortality model, local and systemic complications per the Revised Atlanta Classification, prognostic determinants, severity scoring systems, long-term sequelae (recurrence, progression to chronic pancreatitis, and new-onset diabetes), and vascular complications. Management of complications and severity classification definitions are covered in dedicated microchapters.

Natural History

Clinical Course by Severity

Approximately 80% of AP episodes are mild and self-limiting, resolving within 3–7 days with supportive care.[1][2] Approximately 20% develop moderately severe or severe disease, with prolonged hospitalization and increased mortality.[2]

  • Mild AP: No organ failure or local complications. Symptoms typically improve within 48 hours; patients tolerate oral diet and are discharged within a week.[1][3][2]
  • Moderately severe AP: Transient organ failure (<48 hours) and/or local complications. Mortality is approximately 2%. Course may be prolonged over weeks due to local complications.[3][2]
  • Severe AP: Overall mortality of severe/necrotizing AP is approximately 15%–20%; mortality with persistent organ failure is 25%–46%, and is substantially higher with multiorgan failure.[1][3][4][5]

Two-Phase Mortality Model

Deaths in AP occur in two distinct phases:[5][6]

  1. Early phase (first 1–2 weeks): Deaths result from primary organ failure driven by SIRS and the systemic inflammatory cascade. This is “sterile” organ failure unrelated to infection. The window of opportunity for intervention is narrow, and treatment is largely supportive.[5]
  2. Late phase (after 2 weeks): Deaths result from infected pancreatic necrosis (IPN) and secondary septic organ failure. Among patients with necrotizing pancreatitis, approximately one-third develop infected necrosis, typically after the first 10–14 days. Late mortality is driven by sepsis and its consequences. However, a large Dutch cohort study (n=639) found that mortality among patients with organ failure alone was paradoxically higher than in those with organ failure plus infected necrosis (44% vs. 29%, p=0.04). This difference disappeared after excluding very early deaths within 10 days of admission (28% vs. 34%, p=0.33), suggesting that the paradox is driven by fulminant early sterile organ failure deaths occurring before infection has time to develop, rather than a protective effect of infected necrosis.[7][3]

In a population-based study, the median interval from AP onset to death was 6 days, and from organ failure onset to death was 3 days.[5] Notably, a large multicenter study found that early-onset persistent organ failure was not associated with higher mortality compared with late-onset persistent organ failure, and no association was found between duration of organ failure and mortality — suggesting that the timing of organ failure may be less prognostically important than its persistence.[7] However, data on the prognostic impact of organ failure duration are conflicting. Schepers et al. (2019) found no association between duration of organ failure and mortality, whereas Singh et al. (2021) found that duration was significantly associated with mortality (p=0.006), and that sequential multiple organ failure carried the worst prognosis (mortality 69% vs. 30% for simultaneous and 12% for single organ failure).[8]

Key Determinants of Disease Course

  • Persistent organ failure (>48 hours) is the prime determinant of mortality. Overall mortality in patients with persistent organ failure is approximately 40%.[5]
  • Transient organ failure (<48 hours) carries a mortality of 1.4%–10%.[5]
  • SIRS at admission is highly predictive of organ failure and severe disease.[1]
  • Infected necrosis substantially worsens prognosis — mortality of 15%–35% overall; however, infected necrosis with concomitant organ failure carries approximately 35% mortality whereas infected necrosis without organ failure carries only ~1.4% mortality. Approximately one-third of patients with necrotizing pancreatitis develop infected necrosis, typically 10–14 days after onset. Risk factors include >50% pancreatic necrosis (aOR 3.61), persistent organ failure (aOR 11.71), invasive mechanical ventilation (uOR 12.24, high certainty), gallstone etiology (aOR 2.35), and delayed enteral nutrition (aOR 2.09) (moderate-to-high certainty evidence).[9][1][10][11]
  • Obesity (BMI >30) is independently associated with increased severity and complications.[1]

Complications

Local Complications

Local complications are classified by the Revised Atlanta Classification based on morphology and timing:[1][4]

Timing Fluid collections Necrotic collections
<4 weeks Acute peripancreatic fluid collection (APFC) Acute necrotic collection (ANC)
≥4 weeks (encapsulated) Pancreatic pseudocyst Walled-off necrosis (WON)

Key points:

  • APFCs are common and usually resolve spontaneously.[4]
  • Pseudocysts are encapsulated fluid collections without solid necrotic material, arising from ductal disruption.[4]
  • ANCs contain variable amounts of fluid and necrotic debris. Necrosis is purely peripancreatic in ~50% of cases.[4]
  • WON is a mature, encapsulated collection containing necrotic material; it is the target of intervention when infected.[4][3]
  • Infected necrosis should be suspected when clinical deterioration occurs (new fever, rising inflammatory markers) or when gas is visible within a necrotic collection on CT.[1]
  • Disconnected duct syndrome may occur as a long-term sequela of necrotizing pancreatitis when a segment of viable pancreas is isolated from the main duct by necrosis, predisposing to persistent collections or fistula.[4][3]

Other local complications:

  • Abdominal compartment syndrome: Sustained intra-abdominal pressure >20 mmHg with organ failure; consider in ventilated patients with severe AP.[12]
  • Gastric outlet/duodenal obstruction from inflammatory mass effect.[12]
  • Pancreatic duct disruption leading to pancreatic ascites or fistula.[12]

Vascular Complications

  • Splanchnic vein thrombosis (SVT): Reported incidence varies by population studied: approximately 4%–7% in unselected AP cohorts, 13% (95% CI 7%–23%) in a 2024 meta-analysis with systematic imaging, and 16%–22% in dedicated necrotizing pancreatitis cohorts. Most commonly involves the splenic vein, followed by portal and superior mesenteric veins. Usually asymptomatic; serious complications (variceal bleeding, ascites) are infrequent. The role of anticoagulation remains controversial. A 2022 meta-analysis (Anis et al.) found that anticoagulation improved recanalization rates (OR 0.51), but the largest prospective necrotizing pancreatitis cohort (Sissingh et al. 2024, n=432) found no difference in radiological or clinical outcomes with anticoagulation, with spontaneous recanalization in 62%. A 2025 global Delphi consensus favored anticoagulation for portal vein and SMV thrombosis but reached no consensus for isolated splenic vein thrombosis. Risks of bleeding into necrotic collections must be weighed, particularly in the acute setting. Long-term, patients may develop sinistral portal hypertension and gastric fundal varices.[3][13][14][15][16]
  • Pseudoaneurysm: Incidence 4%–6% in necrotizing pancreatitis; most commonly involves the splenic artery and gastroduodenal artery. Rupture causes life-threatening hemorrhage with mortality historically reported at 34%–52%, though more recent series report 14%–23%.[17]

Systemic Complications

  • Pulmonary: Pleural effusions (most common systemic complication), atelectasis, ARDS.[12]
  • Cardiovascular: Hypotension, hypovolemic shock, nonspecific ST-T changes mimicking MI, pericardial effusion.[12]
  • Renal: Acute kidney injury (prerenal from hypovolemia; intrarenal from systemic inflammation).[12]
  • Hematologic: DIC.[12]
  • Metabolic: Hypocalcemia (fat saponification), hyperglycemia.[12]
  • Other: Abdominal compartment syndrome, intestinal ileus/obstruction, GI bleeding.[12]

Prognosis

Mortality

  • Overall AP mortality: ~1%–2% at the population level, though hospitalized cohort studies report rates up to 5%.[3][1][18]
  • Mild AP: Near-zero mortality.[3]
  • Moderately severe AP: ~2% mortality.[3]
  • Severe AP: Overall mortality of severe/necrotizing AP is approximately 15%–20%; mortality with persistent organ failure is 25%–46%, and is substantially higher with multiorgan failure.[3][4][5]
  • Sterile necrosis with organ failure: ~20% mortality; sterile necrosis without organ failure carries near-zero mortality.[11]
  • Infected necrosis: 15%–35% mortality overall; however, infected necrosis with concomitant organ failure carries approximately 35% mortality whereas infected necrosis without organ failure carries only ~1.4% mortality.[1][10][11]

Post-discharge mortality is clinically significant: in a large multicenter cohort (n=2,613), first-year post-discharge mortality was 5.5%, with 3.0% dying in the first 90 days — nearly matching in-hospital mortality (3.5%). A Danish population-based study (n=28,759) confirmed a 5.0% 90-day post-discharge mortality (aHR 7.62 vs. matched controls), with risk remaining elevated for up to 5 years. Age, comorbidities, severity, and admission creatinine and glucose were independent risk factors for post-discharge death. This underscores the importance of structured post-discharge follow-up.[19][20]

Prognostic Factors

Per the ACG 2024 Guidelines, clinicians should assess multiple risk factors rather than relying on any single test or score:[1]

Patient factors:

  • Age >55 years
  • Obesity (BMI >30)
  • Altered mental status
  • Comorbid disease (especially type 2 diabetes)

Clinical/laboratory markers:

  • SIRS at admission (highly predictive of organ failure)[1]
  • Persistent SIRS >48 hours
  • BUN >20 mg/dL or rising BUN (marker of hypovolemia)
  • Hematocrit >44% or rising hematocrit
  • Elevated/rising creatinine
  • CRP (peaks at 48–72 hours; useful but delayed)[1]

Radiographic markers:

  • Pleural effusions or pulmonary infiltrates
  • Multiple or extensive extrapancreatic collections

Severity Scoring Systems

No single scoring system is established as a gold standard. All have limitations including cumbersomeness and high false-positive rates.[3] Scoring tools should supplement, not replace, ongoing clinical assessment.[3]

Score Variables Timing Key Limitations
BISAP 5 variables (BUN >25, mental status, SIRS ≥2, age >60, pleural effusion) First 24 hours Limited validation in severe disease; does not include imaging
APACHE II 12 physiologic variables + age + chronic health Admission and serial Complex; designed for ICU patients; not routinely obtained in non-ICU setting
Ranson 11 criteria (5 at admission, 6 at 48 hours) Requires 48 hours Cannot be recalculated; delayed; cumbersome
Glasgow/Imrie 8 criteria 48 hours Similar limitations to Ranson
Modified Marshall Respiratory, renal, cardiovascular Serial Used to define organ failure per Atlanta; simple

BISAP scoring: Score ≥3 associated with substantially increased mortality (0: 0.1%, 1: 0.4%, 2: 1.6%, 3: 3.6%, 4: 7.4%, 5: 9.5%).[21]

The ACG 2024 Guidelines emphasize that the presence of SIRS at admission and signs of hypovolemia (rising BUN, elevated hematocrit) are the most practical early predictors of severe disease.[1]

Long-Term Sequelae

Recurrence

The risk of recurrent AP after an index episode is approximately 17%–22% overall, with substantially higher rates in alcohol-associated (~29%), hypertriglyceridemia-associated (~30%), and idiopathic (~15%–25%) etiologies, and lower rates in biliary AP (~12%), which is further reduced to ~7% after cholecystectomy.[22][23][3] Independent risk factors for recurrence include alcohol etiology, smoking, and history of necrosis.[2] Persistent organ failure >48 hours during the index episode independently predicts recurrence (HR 3.52, 95% CI 1.22–10.19).[24]

Progression to Chronic Pancreatitis

  • 10% of patients with a first AP episode progress to chronic pancreatitis (CP).[2][25]
  • 36% of patients with recurrent AP develop CP.[2][25]
  • Risk factors: alcohol use (HR 8.79), smoking (HR 2.50), male sex, CTSI severity, and ≥3 recurrences.[25][24]
  • Nearly three-quarters of patients diagnosed with CP have a prior AP diagnosis.[2]
  • There is an increased lifetime risk of pancreatic cancer in those with AP (adjusted HR ~3.8 for pancreatic cancer mortality in post-pancreatitis diabetes), likely driven by chronic inflammation.[2][26]

New-Onset Diabetes

New-onset diabetes after AP is more common than previously recognized:

  • 23% of patients develop diabetes following a first AP episode (meta-analysis of 24 studies).[4][27]
  • 15% develop diabetes within 12 months, with risk increasing >2-fold at 5 years.[2][27]
  • Earlier meta-analyses suggested that diabetes development was not strongly associated with AP severity; however, a larger 2023 meta-analysis found significantly higher odds of prediabetes/DM after severe and moderately severe AP (OR 4.32). Both immune/inflammatory mechanisms beyond simple beta-cell destruction and necrosis-related injury likely contribute.[2][27][28]
  • Preliminary longitudinal data show that among patients with normal baseline endocrine function after a single AP episode, 54% develop prediabetes or diabetes by year 4, with progression most dynamic in the first 2 years (preliminary data; awaiting full publication).[29]
  • Hyperglycemia during AP (peak glucose >200 mg/dL) is a strong predictor of early-onset diabetes (42.9% vs. 3.5%) (preliminary data; awaiting full publication).[30]

Exocrine Insufficiency

Pooled prevalence of pancreatic exocrine insufficiency is 19% after mild AP and 33% after severe AP.[4] Manifests as steatorrhea, malabsorption, and fat-soluble vitamin deficiency. Diagnosed by fecal elastase-1 or 13C-mixed triglyceride breath test.[4]

Clinically Actionable Recommendations

  1. Assess severity early and serially: Evaluate SIRS criteria, BUN, hematocrit, and mental status at admission and at 24–48 hours. Do not rely solely on scoring systems.[1]
  2. Recognize the two-phase model: Early mortality is driven by sterile organ failure (supportive care); late mortality by infected necrosis (source control).[5]
  3. Suspect infected necrosis when clinical deterioration occurs after initial improvement (typically >7–10 days), particularly new/persistent fever or rising inflammatory markers.[1]
  4. Monitor for vascular complications in necrotizing pancreatitis: consider CT angiography for unexplained hemorrhage (pseudoaneurysm).[2]
  5. Screen for diabetes in the 12 months to 5 years following AP, regardless of severity.[2]
  6. Assess for exocrine insufficiency in patients with persistent GI symptoms after AP, especially after severe/necrotizing disease.[4]

High-Yield Clinical Pearls

  1. Persistent organ failure >48 hours is the single most important prognostic factor — not the extent of necrosis per se.
  2. SIRS at admission is the best early bedside predictor of severe disease.
  3. Rising BUN within 24 hours is a simple, reliable marker of hypovolemia and poor prognosis.
  4. Necrosis cannot be reliably assessed on CT before 72 hours — early CT for severity staging is not recommended.
  5. Infected necrosis typically develops >7–10 days into the disease course; new fever or deterioration in a recovering patient should raise suspicion.
  6. ~1 in 4 patients develops diabetes after AP, with higher risk after severe disease — plan post-discharge metabolic follow-up.
  7. Pseudoaneurysm rupture is a rare but rapidly fatal complication — consider CT angiography for any unexplained drop in hemoglobin in a patient with necrotizing pancreatitis.

Common Pitfalls

  1. Over-relying on scoring systems (e.g., Ranson, APACHE II) instead of serial clinical assessment, SIRS monitoring, and trending BUN/hematocrit.
  2. Obtaining early CT (within 48 hours) to assess severity — necrosis is not yet visible and the CT will likely be falsely reassuring.
  3. Equating “no necrosis on CT” with mild disease — organ failure can occur without necrosis.
  4. Neglecting long-term follow-up — failing to screen for diabetes, exocrine insufficiency, and chronic pancreatitis after discharge.
  5. Anticoagulating isolated splenic vein thrombosis without individual risk-benefit assessment — no consensus exists; bleeding risk into necrotic collections must be weighed.
  6. Using obsolete terminology (phlegmon, abscess, hemorrhagic pancreatitis) rather than current Revised Atlanta Classification terminology.

References

  1. ↑ 1.00 1.01 1.02 1.03 1.04 1.05 1.06 1.07 1.08 1.09 1.10 1.11 1.12 1.13 1.14 1.15 Tenner S, Vege SS, Sheth SG; et al. (2024). "American College of Gastroenterology Guidelines: Management of Acute Pancreatitis". Am J Gastroenterol. 119 (3): 419–437. doi:10.14309/ajg.0000000000002645. PMID 38301252 Check |pmid= value (help).
  2. ↑ 2.00 2.01 2.02 2.03 2.04 2.05 2.06 2.07 2.08 2.09 2.10 2.11 2.12 Mederos MA, Reber HA, Girgis MD (2021). "Acute Pancreatitis: A Review". JAMA. 325 (4): 382–390. doi:10.1001/jama.2020.20317. PMID 33464334 Check |pmid= value (help).
  3. ↑ 3.00 3.01 3.02 3.03 3.04 3.05 3.06 3.07 3.08 3.09 3.10 3.11 3.12 3.13 Trikudanathan G, Yazici C, Evans Phillips A, Forsmark CE (2024). "Diagnosis and Management of Acute Pancreatitis". Gastroenterology. 167 (4): 673–688. doi:10.1053/j.gastro.2024.02.052. PMID 38734348 Check |pmid= value (help).
  4. ↑ 4.00 4.01 4.02 4.03 4.04 4.05 4.06 4.07 4.08 4.09 4.10 4.11 Boxhoorn L, Voermans RP, Bouwense SA; et al. (2020). "Acute Pancreatitis". Lancet. 396 (10252): 726–734. doi:10.1016/S0140-6736(20)31310-6. PMID 32682482 Check |pmid= value (help).
  5. ↑ 5.0 5.1 5.2 5.3 5.4 5.5 5.6 5.7 Garg PK, Singh VP (2019). "Organ Failure Due to Systemic Injury in Acute Pancreatitis". Gastroenterology. 156 (7): 2008–2023. doi:10.1053/j.gastro.2018.12.041. PMID 30802407.
  6. ↑ Baron TH, Morgan DE (1999). "Acute Necrotizing Pancreatitis". N Engl J Med. 340 (18): 1412–1417. doi:10.1056/NEJM199905063401807. PMID 10235545.
  7. ↑ 7.0 7.1 Schepers NJ, Bakker OJ, Besselink MG; et al. (2019). "Impact of Characteristics of Organ Failure and Infected Necrosis on Mortality in Necrotising Pancreatitis". Gut. 68 (6): 1044–1051. doi:10.1136/gutjnl-2017-314657. PMID 29950344.
  8. ↑ Singh AK, Samanta J, Shukla J; et al. (2021). "Impact of Different Patterns of Organ Failure on Mortality in Acute Necrotizing Pancreatitis". Pancreas. 50 (7): 1030–1036. doi:10.1097/MPA.0000000000001880. PMID 34629457 Check |pmid= value (help).
  9. ↑ Tran A, Fernando SM, Rochwerg B; et al. (2022). "Prognostic Factors Associated With Development of Infected Necrosis in Patients With Acute Necrotizing or Severe Pancreatitis-a Systematic Review and Meta-Analysis". J Trauma Acute Care Surg. 92 (5): 940–948. doi:10.1097/TA.0000000000003502. PMID 34936587 Check |pmid= value (help).
  10. ↑ 10.0 10.1 Baron TH, DiMaio CJ, Wang AY, Morgan KA (2020). "American Gastroenterological Association Clinical Practice Update: Management of Pancreatic Necrosis". Gastroenterology. 158 (1): 67–75.e1. doi:10.1053/j.gastro.2019.07.064. PMID 31479658.
  11. ↑ 11.0 11.1 11.2 Leppäniemi A, Tolonen M, Tarasconi A; et al. (2019). "2019 WSES Guidelines for the Management of Severe Acute Pancreatitis". World J Emerg Surg. 14: 27. doi:10.1186/s13017-019-0247-0. PMID 31210778.
  12. ↑ 12.0 12.1 12.2 12.3 12.4 12.5 12.6 12.7 12.8 Oppenlander KE, Chadwick C, Carman K (2022). "Acute Pancreatitis: Rapid Evidence Review". Am Fam Physician. 106 (1): 44–50. PMID 35877133 Check |pmid= value (help).
  13. ↑ Borbély RZ, Szalai EÁ, Philip BM; et al. (2024). "The Risk of Developing Splanchnic Vein Thrombosis in Acute Pancreatitis Increases 3 days After Symptom Onset: A Systematic Review and Meta-Analysis". United European Gastroenterol J. 12 (6): 678–690. doi:10.1002/ueg2.12550. PMID 38400822 Check |pmid= value (help).
  14. ↑ Anis FS, Adiamah A, Lobo DN, Sanyal S (2022). "Incidence and Treatment of Splanchnic Vein Thrombosis in Patients With Acute Pancreatitis: A Systematic Review and Meta-Analysis". J Gastroenterol Hepatol. 37 (3): 446–454. doi:10.1111/jgh.15711. PMID 34657310 Check |pmid= value (help).
  15. ↑ Sissingh NJ, Timmerhuis HC, Groen JV; et al. (2024). "Splanchnic Vein Thrombosis in Necrotizing Pancreatitis: A Post-Hoc Analysis of a Nationwide Prospective Cohort". HPB (Oxford). 26 (4): 548–557. doi:10.1016/j.hpb.2024.01.011. PMID 38336603 Check |pmid= value (help).
  16. ↑ Scott M, Ghazanfar M, Windsor J; et al. (2025). "The Management of Splanchnic Vein Thrombosis in Acute Pancreatitis: A Global DELPHI Consensus Study". HPB (Oxford). 27 (3): 343–351. doi:10.1016/j.hpb.2024.12.002. PMID 39741058 Check |pmid= value (help).
  17. ↑ Trikudanathan G, Wolbrink DRJ, van Santvoort HC; et al. (2019). "Current Concepts in Severe Acute and Necrotizing Pancreatitis: An Evidence-Based Approach". Gastroenterology. 156 (7): 1994–2007.e3. doi:10.1053/j.gastro.2019.01.269. PMID 30986341.
  18. ↑ Iannuzzi JP, King JA, Leong JH; et al. (2022). "Global Incidence of Acute Pancreatitis Is Increasing Over Time: A Systematic Review and Meta-Analysis". Gastroenterology. 162 (1): 122–134. doi:10.1053/j.gastro.2021.09.043. PMID 34687739 Check |pmid= value (help).
  19. ↑ Czapári D, Váradi A, Farkas N; et al. (2023). "Detailed Characteristics of Post-Discharge Mortality in Acute Pancreatitis". Gastroenterology. 165 (3): 682–695. doi:10.1053/j.gastro.2023.05.028. PMID 37211309 Check |pmid= value (help).
  20. ↑ Davidsen L, Knoph CS, Cook ME, Drewes AM, Olesen SS (2025). "Increased Early Post-Discharge Mortality in Patients With Acute Pancreatitis". United European Gastroenterol J. 13 (4): 631–639. doi:10.1002/ueg2.12766. PMID 39918008 Check |pmid= value (help).
  21. ↑ Wu BU, Johannes RS, Sun X; et al. (2008). "The Early Prediction of Mortality in Acute Pancreatitis: A Large Population-Based Study". Gut. 57 (12): 1698–1703. doi:10.1136/gut.2008.152702. PMID 19118453.
  22. ↑ Li S, Gao L, Gong H; et al. (2023). "Recurrence Rates and Risk Factors for Recurrence After First Episode of Acute Pancreatitis: A Systematic Review and Meta-Analysis". Eur J Intern Med. 116: 72–81. doi:10.1016/j.ejim.2023.06.006. PMID 37330318 Check |pmid= value (help).
  23. ↑ Hajibandeh S, Jurdon R, Heaton E; et al. (2023). "The Risk of Recurrent Pancreatitis After First Episode of Acute Pancreatitis in Relation to Etiology and Severity of Disease: A Systematic Review, Meta-Analysis and Meta-Regression Analysis". J Gastroenterol Hepatol. 38 (10): 1718–1733. doi:10.1111/jgh.16264. PMID 37366550 Check |pmid= value (help).
  24. ↑ 24.0 24.1 Park JY, Bang S, Jeon TJ; et al. (2025). "Risk of and Factors Influencing the Progression From Acute to Recurrent Acute to Chronic Pancreatitis". Pancreatology. doi:10.1016/j.pan.2025.04.006. PMID 40280847 Check |pmid= value (help).
  25. ↑ 25.0 25.1 25.2 Sankaran SJ, Xiao AY, Wu LM; et al. (2015). "Frequency of Progression From Acute to Chronic Pancreatitis and Risk Factors: A Meta-Analysis". Gastroenterology. 149 (6): 1490–1500.e1. doi:10.1053/j.gastro.2015.07.066. PMID 26248032.
  26. ↑ Petrov MS, Olesen SS (2023). "Metabolic Sequelae: The Pancreatitis Zeitgeist of the 21st Century". Gastroenterology. 165 (5): 1122–1135. doi:10.1053/j.gastro.2023.07.025. PMID 37625497 Check |pmid= value (help).
  27. ↑ 27.0 27.1 27.2 Das SL, Singh PP, Phillips AR; et al. (2014). "Newly Diagnosed Diabetes Mellitus After Acute Pancreatitis: A Systematic Review and Meta-Analysis". Gut. 63 (5): 818–831. doi:10.1136/gutjnl-2013-305062. PMID 24000203.
  28. ↑ Zahariev OJ, Bunduc S, Kovács A; et al. (2023). "Risk Factors for Diabetes Mellitus After Acute Pancreatitis: A Systematic Review and Meta-Analysis". Front Med (Lausanne). 10: 1257222. doi:10.3389/fmed.2023.1257222. PMID 38264039 Check |pmid= value (help).
  29. ↑ Mikó A, Farkas N, Vincze Á; et al. (2026). "Progression of Pancreatic Morphologic Changes and Endocrine Dysfunction After Acute Pancreatitis: Preliminary Results of the Longitudinal GOULASH-Plus Cohort Study". Gastroenterology.
  30. ↑ Dungan KM, Chinchilli VM, Pichardo-Lowden A; et al. (2026). "Hyperglycemia During Acute Pancreatitis and Progression to Early-Onset Diabetes After Recovery: Preliminary Findings From the DREAM Study". Diabetes Care.
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