Difference between revisions of "Myocarditis laboratory findings"

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===Other Biomarkers===
 
===Other Biomarkers===
 
*Serological markers such as [[Fas]], [[Fas ligand]], [[interleukin]]-10 or antimyosin autoantibodies are of prognostic value in myocarditis.  
 
*Serological markers such as [[Fas]], [[Fas ligand]], [[interleukin]]-10 or antimyosin autoantibodies are of prognostic value in myocarditis.  
**[[Fas]] and [[Fas ligand]] are markers of cell death ([[apoptosis]]) and are associated with [[cardiac dysfunction]].<ref name="pmid16168288">{{cite journal| author=Sheppard R, Bedi M, Kubota T, Semigran MJ, Dec W, Holubkov R et al.| title=Myocardial expression of fas and recovery of left ventricular function in patients with recent-onset cardiomyopathy. | journal=J Am Coll Cardiol | year= 2005 | volume= 46 | issue= 6 | pages= 1036-42 | pmid=16168288 | doi=10.1016/j.jacc.2005.05.067 | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=16168288  }} </ref>  
+
**[[Fas]] and [[Fas ligand]] are markers of cell death ([[apoptosis]]) and are associated with [[cardiac dysfunction]].<ref name="pmid16168288">{{cite journal| author=Sheppard R, Bedi M, Kubota T, Semigran MJ, Dec W, Holubkov R et al.| title=Myocardial expression of fas and recovery of left ventricular function in patients with recent-onset cardiomyopathy. | journal=J Am Coll Cardiol | year= 2005 | volume= 46 | issue= 6 | pages= 1036-42 | pmid=16168288 | doi=10.1016/j.jacc.2005.05.067 | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=16168288  }} </ref>
**Antimyosin autoantibodies are associated with left ventricular systolic dysfunction and diastolic stiffness in patients with chronic myocarditis.<ref name="pmid10636253">{{cite journal| author=Lauer B, Schannwell M, Kühl U, Strauer BE, Schultheiss HP| title=Antimyosin autoantibodies are associated with deterioration of systolic and diastolic left ventricular function in patients with chronic myocarditis. | journal=J Am Coll Cardiol | year= 2000 | volume= 35 | issue= 1 | pages= 11-8 | pmid=10636253 | doi= | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=10636253  }} </ref>  
+
**Antimyosin autoantibodies are associated with left ventricular systolic dysfunction and diastolic stiffness in patients with chronic myocarditis.<ref name="pmid10636253">{{cite journal| author=Lauer B, Schannwell M, Kühl U, Strauer BE, Schultheiss HP| title=Antimyosin autoantibodies are associated with deterioration of systolic and diastolic left ventricular function in patients with chronic myocarditis. | journal=J Am Coll Cardiol | year= 2000 | volume= 35 | issue= 1 | pages= 11-8 | pmid=10636253 | doi= | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=10636253  }} </ref>
 
**High levels of [[interleukin-10]] in fulminant myocarditis patients at admission may be predictive of subsequent development of [[cardiogenic shock]] (requiring mechanical cardiopulmonary support system) and mortality.<ref name="pmid15364334">{{cite journal| author=Nishii M, Inomata T, Takehana H, Takeuchi I, Nakano H, Koitabashi T et al.| title=Serum levels of interleukin-10 on admission as a prognostic predictor of human fulminant myocarditis. | journal=J Am Coll Cardiol | year= 2004 | volume= 44 | issue= 6 | pages= 1292-7 | pmid=15364334 | doi=10.1016/j.jacc.2004.01.055 | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=15364334  }} </ref>
 
**High levels of [[interleukin-10]] in fulminant myocarditis patients at admission may be predictive of subsequent development of [[cardiogenic shock]] (requiring mechanical cardiopulmonary support system) and mortality.<ref name="pmid15364334">{{cite journal| author=Nishii M, Inomata T, Takehana H, Takeuchi I, Nakano H, Koitabashi T et al.| title=Serum levels of interleukin-10 on admission as a prognostic predictor of human fulminant myocarditis. | journal=J Am Coll Cardiol | year= 2004 | volume= 44 | issue= 6 | pages= 1292-7 | pmid=15364334 | doi=10.1016/j.jacc.2004.01.055 | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=15364334  }} </ref>
  
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*Polymerase chain reaction (PCR) may be used in the detection of and identification of viral infections from [[myocardial biopsy]], pericardial fluid or other body fluids. Persistence of a viral genome is indicative of a poor prognosis.<ref name="pmid16172268">{{cite journal| author=Kühl U, Pauschinger M, Seeberg B, Lassner D, Noutsias M, Poller W et al.| title=Viral persistence in the myocardium is associated with progressive cardiac dysfunction. | journal=Circulation | year= 2005 | volume= 112 | issue= 13 | pages= 1965-70 | pmid=16172268 | doi=10.1161/CIRCULATIONAHA.105.548156 | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=16172268  }} </ref>
 
*Polymerase chain reaction (PCR) may be used in the detection of and identification of viral infections from [[myocardial biopsy]], pericardial fluid or other body fluids. Persistence of a viral genome is indicative of a poor prognosis.<ref name="pmid16172268">{{cite journal| author=Kühl U, Pauschinger M, Seeberg B, Lassner D, Noutsias M, Poller W et al.| title=Viral persistence in the myocardium is associated with progressive cardiac dysfunction. | journal=Circulation | year= 2005 | volume= 112 | issue= 13 | pages= 1965-70 | pmid=16172268 | doi=10.1161/CIRCULATIONAHA.105.548156 | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=16172268  }} </ref>
 
 
==Overview==
 
An elevated/reduced concentration of serum/blood/urinary/CSF/other [lab test] is diagnostic of [disease name].
 
 
OR
 
 
Laboratory findings consistent with the diagnosis of [disease name] include [abnormal test 1], [abnormal test 2], and [abnormal test 3].
 
 
OR
 
 
[Test] is usually normal for patients with [disease name].
 
 
OR
 
 
Some patients with [disease name] may have elevated/reduced concentration of [test], which is usually suggestive of [progression/complication].
 
 
OR
 
 
There are no diagnostic laboratory findings associated with [disease name].
 
 
==Laboratory Findings==
 
 
There are no diagnostic laboratory findings associated with [disease name].
 
 
OR
 
 
An elevated/reduced concentration of serum/blood/urinary/CSF/other [lab test] is diagnostic of [disease name].
 
 
OR
 
 
[Test] is usually normal among patients with [disease name].
 
 
OR
 
 
Laboratory findings consistent with the diagnosis of [disease name] include:
 
*[Abnormal test 1]
 
*[Abnormal test 2]
 
*[Abnormal test 3]
 
 
OR
 
 
Some patients with [disease name] may have elevated/reduced concentration of [test], which is usually suggestive of [progression/complication].
 
 
  
 
==References==
 
==References==
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[[Category:Medicine]]
 
[[Category:Medicine]]
 
[[Category:Cardiology]]
 
[[Category:Cardiology]]
[[Category:Up-To-Date]]
+
[[Category:Up-To-Date]]
 
[[Category:Primary care]]
 
[[Category:Primary care]]
 
[[Category:Emergency medicine]]
 
[[Category:Emergency medicine]]

Revision as of 17:26, 16 January 2020

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor(s)-in-Chief: Varun Kumar, M.B.B.S., Maliha Shakil, M.D. [2] Homa Najafi, M.D.[3]

Overview

Laboratory findings consistent with the diagnosis of myocarditis include elevated markers of myonecrosis, inflammatory markers, and other biomarkers. Markers of myonecrosis include creatine kinase (CK-MB), cardiac troponin I (cTnI) or T (cTnT), lactate dehydrogenase (LDH), alanine transaminase (ALT), and aspartate transaminase (AST). Elevated levels of C-reactive protein and erythrocyte sedimentation rate (ESR), and leukocytosis are suggestive of myocarditis. Serological markers such as Fas, Fas ligand, interleukin-10 or antimyosin autoantibodies are of prognostic value in myocarditis. Other auto-antibodies such as ANA and rheumatoid factor may also be detected.

Laboratory Findings

Markers of Myonecrosis

The following markers of myonecrosis are often elevated in myocarditis, particularly early on in the course of the disease:

AST is considered to be the most sensitive marker of myocarditis with the sensitivity of 85%.[4] However, the specificities of AST and ALT are low in patients with myocarditis as they may be elevated secondary to other coexisting systemic or organ dysfunction.[5]

Inflammatory Markers

The following inflammatory markers are often elevated:

Other Biomarkers

  • Serological markers such as Fas, Fas ligand, interleukin-10 or antimyosin autoantibodies are of prognostic value in myocarditis.
    • Fas and Fas ligand are markers of cell death (apoptosis) and are associated with cardiac dysfunction.[6]
    • Antimyosin autoantibodies are associated with left ventricular systolic dysfunction and diastolic stiffness in patients with chronic myocarditis.[7]
    • High levels of interleukin-10 in fulminant myocarditis patients at admission may be predictive of subsequent development of cardiogenic shock (requiring mechanical cardiopulmonary support system) and mortality.[8]
  • Viral antibody titers for coxsackie B virus, human immunodeficiency virus (HIV), cytomegalovirus, Ebstein-Barr virus, hepatitis virus family, and influenza virus may be useful in diagnosing the causative organism. However, the management of myocarditis due to a viral etiology seldom differs depending upon the virus, and therefore, antibody titers are rarely indicated in the diagnostic evaluation of myocarditis.
  • Polymerase chain reaction (PCR) may be used in the detection of and identification of viral infections from myocardial biopsy, pericardial fluid or other body fluids. Persistence of a viral genome is indicative of a poor prognosis.[9]

References

  1. 1.0 1.1 Smith SC, Ladenson JH, Mason JW, Jaffe AS (1997). "Elevations of cardiac troponin I associated with myocarditis. Experimental and clinical correlates". Circulation. 95 (1): 163–8. PMID 8994432.
  2. Lauer B, Niederau C, Kühl U, Schannwell M, Pauschinger M, Strauer BE; et al. (1997). "Cardiac troponin T in patients with clinically suspected myocarditis". J Am Coll Cardiol. 30 (5): 1354–9. PMID 9350939.
  3. Soongswang J, Durongpisitkul K, Ratanarapee S, Leowattana W, Nana A, Laohaprasitiporn D; et al. (2002). "Cardiac troponin T: its role in the diagnosis of clinically suspected acute myocarditis and chronic dilated cardiomyopathy in children". Pediatr Cardiol. 23 (5): 531–5. PMID 12211203.
  4. Freedman SB, Haladyn JK, Floh A, Kirsh JA, Taylor G, Thull-Freedman J (2007). "Pediatric myocarditis: emergency department clinical findings and diagnostic evaluation". Pediatrics. 120 (6): 1278–85. doi:10.1542/peds.2007-1073. PMID 18055677.
  5. Lippi G, Salvagno GL, Guidi GC (2008). "Cardiac troponins in pediatric myocarditis". Pediatrics. 121 (4): 864, author reply 864-5. doi:10.1542/peds.2008-0031. PMID 18381554.
  6. Sheppard R, Bedi M, Kubota T, Semigran MJ, Dec W, Holubkov R; et al. (2005). "Myocardial expression of fas and recovery of left ventricular function in patients with recent-onset cardiomyopathy". J Am Coll Cardiol. 46 (6): 1036–42. doi:10.1016/j.jacc.2005.05.067. PMID 16168288.
  7. Lauer B, Schannwell M, Kühl U, Strauer BE, Schultheiss HP (2000). "Antimyosin autoantibodies are associated with deterioration of systolic and diastolic left ventricular function in patients with chronic myocarditis". J Am Coll Cardiol. 35 (1): 11–8. PMID 10636253.
  8. Nishii M, Inomata T, Takehana H, Takeuchi I, Nakano H, Koitabashi T; et al. (2004). "Serum levels of interleukin-10 on admission as a prognostic predictor of human fulminant myocarditis". J Am Coll Cardiol. 44 (6): 1292–7. doi:10.1016/j.jacc.2004.01.055. PMID 15364334.
  9. Kühl U, Pauschinger M, Seeberg B, Lassner D, Noutsias M, Poller W; et al. (2005). "Viral persistence in the myocardium is associated with progressive cardiac dysfunction". Circulation. 112 (13): 1965–70. doi:10.1161/CIRCULATIONAHA.105.548156. PMID 16172268.



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