Familial amyloidosis laboratory findings: Difference between revisions
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* [[Cardiac biomarkers]] are the most important predictors of outcome in amyloidosis. They provide a quantitative assessment for [[Heart|cardiac]] damage and wall strain.<ref name="pmid21483018">{{cite journal |vauthors=Merlini G, Seldin DC, Gertz MA |title=Amyloidosis: pathogenesis and new therapeutic options |journal=J. Clin. Oncol. |volume=29 |issue=14 |pages=1924–33 |date=May 2011 |pmid=21483018 |pmc=3138545 |doi=10.1200/JCO.2010.32.2271 |url=}}</ref><ref name="pmid23227278">{{cite journal |vauthors=Baker KR, Rice L |title=The amyloidoses: clinical features, diagnosis and treatment |journal=Methodist Debakey Cardiovasc J |volume=8 |issue=3 |pages=3–7 |date=2012 |pmid=23227278 |pmc=3487569 |doi= |url=}}</ref><ref name="pmid25378951">{{cite journal |vauthors=Real de Asúa D, Costa R, Galván JM, Filigheddu MT, Trujillo D, Cadiñanos J |title=Systemic AA amyloidosis: epidemiology, diagnosis, and management |journal=Clin Epidemiol |volume=6 |issue= |pages=369–77 |date=2014 |pmid=25378951 |pmc=4218891 |doi=10.2147/CLEP.S39981 |url=}}</ref> | * [[Cardiac biomarkers]] are the most important predictors of outcome in amyloidosis. They provide a quantitative assessment for [[Heart|cardiac]] damage and wall strain.<ref name="pmid21483018">{{cite journal |vauthors=Merlini G, Seldin DC, Gertz MA |title=Amyloidosis: pathogenesis and new therapeutic options |journal=J. Clin. Oncol. |volume=29 |issue=14 |pages=1924–33 |date=May 2011 |pmid=21483018 |pmc=3138545 |doi=10.1200/JCO.2010.32.2271 |url=}}</ref><ref name="pmid23227278">{{cite journal |vauthors=Baker KR, Rice L |title=The amyloidoses: clinical features, diagnosis and treatment |journal=Methodist Debakey Cardiovasc J |volume=8 |issue=3 |pages=3–7 |date=2012 |pmid=23227278 |pmc=3487569 |doi= |url=}}</ref><ref name="pmid25378951">{{cite journal |vauthors=Real de Asúa D, Costa R, Galván JM, Filigheddu MT, Trujillo D, Cadiñanos J |title=Systemic AA amyloidosis: epidemiology, diagnosis, and management |journal=Clin Epidemiol |volume=6 |issue= |pages=369–77 |date=2014 |pmid=25378951 |pmc=4218891 |doi=10.2147/CLEP.S39981 |url=}}</ref> | ||
:* Troponin I or Troponin T | |||
:* BNP and NT-proBNP | :*[[Troponin I]] or [[Troponin T]] | ||
:*[[BNP]] and [[NT-proBNP]] | |||
'''Hepatic''' | '''Hepatic''' | ||
* Common [[Test|tests]] that are abnormal in [[liver function tests]] including: | * Common [[Test|tests]] that are abnormal in [[liver function tests]] including: | ||
:*AST | :*[[AST]] | ||
:*ALT | :*[[ALT]] | ||
:*Total bilirubin | :*Total [[bilirubin]] | ||
:*Alkaline phosphatase | :*[[Alkaline phosphatase]] | ||
:*Albumin | :*[[Albumin]] | ||
'''Renal''' | '''Renal''' | ||
| Line 35: | Line 36: | ||
* Common [[Test|tests]] that are abnormal in thyroidal involvement of amyloidosis include: | * Common [[Test|tests]] that are abnormal in thyroidal involvement of amyloidosis include: | ||
:*TSH | :*[[TSH]] | ||
:*Free T4 | :*[[Free T4]] | ||
'''Bone marrow''' | '''Bone marrow''' | ||
Revision as of 18:56, 30 October 2019
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Farima Kahe M.D. [2]
Overview
Laboratory findings in amyloidosis include elevated erythrocyte sedimentation rate, increased BUN level, serum creatinine, protein, casts, or fat cast in urine. Serum troponin, B-type natriuretic peptide, and beta-2-microglobulin are prognostic markers for heart failure.
Laboratory Findings
Cardiac
- Cardiac biomarkers are the most important predictors of outcome in amyloidosis. They provide a quantitative assessment for cardiac damage and wall strain.[1][2][3]
- Troponin I or Troponin T
- BNP and NT-proBNP
Hepatic
- Common tests that are abnormal in liver function tests including:
Renal
- Serum creatinine
- Urinary protein
- Glomerular filtration rate
- Albumin to creatinine ratio in the urine
Thyroid
- Common tests that are abnormal in thyroidal involvement of amyloidosis include:
Bone marrow
- Concurrent multiple myeloma can be found in patients with amyloidosis. In such cases laboratory testing include[4]:
- Serum protein electrophoresis
- Immunoglobulin levels
- Serum free light chains
- Beta-2-microglobulin
References
- ↑ Merlini G, Seldin DC, Gertz MA (May 2011). "Amyloidosis: pathogenesis and new therapeutic options". J. Clin. Oncol. 29 (14): 1924–33. doi:10.1200/JCO.2010.32.2271. PMC 3138545. PMID 21483018.
- ↑ Baker KR, Rice L (2012). "The amyloidoses: clinical features, diagnosis and treatment". Methodist Debakey Cardiovasc J. 8 (3): 3–7. PMC 3487569. PMID 23227278.
- ↑ Real de Asúa D, Costa R, Galván JM, Filigheddu MT, Trujillo D, Cadiñanos J (2014). "Systemic AA amyloidosis: epidemiology, diagnosis, and management". Clin Epidemiol. 6: 369–77. doi:10.2147/CLEP.S39981. PMC 4218891. PMID 25378951.
- ↑ Kourelis TV, Kumar SK, Gertz MA, Lacy MQ, Buadi FK, Hayman SR; et al. (2013). "Coexistent multiple myeloma or increased bone marrow plasma cells define equally high-risk populations in patients with immunoglobulin light chain amyloidosis". J Clin Oncol. 31 (34): 4319–24. doi:10.1200/JCO.2013.50.8499. PMC 4881366. PMID 24145344.