Gout laboratory findings: Difference between revisions
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{{CMG}} | {{CMG}} | ||
== Overview == | == Overview == | ||
A definitive [[diagnosis]] of gout is made from [[light microscopy]] of fluid aspirated from the joint | A definitive [[diagnosis]] of gout is made from [[light microscopy]] of the fluid aspirated from the joint. The fluid demonstrates [[intracellular]] negatively bi-refringent monosodium urate crystals and [[polymorphonuclear leukocytes]] in the [[synovial fluid]]. Although [[hyperuricemia]] is a common feature of gout, a high [[uric acid]] level does not necessarily mean a person will develop gout. | ||
== Laboratory Findings == | == Laboratory Findings == | ||
While synovial fluid analysis remains the central pillar of diagnostic work up for all patients with new-onset acute monoarthritis, other laboratory investigations contribute to assist the diagnosis of gout, and in assessing comorbid conditions which affect gout. | |||
{| class="wikitable" align="right" | |||
|+ The serum uric acid level during an attack of gout | |||
! !! Sensitivity !! Specificity | |||
|- | |||
| > 5.88 mg/dl<ref name="pmid20625017" />|| align="center" |95%|| align="center" |53% | |||
|- | |||
| ≥ 6 mg/dl<ref name="pmid19369457" />|| align="center" | 86% || align="center" | ? | |||
|- | |||
| ≥ 8 mg/dl<ref name="pmid19369457" />|| align="center" |68% || align="center" |? | |||
|} | |||
The level | ==== Serum uric acid concentrations<ref name="pmid20625017">{{cite journal| author=Janssens HJ, Fransen J, van de Lisdonk EH, van Riel PL, van Weel C, Janssen M| title=A diagnostic rule for acute gouty arthritis in primary care without joint fluid analysis. | journal=Arch Intern Med | year= 2010 | volume= 170 | issue= 13 | pages= 1120-6 | pmid=20625017 | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=20625017 | doi=10.1001/archinternmed.2010.196 }} </ref><ref name="pmid19369457">{{cite journal |author=Schlesinger N, Norquist JM, Watson DJ |title=Serum urate during acute gout |journal=J. Rheumatol. |volume=36 |issue=6 |pages=1287–9 |year=2009 |month=June |pmid=19369457 |doi=10.3899/jrheum.080938 |url=http://www.jrheum.org/cgi/pmidlookup?view=long&pmid=19369457 |issn=}}</ref><ref name="pmid718280">{{cite journal |vauthors=Brauer GW, Prior IA |title=A prospective study of gout in New Zealand Maoris |journal=Ann. Rheum. Dis. |volume=37 |issue=5 |pages=466–72 |date=October 1978 |pmid=718280 |pmc=1000277 |doi= |url=}}</ref> ==== | ||
* Uric acid level is only useful to assist with clinical diagnosis of gout in symptomatic individuals as hyperuricemia alone is not sufficient. | |||
* It is less significant in diagnosing gout, especially during an acute attack when urate excretion through the kidneys is often increased. | |||
* The levels are important during urate lowering therapy when the goal is to maintain a target urate level. | |||
==== Blood tests: ==== | |||
* Acute phase reactants, such as C-reactive protein, are usually increased during a flare—concentrations can be higher than 100 mg/L.<ref name="pmid2448456">{{cite journal |vauthors=Roseff R, Wohlgethan JR, Sipe JD, Canoso JJ |title=The acute phase response in gout |journal=J. Rheumatol. |volume=14 |issue=5 |pages=974–7 |date=October 1987 |pmid=2448456 |doi= |url=}}</ref> | |||
* Complete blood counts showing neutrophil leukocytosis can also be present depicting degree of systemic inflammation.<ref name="pmid27112094">{{cite journal |vauthors=Dalbeth N, Merriman TR, Stamp LK |title=Gout |journal=Lancet |volume=388 |issue=10055 |pages=2039–2052 |date=October 2016 |pmid=27112094 |doi=10.1016/S0140-6736(16)00346-9 |url=}}</ref> | |||
==== Renal function tests ==== | |||
* Renal function tests are recommended when prescribing and monitoring drugs used for urate lowering therapy. | |||
==References== | ==References== | ||
{{ | {{Reflist|2}} | ||
{{WH}} | {{WH}} | ||
{{WS}} | {{WS}} | ||
[[Category:Arthritis]] | [[Category:Arthritis]] | ||
[[Category:Rheumatology]] | [[Category:Rheumatology]] | ||
[[Category:Disease]] | [[Category:Disease]] | ||
Latest revision as of 21:55, 29 July 2020
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]
Overview
A definitive diagnosis of gout is made from light microscopy of the fluid aspirated from the joint. The fluid demonstrates intracellular negatively bi-refringent monosodium urate crystals and polymorphonuclear leukocytes in the synovial fluid. Although hyperuricemia is a common feature of gout, a high uric acid level does not necessarily mean a person will develop gout.
Laboratory Findings
While synovial fluid analysis remains the central pillar of diagnostic work up for all patients with new-onset acute monoarthritis, other laboratory investigations contribute to assist the diagnosis of gout, and in assessing comorbid conditions which affect gout.
| Sensitivity | Specificity | |
|---|---|---|
| > 5.88 mg/dl[1] | 95% | 53% |
| ≥ 6 mg/dl[2] | 86% | ? |
| ≥ 8 mg/dl[2] | 68% | ? |
Serum uric acid concentrations[1][2][3]
- Uric acid level is only useful to assist with clinical diagnosis of gout in symptomatic individuals as hyperuricemia alone is not sufficient.
- It is less significant in diagnosing gout, especially during an acute attack when urate excretion through the kidneys is often increased.
- The levels are important during urate lowering therapy when the goal is to maintain a target urate level.
Blood tests:
- Acute phase reactants, such as C-reactive protein, are usually increased during a flare—concentrations can be higher than 100 mg/L.[4]
- Complete blood counts showing neutrophil leukocytosis can also be present depicting degree of systemic inflammation.[5]
Renal function tests
- Renal function tests are recommended when prescribing and monitoring drugs used for urate lowering therapy.
References
- ↑ 1.0 1.1 Janssens HJ, Fransen J, van de Lisdonk EH, van Riel PL, van Weel C, Janssen M (2010). "A diagnostic rule for acute gouty arthritis in primary care without joint fluid analysis". Arch Intern Med. 170 (13): 1120–6. doi:10.1001/archinternmed.2010.196. PMID 20625017.
- ↑ 2.0 2.1 2.2 Schlesinger N, Norquist JM, Watson DJ (2009). "Serum urate during acute gout". J. Rheumatol. 36 (6): 1287–9. doi:10.3899/jrheum.080938. PMID 19369457. Unknown parameter
|month=ignored (help) - ↑ Brauer GW, Prior IA (October 1978). "A prospective study of gout in New Zealand Maoris". Ann. Rheum. Dis. 37 (5): 466–72. PMC 1000277. PMID 718280.
- ↑ Roseff R, Wohlgethan JR, Sipe JD, Canoso JJ (October 1987). "The acute phase response in gout". J. Rheumatol. 14 (5): 974–7. PMID 2448456.
- ↑ Dalbeth N, Merriman TR, Stamp LK (October 2016). "Gout". Lancet. 388 (10055): 2039–2052. doi:10.1016/S0140-6736(16)00346-9. PMID 27112094.