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Crystal arthritides - gout and calcium pyrophosphate arthritis Part 2: clinical features, diagnosis and differential diagnostics

Schlee S, Bollheimer LC, Bertsch T, Sieber C, Haerle P (2018)

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Publication Status: Published

Publication Type: Journal article

Publication year: 2018

Journal

Publisher: SPRINGER HEIDELBERG

Book Volume: 51

Pages Range: 579-584

Journal Issue: 5

DOI: 10.1007/s00391-017-1198-2

Abstract

Gout develops in four stages beginning with an asymptomatic increase in blood levels of uric acid. An acute gout attack is an expression of an underlying inflammatory process, which in the course of time is self-limiting. Without therapy monosodium urate crystals remain in the synovial fluid and synovialmembrane and trigger more acute attacks. In the course of the disease monosodium urate crystals form deposits (tophi) leading in severe forms to irreversible joint deformities with loss of functionality. In 20% of cases gout leads to involvement of the kidneys. Overproduction of uric acid can cause nephrolithiasis. These stones can be composed of uric acid or calcium phosphate. Another form of kidney disease caused by gout is uric acid nephropathy. This is a form of abacterial chronic inflammatory response with deposition of sodium urate crystals in the medullary interstitium. Acute obstructive nephropathy is relatively rare and characterized by renal failure due to uric acid precipitation in the tubules because of rapid cell lysis that occurs, for example, with chemotherapy. There is a causal interdependence between the occurrence of hyperuricemia and hypertension. Uric acid activates the renin-angiotensin-aldosterone (RAA) systemand inhibits nitric oxide (NO) with the possible consequence of a rise in systemic vascular resistance or arteriolar vasculopathy; however, uric acid is also an apparently independent risk factor for atherosclerosis. In contrast to young patients, the diagnosis of an acute gout attack in the elderly can be a challenge for the physician. Polyarticularmanifestations and obscure symptoms can make it difficult to differentiate it from rheumatoid arthritis and calcium pyrophosphate deposition disease (CPPD). Aspiration of synovial fluid with visualization of urate crystals using compensated polarized light microscopy is the gold standard for diagnosis of acute gout. Moreover, analysis of synovial fluid enables a distinction from septic arthritis by Gram staining and bacterial culture. Soft tissue ultrasonography is useful to detect affected synovial tissue and monosodium urate crystals within the synovial fluid. Involvement of bone occurs relatively late in the disease so that x-ray images are not useful in the early stages but might be helpful in differential diagnostics. Dual energy computed tomography (CT) and magnetic resonance imaging (MRI) can be used for certain indications.

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APA:

Schlee, S., Bollheimer, L.C., Bertsch, T., Sieber, C., & Haerle, P. (2018). Crystal arthritides - gout and calcium pyrophosphate arthritis Part 2: clinical features, diagnosis and differential diagnostics. Zeitschrift für Gerontologie und Geriatrie, 51(5), 579-584. https://doi.org/10.1007/s00391-017-1198-2

MLA:

Schlee, S., et al. "Crystal arthritides - gout and calcium pyrophosphate arthritis Part 2: clinical features, diagnosis and differential diagnostics." Zeitschrift für Gerontologie und Geriatrie 51.5 (2018): 579-584.

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