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Crystal arthropathies

            Gout is a metabolic disorder that as a consequence of elevated serum uric acid levels (hyperuricemia) although most of the people with hyperuricaemia never develop gout. In cases of hypersaturation of extracellular fluids with uric acid, monosodium urate crystals are formed in joints and other tissues. The incidence of gout increases with aging and with elevation of uric acid serum levels. Its prevalence is over 5-28 cases per 1000 men and 1-6 case per 1000 women. The disease is more frequent in men with male-to-female ratio about 2-7:1. The primary hyperuricaemia may be induced by diminished renal clearance, increased production or both mechanisms. Excessive amounts of uric acid may derive from increased intake of purine-rich food and drinks mainly meat and beer. Secondary gout develops as a consequence of high cell turn-over and metabolism of DNA and RNA such as myelo- and lymphoproliferative haematological malignancies e. g., leukaemia or lymphoma, psoriasis, solid tumors, etc. It may be a consequence of drug-induced decreased renal excretion after intake of diuretics, low-dose aspirin, ciclosporin, etc.


            The asymptomatic hyperuricemia precedes the development of clinically manifested joint inflammation. The classic clinical presentation of gout is acute monoarthritis most often of the first metatarsophalangeal joint of the great toe, which is considered as a hallmark of the disease and is termed podagra. The joint is warm, painful, oedematous with erythema of the overlying skin. In over half of the patients the disease starts in other joints e. g., foot joints (tarsal, subtalar), ankle, knee, elbow, wrist or hand joints (metacarpophalangeal or interphalangeal). The first attacks subside for several days even without treatment with mean duration 5-14 days. Recurrent attacks of joint inflammation and intercritical period free of clinical symptoms is the characteristic pattern of the disease. The disease progression is associated with more frequent gouty attacks, which last longer and tend to be polyarticular. In the evolution of the disorder chronic tophaceous gout may develop.


            Visceral damage caused by the hyperuricemia itself is renal involvement. In highly acidic urine (low pH), uric acid stones are formed, as in alkaline urine the uric acid crystals  are soluble.


            It should be underlined that hyperuricemia often is accompanied by obesity, hypertension, hyper- and dyslipidemia, impaired glucose tolerance or diabetes mellitus type 2, which are the components of the metabolic syndrome. The hyperuricemia is associated with increased risk for atherosclerosis and cardiovascular-related mortality.


            Laboratory and instrumental investigations

            For the proper diagnosis and treatment a complex of blood tests should be performed as well as urine analysis as well as evaluation of renal structure and function, examination of joint fluid via cytological analysis and polarizing microscopy. At the discretion of the physician joint X-ray may be ordered. Definite diagnosis gout is established on the basis of presence of specific crystals on polarizing microscopy.


            The treatment of gouty attack includes nonsteroidal anti-inflammatory drugs (NSAIDs), colchicine, intraarticular and systemic corticosteroids, and in refractory cases – a combination from the above-mentioned drugs. The precise drug choice depends on the severity of the gouty attack, the number of the affected joints, the concomitant diseases. If indicated the hyperuricemia is controlled via administration of uric acid synthesis inhibitors (xanthine oxidase inhibitors) or uricosuric agents. The drug choice should be performed by rheumatologist in every individual case according to the disease severity and the concomitant pathology. The proper hygienic-dietetic regimen, enough intake of alkaline mineral water and alkalizing substances play a key role for disease control.


            Crystal arthropathy associated with calcium pyrophosphate dihydrate crystals

            Crystal arthropathy associated with calcium pyrophosphate dihydrate crystals (CPPD) may be asymptomatic or may manifest in different clinical forms. Arthritis associated with CPPD crystal deposition can be classified as idiopathic and secondary in the context of various systemic diseases (hyperparathyroidism, hemochromatosis, hypothyroidism, amyloidosis, etc.) or trauma.


            The term “pseudogout” refers to the acute gout-like attacks of joint inflammation. Acute pseudogout occurs in over 25% of patients with CPPD deposition disease. The attack of acute inflammation lasts between several days and 2 weeks and is usually self-limited with abrupt onset and profound severity similarly to gout inflammation. Knees are affected in half of the cases, but any other joint may be involved including the most common for gout first metatarsophalangeal joint of the great toe. Similarly to gout, the attack may be provoked by trauma, surgery, myocardial infarction. The patients are asymptomatic between the episodes. The acute pseudogout should be differentiated from gout and septic arthritis via microscopic examination of joint fluid and culture.


            CPPD deposition disease may also manifest as inflammatory arthropathy with low-grade inflammation or as degenerative joint disorder – osteoarthritis. The latter pattern is observed in half of the patients. The knees are most commonly affected, followed by wrists, metacarpophalangeal joints, hips, shoulders, elbows and ankles. The term “chondrocalcinosis” refers to the presence of calcium-containing crystals detected as radiodensities in articular cartilage. 


            Laboratory and instrumental investigations

            In cases of clinical suspicion of secondary form of CPPD disease a complex of laboratory tests is ordered with hyperparathyroidism being a primary consideration.


            Definite diagnosis is established on the basis of visualization of CPPD crystals via polarizing microscopy. Calcium deposits in articular cartilage are demonstrated on joint X-rays and via musculoskeletal ultrasonography.


             The treatment of pseudogout includes NSAIDs, colchicine, intraarticular corticosteroids. In in cases with degenerative joint changes associated with CPPD crystals, the physiotherapy plays a crucial role.


                                                                                              Dr Sevdalina Lambova, MD, PhD