Microcrystalline arthritis

Microcrystalline arthritis is a group of joint diseases caused by the deposition of microcrystals of different composition in them. These include diseases with a fundamentally different etiology and pathogenesis. But they all have one thing in common - the arisen arthritis of one or a few joints, which occurs in the form of attacks. Most often, microcrystalline arthritis is caused by crystals of urate (gout) and calcium pyrophosphate (pyrophosphate arthropathy). A great, if not decisive, significance in the diagnosis of these diseases is the detection of the corresponding crystals in the tissues of the joints (more often in the synovial fluid) by means of polarization microscopy.

Arthropathy pyrophosphate is a disease of deposition of calcium pyrophosphate crystals.

The etiology is unclear. There are known genetic forms of the disease, cases when pyrophosphate arthropathy develops as a bottom from manifestations of such diseases as hemochromatosis, Westphalian disease-Wilson-Konovalov's disease, hyperparathyroidism, etc. But more often no prerequisites to the development of the disease are found. In contrast to the gout of any systemic metabolic disorders of inorganic phosphate or calcium, an increase in these levels in the blood with pyrophosphate arthropathy is not expected. It is suggested that there are local disturbances in the metabolism of pyrophosphate and calcium in the tissues of the joints. Crystals of calcium pyrophosphate are deposited first of all in the cartilage. When the crystals hit the joint cavity, inflammation develops.

Symptoms, course. The disease can proceed as a recurrent mono- or oligoarthritis. The knee joint is most often affected. This form of the disease resembles gout and is therefore called "pseudogout." More often, pyrophosphate arthropathy proceeds differently, reminiscent of osteoarthritis. Typical is moderate, but quite constant pain in the knee, wrist, ankle, and also other joints, whose lesion is atypical for osteoarthritis. Periodically the pain in these joints increases, but never reaches the gouty force. On examination, signs of mild inflammation of the joints may be revealed. The diagnosis becomes obvious during radiography. For pyrophosphate arthropathy, the presence of chondrocalcinosis is almost pathognomonic, calcification of the meniscus (in the region of the knee, wrist joints, lone articulation), as well as articular cartilage. In addition, there are signs characteristic of osteoarthritis. This form of the disease is called "pseudo-osteoarthrosis". Other clinical forms are also known, for example a form resembling rheumatoid arthritis. In this case, persistent inflammation of the small joints of the hands is noted.

Treatment is symptomatic. When developing acute arthritis, non-steroidal anti-inflammatory drugs are used.

Gout is a disease of the deposition of urate crystals in the joints and other tissues, arising from disorders of the metabolism of purine bases and uric acid.

Etiology, pathogenesis. Violations of the metabolism of purine bases (mainly occurring in nucleic acids) arise mainly due to congenital or acquired weakening of the activity of enzymes that regulate this process. Obligatory gout increases the level of uric acid in the blood (hyperuricemia) occurs either due to increased disintegration of purine bases, or because of decreased urinary excretion of uric acid by the kidneys. There can be both these reasons. Diseases or situations are known where gout is only a symptom: for example, with myelogenous leukemia, congenital and acquired heart diseases, with cyanosis, lead toxicity, the use of diuretics, riboxin, etc. Hyperuricemia promotes the accumulation and deposition in various tissues, especially in cartilage Joints, uric acid salts of skurates) in the form of microcrystals. The periodic entry of crystals into the synovial cavity of the joints leads to the development of an acute inflammatory reaction. Hyperuricemia reduces the buffer properties of urine, which contributes to the deposition of microcrystals in the interstitial tissue of the kidneys, as well as in the urinary tract in the form of stones.

Symptoms, course. The disease develops almost exclusively in middle-aged men. Usually there are recurrent acute mono- or oligoarthritis of the joints of the lower limbs with frequent involvement of 1 metatarsophalangeal joint (approximately in 75% of patients), joints of the metatarsal, ankle and knee joints. Less common arthritis of small joints of hands, wrist and elbow joints. Gouty arthritis has characteristic features: it often develops at night, the intensity of pain grows very quickly and within a few hours reaches a maximum. The pain is usually very severe, movements in the joint become impossible, there is hyperemia of the skin and hyperthermia of the tissues over the joint. Body temperature may increase. Independently or under the influence of treatment, arthritis subsides in a few days, leaving no residual changes in most cases. The factors that trigger the onset of an attack of gouty arthritis include: excessive consumption of foods rich in purine bases, mainly meat, alcohol kurtosis, surgery, trauma, taking diuretics, riboxin. In rare cases, chronic gouty polyarthritis with periodic enhancement and weakening of inflammatory phenomena can be observed.

In 15 to 20% of patients with gout, urolithiasis occurs (a stroke of kidney colic can sometimes be the first sign of gout), as well as interstitial nephritis. There is a tendency to deposition of uric acid crystals in the thickness of the skin more often over the joints (elbows, knees) or in the cartilage of the auricles, where there are painless nodules of different sizes - tofusi.

When gout is constantly observed an increase in the level of uric acid in the blood, which is of diagnostic significance.

Treatment. In the treatment of acute gouty arthritis, non-steroidal anti-inflammatory drugs are used at maximum or even elevated daily doses: voltaren (150-200 mg / day), indomethacin (150-200 mg / day), butadione (0.6 g / day). With frequent relapsing arthritis, kidney damage, urolithiasis, tofus, permanent (lifelong) use of allopurinol (milurite) in a daily dose of 0.3-0.4 g is indicated for the normalization of uric acid in the blood. In the absence of gouty kidney damage, uricosuric agents are also used: anthuran (daily dose 0.2-0.6 g) or etamid (courses of 1 week at a daily dose of 2.8 g with interruptions of 1 to 2 weeks). A certain value for gout is dietary restrictions: the exclusion of alcohol, the reduction in the consumption of foods containing a large number of purine bases (meat, fish and products from them).