Patients are prescribed phosphorus and calcium preparations, vitamin complexes and agents for stimulating regeneration (ATP, vitreous body, etc.).
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Aldactone drug methods. Radon baths provide a good effect. UHF, ultrasound and diathermic currents are used among other physiotherapeutic methods. Showing massage and regular exercise therapy. Since Kashin-Beck disease is rarely accompanied by inflammation and intense pain, drugs from the NSAID group are not used. Recommended sanatorium treatment in specialized sanatoriums. Operations are carried out at II and III stages of the disease. The aim of the interventions is to eliminate contractures and other movement obstructions. Depending on the nature and severity of pathological changes, the following are performed:
Removal of intraarticular bodies. It is indicated in the presence of articular mice that are pinched between the surfaces of the joint, causing blockades.
Usually performed using arthroscopic equipment. Redressation. Violent rupture of spironolactone pills tissue of the capsule to increase the range of motion. It is carried out under general anesthesia. It can be performed in addition to the removal of intra-articular bodies or independently. In the latter case, incisions are not required. Arthroplasty. It is recommended for pronounced changes in the articular surfaces that create obstacles to movement.
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It includes the removal of Aldactone tissues, the modeling of the articular ends of the bones and the placement of a pad from the patient's soft tissues between them, which prevents fusion. Endoprosthetics. It is the most effective technique for gross violations of the function of the joint. Allows you to restore range of motion and ability to work. Most often, prostheses are installed for the knee and hip joints, less often for the joints of the upper limbs.
In the postoperative period, therapeutic exercises are prescribed to prevent contractures and muscle atrophy. Apply massage, physiotherapy, multivitamins, mineral preparations. The prognosis is determined by the degree of Kashin-Beck disease. At the initial stage, complete recovery can be achieved in 30% of patients, in other cases, stabilization of the process is observed. At subsequent stages, recovery is impossible due to the presence of spironolactone organic changes, however, treatment can prevent the progression of the disease, maintain working capacity, or achieve a significant improvement in functionality.
- Kashin Beck's disease causes, symptoms, methods of treatment and prevention.
- Kashin Beck's disease is a degenerative disease of the musculoskeletal system, which develops due to a primary violation of the processes of growth of tubular bones and ossification.
- Failure in the body leads to joint deformity and osteophytosis. Some doctors consider Kashin Beck's disease to be deforming osteoarthritis.
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Preventive measures are complex, including soil cultivation, feeding farm animals with mineralized additives, delivery of aldactone pills products and water with a balanced content of minerals to endemic regions. Regular examinations of children are of great importance for the timely detection and treatment of the disease. Children, young people and pregnant women are prescribed preventive courses of vitamins and minerals.
The disease affects children and adolescents at the age of 6-14, that is, during the period of rapid bone growth. In children under 4 years of age, the disease does not occur, and people over 25 are extremely rare. Diagnosis and treatment of the disease are carried out by a pediatrician and a rheumatologist.
The exact causes of the disease have not been established, but doctors put forward several theories: mineral theory says that the disease develops due to an unbalanced content of calcium and trace elements in the body, an excess of strontium, iron and manganese in water and soil in the region of residence; hyposelenism hypothesis suggests that the main cause of the disease is a lack of selenium in soil and water.
The role of a viral or bacterial infection and vitamin A metabolism disorders are unlikely. The presence of familial cases indicates the possible involvement of hereditary factors. Inheritance is presumed to be autosomal recessive.
Tappeiner et al. (1969) believe that the main pathogenesis is the rapid and premature keratinization of cells, which can begin already in the lower rows of the styloid layer. Thus, the boundary between normal and keratinized cells shifts downward, to the basal layer, whose cells can also be involved in this process. At this point, even a minimal mechanical impact is enough for the horny masses to penetrate into the dermis.
The lesions are usually multiple, consisting of hyperkeratotic papules with a distinct follicular tendency. At first they are small, with a pinhead, gradually increase in size and reach a size of 1 cm or more. Papules are greyish, brownish red or yellowish in color. The coloration is more intense along the periphery of the papules.
In the center of them is a hyperkeratotic plug, the size of which increases as the elements grow.
If the layers of horny masses are more or less significant, the surface of the papules may become verrucous. After removal of the horny plugs, a slightly moist or bleeding crater-like depression is found. When the rash merges, sharply defined, often warty plaques of uneven outlines develop, sometimes located in a strip-like manner, mostly in the folds (popliteal, ulnar). The rashes are in different stages of development: along with small ones that have just appeared, there are also large lesions, some of which are already regressing. The Koebner phenomenon can be observed.
In the subcutaneous adipose tissue - cell infiltration, the appearance of acid mucopolysaccharides, a decrease in the number of elastic fibers.
The etiology is unknown. The genetic nature of dermatosis is assumed, great importance is also attached to a violation of the metabolism of vitamin A, disorders of carbohydrate metabolism. 1 Histopathology 2 Clinical picture 3 Diagnosis 4 Treatment.
The differential diagnosis is carried out with lichen planus verruciformis, Devergy's pilaris pilaris, Darier's follicular dyskeratosis, Mibelli's porokeratosis, Flegel's persistent lenticular hyperkeratosis, Miescher-Lutz's serpiginous perforating elastosis, follicular psoriasis, Mibelli's angiokeratosis.
It is characteristic and has diagnostic significance: acanthosis, pronounced follicular hyperkeratosis, horny plugs with parakeratosis, with basophilic cell detritus, penetration into the dermis of horny masses, granulomatous reaction of lymphocytes, epithelioid cells, giant cells of foreign bodies.
Tappeiner et al., who analyzed 28 published cases of Kirle's disease, write that no one observed a complete recovery. Combinations with the presence in patients with diabetes mellitus, functional disorders of the liver, kidneys, doubling of the renal pelvis and ureter are described.
The disease usually develops in adults, after 30 years, but adolescents and children can get sick. It proceeds for a long time, individual rashes can regress after 6-8 weeks from the moment of occurrence without a trace or leaving pigmented scars, but new ones appear to replace them.
The general condition of patients does not suffer, the disease does not cause subjective disorders. There are publications on the defeat of the skin of the face, but this localization, apparently, belongs to the category of rare, like the scalp.
The process can be located on any part of the skin, be common, but more often local, with preferential localization in the region of the legs, buttocks, and forearms. There are no rashes on the palms and soles, or this is considered a rarity.