Polymyositis is an infectious-allergic muscle lesion where, along with inflammatory reactions, degenerative changes develop. According to most authors, polymyositis is a polyetiological disease, but with a single pathogenesis, which is based on allergic reactions with the formation of antibodies to muscle tissue. If antibodies are produced to ectoderm, then a more severe form of the disease develops – dermatomyositis. The manifestation of allergic reactions is an increase in the titer of antistreptolysin and gamma globulins, and an increase in blood fibrinogen and DPA are indicators of tissue destruction. Various infections, in particular sore throat, as well as injuries, massive insolation, abuse of certain medications, such as sulfonamides and antibiotics, can be factors that lead to hypersensitivity or to sensitization of immune reactions. Contributing factors include endocrine shifts; for example, during pregnancy, childbirth, menopause.
Clinic of polymyositis
Polymyositis is more common in two age periods – 5-15 years and 50-60 years. Women suffer 2 times more often than men. The disease can begin acutely, sometimes with an increase in temperature, local or diffuse muscle pains appear, sharp muscle weakness quickly develops, up to tetraplegia . In such cases, visceral symptoms may be observed in the form of pneumonia, damage to the muscles of the heart, and sometimes the kidneys. The course is severe, with severe disability and even death.
In other cases, polymyositis can occur very mildly, without common symptoms and without clinical manifestations of damage to internal organs. Patients have pain, usually moderate, and muscle weakness with localization in the proximal arms and legs and muscles of the shoulder and pelvic girdle. Paresis may be accompanied by moderate muscle hypotrophy, decreased tendon reflexes. Such symptoms are extremely reminiscent of the clinical picture of muscular dystrophy type Erba . With severe forms of polymyositis , seals are palpated in the muscles, sometimes tension and even pronounced induction develop . In rare cases, some difficulty swallowing and hypotension of the muscles of the esophagus develop.
Polymyositis can be part of the so-called dry Sjogren’s syndrome , which is characterized by a sharp decrease in the secretion of the lacrimal, salivary, gastric and intestinal glands, polyarthritis, secondary manifestations in the form of keratitis and swelling of the parotid glands. Sometimes polymyositis syndrome is observed with carcinoma.
Additional studies in severe forms of polymyositis reveal blood changes (leukocytosis, neutrophilia , an increase in ESR), creatine-creatinine metabolism disorders (creatine in the urine, decreased creatinine excretion ). Hyperfermentemia is often noted , especially due to creatine phosphokinase , aldolases and transaminases . The change in protein fractions is characterized by an increase in alpha-2 and gamma globulins. In mild cases, biochemical shifts may not occur.
Specific changes are found on EMG, especially when using needle electrodes: short, low polyphase potentials of motor units, potentials of fibrillation and irrigation to insert an electrode, and bizarre high-frequency discharges are noted. A pathomorphological study of a muscle biopsy reveals necrosis, phagocytosis, atrophy and degeneration of muscle fibers in combination with clear inflammatory infiltrates and vasculitis .
The differential diagnosis is carried out with sporadic forms of progressive muscular dystrophy, spinal amyotrophy , with a muscular form of sarcoidosis , type V glycogenosis ( MacArdl disease ), as well as with endocrine myopathies (with hyperparathyroidism , thyrotoxicosis, menopause – Nevine syndrome ). Of key importance in the diagnosis (in addition to the clinical picture) is a muscle biopsy with the identification of characteristic changes and an electromyographic study.
Polymyositis treatment
In mild forms of myositis, desensitizing therapy, butadion , delagil in combination with ascorbic acid, vitamin B is prescribed . In severe forms with clear biochemical shifts and especially when combined with damage to internal organs, steroid hormone treatment is indicated. The use of prednisone is preferable, as other drugs ( triamcinolone , dexamethasone ) can aggravate muscle damage (steroid myopathy).