Brief clinical and laboratory observation

Progressive fibrosis of the deltoid muscles

Many drugs used in various branches of medicine, as well as alcohol and other substances of addiction, produce muscular symptoms, either through a direct effect on the skeletal muscles or by interfering with neuromuscular transmission or peripheral nerve function. A variety of chemicals, biological toxins, and venoms are also myotoxic. The mechanisms of action of drugs and toxins on muscle are diverse. Some have a direct toxic effect, either locally after intramuscular injection, or more widely after systemic administration or absorption of the agent. In case of drugs that are not inherently myotoxic, muscle damage may be secondary to an immunological process, to hypokalaemia, or to muscle compression and ischemia during periods of unconsciousness and immobility following a drug overdose. A change in ionic conductance and excitability of the plasma membrane is the basis for the myotonia induced by a number of drugs and chemicals, and for the muscular weakness and hypotonia that occurs in patients who become severely hypokalaemic or hyperkalaemic while taking diuretics or certain other drugs. Some drugs interfere with muscle protein synthesis and degradation. This occurs particularly with the natural and synthetic glucocorticoids that inhibit the synthesis of muscle specific proteins as well as increasing protein degradation. Chloroquine, amiodarone, and a number of other amphiphilic cationic compounds cause a myopathy characterized by autophagic degeneration and phospholipid accumulation in muscle. Various drug-induced disorders are discussed such as myalgia and muscle cramps, myotonia, necrotizing myopathies, acute rhabdomyolysis, mitochondrial myopathy, dyskalemic myopathy, dyskalemic myopathy, autophagic myopathies, and alcoholic myopathy.

We performed a radiographic survey on 12 shoulders in 11 patients with a contracture of the deltoid present since childhood (juvenile) but left untreated until adulthood and on 14 shoulders in 10 patients with the same disorder first developed in adulthood (adult type). The greater tuberosity was located either under or near the acromion in all but 1 shoulder. Flattening of the humeral head, a high-positioned greater tuberosity, posterior rotation and vertical disposition of the acromion, inferior angulation of the lateral clavicle, and anterosuperior subluxation of the humeral head were noted in 58%, 33%, 75%, 67%, and 8% of the juvenile cases, respectively. Scoliosis and narrowing of the thoracic cage were each detected in 36% of the patients with juvenile deltoid contracture. Six of the juvenile cases were treated surgically and followed-up for a lengthy period. In these cases, however, the abnormalities persisted, except for subluxation of the humeral head and abnormal proximity of the acromion and greater tuberosity. In the adult-type cases no abnormalities were observed except for scoliosis in 4 patients and anterosuperior subluxation of the humeral head in 1 shoulder. We conclude that treatment by surgical intervention should be performed at an age when spontaneous correction of the bone deformity can prevent future development of secondary arthrosis.

Myositis in man may be divided into infectious and non-infectious forms. The myopathologist more often deals with the latter forms which comprise dermatomyositis/polymyositis, inclusion body myositis, mixed connective tissue disease/collagenoses, and granulomatous myopathies. Modern morphological techniques as enzyme-histochemistry, electron microscopy, immunohistology, and morphometry are of different value in various forms of myositis, but are often indispensable techniques in up-to-date diagnostic work up of a myositis.