Steroids and the skeleton.

Abstract

Harvey Cushing in 1932 first described the syndrome of obesity, hypertension, weakness, and depression of sexual function which has since become classically designated by his name. The condition was attributed by him to overproduction of pituitary adrenocorticotrophic hormone in association with the presence of a basophil adenoma. Although he postulated that the consequent stimulation of the adrenal cortex resulted in endogenous overproduction of the adrenocortical steroids, it has since been shown, largely as a result of the work of Albright, Parson, and Bloomberg (1941), that the presence of such an adenoma is not essential for the development of the syndrome. Primary disease of the adrenal cortex itself, either simple hyperplasia or benign or malignant neoplasia, is the more common cause, without stimulus from the pituitary. The hormones responsible for the skeletal changes in this condition are cortisone and hydrocortisone. During the last decade, these substances and similar steroids have been made available for therapeutic use and a number of instances of iatrogenic disease have resulted from their employment. These untoward sequelae are relatively uncommon, and individual radiologists may not encounter personally all the varieties that may occur. That such therapy may result in fully developed Cushing's syndrome, with its principal skeletal manifestations of osteoporosis, pathological fractures, and abnormal callus formation, is now well recognised. Study of the literature, however, indicates that certain lesser changes may be observed, particularly in connection with intraarticular injections. Diminution of pain sense and suppression of inflammatory reaction as a result of a surfeit of these hormones, whether natural or therapeutic, may cause the diagnosis of such lesions to be delayed. Radiological Changes in the Skeleton in Cushing's Syndrome (a) Osteoporosis: The generalised increase of translucency affecting the bony structures in the majority of patients suffering from Cushing's syndrome results from inability to lay down the osteoid tissue or protein matrix, which is an essential preliminary to the formation of new bone. Such bone as is present is normally calcified. This condition, therefore, is a true example of osteoporosis. In a minority of patients, and in early cases, no radiological bone abnormality can be detected. When only minimal changes of osteoporosis are present, differentiation on radiological grounds from osteoporosis of other origin cannot be made. Cushing recognised osteoporosis as a fundamental feature of the syndrome and this observation was confirmed by Eisenhardt and Thompson (1939) and by Sussman and Copleman (1942). The condition is usually first visible in the spine, where a fine, vertical linear striation becomes apparent, with consequent prominence of the vertebral plates. The skull, ribs, and pelvis become similarly affected.