Apituitarism

APITUITARISM, the absence of the pituitary gland (glandula pituitaria, hypophysis cerebri, pituitary body), denotes in clinical pathology phenomena associated with the loss or suppression of pituitary function. This includes: pituitary dwarfism, pituitary obesity, phenomena of dystrophia adiposogenitalis, pituitary cachexia, and diabetes insipidus. The assertion that existed until recently regarding the impossibility of living without the pituitary gland (the doctrine of pituitary cachexia, or “Simmonds' disease”) has been subjected to criticism. At the present time, thanks to the works of Aschner, Camus and Roussy, as well as the Russian school, it can be considered firmly established that experimental apituitarism (as a result of the complete removal of the pituitary gland) is fully compatible with life. Dogs operated on at the age of two months can live for years without a pituitary gland without showing any signs of cachexia. The inevitable consequences of experimental apituitarism are: growth retardation, obesity, and inhibition of sexual development. Experimental pituitary dwarfism is characterized by a lag of 2-3 times the size of normal siblings serving as controls, proportional development of the skeleton, and premature ossification of the epiphyses. Manifestations of higher nervous activity remain infantile for a long time (pituitary infantilism). Obesity in experimental apituitarism reaches enormous proportions. Fat deposits are often so great that, given the presence of soft long hair usually found in hypophysectomized dogs, and with proportional development of the limbs, the abdomen of the animal in a standing position seems to reach the floor. The cause of obesity is, apparently, a disturbance of oxidative processes and profound changes in carbohydrate metabolism in apituitarism. The short-term hyperglycemia and glycosuria that occur after the removal of the pituitary (as a consequence of the inevitable irritation of the tuber cinereum during the operation) are replaced within a day or two by hypoglycemia and an increase in the limit of carbohydrate assimilation. About two months after the operation, by the time obesity develops, the sugar content in the blood becomes normal; however, the ability of the liver to retain sugar absorbed from the intestine falls below the norm. A major dispute between clinicians and experimentalists is caused by the following question: is diabetes insipidus a consequence of apituitarism (or hypopituitarism)? Experimental pathology resolves this question in the negative. Removal of the pituitary, both complete and partial, does not cause any prolonged polyuria if there was no damage to the tuber cinereum during the operation, in which the vasomotor centers of the kidneys are located. This is in some contradiction with the possibility of symptomatic treatment of diabetes insipidus with pituitary extract (pituitrin). However, there is no more basis to conclude from this that diabetes insipidus is a consequence of the suppression of pituitary function than (according to the witty remark of Camus and Roussy) to claim that, because pituitrin prepared from the pituitary of a bull causes contraction of the pregnant uterus, it performs the same functions in the body of the bull. Clinical phenomena of apituitarism arise as a result of damage to the pituitary gland by neoplasms or inflammatory processes. With these lesions, it is very difficult to exclude their influence on nearby vegetative nerve centers that regulate metabolism in the body. Therefore, it is not always possible to decide whether one or another of the clinical syndromes of apituitarism is caused by the loss of internal secretion of the pituitary or by disturbances of vegetative innervation.