The Bone Changes in Primary Hypogonadism

Abstract

THIS report is based on observations made on nine cases of primary prepuberal hypogonadism. By this term we refer to that condition in which puberty has not taken place (absence of secondary sex characteristics), in which there is every evidence clinically of normal pituitary function, and in which there is no evidence of other endocrine disorders. When the usual and normal physiologic changes caused by a particular gland fail to appear, it is, therefore, natural to assume that the gland is deficient. It must not be forgotten, however, that such changes are produced not only by the activity of the hormone in question but also by the ability of the end organ to react to that hormone. Furthermore, if there is evidence of activity of a certain gland, as determined by biological tests which even now are relatively crude, the product of that gland may fail to produce a reaction in the end organ because the hormone may be present in an inactive form. A clear conception of these principles should simplify diagnosis of endocrine disorders. It is our belief that most endocrine disorders are primarily uniglandular in origin, and that many of the so-called pluriglandular syndromes will eventually be regarded as originating in one endocrine gland. Deficient sex secretion causes different clinical pictures, depending on the time of life at which it occurs. Excluding pituitary disease, hypogonadism may be classified in relation to time of life, as follows: (1) Loss or failure of sex hormone to be secreted in infancy or childhood up to the usual time of puberty. This failure is followed by typical prepuberal or primary hypogonadism. (2) Loss or failure of gonadal secretion to act shortly after puberty. This may result in partial development of secondary sex characteristics and epiphyseal closure, although they may be delayed (Case 5). (3) Loss of gonadal secretions after epiphyseal closure. In this case there may be slight regression of sex characteristics or they may remain unchanged (Case 6, Fig. 1). The gain in weight so often ascribed to the termination of sex secretion, especially at the menopause, may be due to the loss of the special effect of sex hormone which produces that dynamic or energizing difference between a sexed and an unsexed person. Apparently the true sex hormones of the gonads bring about epiphyseal closure, at least this phenomenon is closely associated with sex maturity. Longitudinal growth at the usual time of puberty cannot be attributed to sex hormones since it continues when these hormones are absent. Thus, open epiphyses are present in true primary hypogonadism and growth continues. This combination is practically pathognomonic of primary hypogonadism, providing growth does not proceed at an abnormal rate. Growth of long bones continues, resulting in time in disproportionate measurements, the span equalling and occasionally markedly exceeding the height.