NORMAL secretion of milk in humans and animals is controlled by the well-balanced action of hormones from the pituitary, the adrenals, the ovaries and the thyroid gland. Though many details in our understanding of this process are still lacking, it appears that the anterior pituitary hormone production is essential in the initiation and maintenance of normal lactation. Even less well known is the mechanism of non-puerperal galactorrhoea which has been named “one of the riddles of endocrinology” (Gordan, 1958). Any milk-like secretion, either spontaneous or after pressure on the nipples outside the normal period of lactation, is termed galactorrhoea. Such milk secretion is usually a sign of endocrine disturbance. It is found in the ChiariFrommel syndrome, in tumours of the pituitary, after use of certain drugs which act on the central nervous system, following thorax operations, as well as due to various miscellaneous causes. The syndrome of Chiari-Frommel was first described by Chiari, Braun and Spaeth (1855) and again by Frommel (1882) who added a detailed description of this disease which consists of non-puerperal galactorrhoea, amenorrhoea and ovarian uterine atrophy. Argonz and del Castillo (1953) separated from this syndrome a group of women in whom galactorrhoea was not connected with pregnancy. This syndrome, as well as the ChiariFrommel syndrome, can occur in the presence or absence of signs of a pituitary tumour. In those cases in which no tumour is present, a functional disturbance in the pituitary-ovarian axis has to be incriminated as the cause for the disorder. It can, however, not be excluded that small adenomata are also present in these cases which do not cause an enlargement of the sella or give rise to other clinical signs of a pituitary tumour. The tumours found in the Chiari-Frommel and the Argonz-del Castillo syndrome are as a rule chromophobe adenomata of the pituitary (Forbes et al., 1954; Greenblatt et al., 1956). Though the elaboration of prolactin is attributed to the eosinophilic cells of the pituitary, it is very possible that chromophobe cells, too, which were described by Cushing (1934) as being preeosinophilics, have the power of prolactin secretion. On the other hand, it is claimed by others (Hirsch, 1959) that galactorrhoea is not necessarily the result of the excessive secretion of a lactogenic factor, but may rather be the result of the hypopituitary state itself. Not many cases of Chiari-Frommel syndrome have been described in the literature until lately, but it appears that this condition is not at all rare (Gordan, 1958). The appearance of the Chiari-Frommel syndrome in the post-lactation period has been explained as a continuation of a physiological situation (milk secretion, amenorrhoea and ovarian uterine atrophy-as it is found during the puerperium) which becomes pathological by its continuation beyond the usual time limit. This explanation does not, of course, hold for that group of patients with galactorrhoea that was separated from the syndrome by Argonz and del Castillo in whom the same clinical manifestations appeared without previous pregnancy. Not only chromophobe adenomata of the pituitary, but also eosinophilic adenomata which cause acromegaly or gigantism are sometimes accompanied by galactorrhoea (Putnam
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