Abstract
THE occurrence of familial and nonfamilial cases of hypogonadotrophic hypogonadism and hyposmia or anosmia (Kallman's syndrome) has been well documented1,2. Because the disease has been found only in humans, little is known about the site of the gonadotrophic lesion. Pathological examination of the pituitary glands of these patients has not revealed any abnormality3. No estimates of pituitary gonadotrophin content in patients with hypogonadotrophic hypogonadism are available, although patients who have normal amounts of circulating follicle stimulating hormone but who lack luteinizing hormone (LH)—the so-called “fertile eunuch syndrome”—have been described. In contradistinction to the Kallman syndrome, these (potentially) fertile patients have a normal sense of smell and testicular development with varying degrees of spermatogenesis4. Injections of gonadotrophic substances cause an appropriate gonadal response in patients with Kallman's syndrome5 and the lesion is considered to be central in origin6. Attempts to stimulate the release of gonadotrophin in these patients by the use of the antioestrogen clomiphene citrate have been unsuccessful7.
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NAFTOLIN, F., HARRIS, G. & BOBROW, M. Effect of Purified Luteinizing Hormone Releasing Factor on Normal and Hypogonadotrophic Anosmic Men. Nature 232, 496–497 (1971). https://doi.org/10.1038/232496a0
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DOI: https://doi.org/10.1038/232496a0
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