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PLASMA STEROID CONCENTRATIONS IN PATIENTS WITH HYPOPITUITARISM AND KALLMAN'S SYNDROME: EFFECTS OF TESTOSTERONE REPLACEMENT THERAPY
Author(s) -
SAGEL J.,
LEVINE J. H.,
MATHUR R. S.,
ROSEBROCK G.,
GONZALEZ J.,
VILLIER C. DE,
NAIR R. M. G.
Publication year - 1982
Publication title -
clinical endocrinology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.055
H-Index - 147
eISSN - 1365-2265
pISSN - 0300-0664
DOI - 10.1111/j.1365-2265.1982.tb01584.x
Subject(s) - endocrinology , medicine , hypopituitarism , dehydroepiandrosterone , androstenedione , pregnenolone , testosterone (patch) , hydrocortisone , hormone , androgen , steroid
SUMMARY To determine the adrenal contribution to plasma concentrations of steroids potentially derived from both the adrenal and the testes, plasma levels of pregnenolone (Δ 5 P), progesterone (P), dehydroepiandrosterone and its sulphate (DHA and DHAS) and androstenedione (Δ 4 A) were measured in four men with isolated gonadotrophin deficiency and anosmia (Kallman's syndrome). A comparison of these levels with those seen in ten patients with both adrenal and testicular failure (hypopituitarism) and in sixteen normal age‐matched men was made. As expected, the basal plasma levels of most steroids were low in patients with hypopituitarism. An exception was the normal Δ 5 P levels in most patients. In the patients with Kallman's syndrome both DHA and Δ 5 P were elevated whereas Δ 4 A and P were low. When expressed as ratios, Δ 5 P/P was increased in both groups. DHA/Δ 4 A was increased in Kallman's syndrome but not in hypopituitarism. Following ACTH infusion, no significant changes in these ratios were observed. To determine whether testosterone deficiency was in part responsible for the abnormal Δ 5 /Δ 4 ratios, three patients with hypopituitarism and two with Kallman's syndrome were treated for 3 months with intramuscular testosterone. A decrease in the DHA/Δ 4 A ratio was seen in all patients and a decrease in Δ 5 P/P in all but one patient. In most cases these changes were produced by a fall in the Δ 5 steroids as well as an increase in Δ 4 steroids. These findings suggest that a defect in the metabolism of Δ 5 steroids exists in patients with hypopituitarism and Kallman's syndrome. In hypopituitarism the defect involves the metabolism of Δ 5 P to both DHA and P. In Kallman's syndrome only the metabolism of Δ 5 P to P is defective. Testosterone therapy alone or in combination with other appropriate hormonal replacement increases the metabolism of Δ 5 to Δ 4 steroids.