Bone tissue in patients with hyperprolactinemic hypogonadism

Sixteen women with hyperprolactinemia were examined for Ca metabolism, osseous metabolism, mineral saturation of bone tissue in the thoracic portion of the spine and radius. Lowered mineral saturation of the thoracic vertebrae was detected in 69% of the examinees, that of the distal segment of the r...

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Published inProblemy ėndokrinologii Vol. 38; no. 6; p. 17
Main Authors Rozhinskaia, L Ia, Marova, E I, Dzeranova, L K, Rassokhin, B M, Purtova, G S, Goncharov, N P, Mishchenko, B P, Ilovaĭskaia, I A
Format Journal Article
LanguageRussian
Published Russia (Federation) 01.11.1992
Subjects
Adolescent
Adult
Bone and Bones - metabolism
Bone Density - physiology
Bone Diseases, Metabolic - etiology
Calcium - metabolism
Estradiol - blood
Female
Humans
Hyperprolactinemia - complications
Hyperprolactinemia - metabolism
Hyperprolactinemia - physiopathology
Hypogonadism - etiology
Hypogonadism - metabolism
Hypogonadism - physiopathology
Osteoblasts - physiology
Osteocalcin - blood
Osteoporosis - etiology
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Summary:Sixteen women with hyperprolactinemia were examined for Ca metabolism, osseous metabolism, mineral saturation of bone tissue in the thoracic portion of the spine and radius. Lowered mineral saturation of the thoracic vertebrae was detected in 69% of the examinees, that of the distal segment of the radius in 44%. Reduction of the mineral saturation of the spine was in negative correlation with the blood prolactin level and length of amenorrhea. No changes in the bone resorption biochemistry or Ca metabolism were detected. A marked reduction of blood osteocalcin level that reflects osteoblast function was detected, its blood concentration being in negative correlation with prolactin level. No relationships between mineral saturation of bone tissue, prolactin, and osteocalcin, on the one hand, and blood estradiol level, on the other, were observed. These data suggest that osteopathy in hyperprolactinemic hypogonadism is due to reduced bone formation and not to reduced estradiol production.
ISSN:0375-9660