Osteoporosis in hypogonadal men: Role of decreased plasma 1,25-dihydroxyvitamin D, calcium malabsorption, and low bone formation

R. M. Francis, Munro Peacock, J. E. Aaron, P. L. Selby, G. A. Taylor, J. Thompson, D. H. Marshall, A. Horsman

Research output: Contribution to journalArticle

182 Citations (Scopus)

Abstract

To investigate the pathogenesis of osteoporosis in male hypogonadism we have investigated a heterogeneous group of 13 men with hypogonadism: 7 men (median age 60, range 31-79) with two or more vertebral crush fractures and 6 men (median age 61.5, range 28-76) without vertebral fractures. The group with crush fractures had trabecular and cortical osteoporosis as assessed by Singh grade, iliac crest trabecular bone volume, and metacarpal cortical area/total area. This was accompanied by an altered trabecular architecture with a reduction in number of trabeculae but no change in trabecular width, which contrasts with age-related bone loss in men where there is no reduction in trabecular number but thinning of trabeculae. The fracture group had significantly lower plasma 1,25-dihydroxyvitamin D [1,25(OH)2D] concentrations than the nonfracture group, and this was associated with malabsorption of calcium. Irrespective of the presence or absence of osteoporosis, treatment with testosterone led to a significant increase in total and free plasma 1,25(OH)2D and an improvement in calcium absorption measured with radiocalcium and by balance techniques. In addition, urine biochemistry, metabolic balance studies, and bone biopsy suggest that skeletal retention of calcium and bone formation are increased by testosterone treatment. We conclude that male hypogonadism causes both cortical and trabecular osteoporosis and altered trabecular architecture. A major risk factor for the development of osteoporosis is reduction in plasma 1,25(OH)2D, leading to malabsorption of calcium and reduced bone formation.

Original languageEnglish (US)
Pages (from-to)261-268
Number of pages8
JournalBone
Volume7
Issue number4
DOIs
StatePublished - 1986
Externally publishedYes

Fingerprint

Osteogenesis
Osteoporosis
Calcium
Eunuchism
Testosterone
Metacarpal Bones
Hypogonadism
Biochemistry
1,25-dihydroxyvitamin D
Urine
Biopsy
Bone and Bones
Therapeutics

Keywords

  • Bone Formation
  • Hypogonadal Men
  • Osteoporosis Calcium Maiabsorption
  • Plasma 1,25(OH) Vitamin D

ASJC Scopus subject areas

  • Physiology
  • Hematology

Cite this

Osteoporosis in hypogonadal men : Role of decreased plasma 1,25-dihydroxyvitamin D, calcium malabsorption, and low bone formation. / Francis, R. M.; Peacock, Munro; Aaron, J. E.; Selby, P. L.; Taylor, G. A.; Thompson, J.; Marshall, D. H.; Horsman, A.

In: Bone, Vol. 7, No. 4, 1986, p. 261-268.

Research output: Contribution to journalArticle

Francis, RM, Peacock, M, Aaron, JE, Selby, PL, Taylor, GA, Thompson, J, Marshall, DH & Horsman, A 1986, 'Osteoporosis in hypogonadal men: Role of decreased plasma 1,25-dihydroxyvitamin D, calcium malabsorption, and low bone formation', Bone, vol. 7, no. 4, pp. 261-268. https://doi.org/10.1016/8756-3282(86)90205-X
Francis, R. M. ; Peacock, Munro ; Aaron, J. E. ; Selby, P. L. ; Taylor, G. A. ; Thompson, J. ; Marshall, D. H. ; Horsman, A. / Osteoporosis in hypogonadal men : Role of decreased plasma 1,25-dihydroxyvitamin D, calcium malabsorption, and low bone formation. In: Bone. 1986 ; Vol. 7, No. 4. pp. 261-268.
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AU - Aaron, J. E.

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AU - Marshall, D. H.

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N2 - To investigate the pathogenesis of osteoporosis in male hypogonadism we have investigated a heterogeneous group of 13 men with hypogonadism: 7 men (median age 60, range 31-79) with two or more vertebral crush fractures and 6 men (median age 61.5, range 28-76) without vertebral fractures. The group with crush fractures had trabecular and cortical osteoporosis as assessed by Singh grade, iliac crest trabecular bone volume, and metacarpal cortical area/total area. This was accompanied by an altered trabecular architecture with a reduction in number of trabeculae but no change in trabecular width, which contrasts with age-related bone loss in men where there is no reduction in trabecular number but thinning of trabeculae. The fracture group had significantly lower plasma 1,25-dihydroxyvitamin D [1,25(OH)2D] concentrations than the nonfracture group, and this was associated with malabsorption of calcium. Irrespective of the presence or absence of osteoporosis, treatment with testosterone led to a significant increase in total and free plasma 1,25(OH)2D and an improvement in calcium absorption measured with radiocalcium and by balance techniques. In addition, urine biochemistry, metabolic balance studies, and bone biopsy suggest that skeletal retention of calcium and bone formation are increased by testosterone treatment. We conclude that male hypogonadism causes both cortical and trabecular osteoporosis and altered trabecular architecture. A major risk factor for the development of osteoporosis is reduction in plasma 1,25(OH)2D, leading to malabsorption of calcium and reduced bone formation.

AB - To investigate the pathogenesis of osteoporosis in male hypogonadism we have investigated a heterogeneous group of 13 men with hypogonadism: 7 men (median age 60, range 31-79) with two or more vertebral crush fractures and 6 men (median age 61.5, range 28-76) without vertebral fractures. The group with crush fractures had trabecular and cortical osteoporosis as assessed by Singh grade, iliac crest trabecular bone volume, and metacarpal cortical area/total area. This was accompanied by an altered trabecular architecture with a reduction in number of trabeculae but no change in trabecular width, which contrasts with age-related bone loss in men where there is no reduction in trabecular number but thinning of trabeculae. The fracture group had significantly lower plasma 1,25-dihydroxyvitamin D [1,25(OH)2D] concentrations than the nonfracture group, and this was associated with malabsorption of calcium. Irrespective of the presence or absence of osteoporosis, treatment with testosterone led to a significant increase in total and free plasma 1,25(OH)2D and an improvement in calcium absorption measured with radiocalcium and by balance techniques. In addition, urine biochemistry, metabolic balance studies, and bone biopsy suggest that skeletal retention of calcium and bone formation are increased by testosterone treatment. We conclude that male hypogonadism causes both cortical and trabecular osteoporosis and altered trabecular architecture. A major risk factor for the development of osteoporosis is reduction in plasma 1,25(OH)2D, leading to malabsorption of calcium and reduced bone formation.

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