BACKGROUND: The discovery of osteoporosis in a male requires a careful search for a cause. OBJECTIVE: To evaluate etiologic factors in male osteoporosis. PATIENTS AND METHODS: Males admitted to our department for osteoporosis were included if they had a nontrauma-related vertebral or peripheral fracture and/or a spinal or femoral neck bone mineral density value 2.5 standard deviations or more below the mean in young subjects. The study was retrospective from 1990 to 1995 and prospective from 1996 to 1997. During the prospective part of the study, each subject underwent a standardized battery of laboratory tests including renal tubular function parameters. Causes identified during these two periods were compared. RESULTS: Of the 160 patients included in the study, 28.1% had idiopathic osteoporosis, 22.5% had alcoholic osteoporosis, 19.4% had glucocorticoid-induced osteoporosis, 12.5% had osteoporosis due to moderate idiopathic proximal tubule dysfunction, and 8.8% had senile osteoporosis. The proportion of patients with idiopathic osteoporosis was 30% (23/76) during the retrospective part of the study and 26% (21/84) during the prospective part (nonsignificant difference). Moderate idiopathic proximal tubule dysfunction was found in 2.6% (2/76) and 21.4% (18/84) of patients during these two parts of the study, respectively, a difference ascribable to the routine determination of tubule function parameters during the second part of the study. CONCLUSION: An exhaustive search for a cause decreases the proportion of male osteoporosis cases that remain idiopathic. In our study, only 28% of cases were classified as idiopathic, a term that probably indicates involvement of multiple interrelated factors.

Adrenal Cortex Hormones↗

PubMedDate not supplied

Axial osteomalacia with sacroiliitis and moderate phosphate diabetes: report of a case.

We report a new case of axial osteomalacia diagnosed in a 51-year-old white Caucasian male, made particular by its association with sacroiliitis, positive HLA-B27 antigen, and also moderate phosphate diabetes responsible for a decreased appendicular bone mass. The diagnosis was suspected when X-ray evaluation showed increased density and coarse trabeculation mainly involving the pelvis and spine. Dual energy X-ray absorptiometry confirmed the elevated bone density at the lumbar spine (T score: +1.92) contrasting with a decreased bone mass at the femoral neck (T score: -2.33). The diagnosis was confirmed by histomorphometry of the iliac crest showing marked thickening of the cortices (2190 microns +/- 0.574, N = 780 +/- 40) and an increased trabecular bone volume (33.24%, N = 14 +/- 3). Osteoid parameters were also markedly increased with an osteoid volume of 2.1% (N = 1.2 +/- 0.5) and a mean osteoid thickness of 28.7 microns (N = 13 +/- 2.5), with a normal bone fluoride content (0.082%, N < 0.10). Bone resorption as assessed on bone biopsy and by the measurement of markers of bone remodeling (serum procollagen type I C-terminal telopeptide and 24 hr urinary cross-laps to creatinine ratio) was increased. This latter finding was not necessarily due to axial osteomalacia and could be the consequence of moderate phosphate diabetes. The patient was treated with calcitriol which was promptly discontinued due to gastrointestinal symptoms and replaced by calcidiol without any significant effect on the low back pain.

Absorptiometry, Photon↗

PubMedDate not supplied

Factors influencing bone loss in rheumatoid arthritis: a longitudinal study.

OBJECTIVES: To assess the occurrence of bone loss in rheumatoid arthritis (RA) and to determine the factors influencing bone loss (particularly the usefulness of bone turnover markers) over an 18-month period. METHODS: A total of 51 patients were studied, 6 men and 45 females (of whom 35 were menopausal). Their mean age was 56 +/- 10 years and the mean RA duration was 12 +/- 10 years. Twenty-eight (55%) were receiving corticosteroids (10 mg/day for a mean duration of 6 +/- 5 years). Several clinical and biological parameters reflecting disease activity or severity were recorded both at the 0 and 18-month investigations. Bone turnover was assessed at baseline by measuring the serum levels of 4 biological markers. Three of them reflected bone formation, i.e., procollagen type I C-terminal propepeptide (PICP), procollagen type I N-terminal propeptide (PINP) and osteocalcin (OC). The fourth, procollagen type I-C terminal telopeptide (ICTP), reflected bone resorption. Bone mineral density (BMD) was measured by dual energy X-ray absorptiometry both at the lumbar spine (LS) and femoral neck (FN) at baseline and 18 months later. RESULTS: Bone loss occurred both at the LS: 2.1%, [95% CI: 0.8%-3.4%, P < 0.005] and femoral neck: 3.1%, [95% CI: 1.1%-5.1%, P < 0.005]. Bone loss was markedly increased for postmenopausal women at the FN: 5.3% [95% CI: 2.9%-7.6%, P < 0.005]. Bone loss was not statistically significantly different between users and non-users of steroids. Bone loss at the LS was significantly correlated with both osteocalcin (r = 0.51, P < 0.01) and ICTP levels (r = 0.32, P < 0.05). FN bone loss was correlated with the osteocalcin level only (r = 0.34, P < 0.05). Fast losers (bone loss at the LS above the median) had higher OC (P < 0.01) and ESR (P < 0.05) levels at baseline as compared with slow losers (bone loss at the LS below the median). CONCLUSION: Bone loss occurs in RA particularly at the FN and seems to be influenced by increased bone turnover and high levels of inflammation.

Adrenal Cortex Hormones↗