The natural history of kyphosis in postmenopausal women.

A cross-sectional study of vertebral morphometry in 449 unscreened postmenopausal women, from the ages of 40 to 80, is reported. The wedge angles of thoracic vertebrae T4-12 were found to increase exponentially as a function of age, up to 70 years. In addition to age, the wedging phenomenon was found to be accentuated by increased bone turnover due to low calcium intake, reduced physical activity, each successive delivery, and breast feeding. Most of these variables were not correlated with isolated vertebral wedge angles, but rather with the sum of them (Sigma, sigma), assumed to assess the impact of those variables on thoracic kyphosis. In a subset of women, sigma was found to be inversely correlated with low spinal mineral density at L2-4. T-11 and T-12 were the vertebrae most frequently deformed (wedge angle exceeding mean +/- 3 SD in a group of 50 young healthy women, 25-45 years old). The distribution of deformed vertebrae was found to be significantly different from those qualified as "fractured" according to Kleerekoper et al.'s (1984) and Melton et al.'s (1989) criteria. The overall information afforded by past and present data indicates that in postmenopausal women, vertebral deformation may occur with the help of mechanical solicitations plus high bone remodeling rates, as well as by structural collapse (fracture). The information obtained does not allow one to quantify the relative contribution of each set of factors to the wedging phenomenon.

Hypercalciuria and urinary saturation measurements in climacteric women.

Fifteen percent (20/130) of a group of climacteric women on diets of their choice had urinary calcium (Ca) levels exceeding 4 mg/kg per day. Most of these hypercalciuric subjects had a daily Ca intake of 0.4-0.5 g. Their bone turnover rates were raised and high Ca absorption was observed in 4 cases. Serum Ca and total protein and glomerular filtration rates were normal in all the hypercalciuric patients. The calcium/creatinine (Ca/Cr) ratio (mg l-1/mg l-1, fasting, 09:00-10:00 h) was measured in 72 climacteric women, 35 of whom (49%) had ratios > 0.1. The latter defines a relative hypercalciuria as compared with premenopausal Ca excretion levels. Only 5 of the 35 subjects had calciuria levels above 4 mg/kg per day. The Ca/Cr ratio cannot replace daily urinary Ca measurements for the screening of subjects in whom calciuria may exceed net Ca absorption. Urinary saturation measurements were carried out in 70 women. Supersaturation was observed only in the case of Ca oxalate (CaOx) among several calcium salts usually found in urinary stones. CaOx supersaturation was observed in 95% of the hypercalciuric subjects and in 48% of the rest of the women investigated. The relatively high frequency of CaOx supersaturation can be attributed in part to the decreased excretion of citrate associated with ovarian failure. Oestrogen replacement therapy increased citrate excretion and lowered the level of CaOx supersaturation. Ca supplementation (1 g Ca/day) reduced the degree of supersaturation as a result of the concurrent reduction in oxalate excretion.

The effect of alkalosis on the glucose-mediated insulin release by the rat.

Bicarbonate loaded (alkalotic) rats had reduced plasma phosphate and ionized Ca concentrations and increased urinary cAMP excretion, phosphate clearance and pancreatic tissue uptake of extracellular calcium, all known effects of increased parathyroid hormone (PTH) secretion. Total insulin secretion after glucose challenge was enhanced in these animals. The response of alkalotic thyroparathyroidectomized rats, on the other hand, suggested exhaustion or inhibition of insulin secretion. The hypothesis is advanced that PTH, enhancing the permeability to calcium of the beta-cell membrane, compensated the effect of decreased calcium concentration in the extracellular fluid caused by alkalosis. PTH appears instrumental for homeostatic adjustments of insulin secretion.

The effect of alkalosis on the glucose-mediated insulin release by the rat.

Bicarbonate loaded (alkalotic) rats had reduced plasma phosphate and ionized Ca concentrations and increased urinary cAMP excretion, phosphate clearance and pancreatic tissue uptake of extracellular calcium, all known effects of increased parathyroid hormone (PTH) secretion. Total insulin secretion after glucose challenge was enhanced in these animals. The response of alkalotic thyroparathyroidectomized rats, on the other hand, suggested exhaustion or inhibition of insulin secretion. The hypothesis is advanced that PTH, enhancing the permeability to calcium of the beta-cell membrane, compensated the effect of decreased calcium concentration in the extracellular fluid caused by alkalosis. PTH appears instrumental for homeostatic adjustments of insulin secretion.