To determine the life expectancy of patients with primary biliary cirrhosis, we analyzed survival data from 280 patients with either symptomatic (243) or asymptomatic (37) disease. Patients were followed for up to 19 years (mean, 6.9 years). The average length of survival was 11.9 years--nearly twice that reported in other studies. In contrast, over a 12-year period the survival of the asymptomatic patients after diagnosis did not differ from that of a control population matched for age and sex. Jaundice, weight loss, hepatomegaly, splenomegaly, and ascites were each associated with a poor prognosis. Prognosis also correlated with the histologic stages of hepatic fibrosis, cholestasis, and periportal-cell necrosis. A multivariate analysis of clinical features revealed that at the onset of disease, age, hepatomegaly, and elevated levels of serum bilirubin were independent discriminators of a poor prognosis. A histologic finding of fibrosis limited to portal areas improved this discrimination, correlating with prolonged survival. No other factors enchanced the prediction of risk.

Purpose Exercise is associated with a decrease in bone mineral density under certain conditions. One potential mechanism is increased bone resorption due to an exercise-induced increase in parathyroid hormone (PTH), possibly triggered by dermal calcium loss. The purpose of this investigation was to determine whether calcium supplementation either before or during exercise attenuates exercise-induced increases in PTH and C-terminal telopeptide of type I collagen (CTX; a marker of bone resorption). Methods Male endurance athletes (n=20) completed three 35-km cycling time trials under differing calcium supplementation conditions: 1) 1000 mg calcium 20 minutes before exercise and placebo during, 2) placebo before and 250 mg calcium every 15 minutes during exercise (1000 mg total), or 3) placebo before and during exercise. Calcium was delivered in a 1000 mg/L solution. Supplementation was double-blinded and trials were performed in random order. PTH, CTX, bone-specific alkaline phosphatase (BAP; a marker of bone formation), and ionized calcium (iCa) were measured before and immediately after exercise. Results CTX increased and iCa decreased similarly in response to exercise under all test conditions. When compared to placebo, calcium supplementation before exercise attenuated the increase in PTH (55.8 ± 15.0 vs. 74.0 ± 14.2; mean ± SE; p=0.04); there was a similar trend (58.0 ± 17.4; p=0.07) for calcium supplementation during exercise. There were no effects of calcium on changes in CTX, BAP, and iCa. Conclusions Calcium supplementation before exercise attenuated the disruption of PTH. Further research is needed to determine the effects of repeated increases in PTH and CTX on bone (i.e., exercise training), and whether calcium supplementation can diminish any exercise-induced demineralization.

Male cyclists have been found to have low BMD in cross-sectional studies. Changes in BMD values over 1 yr of training and competition were studied in 14 male cyclists. BMD decreased significantly at the total hip, neck, trochanter, and shaft regions but not the lumbar spine. This first prospective study of cyclists showed a decrease in BMD over the course of 1 yr. Introduction: Cross-sectional studies have shown that some endurance athletes, and cyclists in particular, have low BMD. Whether vigorous cycle training is causally related with low BMD remains unknown. Materials and Methods: Changes in BMD values over 1 yr of training and competition were studied in 14 male road cyclists, 27-44 yr of age. Subjects were randomized to receive 1500 (500 mg with meals) or 250 mg of supplemental calcium citrate daily. BMD measurements were obtained at pre-, mid-, post-, and off-season time points over 1 yr. Dermal calcium loss during exercise was estimated using a patch collection technique to examine calcium loss as a potential mediator of changes in BMD. Results: Using paired t-tests, BMD was found to decrease significantly from pre-to off-season at the total hip, neck, shaft, and trochanter regions (relative changes of −1.5 ± 2.1%, −0.7 ± 2.1%, −0.9 ± 2.1%, and −1.0 ± 1.2%, respectively, all p < 0.05). The 1.0 ± 1.2% decrease in BMD at the lumbar spine failed to reach statistical significance (p ‫ס‬ 0.079). There were no differences in changes in BMD between the calcium supplementation groups. The 2-h dermal calcium loss was estimated at 136.5 ± 60.5 mg. Higher dermal calcium losses were associated with lower baseline BMD values at the total hip, neck, and shaft (all p < 0.05), but were not significantly associated with changes in BMD. Conclusions: This study suggests that high intensity cycle training may adversely affect BMD. Excessive dermal calcium loss during exercise may be a contributing factor, but mechanisms remain to be elucidated.

T supplementation was well tolerated and improved body composition but had no effect on functional performance. T supplementation improved upper body strength only in nonexercisers compared with placebo.

Previous studies have found that serum parathyroid hormone (PTH) increases in response to relatively short (<60 minutes), intense bouts of exercise, possibly as a result of decreases in serum calcium. Whether longer, less intense exercise also stimulates an increase in PTH is not known. The effects of 2 hours of moderate-intensity cycling on serum PTH and calcium were investigated in 20 competitive male cyclists, aged 22-45 years. Serum concentrations of PTH and calcium were measured before and after exercise. Dermal calcium loss was estimated using patch collections and loss of sweat. There were increases in PTH from 40.6 +/- 15.6 to 69.5 +/- 25.5 pg/mL (P < 0.001) and in serum calcium from 9.3 +/- 0.3 to 9.6 +/- 0.5 mg/dL (mean +/- standard deviation, P = 0.001) in response to exercise. Contraction of plasma volume explained the rise in calcium but not PTH. Dermal calcium loss was estimated at 138.0 +/- 71.9 mg for the 2-hour exercise bout. Neither the change in serum calcium nor the dermal calcium loss was significantly related to the increase in PTH. The study demonstrated that prolonged exercise stimulates PTH secretion. The effects of such transient increases in PTH on bone metabolism are not known.