Abstract. Several metabolic derangements, including enhanced protein catabolism, have been suggested to be associated with increased circulating parathyroid hormone (PTH) in patients with secondary hyperparathyroidism (HPT). Such conditions, therefore, might lead to an increase in energy expenditure. The present study examined by indirect calorimetry the resting energy expenditure (REE) of 15 hemodialysis patients who have severe HPT (PTH ϭ 1457 Ϯ 676 pg/ml) and were pair-matched for age and gender to 15 hemodialysis patients with mild to moderate HPT (PTH ϭ 247 Ϯ 196 pg/ml). Both groups were also pair-matched for age and gender to a group of 15 healthy adult subjects (control). In six patients from the severe HPT group submitted to total parathyroidectomy, REE was determined 6 mo after the surgery. The groups were not different regarding lean body mass (LBM) measured by bioelectric impedance, serum C-reactive protein, and bicarbonate. Thyroid-stimulating hormone was within the normal range in all groups. Nonadjusted REE was significantly higher in the severe HPT group (1674 Ϯ 337 kcal/d) compared with patients with mild to moderate HPT (1388 Ϯ 229 kcal/d; P Ͻ 0.05). Both groups did not differ from the control group (1468 Ϯ 323 kcal/d). When adjustment of REE for LBM was performed using the multiple regression analysis, patients with mild to moderate HPT and control subjects had significantly lower REE (Ϫ231 and Ϫ262 kcal, respectively) than that of the severe HPT group. Considering all patients together, nonadjusted REE correlated directly with LBM (r ϭ 0.61; P Ͻ 0.01). PTH correlated strongly with LBM in the severe HPT group (r ϭ Ϫ0.82; P Ͻ 0.01). In the multiple linear regression analysis, only LBM and PTH were independent determinants of REE (n ϭ 30; R 2 ϭ 0.47). REE decreased significantly in the six patients who were evaluated 6 mo after parathyroidectomy (from 1617 Ϯ 339 to 1226 Ϯ 253; P ϭ 0.02). These results demonstrate that hemodialysis patients with severe HPT have increased REE that might be reduced after parathyroidectomy.Reasonable evidence exists to support the notion that parathyroid hormone (PTH) is a uremic toxin (1). Indeed, in excess, the hormone can contribute to many of the cellular and metabolic abnormalities frequently observed in patients with chronic kidney disease (CKD) (2). Increased circulating PTH may cause wasting, weight loss, weakness, muscle atrophy, and negative nitrogen balance in patients with primary and secondary hyperparathyroidism (HPT) (3-5). These observations suggest that PTH may exert its effect by affecting protein metabolism and/or bioenergetics of skeletal muscle. In fact, a study has shown that PTH impairs energy production, transfer, and utilization of skeletal muscle (6). In addition, Garber (7) demonstrated in vitro that PTH enhances muscle proteolysis and increases the release of alanine and glutamine. Increased protein catabolism, therefore, might increase energy expenditure and adversely affect the nutritional status of patients with secondary HPT. Actually,...
Osteopenia is frequently found among calcium stone forming (CSF) patients with hypercalciuria. We investigated the effect of a 2-year therapeutic course of etidronate, a bone-sparing agent, in 7 young male CSF patients. The treatment consisted of a cyclic intermittent administration of phosphate followed by sodium etidronate and calcium supplementation every 74 days. Bone mineral density (BMD) measured at 12-month intervals and bone biopsies performed at baseline and after 2 years were the primary efficacy parameters. Mean lumbar spine BMD increased significantly after the 1st year by 2.6 ± 1.0% (mean ± SE, p < 0.05) and nonsignificantly after the 2nd year by 5.6 ± 2.6%. Nonsignificant changes were observed for femoral neck mean BMD after either the 1st or the 2nd year (decrease of 2.0 ± 1.0% and 2.0 ± 3.0%, respectively). Mean histomorphometric parameters showed that bone volume, osteoid volume, and eroded surfaces did not differ from baseline (13.9 ± 2.2 vs. 12.2 ± 1.1%, 1.2 ± 0.7 vs. 2.6 ± 0.7%, and 20.7 ± 6.2 vs. 13.7 ± 1.3%, respectively). Osteoid surface was significantly lower than baseline values (9.5 ± 5.2 vs. 18.8 ± 5.3%, p < 0.05). These data suggest that etidronate given to young male CSF patients presenting with hypercalciuria and osteopenia led to a significant amelioration of BMD, evident only in the lumbar spine after 1 year of treatment. There was no histological evidence of long-term improvement in bone remodeling.
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