Body composition study in the elderly: comparison between tritium dilution method and dual photon absorptiometry.

BACKGROUND: The methods commonly employed in body composition study in elderly persons derive fat-free mass (FFM) by measures of total body water (TBW); these methods assume FFM hydration constant (TBW/FFM = 0.732). The aim of our study was to verify the accuracy of the TBW method in FFM estimation and to study the variability of fat-free mass hydration (TBW/FFM) in healthy elderly subjects. METHODS: We assessed FFM in 27 healthy old subjects (76 +/- 7 yrs) by dual photon absorptiometry (DPA) and by TBW measured by 3H2O. Furthermore, to verify the accuracy in FFM estimation by our methods, we measured resting metabolic rate (RMR) by indirect calorimetry. RESULTS: FFM hydration was 71.9 +/- 4.9 (range 63.6-80.4%), a range larger than that reported by direct chemical analysis in adults. The FFM hydration measured in our subjects was not different from the 73.2 value currently used in healthy adults. FFM values derived by TBW (assuming TBW/FFM = 0.732) were not significantly different from FFM measured by DPA. We correlated FFM with resting metabolic rate and found a similar correlation between RMR and FFM-DPA (r = .89, p < .001) and FFM-TBW (r = .85, p < .001). CONCLUSIONS: Both methods employed in our study have proved to be accurate in estimating FFM in elderly persons; particularly, the value of 0.732 assigned to FFM hydration to derive fat-free mass in adults can be employed also in body composition study of the elderly.

Effects of one-year cyclical treatment with clodronate on postmenopausal bone loss.

We studied 60 women with postmenopausal bone loss randomly allocated to the following treatments: Group 1 (20 patients), no treatment; Group 2 (20 patients), clodronate 400 mg daily by mouth for 30 consecutive days, followed by 60 days of no treatment; Group 3 (20 patients) oral calcitriol 2 mcg by mouth for 5 days and oral clodronate 400 mg daily for additional 25 days, followed by 60 days of no treatment. The therapeutic cycles were repeated four times in the 12-month study period. In the 36 treated patients of Groups 2 and 3 who completed the study period we observed a progressive and significant increase in lumbar bone density both at 6 and 12 months of therapy, without significant differences between the two treatment protocols (+3.88 +/- 0.65%, P < 0.001 and +3.21 +/- 0.89%, P < 0.005 in Groups 2 and 3, respectively, at the end of the study). In contrast, there was a progressive and significant decline of bone mineral density in untreated patients (-2.34 +/- 0.49%, P < 0.001). After 12 months serum calcium values in treated subjects were higher than in untreated patients (P < 0.05). Serum phosphate was raised only in Group 2, mean values being higher after 12 months than before treatment (P < 0.05); parathyroid hormone (PTH) declined in all treated patients, the fall being significant in Group 2 (P < 0.02). No important side effects were observed with treatment and no patient withdrew because of these. We conclude that cyclical low dose clodronate therapy induced a gain in lumbar spine bone mass in patients with postmenopausal osteoporosis.

Hyperparathyroidism: cause or consequence of recurrent calcium nephrolithiasis?

Primary hyperparathyroidism (PHP) might be characterized by either prevailing bone or renal stone patterns with different metabolic features. To explore the possibility of different hormonal patterns we studied 129 patients with PHP: 95 stone formers (SF) and 34 nonstone formers (NSF). Females prevailed over males in both groups. Severe and specific bone lesions were more evident in NSF than SF. Parathyroid gland histology displayed a prevalence of adenoma in NSF, whereas isolated hyperplasia prevailed in SF. SF had lower levels of serum Ca, urinary Ca, ALP and serum PTH than NSF. As expected serum 1,25-dihydroxyvitamin D [1,25(OH)2 D] levels were greater in both groups of patients than in controls but we found no difference between the two groups. 25-Hydroxyvitamin D was neither increased with respect to controls nor different between groups. We conclude that patients with PHP may represent well separated metabolic and clinical entities, but we cannot confirm that serum 1,25(OH)2D levels play a key role in discriminating the different clinical features. In addition, the findings of predominant parathyroid hyperplasia in SF and the clinical evidence of recurrent hyperparathyroidism only in these patients suggest the possibility that the endocrine disorder might be the consequence over time rather than the cause of nephrolithiasis.

Longitudinal study on osteodystrophy in primary biliary cirrhosis (PBC) and a pilot study on calcitonin treatment.

The aims of this study were to evaluate bone metabolism in primary biliary cirrhosis (PBC) and the effect of ADFR (activate, depress, free, repeat) therapy with vitamin D, calcium and calcitonin in preventing bone resorption. Sixty-nine female subjects entered the study: 38 PBC (AMA + ve) patients, 11 AMA-negative chronic liver disease patients and 20 age-matched healthy controls. Bone metabolism was evaluated by biochemical parameters and dual-photon absorptiometry of the lumbar spine at time 0, 6 and 18 months. Both PBC and chronic liver disease (CLD) patients showed low levels of serum 25-hydroxyvitamin D, osteocalcin and bone mineral content expressed as AAD (average area density) compared to healthy controls. Serum parathyroid hormone in PBC patients was at the lower limit of the normal range and was significantly lower than patients with chronic liver disease. At a 6-month interval, AAD significantly decreased in PBC patients (p less than 0.005). At the 6-month period PBC patients were allocated into two groups according to a cut-off AAD of 0.800 g/cm2: group A (no treatment, AAD greater than 0.800, n = 11), group B (treatment, AAD less than 0.800, n = 13). The latter group received a 4-week course with oral calcium carbonate (1500 mg daily) + oral 1,25-dihydroxyvitamin D (0.5 micrograms twice a day for 5 days) + carbocalcitonin (40 U MRC) i.m. thrice a week. The treatment was repeated with the same protocol at 2-month intervals for 12 months.(ABSTRACT TRUNCATED AT 250 WORDS)

Efficacy of captopril in hypertensive diabetic patients.

Twenty hypertensive diabetic patients (10 with type I and 10 with type II) were treated with captopril, 50 mg twice a day, for three months. The drug was effective as monotherapy in 16 patients. An additional nine months of follow-up was obtained in 12 of these patients (four with type I and eight with type II) who did not need the addition of diuretics to achieve normal blood pressure. For these patients with long-term treatment, since there was no substantial difference between those with type I and those with type II, the data were pooled. Mean arterial pressure significantly decreased shortly after treatment was begun and the reduction was maintained. No significant change was induced by captopril in urine volume, osmolar clearance, and serum and urinary values of sodium, chloride, calcium, and magnesium, whereas significant reduction was found in fractional excretion of potassium and phosphate. The baseline levels of proteinuria were only slightly elevated, yet they fell in all patients during treatment. All patients maintained satisfactory control of carbohydrate metabolism, and none of them required substantial changes in hypoglycemic treatment. The administration of captopril as monotherapy appears to be an effective and safe way of lowering blood pressure in diabetic hypertensive patients, even in the long term, without effects on renal function and in carbohydrate metabolism.

Exogenous calcitonin protects against renal bone disease in rats with early renal failure.

Chronic renal failure was induced in four groups of male Sprague-Dawley rats by unilateral nephrectomy followed by removal of the outer poles and cautery of the remnant kidney. The four groups of animals received isocaloric diets with normal (groups 1 and 4) or low (groups 2 and 3) phosphate contents and variable amounts of calcium. In addition, rats in group 4 were given salmon calcitonin. After 90-160 days the 4 groups of rats had developed comparable levels of chronic renal failure. The serum phosphate values were significantly lower in rats on low phosphate intake than in those on normal phosphate diet. Bone histology was evaluated on tibiae, lumbar vertebrae and ribs. The rats kept on low phosphate diet (groups 2 and 3) had significantly lower frequency of osteomalacia and bone resorption than those fed a normal phosphate diet. Rats treated with calcitonin (group 4) had the lowest frequency of osteomalacia and virtually no association with bone resorption, despite normal phosphate intake. The serum levels of parathyroid hormone were not significantly different in rats in groups 1 and 4 as compared to controls. Serum 1,25-dihydroxycholecalciferol levels were significantly lower in group 1 than in controls and were significantly higher in group 4 than in group 1. These data show that calcitonin effectively prevents bone lesions in rats with early chronic renal failure.

Captopril in the treatment of hypertension in type I and type II diabetic patients.

This investigation was performed in two groups of adult patients, 10 with type I and 10 with type II diabetes mellitus, all with arterial hypertension (160 to 200 mm Hg systolic and 95 to 120 mm Hg diastolic). Captopril, 50 mg twice a day, was administered for 12 weeks and was effective as monotherapy in 16 patients. Mean arterial pressure (+/- s.d.) in type I patients changed from 121.4 +/- 9.6 to 100.2 +/- 10.1 after 4 weeks and to 102.0 +/- 3.8 mm Hg after 12 weeks; in type II patients it changed from 132.8 +/- 5.7 to 123.9 +/- 13.5 after 4 weeks and to 109.1 +/- 11.1 mm Hg after 12 weeks. The differences were statistically significant. In only 4 patients was it necessary to add a thiazide after the first month of therapy. No significant change was induced by captopril in urine output, osmolar clearance, free water clearance inulin, and PAH clearances. No significant change was observed in serum and urine Na+, Cl-, Ca++ and Mg++, whereas a statistically significant reduction was found in the renal clearances of K+ and PO4-. No important change in serum aldosterone was found, while plasma renin activity was increased, as expected. No alterations in urine protein, glucosaminoglycans, gamma GT, and N-acetyl-beta-glucosaminidase were observed during follow-up. All patients maintained good metabolic control of their disease. No neutropenia and orthostatic hypotension were seen. Captopril appears to be an effective and safe drug for lowering blood pressure in diabetic patients, without affecting renal function, electrolyte balance and the metabolic control of diabetes.

Mineral metabolism and bone mineral content in rheumatoid arthritis. Effect of corticosteroids.

An evaluation of mineral metabolism was performed in 41 patients with RA and the pertinent data were compared to bone mineral content in patients either untreated or treated with different doses of corticosteroids. Our study confirms that osteoporosis is a common finding even in rheumatoid patients never treated with corticosteroids. Moreover, in patients treated with such drug the loss of bone mineral content was related to the dosage rather than to the length of treatment. In all cases no overt biochemical derangement was observed. According to our study, parathyroid hormone does not seem to influence the development of osteoporosis in rheumatoid arthritis, while a relative deficiency of calcitonin along with an inadequate vitamin D metabolism could play some role.