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Biomedical subjects

M Fuss

Publications and source records attributed to M Fuss.

At least 19 recordsLinked to original sources
PubMed1992

Longitudinal study of bone metabolism after ethanol withdrawal in alcoholic patients.

The pathogenesis of osteopenia in chronic alcoholism remains unclear, and many ethanol-related abnormalities have been advocated to explain bone loss. A direct inhibitory effect of ethanol on osteoblast function was suggested by in vivo and in vitro studies. We measured biochemical markers of bone turnover in 12 alcoholic men before and during a 2 week period of alcohol withdrawal, and we compared the results with those obtained in 15 nonalcoholic men. Our alcoholic patients presented with (1) decreased serum concentrations of bone gla protein (BGP), suggesting decreased bone formation; (2) increased urinary excretion of hydroxyproline, suggesting increased bone resorption; (3) increased renal threshold of phosphate excretion without modification of serum PTH concentration, suggesting a direct effect of ethanol on the renal handling of phosphate. The rapid increase in serum BGP concentrations following ethanol withdrawal suggests that low serum BGP concentrations in alcoholics may result from a direct toxic effect of ethanol on osteoblast function and/or numbers.

Adult↗
PubMed1992

Calcium and vitamin D metabolism in granulomatous diseases.

Overproduction of the active metabolite of vitamin D 1,25-dihydroxyvitamin D (1,25(OH)2D) has been described in sarcoidosis and other granulomatous diseases. High circulating concentrations of 1,25(OH)2D lead to increased intestinal absorption of calcium, possibly to enhanced bone resorption, and may result in hypercalcaemia and/or hypercalciuria. Data obtained in vivo and in vitro demonstrated that the unregulated production of 1,25(OH)2D lies within the granulomatous tissue and is controlled by glucocorticoids. This abnormal production of 1,25(OH)2D seems to be a general phenomenon of granulomatous processes, which is not exceptional in sarcoidosis, but appears seldom in tuberculosis. These abnormalities, however, are not pathognomonic of granulomatous processes, since they have been described in other diseases such as lymphomas.

Calcium↗
PubMed1992

[Persistent and recurrent hyperparathyroidism following parathyroidectomy].

In a series of 416 parathyroidectomies for primary or secondary hyperparathyroidism, 19 were reoperations for persistence (17 cases) on recurrence (2 cases) of the disease. (1) Preoperative localisation studies were useless in half of the cases. (2) In re-explorations, 72% only of parathyroid glands were discovered, 46% of them in ectopic locations. In reoperations for primary hyperparathyroidism, 56% of cases had more than one pathological gland. (3) Long term results have been less satisfactory after re-explorations than after the first operations.

Adult↗
PubMed1991

Calcitonin secretion in idiopathic renal stone formers.

Several studies demonstrated a reduction in bone mineral content (BMC) in idiopathic renal stone formers (RSF). We found this reduction in association with a chronic low-calcium diet. Low calcium intake could theoretically result in calcitonin deficiency, responsible for increased bone resorption. This hypothesis was tested in 22 male RSF eating a low-calcium diet (350 +/- 72 SD mg/day) for 2 years or more, who showed a significant reduction in their BMC. When compared to 15 normal male subjects eating a free diet, RSF showed increases in serum alkaline phosphatase activity and fasting urinary excretion of hydroxyproline and calcium, suggesting increased bone turnover. Plasma calcitonin levels were measured by radioimmunoassay following an extraction-concentration technique (exCT). Basal plasma exCT levels were higher (P less than 0.005) in RSF (4.1 +/- 0.8 SEM pg/ml) than in normal subjects (2.8 +/- 0.4). Following a 5 minute infusion of 2 mg elemental calcium per kg, levels of plasma exCT tended to increase more, although not significantly, in RSF (51.3 +/- 9.4 pg/ml) than in normal subjects (36.6 +/- 9.7). The CT secretory response, taking into account changes in serum calcium concentration (delta exCT/delta Ca), was higher (P less than 0.05) in RSF (50.0 +/- 10.0) than in normal subjects (25.6 +/- 6.6). Our study thus demonstrates that RSF chronically fed a low-calcium diet have increased basal plasma CT levels and increased CT cells responsiveness. CT deficiency cannot therefore be considered a cause for the low BMC associated with a chronic low-calcium diet in RSF.

Adult↗
PubMed1991

Stimulation of calcitonin secretion by an oral calcium load test in normal subjects and in idiopathic renal stone formers.

Circulating concentrations of calcitonin (CT) have been found high in idiopathic renal calcium stone formers (RSF). It has been postulated that this could result from increased serum calcium concentrations following calcium-containing meals. To verify this hypothesis, 15 male idiopathic RSF and 15 male normal subjects underwent plasma CT measurements, following an extraction-concentration technique (exCT), in basal state and during an oral calcium load test. Most RSF exhibited increased excretion of calcium following oral calcium loading, suggesting overabsorption of calcium, but serum calcium did not increase more in RSF than in normal subjects. Basal plasma exCT concentrations were normal in RSF. ExCT plasma concentrations following calcium loading, and the area under the curve of exCT levels, tended to be higher in RSF than in normal subjects, but not significantly. Our results thus do not support the hypothesis that increased plasma CT levels in RSF result from increased serum calcium concentrations following calcium-containing meals.

Administration, Oral↗
PubMed1991

The natural history of renal stone disease after parathyroidectomy for primary hyperparathyroidism.

The evolution of renal stone disease has been followed, before and after parathyroidectomy, in 197 patients with primary hyperparathyroidism. Before operation, 120 patients had had a previous history of renal colics or stones, or both, demonstrated on roentgenograms of the urinary tract. In 36 patients with stones that had been passed or removed before exploration of the neck, no recurrence of lithiasis has been observed. In 84 patients who still had stones at the time of the operation, the stones dissolved and disappeared within ten years in 88 per cent of those with urolithiasis and in 77 per cent with nephrocalcinosis. The rate of stone disappearance was similar in those with or without preoperative urinary tract infection and in patients operated upon for adenoma of the parathyroid gland or primary hyperplasia. This rate was slower for patients with a postoperative urinary infection. The frequency of renal colics, 0.66 per patient per year before parathyroidectomy, decreased to 0.02 per patient per year after the first postoperative year.

Adult↗
PubMed1990

Involvement of low-calcium diet in the reduced bone mineral content of idiopathic renal stone formers.

The possibility that low-calcium intake in renal stone formers could lead to reduced bone mineral content was investigated in 123 male patients with idiopathic urolithiasis. Radius bone mineral content (BMC) was measured by single photon absorptiometry. Two groups of patients were analyzed: group 1 (n = 63) maintained on a free diet; group 2 (n = 60) maintained on a low-calcium diet (350 mg/day +/- 20 SEM) for 3.9 years +/- 0.6 SEM. The two groups of patients were investigated after a standard reduction of calcium intake for at least 1 week. The urinary excretion of calcium and of hydroxyproline, and the serum alkaline phosphatase activity were higher in both groups than in normal subjects submitted to the same low-calcium diet. Both groups of stone formers showed lowered radius BMC values at 3 cm (distal) and 8 cm (proximal) above the styloid process, but distal BMC was significantly lower in group 2 than in group 1. The results suggest that low-calcium intake could worsen the already decreased BMC of idiopathic renal stone formers.

Adult↗
PubMed1990

Low calcium diet in idiopathic urolithiasis: a risk factor for osteopenia as great as in primary hyperparathyroidism.

The bone mineral content of the radius was measured in 32 male renal stone formers, 18 of them presenting with idiopathic urolithiasis and 14 with primary hyperparathyroidism, a disease known to disturb bone metabolism. The idiopathic stone formers had been on regular treatment with a low calcium diet. The bone mineral content of the radius was reduced to a similar level in both groups of patients. The data suggest that idiopathic stone formers on a low calcium diet are at risk of osteopenia; the factors which could lead to a negative calcium balance included uncompensated renal hypercalciuria, hypophosphataemia and exaggerated serum levels of 1,25-dihydroxyvitamin D. To treat idiopathic hypercalciuria, thiazide diuretics, which reduce the renal excretion of calcium and have been shown to be beneficial for bone, seem safer than a low calcium diet.

Adult↗
PubMed1990

Long-term irreversibility of bone loss after surgery for primary hyperparathyroidism.

We reported previously that radial bone mineral content was decreased in patients with primary hyperparathyroidism and remained subnormal 1 year after surgery. In this study, we reviewed the results of sequential measurements of the radial bone mineral content, performed up to 107 months after removal of the parathyroid adenoma in 71 patients suffering from primary hyperparathyroidism. Bone mineral content increased during the first year after surgery. During the period 1 to 8 months after removal of the adenoma, the mean monthly increment was 0.009 +/- 0.0022 g/cm for the radial epiphysis and 0.0084 +/- 0.0023 g/cm for the shaft. However, in 39 patients seen at the end of 1 year after surgery, the bone mineral content of the epiphysis remained more than 1 SD below the normal mean in 61% (24) of the patients and more than 2 SDs in 36% (14) of the patients. For the shaft, those percentages were 59% (23) and 26% (10), respectively. Thereafter, the monthly increment rate of bone mineral content decreased rapidly with time, so that only minor further increase could be expected. Data show that patients with a low bone mineral content when diagnosed with primary hyperparathyroidism will conserve life long an irreversible loss of bone as compared with a matched control population.

Adenoma↗
PubMed1989

Correction of low circulating levels of 1,25-dihydroxyvitamin D by 25-hydroxyvitamin D during reversal of hypomagnesaemia.

The effect of 25-hydroxyvitamin D (25OHD), given orally during the reversal of hypomagnesaemia, was studied in five patients with hypomagnesaemic hypocalcaemia and low serum levels of 25OHD and 1,25-dihydroxyvitamin D (1,25(OH)2D). The results were compared to those obtained in five other patients with similar initial levels of magnesium, calcium, 25OHD and 1,25(OH)2D who did not receive 25OHD. Serum levels of 1,25(OH)2D in the ten hypomagnesaemic patients were lower than in ten control subjects with low serum levels of 25OHD. The reversal of hypomagnesaemia was similar in the two groups of patients and elicited a similar increase of circulating iPTH levels. The expected increase of circulating 25OHD was observed in patients supplemented with 25OHD; their circulating 1,25(OH)2D rose within 48 h to normal levels, contrasting with the delayed and poor increase of 1,25(OH)2D in patients receiving no 25OHD. The evolution of serum calcium was however identical in the two groups. Our results suggest that vitamin D deficiency was a significant factor leading to low circulating levels of 1,25(OH)2D in hypomagnesaemic hypocalcaemic patients. The biological consequences of low serum 1,25(OH)2D in these patients remain unclear, but clearly, normal levels of 1,25(OH)2D are not essential for the correction of hypomagnesaemic hypocalcaemia.

Adult↗
PubMed1989

Hyperuricemia and renal handling of urate in primary hyperparathyroidism.

Serum urate and the renal handling of urate were measured in 37 patients with primary hyperparathyroidism and in normal sex- and age-matched subjects. Serum urate was increased in the hyperparathyroid group compared to the control group (6.23 +/- 1.46 versus 4.64 +/- 1.24 mg/100 ml; p less than 0.005), whereas the fractional excretion of urate was decreased in hyperparathyroid patients compared to the controls (6.80 +/- 2.69 versus 8.73 +/- 3.47%; p less than 0.005). Twenty-four of these hyperparathyroid patients were studied 6 months after surgical correction of their disease. Serum urate decreased after surgery (5.14 +/- 1.65 mg/100 ml) compared to the preoperative state (5.92 +/- 1.46 mg/100 ml) and was no longer different from the normal values. The possible mechanisms of hyperuricemia associated with the hyperparathyroid state are discussed.

Adolescent↗
PubMed1988

Infrequency of primary hyperparathyroidism in renal stone formers.

Repeated measurements of serum calcium and immunoreactive parathyroid hormone were performed in 1433 renal stone formers systematically referred from Accident and Emergency Departments and from Departments of Urology and Nephrology, irrespective of their serum calcium. Primary hyperparathyroidism was found in 23 patients and confirmed in 19/20 patients who underwent neck surgery, including 8 with intermittent hypercalcaemia. Our data suggest that when selection bias is minimised, primary hyperparathyroidism is found in about 2% of renal stone formers in a western country such as Belgium.

Calcium↗
PubMed1988

[Sequential development of vitamin D metabolites under isoniazid and rifampicin therapy].

A sequential study of 25-hydroxy vitamin D (25-OH-D), 1.25 dihydroxy vitamin D [1.25 (OH)2-D], PTH, alkaline phosphatase and gammaglutamyl transpeptidase (gamma GT) was undertaken in a series of 46 children with asymptomatic tuberculosis treated by isoniazid (INH) alone or associated with rifampin (RMP). These parameters were measured before treatment, 1 month, 3 months after the onset and at the end of treatment (6 months). In order to reduce the influence of the time of the year on the 25-OH-D levels, 22 patients were selected for whom the whole treatment took place between October and May of the following year. In this group, 13 children were treated by INH and RMP, 9 by INH alone. A statistically significant decrease in 25-OH-D levels could be demonstrated after 3 months of treatment in 13 patients under INH and RMP as well as a significant increase in alkaline phosphatase and gamma GT levels. In 9 patients given INH alone, 1.25 (OH)2-D levels decreased after 3 months without significant changes in 25-OH-D, alkaline phosphatase or gamma GT levels. These results emphasize the need for regular biochemical supervision, even if no sign of rickets is observed in these patients.

Adolescent↗
PubMed1988

Are tuberculous patients at a great risk from hypercalcemia?

The risk of tuberculous patients to develop hypercalcemia was investigated in 33 patients aged 19 to 80. Twenty-two of the 33 received no vitamin D supplements. Before antituberculous chemotherapy serum calcium corrected for albumin and urinary calcium levels were normal, serum 25-hydroxyvitamin D (25(OH)D) levels were low, but serum 1,25(OH)2D levels, oral calcium load test and intestinal 47Ca absorption were normal. After 17 to 34 days of chemotherapy serum calcium corrected for albumin and 1,25(OH)2D levels were lower without change in serum D-binding protein. In 11 patients 25(OH)D, 50 micrograms/day, was given orally for two months. 25(OH)D given three days before chemotherapy in five patients induced an increase of levels of 1,25(OH)2D which was greater than in 10 control patients with similar serum levels of 25(OH)D. When chemotherapy was added to 25(OH)D, the five patients showed high normal 1,25(OH)2D levels. The last six patients received 25(OH)D together with or after starting chemotherapy. None of the 33 patients developed hypercalcemia, even when supplemented with 25(OH)D for two months. It appears that hypercalcemia is uncommon in tuberculosis.

Adult↗