Search PubMed⌕ Search

Biomedical subjects

J Corvilain

Publications and source records attributed to J Corvilain.

At least 37 records · Page 2Linked to original sources

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↗

Low basal thyrotropin with normal thyroid function in primary hyperparathyroidism.

TSH serum levels and thyroid function in 32 patients with primary hyperparathyroidism and hypercalcemia were compared to those of 30 age and sex-matched normal subjects. Serum T3 and T4 concentrations in hyperparathyroidism were not different from normal. However, basal serum TSH concentrations measured with an ultrasensitive immunoradiometric assay were significantly lower than normal (1.09 +/- 0.49 vs 2.06 +/- 0.85 mU/l, p less than 0.001). In hyperparathyroidism, TSH, but not T4 or T3, was negatively correlated with serum calcium, not with iPTH. The increase in TSH (delta TSH) 30 min after the iv injection of TRH was also significantly blunted in patients with primary hyperparathyroidism; delta TSH was highly correlated with basal TSH in hypercalcemic patients. The basal TSH concentration was higher and no longer different from normal (1.70 +/- 1.2 mU/l) 2 to 12 months after removal of the parathyroid adenoma, when serum calcium was normalized, whereas T3 and T4 did not change. A low basal TSH with normal T4 and low T3 was found in 13 patients with hypercalcemia of malignancy. In these patients, TSH increased after treatment of hypercalcemia with 3-amino-l,hydroxypropylidene-1, 1-bisphosphonate, whereas T4 did not change. The results suggest that the set point of pituitary thyroid feedback control could be decreased in chronic hypercalcemia and that hypercalcemia could render the thyroid more sensitive to TSH.

Adenoma↗

Ethanol increases and vitamin D metabolites decrease the production of cyclic AMP by canine renal cortical membranes.

Ethanol 0.16% increased cyclic AMP production by canine renal cortical membranes in the basal state and when challenged with different parathyroid hormone or fluoride concentrations. 1,25-dihydroxycholecalciferol (1,25(OH)2D3) 40 pM completely inhibited this effect of ethanol and reversed cyclic AMP production to the level observed in buffer alone. The same inhibitory effect was observed with 25OHD3 and with 24,25-dihydroxycholecalciferol (24,25(OH)2D3). The inhibitory effect was related to the vitamin D metabolites' concentration and was maximal for 160 pM; it was independent of their biological activity. This suggests that the effect is mediated through an interaction with the membrane lipids. The effect of vitamin D metabolites on cyclic AMP production was also observed in the presence of serum proteins and should be taken into account if unextracted plasma is assayed in the renal cortical membrane system for PTH bioactivity.

Animals↗

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↗

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↗

Cationized serum albumin enhances basal and stimulated adenylate cyclase activity in canine renal membranes.

We examined the effects of cationized serum albumin on the canine renal membrane adenylate cyclase in the basal state and when stimulated with guanylyl-imidodiphosphate, PTH or NaF. Human albumin was cationized to an isoelectric point greater than 9.5 by the addition of hexamethylene diamine. Cationized albumin increased basal and stimulated cAMP production by the membranes and increased the sensitivity of the system to low doses of PTH (0.25 pmol/l), being usually inactive in buffer alone or in human serum albumin. These observations are comparable to those previously reported on thyroid membranes and cells from adrenal tumours and confirm that positively charged macromolecules can increase adenylate cyclase activity. A decrease in non-specific binding of PTH is only partly responsible for the increased sensitivity to the hormone. Though this increase in sensitivity is small, it could nevertheless be useful in the detection of biologically active PTH after extraction from the serum.

Adenylyl Cyclases↗

Calcitonin deficiency in primary hypothyroidism.

The relative lack of sensitivity and specificity of current assays for plasma calcitonin (CT) have made it difficult to study possible CT deficiency conditions. Using a new extraction method that considerably improves the sensitivity of the assay for CT monomer, CT levels were measured before and after a short calcium (Ca) stimulation test (2 mg Ca/kg over 5 min) to determine C-cell secretory reserve in women with autoimmune primary hypothyroidism and normal women. Mean basal plasma CT concentrations were lower in the hypothyroid women [0.9 +/- 0.1 (+/- SEM) pg/ml] than in the normal women (1.5 +/- 0.2 pg/ml; P less than 0.01). Serum Ca increased similarly in both groups, but postinfusion CT levels were lower in the women with primary hypothyroidism (3.8 +/- 1.3 pg/ml) than in normal women (15.9 +/- 3.0 pg/ml; P less than 0.001). The functional thyroid status at the time of the study did not influence CT levels; both hypothyroid patients (n = 10) and patients who were euthyroid during T4 treatment (n = 11) were CT deficient to the same extent. Unlike that in primary hypothyroidism, CT secretion was normal in four patients with hypothyroidism of pituitary origin. We conclude that the process that causes hypothyroidism in patients with autoimmune thyroid disease can also cause marked CT deficiency. This first demonstration of spontaneous CT deficiency in adults should contribute to the understanding of CT physiology; it also suggests that bone metabolism should be closely monitored during the treatment of primary hypothyroidism.

Calcitonin↗

Partially reversible osteopenia after surgery for primary hyperparathyroidism.

Bone mineral content of the radius in 30 patients with primary hyperparathyroidism was determined by single-photon absorptiometry before and one year after the removal of a parathyroid adenoma. When compared with normal age- and sex-matched subjects, preoperative bone mineral content was decreased by more than 1 SD in 24 patients 3 cm from the styloid apophysis (distal site) and in 23 patients 8 cm from the styloid apophysis (proximal site). The decrease at the distal site, where there is more trabecular bone, was significantly greater than at the proximal site (74% +/- 13% of the normal mean vs 79% +/- 13%). Bone mineral content values were not different in the female and male populations. One year after surgery, the bone mineral content was significantly increased but was still lower than normal at both sites (81% and 84% of the normal mean, respectively). In some patients, seen up to three years after surgery, the bone mineral content remained lower than normal. We conclude that primary hyperparathyroidism causes an osteopenia that affects both cortical and trabecular bone and that is only partially reversible, even in the long term.

Adenoma↗

Magnesium administration reverses the hypocalcaemia secondary to hypomagnesaemia despite low circulating levels of 25-hydroxyvitamin D and 1,25-dihydroxy vitamin D.

The effect of parenteral administration of magnesium was studied in five patients with hypomagnesaemic hypocalcaemia. The initial metabolic state was characterized by a normal level of serum immunoreactive parathyroid hormone (iPTH), and by low or undetectable serum 25-hydroxyvitamin D (25OHD) and 1,25-dihydroxyvitamin D (1,25 (OH)2D). A parathyroid response was elicited by the acute intravenous injection of magnesium chloride. In contrast, 1,25(OH)2D did not change up to 24 h after the injection. Intramuscular magnesium sulphate restored serum magnesium and calcium to normal, whereas iPTH was transiently increased. 25OHD remained low and unchanged. 1,25(OH)2D rose very slowly, but the correction of hypocalcemia began before any change in 1,25(OH)2D levels could be demonstrated. Thus, the early correction of hypocalcemia mainly depended on the restoration of an adequate parathyroid function independently of the secretion of 1,25(OH)2D.

25-Hydroxyvitamin D 2↗

[Familial hypocalciuric hypercalcemia. A new family].

A new example of familial hypocalciuric hypercalcaemia is reported. The family studied consists of 19 members over four generations. The first patient described in this study had already undergone a classical surgical operation for "primary hyperparathyroidism" before the correct diagnosis was established: that of a new syndrome described for the first time by Foley in 1972 and subsequently studied by Marx since 1977. The features of this syndrome are: hypercalcaemia accompanied by hypocalciuria, autosomal dominant transmission with strong penetrance, with early appearance of hypercalcaemia, absence of signs of familial multiple endocrine neoplasia, benign course and persistence of the hypercalcaemia despite classical sub-total parathyroidectomy. Following a family survey, the authors discovered eight other members of the family who also presented this syndrome.

Adult↗