SEARCH · PubMed Health

Results for “Hypoparathyroidism”

Explore indexed PubMed citations for clinical trials, systematic reviews and public health research. Read source abstracts and follow each citation to its original PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 19 recordsLinked to original sources

PubMed1976

Effect of postoperative hypoparathyroidism on bone density.

The mean radiographic vertebral density of permanently hypoparathyroid patients was elevated above the normal-for-age, while the vertebral density of transiently hypoparathyroid patients was normal. Of the patients who received desiccated thyroid, both the transient and permanent hypoparathyroid patients had significantly higher-than-normal vertebral densities (P less than 0.01 and P less than 0.02, respectively). The duration of thyroid treatment corresponded with the degree of hypermineralized vertebral density in the patients with permanent hypoparathyroidism and permanent hypothyroidism (r = .728, P less than 0.01). However, in the transient hypoparathyroid patients, no significant relationship was found between the duration of thyroid treatment and vertebral density. Visual assessment of spinal radiographs for incidence of vertebral compressions revealed no significant differences between hypoparathyroid patients and the controls. In the patients with transient and permanent hypoparathyroidism who received calcium and vitamin D, the initially depressed blood calcium levels were within normal limits at the follow-up observation, but the untreated permanent hypoparathyroid patients were still depressed.

Calcium↗

PubMed1976

Post-thyroidectomy hypoparathyroidism.

The incidence of hypoparathyroidism following thyroid surgery in the series reported was 7.8 per cent. Temporary hypoparathyroidism was present in 15 patients (4.6%) and permanent hypoparathyroidism in 10 (3.2%). Persistently low levels of serum calcium and high levels of serum phosphorus at six to 10 weeks after thyroid operation in patients with temporary hypoparathyroidism, with no tendency toward normalization, suggests permanent hypoparathyroidism. Serum calcium below 5 mg per cent suggests permanent hypoparathyroidism.

Calcium↗

PubMed1975

Dissociation of calcium and sodium clearances in patients with hypoparathyroidism by infusion of chlorothiazide.

Previous reports have identified a deficient hypocalciuric response to chronic treatment with thiazide diuretics in patients with hypoparathyroidism. The present study was designed to ascertain if the acute response to thiazide diuretics is impaired in hypoparathyroidism. Five normal subjects and five patients with hypoparathyroidism were studied with the renal clearance technique during water diuresis. In normal subjects the clearance of calcium/clearance of sodium was 0.98 +/- 0.14 before, and 0.33 +/-0.03 during the intravenous infusion of chlorothiazide. In patients with hypoparathyroidism the corresponding ratios were 1.69 +/- 0.27 and 0.57 +/- 0.10. In both groups the drug-induced fall in clearance was 65% of control. The concentration of chlorothiazide in plasma and its rate of excretion were comparable in both groups. It is concluded that the acute action of thiazides is not impaired in hypoparathyroidism.

Adolescent↗

PubMed1979

Hypoparathyroidism.

Recent advances in our understanding of the physiologic actions of PTH and vitamin D have clarified certain aspects of the pathogenesis, classification, and management of hypoparathyroidism. Central to pathogenesis and categorization is the recognition that hypoparathyroidism may result from PTH deficiency, ineffectiveness, or resistance, with a resultant inability to stimulate adenylate cyclase in target tissues. This aberration in adenylate cyclase activity impairs certain physiologic responses such as renal phosphate excretion and renal calcium reabsorption that are required for proper calcium homeostasis. Also critical is the subnormal production of 1 alpha,25-dihydroxycholecalciferol (1,25-DHCC). Although the precise mechanism for the deficiency of 1,25-DHCC remains unclear, one may hypothesize that in hormone-deficient or hormone-ineffective hypoparathyroidism, decreased synthesis results from the absence of the two recognized stimuli for 1 alpha-hydroxylase--bioactive PTH and hypophosphatemia. Provision of either one of these stimuli would then be expected to restore 1,25-DHCC to normal levels, which could explain the calcemic response to PTH in these patients. There is some evidence that the synthesis of 1,25-DHCC may be "primarily" affected in PTH-resistant hypoparathyroidism, and thus may be unresponsive to any of the known stimuli. It remains conceivable, however, that during normocalcemic phases, such patients may improve their renal cyclic AMP and phosphaturic responses to PTH, with associated improvement in 1,25-DHCC synthesis. Certain acquired forms of PTH resistance such as hypomagnesemia and end-stage renal disease may also be associated with defective 1-hydroxylation. Whether occurring primarily or as a secondary process, the subnormal production of 1,25-DHCC may influence calcium and skeletal metabolism directly or by modifying response to PTH. The availability of 1,25-DHCC provides an effective and physiologically meaningful mode of therapy for most cases of hypoparathyroidism.

Acetazolamide↗

PubMed1975

Effects of 1alpha-hydroxy-vitamin D3 and 1,25-dihydroxy-vitamin D3 on calcium and phosphorus metabolism in hypoparathyroidism.

The effects of 1alpha-OH D3 or 1,25-(OH)2D3 on calcium and phosphorus metabolism have been evaluated in five hypoparathyroid patients to establish the direct effects of these compounds in adult humans, uncomplicated by compensatory changes in parathyroid hormone secretion. Doses of 1-2.5 mug/day in four patients (5 mug/day in a fifth patient on diphenylhydantoin and phenobarbital) caused a marked increase in serum calcium concentration and urinary calcium excretion, without significant changes in renal calcium clearance or urinary hydroxyproline excretion. These results suggest that the correction of hypocalcemia involved primarily a stimulation of intestinal calcium absorption rather than a stimulation of skeletal calcium resorption. Simultaneously, there were increases in urinary phosphorus excretion and variable changes in serum inorganic phosphate concentration. These effects were produced by doses of 1alpha-OH D3 and 1,25-(OH)2D3 which approach the dose needed to prevent rickets, in contrast to the very large doses of vitamin D or 25-OH D3 required for comparable effects in hypoparathyroid patients. The increased relative effectiveness of these one-hydroxylated forms of vitamin D reveals a deficiency of vitamin D one-hydroxylation in hypoparathyroidism. The rapidity of action of 1alpha-OH D3 and 1,25-(OH)2D3 was also striking. Apart from its physiologic implications, the potency of the one-hydroxylated forms of vitamin D offers significant therapeutic advantages in some patients whose hypoparathyroidism is difficult to control with vitamin D itself.

Adult↗

PubMed1992

T-lymphocyte activation in adult-onset idiopathic hypoparathyroidism.

PURPOSE: Patients with adult-onset idiopathic hypoparathyroidism (AOIH) often have antibodies against the parathyroid glands and other tissues, suggestive of immune activation. The purpose of this study was to determine whether T-cell activation is also a component of the endocrine disease. PATIENTS AND METHODS: We identified eight patients with idiopathic hypoparathyroidism diagnosed after the age of 30 years at two tertiary care centers and evaluated peripheral blood lymphocyte subset phenotype frequencies using monoclonal antibodies and flow cytometry. Control subjects were 13 patients with Graves' disease (five thyrotoxic and eight euthyroid) and 110 healthy volunteers. In two of the patients with AOIH, we also determined the mitogenic response to parathyroid cell membranes in peripheral lymphocytes. RESULTS: Patients with AOIH had higher than normal frequencies of the following phenotypes (p less than 0.05 versus controls, one-way analysis of variance): CD4, helper T cells; CD29/CD4, inducer of helper T cells; CD16 and CD56, natural killer cells; and CD3/DR, activated T cells coexpressing DR. Patients with Graves' disease had significantly higher than control frequencies of CD25 (T cells bearing the interleukin-2 receptor), CD3/DR, and CD26 (also a marker of T-cell activation); whereas the frequency of CD29/CD4 was significantly less than the control frequency. Neither of the two AOIH patients tested showed lymphocyte proliferation in response to parathyroid or thyroid cell membrane fractions. CONCLUSIONS: Generalized T-cell activation represents a novel feature associated with AOIH. Although we could not demonstrate parathyroid-specific lymphocyte clonal expansion, these data are suggestive of a generalized immune disturbance possibly related to autoimmunity, in which one of the manifestations is hypoparathyroidism.

Adult↗

PubMed1977

Keratitis with hypoparathyroidism.

Chronic kiratitis developed in two children with nonsurgical hypoparathyroidism, as part of an autosomal recessive syndrome that included adrenal insufficiency and moniliasis in what was postulated to be an autoimmune disease. The corneal changes may also have been caused by autoimmune mechanism. Activity of the keratitis diminished once the hypoparathyroidism had been brought under control. However, these patients were thought to be at risk for adrenal insufficiency: neither had moniliasis or adrenocortical insufficiency at present, but the features of the hypoparathyroidism adrenal insufficiency-moniliasis syndrome appeared at different ages and in differing sequences.

Adolescent↗

PubMed1992

The dose-dependency of alcohol-induced hypoparathyroidism, hypercalciuria, and hypermagnesuria.

Ingestion of alcohol evokes hypoparathyroidism, hypercalciuria, and hypermagnesuria. The dose-dependency of these changes has not been assessed before. We measured the serum concentrations of intact parathyroid hormone (PTH), and serum and urine calcium and magnesium in six normal men before and at intervals up to 6 h after the ingestion of fruit juice (control) and 0.5, 1.0 and 1.3 g of alcohol per kg of body weight. As compared with the control experiment the maximum reductions in the mean PTH concentration were 31% (P = 0.19), 31% (P = 0.20) and 45% (P = 0.01) with the three alcohol doses, respectively. After stopping drinking, the urinary excretion of calcium was 85%, 142% and 207% higher during the three alcohol experiments than during the control session (P < 0.05, < 0.01 and < 0.01, respectively), also urinary magnesium increased up to threefold. We conclude that in nonalcoholic subjects acute alcohol intake induces hypoparathyroidism, hypercalciuria, and hypermagnesuria, the latter two being dose-dependent. The direct renal effects of alcohol are the major mechanisms for hypercalciuria and hypermagnesuria, but hypoparathyroidism contributes to hypercalciuria at high levels of alcohol intoxication.

Adult↗

PubMed1976

A simplified assessment of response to parathyroid hormone in hypoparathyroid patients.

Hightly purified bovine parathyroid hormone (B.P.T.H) was given by injection and/or infusion to six normal volunteers and to patients with surgical hypoparathyroidism (five cases), idiopathic hyparathyroidism (five cases), or poeudo-hypoparathyroidism (six cases). Infusion and injection of B.P.T.H. produced very similar patterns of response in plasma adenosine 3' 5' cyclic monophosphate (cyclic A.M.P.) In all six normal volunteers and in the patients with surgical (five cases) or idiopathic (four cases) hypoparathyroidism who had injections of B.P.T.H., plasma-cA.M.P. had risen significantly within 5 min and the peak response was genereally observed 10 min after injection of hormone. In the five pseudohypoparathyroid patients who received injections of B.P.T.H., plasma-c?A.M.P. concentration increased only slightly or not at all after the hormone was administered. Unlike the traditional test for the investigation of hypocalcaemia, the test described here does not require collections of urine samples.

Adolescent↗

PubMed1975

Treatment of hypoparathyroidism and pseudohypoparathyroidism with metabolites of vitamin D: evidence for impaired conversion of 25-hydroxyvitamin D to 1 alpha,25-dihydroxyvitamin D.

In hypoparathyroidism and pseudohypoparathyroidism, pharmacologic doses of vitamin D correct hypocalcemia, but the mechanism is unknown. In two children with hypoparathyroidism and one with pseudohypoparathyroidism we tested the hypothesis that in these conditions there is a defect in synthesis of 1 alpha,25-dihydroxyvitamin D3, the principal active metabolite of vitamin D. In both conditions, minute doses of the metabolite (0.04 to 0.08 mug per kilogram of body weight per day) quickly corrected hypocalcemia and increased intestinal calcium absorption. On the other hand, the effective dose of 25-hydroxyvitamin D3 to maintain normocalcemia was 3 to 4 mug per kilogram per day in the two conditions. Thus, the dosage ratio of 25-hydroxyvitamin D3 to 1 alpha,25-dihydroxyvitamin D3 approximated 100:1. By contrast this ratio was approximately 3:1 in two infants with vitamin D deficiency, a condition in which optimal metabolism of vitamin D would be expected. These findings suggest an impaired conversion of 25-hydroxyvitamin D to 1 alpha,25-dihydroxyvitamin D in both hypoparathyroidism and pseudohypoparathyroidism.

Administration, Oral↗

PubMedDate not supplied

Case report: hypoparathyroidism and iron storage disease. Treatment with 25-hydroxy-vitamin D3.

A patient in whom hypoparathyroidism developed as a complication of posttransfusional iron storage disease is described. The hypoparathyroidism occurred after more than 15 years of receiving blood transfusions at frequent intervals. In this patient with thalassemia major the serum PTH levels were undetectable. 25-hydroxy-vitamin D3 corrected the hypocalcemia that was resistant to vitamin D2, probably due to the associated liver dysfunction. Other cases reported in the literature are reviewed. It is suggested that hypoparathyroidism occurs more frequently than usually suspected in patients with iron storage disease.

Adult↗

PubMed1977

Paroxysmal choreoathetosis as a presenting symptom in idiopathic hypoparathyroidism.

A patient with idiopathic hypoparathyroidism presenting with spells of paroxysmal choreoathetosis is described. The possible mechanisms by which hypoparathyroidism induces choreoathetosis and other extrapyramidal motor dyfunctions are discussed. The need for screening patients with extrapyramidal disease for hypoparathyroidism is stressed.

Adolescent↗

PubMed1976

Optic nueritis in hypoparathyroidism.

Disk swelling in patients with hypoparathyroidism has often been attributed to papilledema but rarely to optic neuritis. Although we are reporting a patient with hypoparathyroidism in whom optic neuritis developed, a causal relationship is not yet clear. The patient may have had ischemic optic neuropathy concomitant with hypoparathyroidism or caused by tetanic vasospasm or calcification of optic nerve nutrient vessels.

Calcinosis↗

PubMedDate not supplied

[Use of the test with disodium salt of ethylenediaminetetraacetic acid for diagnosis of latent forms of hypoparathyroidism].

A test with disodium salt of ethylenediaminetetraacetic acid was conducted in 29 individuals--9 healthy ones, 5 patients with latent hypoparathyroidism, 7 with manifest hypoparathyroidism given vitamin D 2, and 8 patients who sustained an operation on the thyroid gland. Primary reduction of the calcium level in patients with latent hypoparathyroidism was in 12 hours combined with a low calcium level, not exceeding 8.5% mg. Along with this in the mentioned group of patients, and also in the patients operated for goiter and in some of the patients given vitamin D 2 there were observed peculiarities of the calciemic curves during the first hours of the test differentiating them from the normal. The diagnostic significance of this is discussed.

Adolescent↗

PubMedDate not supplied

Hypoparathyroidism secondary to surgery for carcinoma of the pharynx and larynx.

Hypoparathyroidism occurs secondary to surgery for carcinoma of the pharynx and larynx in which a total thyroidectomy is required. The indications for partial and total thyroidectomy are presented. Hypoparathyroidism is an important and complex problem with the clinical presentation ranging from tetany to latent chronic hypoparathyroidism. Serum calcium, phosphate, magnesium, and protein levels are important parameters to monitor. A therapeutic strategy is presented and its complications are discussed. The role of magnesium in calcium metabolism is emphasized.

Adult↗

PubMed1977

Oculocraniosomatic neuromuscular disease with hypoparathyroidism.

During a six-year period, an adolescent girl developed a polyglandular disease characterized by hypoparathyroidism, chemical diabetes, growth failure and pubertal delay, hypercholesterolemia, and hypomagnesemia. A slowly progressive neurological disorder occurred simultaneously, consisting of progressive external ophthalmoplegia, mitochondrial myopathy, ataxia, neural deafness, mental subnormality, atypical retinitis, corneal dystrophy, cataract, and increased protein level in the cerebrospinal fluid. An intracardiac conduction defect was also found. This disorder, the cause of which is uncertain, is termed oculocraniosomatic disease. Our patient is apparently unique in that there was an associated hypoparathyroidism.

Adolescent↗

PubMed1977

Familial nephrosis, nerve deafness, and hypoparathyroidism.

Two male siblings with nephrotic syndrome, nerve deafness, and hypoparathyroidism are described. Each child, one at five years of age and the other at eight years, died in renal failure. At autopsy the parathyroid glands were absent in one child and hypoplastic in the other one. Two twin male siblings presented with similar findings and died at the age of three years. At autopsy their parathyroid glands were fibrotic, and glomerular basement membranes were thickened. This may be the first recorded association of familial nephrosis, nerve deafness, and hypoparathyroidism. The mode of transmission is compatible with autosomal recessive inheritance.

Child, Preschool↗

PubMed1977

Vitamin D therapy in hypoparathyroidism and pseudohypoparathyroidism: weight-related dosages for initiation of therapy and maintenance therapy.

The aims of this study were to determine the dose of vitamin D2 that maintains the serum calcium level within the normal range in hypoparathyroid and pseudohypoparathyroid children and to establish a safe and quickly acting dose for initiating therapy in symptomatic patients. The dose requirement for maintenance therapy was studied in 11 patients and initiation therapy was studied in five newly diagnosed hypocalcemic patients. The results show that (1) the maintenance requirement of vitamin D2 is proportional to body weight and averages 2,000 IU (50 microgram)/kg/day for children of all ages and with all types of hypoparathyroid disorders and the (2) in newly diagnosed symptomatic patients, carefully controlled administration of 8,000 IU (200 microgram) vitamin D2/kg/day for the first one to two weeks corrects hypocalcemia quickly and safely.

Adolescent↗