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Results for “PARATHYROID, HYPOPARATHYROIDISM”

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At least 19 recordsLinked to original sources
PubMed1990

[Hypomagnesemia-induced hypocalcemia: functional hypoparathyroidism, parathyroid hormone- and vitamin D-resistant].

In four patients with severe hypomagnesemia, hypocalcemia, and functional hypoparathyroidism (three patients with shortened bowel, one with alcoholism), sequential measurements of parameters of calcium metabolism were performed before and during intravenous administration of magnesium. Parathyroid hormone was immeasurably or inadequately low in all patients before magnesium injection, but rapidly rose to elevated values thereafter. Even without calcium supplements, serum calcium rose to normal levels within 2-5 days, although 1,25(OH)2-Vitamin D levels did not rise significantly. In the patient with alcoholism, hypophosphatemia developed during the first days after admission; the rise of serum calcium preceded the elevation of cyclic adenosine monophosphate in urine. A transient rise of urinary calcium was observed in two patients after initiation of magnesium therapy, with a subsequent fall to subnormal levels in spite of normal serum calcium concentrations. The findings were considered to be due to partial parathyroid hormone resistance during the phase of magnesium replenishment.

Adult↗
PubMed1985

Parathyroid allotransplantation in the treatment of complicated idiopathic primary hypoparathyroidism.

Parathyroid allotransplantation was performed in a 25-year-old woman with idiopathic hypoparathyroidism that had been diagnosed at age 4 years. Long-term medical management of the primary condition with vitamin D and oral calcium supplementation was complicated by multiorgan calcinosis and renal failure. At the age of 21 years she received a successful cadaver renal allograft. Four years later she developed calcinosis cutis with widespread skin necrosis. Medical control of calcium and phosphate metabolism was unsatisfactory and the skin necrosis became progressive and life threatening. A parathyroid allograft that was performed with tissue from a parathyroid adenoma resulted in normalization of the serum calcium and phosphorus levels with arrest and subsequent healing of the skin necrosis. Later failure of the parathyroid allograft was followed by successful retransplantation of normal parathyroid tissue from a cadaver organ donor.

Adult↗
PubMed1996

Mutations in the Ca(2+)-sensing receptor gene cause autosomal dominant and sporadic hypoparathyroidism.

Parathyroid hormone secretion is negatively regulated by a 7-transmembrane domain, G-protein coupled Ca(2+)-sensing receptor. We hypothesized that activating mutations in this receptor might cause autosomal dominant hypoparathyroidism (ADHP). Consistent with this hypothesis, we identified, in two families with ADHP, heterozygous missense mutations in the Ca(2+)-sensing receptor gene that cosegregated with the disorder. None of 50 normal controls had either mutation. We also identified a de novo, missense Ca(2+)-sensing receptor mutation in a child with severe sporadic hypoparathyroidism. The amino acid substitution in one ADHP family affected the N-terminal, extracellular domain of the receptor. The other mutations involved the transmembrane region. Unlike patients with acquired hypoparathyroidism, patients with these mutations had hypercalciuria even at low serum calcium concentrations. Their greater hypercalciuria presumably reflected activation of Ca(2+)-sensing receptors in kidney cells, where the receptor negatively regulates calcium reabsorption. This augmented hypercalciuria increases the risk of renal complications and thus has implications for the choice of therapy.

Adult↗
PubMed1976

Experimental induction of hypoparathyroidism with parathyroid hormone antibodies.

This study describes the effect of a single injection of parathyroid hormone antiserum on the serum calcium, serum phosphate, urinary cyclic AMP, and urinary phosphate levels in the intact perfused rat. A significant decline in serum calcium level with concomitant elevation in serum phosphate level and decreased urinary excretion of phosphate and cyclic AMP was noted. These findings strongly suggest that a transient hypoparathyroid state was induced by the parathyroid hormone antiserum.

Animals↗
PubMed2006

Hypoparathyroidism and pseudohypoparathyroidism.

The principal function of the parathyroid hormone (PTH) is maintenance of calcium plasmatic levels, withdrawing the calcium from bone tissue, reabsorbing it from the glomerular filtrate, and indirectly increasing its intestinal absorption by stimulating active vitamin D (calcitriol) production. Additionally, the PTH prompts an increase in urinary excretion of phosphorus and bicarbonate, seeking a larger quantity of free calcium available in circulation. Two mechanisms may alter its function, limiting its control on calcium: insufficient PTH production by the parathyroids (hypoparathyroidism), or a resistance against its action in target tissues (pseudohypoparathyroidism). In both cases, there are significantly reduced levels of plasmatic calcium associated with hyperphosphatemia. Clinical cases are characterized by nervous hyperexcitability, with paresthesia, cramps, tetany, hyperreflexia, convulsions, and tetanic crisis. Abnormalities such as cataracts and basal ganglia calcification are also typical of these diseases. Treatment consists of oral calcium supplementation associated with increased doses of vitamin D derivatives.

Calcitriol↗
PubMed1976

Functional hypoparathyroidism and parathyroid hormone end-organ resistance in human magnesium deficiency.

Hypocalcaemia is a well-recognized manifestation of magnesium deficiency. We have studied seventeen patients with this syndrome in an attempt to determine the pathogenesis of the hypocalcaemia. Mean initial serum calcium concentration was 5-6 mg/dl and mean initial serum magnesium concentration was 0-75 mg/dl. Serum immunoreactive parathyroid hormone (IPTH) was measured in sixteen patients in the untreated state. Despite severe hypocalcaemia, serum IPTH was either undetectable (less than 150 pg/ml) or normal (less than 550 pg/ml) in all but two patients. Serial measurements made during the initial 4 days of magnesium therapy in four patients showed an increase in serum IPTH within 24h, but a delayed increase in serum calcium, which required approximately 4 days to reach normal values. The effect of the rapid normalization of serum magnesium on serum IPTH and serum calcium concentration was studied in three patients. Within 1 min after 144-300 mg of elemental magnesium was administered i.v., serum IPTH had risen from undetectable to 3600 pg/ml and 1725 pg/ml in two patients and from 425 pg/ml to 937 pg/ml in the third. Serum calcium concentrations were unchanged after 30-60 min. These data provide evidence for impaired parathyroid gland function in most of the magnesium deficient patients. The rapidity with which serum IPTH rose in response to magnesium therapy indicates that this may reflect a defect in parathyroid hormone (PTH) secretion rather than its biosynthesis. The failure of serum calcium concentration to increase during the initial days of magnesium repletion, at a time when serum IPTH concentrations were normal or elevated, suggests end-organ resistance to PTH in these patients. The renal response to PTH was examined in two magnesium deficient patients by measurement of urinary cyclic AMP excretion following administration of parathyroid extract. In both patients there was a minimal increase in urinary cyclic AMP concentrations. In contrast, when the hepatic response to glucagon was tested on the same patients by measurement of plasma cyclic AMP concentrations following administration of glucagon, normal increases were observed. These results suggest that adenylate cyclase systems of various organs may be affected differentially by a state of magnesium deficiency. It is suggested that magnesium deficiency may result in defective cyclic AMP generation in the parathyroid glands and in the PTH target organs. This could be the principal mechanism operative in both impaired PTH secretion and end-organ resistance to PTH which together contribute to the development of hypocalcaemia.

Adult↗
PubMed1995

Resetting of parathyroid hormone secretion after vitamin D3 treatment in hypoparathyroidism and after parathyroid adenectomy in primary hyperparathyroidism.

The relationship between parathyroid hormone (PTH) secretion and extracellular calcium (Ca) level is reciprocal causality. The equilibrium operating point determines basal PTH secretion rate and basal extracellular Ca level. We studied how this equilibrium was achieved in the subjects with decreased PTH secretion or decreased parathyroid glands number. Basal/maximum ratio of serum PTH, which reflects the basal secretory state of parathyroid glands, was increased in 9 hypoparathyroid patients treated with vitamin D3 (VD3) [7 patients with idiopathic hypoparathyroidism] and in seven of nine parathyroid adenectomized patients. There was a negative correlation between the ratio and basal serum Ca level in the patients with IHP after VD3 treatment (r = 0.7167, P < 0.05) and in the patients after parathyroid adenectomy (r = 0.7760, P < 0.05). The regression curves in these two groups coincided regardless of the difference in maximum PTH secretion rate, which suggested that the basal secretory state of parathyroid glands was determined by extracellular Ca level in a similar manner in these subjects. There was a sigmoidal relationship between basal/maximum ratio of serum PTH and basal serum Ca level, when the data were collected from 15 hypoparathyroid patients before or after VD3 treatment, 9 parathyroid adenectomized patients, and 10 normal subjects (r = 0.9057, P < 0.001). This sigmoidal curve is thought to represent the fundamental relationship between the basal secretory state of parathyroid glands and extracellular Ca level.

Adenoma↗
PubMed2005

Plasma osteoprotegerin is associated with mortality in hemodialysis patients.

Expression of bone proteins resulting from transdifferentiation of vascular smooth muscle cells into osteoblasts suggests that vascular calcifications are a bioactive process. Regulating molecules such as osteoprotegerin (OPG) and receptor activator of NF-kappaB ligand (RANKL) could play a key role in bone-vascular calcification imbalance. This study investigated the contribution of these proteins as well as mineral metabolism disorders in hemodialysis (HD) patient outcome. A total of 185 HD patients were followed up prospectively for 2 yr. In addition to clinical characteristics, mineral metabolism markers as well as OPG and soluble RANKL (sRANKL) were measured at baseline. After 2 yr, survival rates were described with Kaplan-Meier and compared with Cox regression analyses; 50 patients died (27 from cardiovascular diseases). Calcium, phosphate, and calcium x phosphate product were not associated with mortality. Both hyperparathyroidism (parathyroid hormone > or =300 pg/ml) and hypoparathyroidism (parathyroid hormone <150 pg/ml) were poorly associated with all-cause and cardiovascular mortality. By contrast, elevated OPG levels predicted all-cause (relative risk [RR] 2.67; 95% confidence interval [CI] 1.32 to 5.41; P = 0.006) and cardiovascular mortality (RR 3.15; 95% CI 1.14 to 8.69; P = 0.03). Low levels of sRANKL were associated with a protective effect for all-cause mortality (RR 0.45; 95% CI 0.21 to 0.94; P = 0.03). The association of OPG with all-cause mortality was stronger in patients with C-reactive protein > or =12.52 mg/L. In this condition, both highest (RR 5.68; 95% CI 1.48 to 22.73; P = 0.01) and lowest tertiles (RR 5.37; 95% CI 147 to 1968; P = 0.01) significantly predicted poor outcome. These results show that regulating-bone molecules, especially OPG, are strong predictors of mortality in HD patients, suggesting that OPG is a vascular risk factor, in particular in patients who have high C-reactive protein levels. OPG determination therefore should be added to the biologic follow-up of these patients.

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↗