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Query: UMLS:C0221002 (primary hyperparathyroidism)
 4,921 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Plasma insulin dynamics were evaluated in 10 patients with primary hyperparathyroidism before and after parathyroidectomy and correction of hypercalcemia. Before surgery fasting plasma insulin concentrations and insulin responses to administered glucose, tolbutamide, and glucagon were significantly greater than postoperative values. Hyperinsulinemia was not associated with altered glucose curves during glucose or glucagon tolerance tests, but a relatively greater insulin response to tolbutamide resulted in an increased hypoglycemic effect following its administration. The glucose-lowering action of intravenous insulin was slightly impaired before treatment. Intramuscular injections of parathormone to six normal men for 8 days induced mild hypercalcemia and hypophosphatemia and reproduced augmented plasma insulin responses to oral glucose and intravenous tolbutamide. 4-hr intravenous infusions of calcium to another group of six normal men raised serum calcium concentrations above 11 mg/100 ml. This did not alter glucose or insulin curves during oral glucose tolerance but markedly accentuated insulin responses to tolbutamide and potentiated its hypoglycemic effect. When highly purified parathormone was incubated with isolated pancreatic islets of male rats, glucose-stimulated insulin secretion was unaffected. These findings suggest that chronic hypercalcemia of hyperparathyroidism sustains a form of endogenous insulin resistance that necessitates augmented insulin secretion to maintain plasma glucose homeostasis. This state is insufficient to oppose tolbutamide-induced hypoglycemia because of an additional direct, selective enhancement of hypercalcemia on pancreatic beta cell responsiveness to the sulfonylurea. The possible direct role of parathormone in these events has not been established.
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PMID:Plasma insulin disturbances in primary hyperparathyroidism. 512 11

We describe a patient with multiple endocrine adenomatosis Type I, characterized by pituitary-dependent Cushing's Syndrome, marked hyperprolactinaemia, primary hyperparathyroidism and hyperinsulinism leading to hypoglycaemia. The patient subsequently developed an exocrine pancreatic carcinoma at the age of 32 years from which she died. An additional finding was the demonstration by immunocytochemistry of nesidioblastosis in the pancreas.
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PMID:A case of multiple endocrine adenomatosis (Type 1) with nesidioblastosis, terminating with an exocrine pancreatic carcinoma. 613 20

Carbohydrate metabolism was investigated in 9 patients with symptomatic primary hyperparathyroidism. Before and after parathyroidectomy intravenous and oral glucose tolerance test, tolbutamide test, arginine infusion test and insulin tolerance test were performed. During intravenous and oral glucose tolerance tests, patients with primary hyperparathyroidism exhibited hyperinsulinemia and impaired glucose tolerance without normalization after surgery. Tolbutamide-induced induced insulin release did not differ pre- or postoperatively. After restoration of normocalcemia and normocalcemia and normophosphatemia we found significantly lower glucose and insulin levels following arginine infusion and a significantly increased hypoglycemic response to parenterally administered insulin, probably indicating partial improvement of glucose tolerance after surgery. Our findings suggest that biochemical abnormalities associated with primary hyperparathyroidism, like hypercalcemia, hypophosphatemia, and elevated parathyroid hormone levels may cause and sustain a form of endogenous insulin resistance, which consequently leads to hyperinsulinemia and to impaired glucose tolerance. Since hyperinsulinemia as well as impaired glucose tolerance seem to be only slowly and partially reversible in symptomatic primary hyperparathyroidism, these data could be considered as an additional argument for early surgical intervention in this disorder.
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PMID:Peripheral insulin resistance in primary hyperparathyroidism. 634 5

We studied insulin receptor-binding and carbohydrate and metabolism in 15 patients with symptomatic primary hyperparathyroidism in comparison with 20 healthy controls. Insulin binding to monocytes and erythrocytes was measured by radioreceptor-ligand-assay. Furthermore, patients and controls were characterized by testing oral (100 g glucose load) glucose tolerance as well as insulin tolerance (0.1U insulin/kg body weight). Compared with controls, patients with primary hyperparathyroidism exhibited marked hyperinsulinemia (P less than 0.01) and significantly higher glucose levels (P less than 0.01) after an oral glucose load. The glucose lowering effect of intravenous insulin was significantly diminished in primary hyperparathyroidism compared with controls (P less than 0.01). Receptor studies revealed a significantly lower (P less than 0.01) insulin binding to monocytes and to erythrocytes in patients with primary hyperparathyroidism compared with controls. The present data indicate an insulin-resistant state in primary hyperparathyroidism, which is caused at least in part, by a downregulation of insulin receptors.
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PMID:Primary hyperparathyroidism is associated with decreased insulin receptor binding and glucose intolerance. 643 88

It is generally known that patients with primary hyperparathyroidism (pHPT) feature disturbances in carbohydrate metabolism and hypertension. The incidence and prevalence of frank diabetes mellitus is significantly increased in these patients. The etiology and pathogenesis of the vascular and metabolic aberrations in this condition are still unclear. Glucose intolerance in pHPT is characterized by severe insulin resistance associated with pancreatic beta cell hypersecretion of insulin. Hypercalcemia is thought to be mainly responsible for the impaired glucose metabolism. However, several studies demonstrated that hypophosphatemia can also induce insulin hypersecretion and impair peripheral glucose uptake. Hypertension in primary hyperparathyroidism is mainly attributed to hypercalcemia. However, high peripheral insulin levels are also proposed to contribute to the development of essential hypertension and hyperinsulinemia per se is regarded as an important independent cardiovascular risk factor. After parathyroidectomy and decrease of the calcium levels to within the normal range, the blood pressure levels of the patients with pHPT normalised very quickly, whereas normalization of the high peripheral insulin levels was only found in a subgroup of patients. Thus, hypercalcemia seems to be mainly responsible for hypertension in primary hyperparathyroidism. Another important, yet unresolved issue is the question as to whether or to which extent the disturbances in glucose homeostasis are reversible after surgical correction of pHPT. At an early stage of the disease, insulin resistance and insulin hypersecretion are fully reversible after parathyroidectomy, whereas in patients with long-standing primary hyperparathyroidism and severely impaired glucose tolerance the metabolic disturbances will only partially improve. These results argue for improved screening to identify asymptomatic patients with primary hyperparathyroidism and for early surgical intervention in this disease.
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PMID:[Diabetes mellitus and carbohydrate metabolism in primary hyperparathyroidism]. 847 26

Disturbances of glucose metabolism with hyperinsulinism and peripheral insulin resistance are frequently observed in patients with hyperparathyroidism. The mechanism of how hyperparathyroidism affects glucose metabolism is not known. Hypercalcemia, hypophosphatemia and the parathyroid hormone itself seem to be involved. However, parathyroidectomy exerted rather variable effects on glucose metabolism: In patients with fully developed diabetes mellitus both, a complete normalisation of glucose tolerance as well as no change in the metabolic situation have been observed. We report a 64-year old female patient with primary hyperparathyroidism and diabetes mellitus. The patient had severe insulin resistance with insulin requirements of 200 IU/day. Fasting insulin and C-peptide levels were elevated. After successful operation of a parathyroid adenoma there was a marked improvement in diabetes, and the patient's insulin requirement decreased to one third of the preoperative dose. This case further illustrates the association between primary hyperparathyroidism and diabetes mellitus and the potential improvement of the metabolic situation after parathyroidectomy.
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PMID:[Improvement of diabetes mellitus after excision of a parathyroid adenoma]. 1002 37

The possible hormonal interactions of parathormone and extracellular calcium level with other endocrine systems were studied. Primary hyperparathyroidism was used first as a clinical model, in which hypercalcemia and normocalcemia occurs before and after surgery, respectively. An increased activity of renin-aldosterone system related to parathormone was found in hyperparathyroidism, and surgery resulted in a small decrease in blood pressure. This change was accompanied by a significant decrease in the activity of the renin-aldosterone system indicating the cessation of the secondary hyperaldosteronism. The role of a relative hyperinsulinism, occurring in hyperparathyroidism, in the pathogenesis of hypertension was not proved. The basal and stimulated secretion of thyreotrophin, the basal growth hormone level, and the stimulated prolactin secretion increased after surgery. Follicle stimulating hormone and luteinizing hormone secretions remained unchanged. The results suggest that extracellular calcium may reversibly modify the secretion of certain anterior pituitary hormones and their stimulus-induced responses. In the second disease, growth hormone deficiency syndrome, studied, long-term growth hormone replacement therapy results in significant but transient changes in bone metabolism: calcium-, alkaline phosphatase-, and phosphate levels increase until 6 to 18 months as compared to the initial values; then these parameters decrease to the baseline level. Parathormone decreases until the first year then returns to the baseline level. Osteocalcin shows similar temporary changes. In spite of the above transient changes, osteodensity increases after 12 months of treatment, and further improvement can be seen after 18 and 24 months, i.e. GH treatment exerts a biphasic effect on bones; resorption increases first followed by an increase in formation. Based on the above results, it can be concluded that both parathormone and extracellular calcium are able to influence the secretion of certain hormones; and--as it is shown in growth hormone replacement therapy--other hormones may cause certain effect on them, too. The better understanding of these interactions may result in a better understanding of the pathomechanism of certain diseases and the improvement of their treatment.
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PMID:[Hormonal interactions of parathormone and calcium metabolism]. 1263 47

Although veterinary clinicians commonly rely on panels of laboratory tests with individual results flagged when abnormal, care should be taken in interpreting normal test results as well. There are several examples of this in evaluating patients with endocrine disease. The finding of a normal leukogram (absence of a stress leukogram) can be indicative of adrenal insufficiency in dogs, and this disorder can be especially elusive when there are no overt indicators of mineralocorticoid deficiency. Cats with hyperthyroidism can have normal serum thyroid hormone concentrations, normal hematocrits, and normal serum concentrations of creatinine despite the presence of disease that affects these parameters. A normal serum phosphorus concentration, in the face of azotemia, isosthenuria, and hypertension can point a clinician toward a diagnosis of primary hyperaldosteronism rather than primary renal disease. A normal serum parathyroid hormone concentration in the face of hypercalcemia is inappropriate and can indicate the presence of primary hyperparathyroidism. Similarly, hypoglycemia accompanied by a normal serum insulin concentration can be found in cases of hyperinsulinism. These normal findings in abnormal patients, and their mechanisms, are reviewed.
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PMID:When normal is abnormal: keys to laboratory diagnosis of hidden endocrine disease. 2159 44

Hypoglycemia is a well recognized cause of acute symptomatic seizures. The fact that hypoglycemia can cause peripheral neuropathy is less appreciated. We describe a case of insulinoma associated peripheral neuropathy. A 17 year-old previously healthy man was referred for investigation of refractory epilepsy. A history of recurrent seizures, slowly progressive weakness of his feet and hands, and weight gain was obtained. Physical examination showed signs of a chronic sensory-motor polyneuropathy. He was diagnosed with insulinoma and primary hyperparathyroidism, characterizing multiple endocrine neoplasia, type 1 syndrome. Cases of insulinoma associated peripheral neuropathy are very rare. The more characteristic clinical picture appears to be distal weakness, worse in the intrinsic hand and feet muscles, and no or mild sensory signs. Peripheral nervous system symptoms may not completely resolve, despite removal of the cause of hyperinsulinism/hypoglycemia and full reversion of central nervous system symptoms. Mechanisms underlying hypoglycemic neuropathy are still poorly understood.
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PMID:Multiple endocrine neoplasia type 1 presenting as refractory epilepsy and polyneuropathy--a case report. 2213 26