Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0221002 (primary hyperparathyroidism)
 4,921 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Serum parathormone (PTH) values are believed useful in diagnosing hyperparathyroidism and in evaluating patients before parathyroid operation. From 1975 through 1983, 328 adults patients with persistent hypercalcemia and normal renal function underwent cervical exploration for presumed primary hyperparathyroidism. Preoperative serum PTH values were obtained in 137 patients. Eight had negative explorations (5.8%): serum PTH values were normal in three patients and elevated in five. Serum PTH values were normal or low in 31 of the other 129 patients (false-negative rate = 24%). Of 191 patients for whom neither serum PTH nor nephrogenic cyclic adenosine-3',5'-monophosphate values did not were obtained preoperatively serum PTH values did not reduce the incidence of negative cervical explorations and, when obtained, they were misleading in one fourth of patients who benefitted from parathyroid exploration.
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PMID:Is serum parathormone assay necessary in evaluating primary hyperparathyroidism? 395 65

Dual tracer parathyroid imaging (DTPI) using Tc-99m and TI-201 has a reported sensitivity of 92% for the detection of parathyroid adenomas. A patient with biopsy-proven parathyroid adenoma as well as papillary thyroid carcinoma is presented. To date, this is the first such case ever to be reported and implies that DTPI, although a sensitive diagnostic modality for parathyroid adenoma detection, is not specific. The diagnosis of primary hyperparathyroidism has recently been established more frequently than in the past due to detection of elevated serum calcium levels on routine blood samples, relatively sensitive parathormone (PTH) assays, and noninvasive imaging modalities such as nuclear medicine, CT scanning, and ultrasonography. At our institution, we have successfully detected the location of parathyroid adenomas in many cases, using the dual tracer method with TI-201 and Tc-99m, confirmed at surgery. We present a case of primary hyperparathyroidism in which two distinct lesions were detected by nuclear imaging: one lesion was proven at surgery to be a parathyroid adenoma, while the other represented thyroid carcinoma.
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PMID:Co-existent parathyroid adenoma and thyroid carcinoma. Nonspecificity of dual tracer parathyroid imaging for parathyroid lesions. 404 7

Uncomplicated bilateral percutaneous subclavian venous sampling for parathormone estimation was performed preoperatively in 10 patients with primary hyperparathyroidism. In 7 cases there was correlation of the higher parathormone level with the side of the parathyroid tumour subsequently found at operation. In conjunction with the "Tibblin strategy of unilateral parathyroidectomy" (1) a dual approach is suggested that may provide a simple, accurate method of treating patients with hyperparathyroidism.
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PMID:Preoperative percutaneous localisation of parathyroid tumours: a preliminary report. 405 21

After the operation of hyperparathyroidism not only the level of calcium but also the postoperative course of the parathormone is a very informative parameter. In contrast to the serum calcium there is a very delayed normalisation of the values of parathormone in single cases of primary hyperparathyroidism. In cases of recurrent primary hyperparathyroidism the value of parathormone increases much earlier than the value of serum calcium and before the patient has any complaints. So the parathormone enables the recurrent or persistening hyperparathyroidism to be early recognized or differentiated respectively. In the course of the operative therapy in secondary hyperparathyroidism the recrudescence of the level of parathormone points to a successful replantation of the epithelial bodies. In general increased postoperative values are not to be equated with the recurrence of the disease.
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PMID:[The course of parathyroid hormone following an operation for hyperparathyroidism]. 409 Jul 86

Two cases of primary hyperparathyroidism due to single parathyroid adenomas presented with the additional feature of hyperchloremic acidosis. The defect in urinary acidification responsible was not of the distal or gradient-limited type since both patients could lower urine pH adequately. However, there was a defect of bicarbonate reabsorption, an abnormality referred to as the proximal or rate-limited type of renal tubular acidosis. It is suggested that this defect represents an exaggeration of the physiological effect of parathormone on bicarbonate reabsorption and may be responsible for the frequent finding of hyperchloremia in association with primary hyperparathyroidism as well as for the urinary bicarbonate-wasting associated with a variety of causes of secondary hyperparathyroidism.
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PMID:Primary hyperparathyroidism and proximal renal tubular acidosis: report of two cases. 501 29

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

A retrospective study of the case-reports of 263 patients explored surgically for primary hyperparathyroidism demonstrated the cause to be: an adenoma (206 cases), a primary hyperplasia (29 cases), or a cancer (3 cases), exploration was negative in 25 cases. Presenting symptoms were mainly urinary, but 15 p. 100 of patients seen during the last two years had been asymptomatic. Nine patients required emergency surgery and 29 had a primary normocalcemic hyperparathyroidism. The two most useful laboratory examinations, apart from measurement of blood calcium and phosphorus levels, were parathormone assay (elevated levels were present in 80 p. 100 of cases) and quantitative bone biopsy (positive in over 80 p. 100 of patients). The surgical approach was mainly cervical, except for repeat operations when ten sternotomies were performed with successful results in 4 cases. Immediate postoperative mortality was quite high (3 p. 100), particularly in the acute forms or those with multiple adenomas, and in patients over 70. Morbidity (hypocalcemia, recurrent nerve palsy) was increased after repeat surgery. Analysis of long-term results, particularly with respect to urinary symptoms, showed marked differences between lesions of single glands (adenoma) and hyperplasia. The most difficult problem to resolve with this surgery is the importance to attach to excision of the parathyroids when lesions are present in several glands.
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PMID:[Surgical treatment of primary hyperparathyroidism. Evaluation of 263 cases]. 614 97

An increased calcium excretion in 24-hour urine was found in 32 of 42 out-patients with recurrent calcium nephrolithiasis (calcium excretion > 300 mg in males, > 250 mg in females). Subsequent hospitalization of the 32 patients revealed the following diagnosis after a calcium tolerance test: absorptive hypercalciuria in 18, renal hypercalciuria in 4, primary hyperparathyroidism in 2 and dietary hypercalciuria in 7. Normocalciuria in 10 out-patients was confirmed in 6; in one instance there was, however, primary hyperparathyroidism, in 3 there was absorptive hypercalciuria. In one patient it was not possible to classify the hypercalciuria. Total as well as nephrogenic cAMP showed wide scatter and was unsuitable, therefore, in differential diagnosis. In 2 of 3 cases of hyperparathyroidism the serum level of parathormone was distinctly elevated.
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PMID:[Diagnosis of hypercalciuria in calcium nephrolithiasis (author's transl)]. 625 Jul 84

In three out of four patients with primary hyperparathyroidism, 2 000 mg of cimetidine daily caused a reduction of immunoreactive parathormone (iPTH) when measured at 8.30 and 11.30 on days 16 and 17 on treatment. Serum Ca, PO4 and maximal tubular reabsorption of PO4 remained unchanged. Excretion of cAMP/100 ml GFR remained elevated to at least the same extent as before treatment. Two patients, in whom cimetidine treatment was continued for an additional 4 weeks, did not show further hormonal or biochemical changes compared with the evaluation on days 16 and 17. We conclude that reduction of iPTH is not accompanied by any change in biological activity of this hormone. The reason for this discrepancy remains unclear.
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PMID:Dissociation between changes in immunoreactive parathormone and its biological indices induced by cimetidine in primary hyperparathyroidism. 627 60

Since Sherwood's report in 1979, contradictory findings have been published with regards to the treatment of primary hyperparathyroidism with cimetidine. We studied 16 patients with primary hyperparathyroidism treated with 1,200 mg of Cimetidine and followed-up clinically and biochemically. A decrease in serum calcium and urinary CAMP was observed after the fourth week of cimetidine therapy with no significant change in parathormone levels. In none of the cases did Cimetidine seem to provide a treatment of hyperparathyroidism, a condition which remains curable with surgery.
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PMID:[Cimetidine treatment of primary hyperparathyroidism]. 632 36


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