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)

Plasma hCT levels were less than 50 pg/ml in 50 normal subjects. In 16 patients with medullary carcinoma of the thyroid (MCT), plasma hCT levels were distinctively elevated and they fell significantly after total thyroidectomy, but in 11 of them plasma levels were still high, indicating the presence of metastases. In 74 patients with the other types of malignancy, plasma hCT levels were found to be high in 9 cases (3 oat cell carcinoma of the lung, 4 malignant carcinoids, one malignant pheochromocytoma and one acute myelocytic leukemia). Except for the leukemic case, all these tumors were derived from neural crest. In 12 patients with primary hyperparathyroidism, plasma hCT levels were less than 20 pg/ml. In 13 hypoparathyroid patients, two with pseudohypoparathyroidism and one with pseudoidiopathic hypoparathyroidism, plasma hCT levels were slightly elevated. Some patients with uremia had elevated plasma hCT levels, but there was no relation between plasma levels of hCT and those of PTH, urea nitrogen or creatinine. In response to Ca (4.5 mg/kg/10 min) or tetragastrin (4 mug/kg/5 min) infusion, a marked increase in plasma hCT was observed in all patients with MCT, but not in normal subjects. In 5 hypoparathyroid patients, a significant increase to both stimuli was also observed in all cases. Two patients with pseudopseudohypoparathyroidism responded to the Ca load. These results indicate that the determination of plasma hCT levels especially after a short Ca or tetragastrin infusion is important to study various pathological conditions.
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PMID:Plasma human calcitonin (hCT) levels in normal and pathologic conditions, and their responses to short calcium or tetragastrin infusion. 19 Dec 50

Twenty-five patients with end-stage renal disease, nine of whom were receiving pharmacologic doses of vitamin D, and seventeen patients with primary hyperparathyroidism underwent bone biopsy following a three-day course of tetracycline administration. The mean width of the fluorescent tetracycline bands were significantly greater in the bones of patients with uremia than in those with primary hyperparathyroidism. This difference was due to wide labels present in the patients with uremia who had not been treated with vitamin D, as no differences existed in mean label widths of patients with uremia who had received this compound and the patients with primary hyperparathyroidism. Comparison of the maximum label widths distinguished not only primary hyperparathyroid patients from those with uremia, but uremic patients who had recieved vitamin D from those who had not been so treated. Quantitative microscopy of standard, nonfluorescent histologic features failed to make this latter distinction. These data are consistent with the presence of a wide zone of instantaneously fluorescing material in uremic bone following tetracycline administration, which does not relate to bone apposition occurring during antibiotic administration. This phenomenon probably represents a delay in mineral maturation which is normalized by vitamin D. Furthermore, it is apparent that the use of a continuously administered (single) tetracycline label will result in an overestimation of bone formation rates, particularly in osteomalacic states.
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PMID:Tetracycline fluorescence in uremic and primary hyperparathyroid bone. 60 25

Although anemia has not been widely appreciated as a complication of primary hyperparathyroidism, 5.1% of the individuals with this disorder seen at the Massachusetts General Hospital since 1962 had a normochromic, normocytic anemia that could not be related to blood loss,a deficiency state, or uremia. The anemic group had more advanced bone disease and higher levels of serum calcium, alkaline phosphatase, and parathyroid hormone than the nonanemic group. Results of bone marrow biopsies performed in five patients showed variable degrees of myelofibrosis. However, none of the patients had hepatosplenomegaly, a myelophthisic peripheral blood smear, leukopenia, or thrombocytopenia. Removal of the abnormal parathyroid glands led to improvement or correction of the anemia.
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PMID:Anemia in primary hyperparathyroidism. 85 57

The serum calcium level measured in the research laboratory was 10.8 mg/100 ml or more in all of 73 patients with primary hyperparathyroidism, though many of the values were normal when measured in the hospital laboratories. Postoperatively, all patients successfully operated on showed an immediate increase in renal phosphorus reabsorption to 95% to 100%, and a decrease, which averaged 54%, in urinary hydroxyproline levels. Seven patients who had hyperplasia had no clinical or laboratory features distinguishing them from those with adenomas. Uremia, an ominous sign, was found in six patients, five of whom died.
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PMID:Primary hyperparathyroidism. Laboratory and clinical data in 73 cases. 117 65

Derangements in leukocyte function occur in patients with primary hyperparathyroidism and in those with uremia, which is a state of secondary hyperparathyroidism, suggesting that parathyroid hormone (PTH) may affect leukocyte function. We examined the interaction between PTH and random migration of human polymorphonuclear leukocytes (PMNL) utilizing a modified Boyden chamber. Intact 1-84 PTH but not its amino-terminal (1-34 PTH) or its carboxy-terminal (53-84 PTH) fragments produced marked and significant (p less than 0.01) stimulation of random migration in a dose-dependent manner. Inactivation of 1-84 PTH abolished its effect and other peptide hormones (calcitonin, glucagon, insulin and vasopressin) did not stimulate migration of PMNL. The effect of PTH on migration was not due to action of the hormone on chemotaxis. PTH did not enhance cAMP or cGMP production by PMNL. The stimulation of PMNL motility by PTH was independent of calcium concentration in media, was not mimicked by calcium ionophore and was not blocked by verapamil. Quinidine also produced significant (p less than 0.01) increase in random migration of PMNL and this effect was not additive to that of PTH. Prolonged exposure to PTH (16-20 h) was associated with significant inhibition of random migration of PMNL. The migration of PMNL from patients with advanced renal failure was significantly (p less than 0.01) reduced and there was a significant (p less than 0.01) inverse relationship between random migration of PMNL and serum levels of PTH. Also PTH produced only modest stimulation of random migration of PMNL in most patients with renal failure.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Effect of parathyroid hormone on random migration of human polymorphonuclear leukocytes. 285 73

During 1974-1984 altogether 481 patients were treated for end-stage renal disease (ESRD). Eight patients, five women and three men, with chronic pyelonephritis as the primary cause of ESRD, had staghorn urinary calculi as a predisposing factor for renal failure. These eight patients were studied retrospectively concerning epidemiological and bacteriological aspects, the treatment of the stone disease, and the development of uraemia. Anatomical and metabolic abnormalities such as bladder outlet disturbances, primary hyperparathyroidism, phenacetin abuse or metabolic stone disease were found in six patients. The women had all been infected with Proteus mirabilis, whereas the men had been infected with various microorganisms. The average time taken for the development of ESRD, estimated from the first sign of renal impairment, was 7.4 +/- 2.9 (SD) years. Five patients had died before this study commenced. One of the patients still alive was on dialysis treatment. Two patients who were doing well without dialysis were stone free and had sterile urine after successful pyelolithotomy. It is concluded that the prevalence of infectious urinary calculi as a cause of uraemia in patients with ESRD is low. The time taken for uraemia to develop is short in these patients and they often have anatomical abnormalities. Proteus is commonly found in this group of patients. Patients with staghorn calculi, urinary tract infection and impairment of renal function are at risk of developing uraemia.
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PMID:Infection-induced urinary calculi and renal failure. 332 3

The long-term clinical results of parathyroidectomy for primary hyperparathyroidism were analyzed in 176 patients. Preoperatively 152 patients (86%) showed classic symptoms, 15 (9%) were classified as minimally symptomatic (only hypertension, diffuse osteopenia or manifestations of the hypercalcemic syndrome), and nine (5%) were asymptomatic. All patients were normocalcemic at follow-up, but renal, skeletal or gastrointestinal symptoms were eliminated in only 88-91%. Preoperatively impaired renal function and hypertension were seldom improved by parathyroidectomy. Deterioration of renal function and hypertension occurred only in the symptomatic and minimally symptomatic patients, in whom the course was varied and unpredictable. During observation periods up to 22 years, 7% of the patients died of acute/chronic renal failure or consequences of hypertension. Death from uremia was more common when there was also skeletal involvement. Acute pancreatitis could occur without preoperative symptoms, but other gastrointestinal disorders responded to normalization of parathyroid metabolism. Multiple bone lesions responded functionally and lacked prognostic significance. Hypercalcemic syndrome was rapidly and lastingly relieved by parathyroidectomy.
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PMID:Clinical long-term results after parathyroidectomy for primary hyperparathyroidism. 342 99

The long-term clinical courses of 212 "cured" (normocalcemic) patients were analyzed for 1 to 25 years (mean, 6.8 +/- 5.4 years). Preoperatively, 181 patients (85%) were classified as having typical symptoms, 22 patients (11%) as having minimal symptoms, and nine patients (4%) as having no symptoms of primary hyperparathyroidism (PHP). Although the formation of urinary calculi was stopped in 91% of patients, deteriorated renal function and hypertension were seen in patients with symptoms (14% and 8%, respectively) and patients with minimal symptoms of PHP (6% and 15%, respectively). Renal function changes and hypertension were unpredictable despite normalization of the hyperactive parathyroid metabolism and had decisive results: 7% of the patients died of uremia or of the consequences of hypertension (stroke). Large, multiple bone lesions healed functionally and were of no prognostic significance. In the majority of patients with symptoms of PHP, gastrointestinal manifestations healed postoperatively, but two patients who had no preoperative gastrointestinal complaints died of acute pancreatitis. Almost all symptoms of the hypercalcemia syndrome disappeared immediately and permanently in patients with symptoms and patients with minimal symptoms of PHP. Neither deterioration of renal function nor elevation of blood pressure were observed postoperatively in "cured" patients who showed no symptoms of PHP preoperatively. Even in these patients, immediate surgical treatment may have avoided the complications of chronic renal failure or hypertension. As soon as organic manifestations, even in mild form, have been established, it seems impossible to predict the course and to prevent an unfavorable clinical outcome.
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PMID:Successful parathyroidectomy in primary hyperparathyroidism: a clinical follow-up study of 212 consecutive patients. 368 53

A procedure for bioassaying parathyroid hormone-like activity in human urine has been developed. 24-hr urine samples were concentrated with dry Sephadex G-25 and bioassayed in the young thyroparathyrocauterized mouse by the measurement of whole blood calcium. Recovery of biological activity and radioiodinated beef parathyroid hormone was over 80%. Normal subjects usually excreted less than 30 U (USP) of activity per day while 18 patients with proven primary hyperparathyroidism excreted a mean of 182 U/day (USP). The activity was not found in 7 patients with hypoparathyroidism or in 5 patients with carcinoma of the breast, but was present in 9 patients with uremia and in 5 with carcinoma of the lung and hypercalcemia.
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PMID:A study of urinary excretion of parathyroid hormone in man. 565 89

The suggestion that parathyroid hormone (PTH) is a major uraemic toxin was examined by testing the effects of synthetic human PTH fragments and synthetic bovine PTH on ADP-induced and collagen-induced platelet aggregation. Whereas the bovine parathyroid-gland extracts inhibited platelet aggregation in a dose-dependent manner, none of the synthetic compounds was effective even at high concentrations. It is suggested that the inhibition of platelet aggregation by extracts of bovine parathyroid glands is not caused by PTH fragments and is probably an effect of other constituents contained in the extract. These findings argue against a role of PTH in the pathogenesis of platelet dysfunction and bleeding tendency in uraemia and were supported by platelet-aggregation studies in 6 patients with primary hyperparathyroidism. Platelet aggregation was normal before and unchanged after surgery of the parathyroid glands.
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PMID:Parathyroid hormone does not inhibit platelet aggregation. 614 27


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