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

We treated a diabetic patient with familial multiple endocrine neoplasia type 1 (MEN 1) who had undergone total pancreatoduodenectomy. The patient received insulin and showed signs of symptomatic primary hyperparathyroidism (PHPT). The insulin requirement to control blood glucose before and after parathyroidectomy was compared by using an artificial pancreas. The insulin infusion rate during the day and at night was reduced to about one-third and half, respectively, after parathyroidectomy with autotransplantation of parathyroid tissues into the forearm. The daily insulin dose was reduced from 36 units to 14 units 2 weeks after surgery, and glycemic control showed further improvement 2 months after surgery with the same dose of insulin for up to 6 months. These observations suggest that insulin sensitivity increases after surgical correction of PHPT.
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PMID:Insulin sensitivity and glycemic control before and after parathyroidectomy in a diabetic patient with familial multiple endocrine neoplasia type 1. 770 99

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

Amylin, also named islet amyloid polypeptide (IAPP), is a protein that is processed and released from pancreatic beta-cells in parallel with insulin. Islet amyloid polypeptide is currently studied with regard to a role for insulin resistance in non-insulin-dependent diabetes. To elucidate a possible function of IAPP for impaired glucose tolerance in primary hyperparathyroidism (pHPT), we studied plasma IAPP levels during an oral glucose tolerance test (OGTT) in seven pHPT patients before and 8 weeks after surgery and in six healthy subjects. The B-glucose level of the patient groups was 4.34 +/- 0.12 mmol/l before and 3.97 +/- 0.16 mmol/l after surgery (NS), while the serum level of insulin was significantly higher before (16.9 +/- 2.8 mlU/l) than after (8.9 +/- 1.9 mlU/l) the operation (p < 0.05), indicating a moderately increased insulin resistance in pHPT. The basal plasma levels of IAPP were significantly higher in pHPT patients before than 8 weeks after surgery (9.71 +/- 1.05 and 4.30 +/- 0.82 pmol/l, respectively: p < 0.01). When compared to the plasma IAPP level of the controls at 1.80 +/- 0.38 pmol/l, pHPT patients had higher IAPP values both before (p < 0.01) and at 8 weeks after (p < 0.05) operation. There was a significant correlation between the serum levels of insulin and plasma levels of IAPP in pHPT patients before (r = 0.87, p < 0.01) as well as 8 weeks after surgery (r = 0.69, p < 0.05). The area under the curve for IAPP during OGTT in pHPT patients was 1872.4 +/- 187.7 pmol.min/l, which is significantly higher than after surgery (1010.8 +/- 93.7 pmol.min/l) (p<0.05) and compared to the area for the controls at 840.3 +/- 49.9 pmol.min/l (p<0.01). In conclusion, pHPT is associated with an increased plasma level of IAPP, correlated to the serum insulin level, but persistently higher than in controls also 8 weeks after surgery. Possibly, increased IAPP levels can have a role for impaired glucose tolerance in pHPT. The hyperparathyroid state might have a specific role for the release of this peptide, otherwise closely connected to insulin secretion
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PMID:Increased plasma levels of islet amyloid polypeptide in patients with primary hyperparathyroidism. 861 29

This paper presents a 59-year-old man who was admitted to our hospital because of abdominal pains in 1973. He had pancreatic calcification and showed high levels of serum amylase, Ca, and PTH. He was diagnosed as primary hyperparathyroidism with chronic pancreatitis. After excision of an ectopic parathyroid adenoma, serum Ca levels were decreased and normalized by dihydrotachysterol p.o. At the same time his symptoms disappeared. The exocrine and endocrine pancreatic functions, however, decreased gradually. Diabetes mellitus appeared in 1975 and he required insulin injection since 1983. In spite of the treatment, his diabetic control was poor. Seventeen years later in 1992, he showed hypertension and edema (nephrotic syndrome). Because of renal failure, he underwent hemodialysis and passed away due to myocardial infarction in 1993. Autopsy findings showed existence of diabetic nephropathy as the cause of renal failure. Clinical course of this patient suggests that severe complications occur even in pancreatic diabetes and that we have to control diabetes strictly in pancreatic diabetes as well as in primary diabetes.
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PMID:[An autopsy case of renal failure as its cause of death in a patient with primary hyperparathyroidism associated with chronic pancreatitis]. 894 Aug 1

The prevalence of previous or current primary hyperparathyroidism in 704 patients (390 male) with proven diabetes mellitus was 0.99% (7 patients, all female). One patient was known to have both disorders when the study commenced and 6 were discovered from the past history or by screening for hypercalcaemia. Diabetes was diagnosed at age 12 years or later, hyperparathyroidism from 45 years. Two patients were insulin-dependent. Diabetes preceded hyperparathyroidism in 3 patients, followed it in 2, and occurred during the same year in 2. The prevalence is significantly greater (p < 0.02 to <0.001) than that of hyperparathyroidism in general populations (0.10-0.36%). When adjusted for the age and sex distribution of the population of the Halton Health District the expected prevalence of 0.82% remains significantly greater, except for the general population with 0.36% prevalence (0.1 > p > 0.05). This increased three- to fourfold prevalence of hyperparathyroidism in diabetes arises mainly from females, in whom the prevalences at age 15 years or over and at age 45 years or over are 2.23% and 2.54%, respectively.
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PMID:Prevalence of primary hyperparathyroidism in patients with diabetes mellitus. 917 Dec 55

The aim of the present study was to test a mathematical model of the biochemical processes in the parathyroid glands responsible for the secretion of parathyroid hormone resulting from extracellular calcium reduction. A double exponential curve described the parathyroid hormone secretion induced by rapid lowering of blood-ionized calcium in humans with normal as well as abnormal parathyroid tissue. Our data show that it was possible to establish a simple mathematical model of the parathyroid hormone response to blood-ionized calcium lowering, sufficient to fit experimental data obtained from patients with abnormal and normal parathyroid tissue. The fitted parameters showed no significant differences between patients with insulin-dependent diabetes mellitus and controls. In primary hyperparathyroidism, the parathyroid hormone production and steady-state transport across the cell membrane were increased, probably due to the larger amount of parathyroid tissue in these patients. These observations reveal a striking functional similarity between abnormal and normal parathyroid tissue. Furthermore, an apparently linear relationship between the rate of parathyroid hormone elimination from the blood plasma and the rate of cellular production/secretion was observed. This could be interpreted as an adaptation of the parathyroid gland's ability to produce parathyroid hormone depending on the average demand from the body.
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PMID:A mathematical/physiological model of parathyroid hormone secretion in response to blood-ionized calcium lowering in vivo. 927 63

Multiple endocrine neoplasia type 1 (MEN-1) is a well characterized hereditary syndrome with the occurrence of primary hyperparathyroidism (HPT) in combination with pancreatic-duodenal endocrine and anterior pituitary tumours. The diagnosis of MEN-1, the possible probands, necessitates the recognition of at least two or three lesions classically associated with the syndrome whilst only one of them is required for individuals belonging to established MEN-1 kindreds. A distinct feature of MEN-1 comprises the multiplicity of organ involvement, the multicentricity of tumours within the affected organs as well as the complex pattern of the clinical signs of these tumours and their sometimes temporarily variable profile of hormone excess. Thorough screening studies have demonstrated that the MEN-1 trait is biochemically detectable virtually two decades prior to clinically overt disease. The primary biochemical screening programme for MEN-1 includes serum prolactin and insulin growth factor 1 (IGF-1) for pituitary lesions, intact PTH and albumin corrected total serum calcium for the parathyroids and for duodenal/pancreatic tumours serum glucose, insulin, proinsulin, pancreatic polypeptide, glucagon, gastrin and plasma chromogranin A. Furthermore a standardized meal stimulatory test analysing serum polypeptides (PP) and gastrin is recommended. Our current primary screening procedure has yielded about 10% false positives when compared with RFLP data. Pancreatic endocrine tumour diagnosis must be biochemically established since radiology fails to show lesions in half of the patients. Pancreatic involvement in young MEN-1 patients is most consistently demonstrated by analysing serum insulin, proinsulin, PP as well as plasma glucagon chromogranin A levels, which have exhibited sensitivities of 56, 67, 37 and 60%, respectively. Serum PP is a non-specific marker of islet cell tumours that should be applied in conjunction with other peptide markers. Elevation of basal serum gastrin generally indicates the presence of advanced pancreatic tumour involvement or duodenal carcinoids. Early diagnosis of pancreatic endocrine tumours in MEN-1 is enhanced by the use of a standardized meal stimulation test with measurements of serum PP and gastrin response. This test was the most sensitive test and substantiated the presence of tumour in 75% of individuals whose mean age was 25 years. False-positive stimulation due to the meal test has been found in about 10% of previous investigated individuals. The diagnosis of MEN-1 pancreatic tumours is based on biochemical screening alone and it has been substantiated that an unequivocal rise in pancreatic tumour markers precedes radiological detection of these lesions by at least five years.
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PMID:The ultimate biochemical diagnosis of endocrine pancreatic tumours in MEN-1. 968 45

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

This study deals with the setting up of human serum calcitonin radioimmunoassay (hCT-RIA) using the high titer and specific antibody which was prepared by our own laboratory. The final dilution of the antibody titer was 1:1,200,000 when the binding rate of Bo/T was 30%. The antibody's affinity constant (Kd) was 2.25 x 10(11) L/M. No cross reaction was found between the antibody and the following eight different peptide hormones and proteins, viz.: TSH, T3, T4, ACTH, PTH, BGP, Insulin and Gastrin. The coefficients variation of intra and inter assay were 3.2% and 9.0%, respectively. The mean recovery rate of CT was 99.8%. The sensitivity of this assay was 9.4 pg/ml. The examination of this methodology showed that all its indices met the demands of RIA. There was no difference in the mean value of serum CT between the two sexes in 232 normal subjects, but the serum CT concentration in those aged of sixty and over of men and women, were much lower than those aged of fourty group. Mean CT concentration was low in the patients with primary osteoporosis, but were significantly higher in those suffering from medullary thyroid carcinoma, primary hyperparathyroidism crisis and chronic renal failure.
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PMID:[The setting up of human serum calcitonin radioimmunoassay and its clinical application]. 1045 98

Primary hyperparathyroidism (PHPT) is associated with increased cardiovascular risk, although the mechanisms involved remain unclear. Recent evidence has shown increased pulse pressure to be a powerful predictor of cardiovascular events. As increases in pulse pressure are due largely to arterial stiffening, we measured arterial stiffness in 21 subjects with PHPT (18 women and 3 men; 46-71 yr old) and 21 age- and sex-matched healthy controls using pulse wave analysis, a technique that measures peripheral arterial pressure waveforms and generates corresponding central aortic waveforms. This allows determination of the augmentation of central pressure resulting from wave reflection and augmentation index, a measure of vessel stiffness. Metabolic parameters were also measured. The serum calcium level among PHPT subjects was (mean +/- SD) 2.74+/-0.14 mmol/L. pulse wave analysis showed that both augmentation and the augmentation index were significantly higher in the PHPT group vs. controls [16+/-5 vs. 10+/-4 mm Hg (P < 0.001) and 36+/-9% vs. 25+/-6% (P < 0.001)] despite comparable brachial systolic pressures between groups (136+/-13 vs. 134+/-18 mm Hg). Patients with PHPT had higher fasting serum insulin levels [median (range), 15.8 (7.4-39.4) vs. 11.6 (5.1-23) mU/L; P < 0.05] and triglyceride (1.6+/-0.6 vs. 1.2+/-0.4 mmol/L; P < 0.05), but lower high density lipoprotein cholesterol (1.4+/-0.4 vs. 1.6+/-0.3 mmol/L; P < 0.05). These data indicate that subjects with mild PHPT (calcium, <3.0 mmol/L) have increased arterial stiffness, as evidenced by higher augmentation of central aortic pressures. Enhanced vessel stiffness may arise from a combination of structural and functional vascular changes due to hypercalcemia and/or metabolic abnormalities. Increased vascular stiffness in subjects with PHPT may account in part for the increased cardiovascular risk in this group.
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PMID:Augmentation of central arterial pressure in mild primary hyperparathyroidism. 1106 92


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