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

Hypertension is frequently associated with primary hyperparathyroidism, yet the mechanism of such hypertension is unknown. Parathyroid hypertensive factor (PHF) is a circulating hypertensive factor found in a proportion of human essential hypertensive patients as well as in spontaneously hypertensive rats (SHR). In the latter case, PHF has been shown to be secreted by the parathyroid gland. The purpose of this study was to determine if PHF expression might be responsible for the hypertension seen in primary hyperparathyroidism. Ten hypertensive and 10 normotensive primary hyperparathyroid patients underwent measurement of blood pressure and PHF pre- and post-parathyroidectomy. Cases reported are those of parathyroid adenomas. There were no significant differences between the hypertensive and normotensive groups preoperatively except that 9 out of 10 of the hypertensive group had significant PHF levels (mean 11 +/- 2 mm Hg vs 0.6 +/- 2 mm Hg, respectively, p = 0.003). Post-operative change in mean arterial pressure could be predicted by pre-operative PHF level, with all PHF-positive patients showing a fall in blood pressure (r = -0.73, p < 0.01). Post-operatively, PHF was undetectable in PHF-positive patients. These results suggest that the parathyroid gland can express PHF in humans and that such expression may be responsible for a proportion of the high reported incidence of hypertension in primary hyperparathyroidism.
 ...
PMID:Expression of parathyroid hypertensive factor in hypertensive primary hyperparathyroid patients. 819 29

Primary hyperparathyroidism (HPT) is characterised by a defective calcium sensitivity of the parathyroid glands. HPT is, furthermore, associated with a high prevalence of hypertension. In the present study BP was measured before operation, during surgery and after operation in 42 HPT patients and in 15 control subjects operated for non-toxic goitre. Parathyroid tissue was removed from all patients and the concentration of cytoplasmic calcium [Ca2+]i was determined in vitro in dispersed single cells by means of microfluometry at extracellular calcium concentrations of 0.5 mM and 3.0 mM. The SBP levels were found to be raised both before (158 +/- 23 (SD) mmHg vs. 144 +/- 24 mmHg in controls, P < 0.05), during surgery (maximal level 167 +/- 22 mmHg vs. 146 +/- 16 mmHg in controls, P < 0.01) and after operation (maximal level 180 +/- 26 mmHg vs. 148 +/- 20 mmHg in controls, P < 0.001) in the HPT subject when compared with controls. SBP during surgery was found to be related to the in vitro measured [Ca2+]i in the parathyroid cells at 3.0 mM extracellular calcium concentration or to the ratio of [Ca2+]i at 3.0 mM-0.5 mM (r = -0.25 and -0.27, respectively; P < 0.05). The degree of suppression of PTH release in vitro at 3.0 mM extracellular calcium was found to be related to both systolic and diastolic BP (r = 0.57 and r = 0.53, respectively; P < 0.05) before surgery. In conclusion, BP was found to be raised in HPT patients both before operation as well as during surgery and after operation.(ABSTRACT TRUNCATED AT 250 WORDS)
 ...
PMID:Relationship between abnormal regulation of cytoplasmic calcium and elevated blood pressure in patients with primary hyperparathyroidism. 820 37

A patient with hypertension (female: aged 48 years) associated with primary hyperparathyroidism and left renal artery thrombosis is described. Taking into account that the patient was treated on the left side by lithotripsy about two years before the development of hypertension while assuming an oral dose of an estro-progestinic compound, a possible role of these two conditions is discussed in the genesis of renal artery thrombosis and development of renal hypertension.
 ...
PMID:[Observations on a case of arterial hypertension associated with primary hyperparathyroidism and renal artery thrombosis]. 825 37

The classical presentation of primary hyperparathyroidism, "moans, bones, groans," is no longer commonly seen since the diagnosis of hypercalcemia is now made much earlier with the routine use of the SMA 12. In the past 8 1/2 years, 85 patients underwent cervical exploration in our institution for primary hyperparathyroidism. There were 34 male and 51 female patients, ranging in age from 18-84 years. The specific symptoms included hypertension in 40 patients, generalized weakness in 25, renal stones in 14, psychiatric problems in 2, and bone changes on X-ray in 4. Forty-one patients were totally asymptomatic. The diagnosis was made mainly on the basis of history, serum calcium and phosphorous levels, parathormone assay, and 24-hour urinary calcium studies. Preoperative localization studies were performed in 38 patients. Thallium technetium subtraction scans, when positive, were very helpful. The surgical approach involved stepwise exploration of both sides of the neck with identification of all four parathyroid glands. In patients with uniglandular pathology (87%), the adenoma was removed with biopsy of at least one normal gland. In multiglandular disease, the abnormal glands were removed. Frozen section was routinely performed to confirm the presence of parathyroid tissue and no attempt was made to pathologically distinguish adenoma from hyperplasia. Two patients had parathyroid carcinoma. In three patients, serum calcium levels did not fall, resulting in an operative success rate of 96%. One patient treated by subtotal parathyroidectomy developed permanent hypoparathyroidism and one other patient developed temporary hypocalcemia. Only a single patient developed vocal cord palsy. Early exploration in patients with primary hyperparathyroidism is indicated. The basic diagnostic workup is sufficient for initial exploration. It is important to distinguish uniglandular from multiglandular pathology after careful bilateral exploration and identification of all four parathyroid glands.
 ...
PMID:Cervical exploration for primary hyperparathyroidism. 844 Dec 55

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.
 ...
PMID:[Diabetes mellitus and carbohydrate metabolism in primary hyperparathyroidism]. 847 26

Free intracellular calcium is increased in primary hyperparathyroidism (HPT) and may be related to the higher incidence of hypertension in this disease. This elevation returns to normal when primary HPT is corrected. In essential hypertension, an alteration in calcium channels allows a intracellular accumulation of calcium. Aiming to asses if a similar mechanism operates in primary HPT, we measured intracellular calcium concentrations using QUIN-2-AM, before and after a 10 mg sublingual dose of nifedipine, in 9 subjects with primary HPT, 12 subjects with essential hypertension and 17 normal controls. Intracellular calcium was higher in subjects with primary HPT and with essential hypertension than in normal controls (276 +/- 56, 343 +/- 50 and 113 +/- 12 nM respectively). Among patient with primary HPT, intracellular calcium correlated with plasma PTH (r = 0.82). Nifedipine reduced intracellular calcium to 173 +/- 36 nM in subjects with primary HPT and to 188 +/- 35 nM in those with essential hypertension. In the latter, the decreased in intracellular calcium and blood pressure correlated significantly (r = 0.65 p < 0.03). We conclude that increased intracellular calcium in primary HPT and essential hypertension seems to depend on an increased inflow through specific channels. However in primary HPT, this alteration is related to PTH levels.
 ...
PMID:[Nifedipine reduces the increase of free intracellular calcium in primary hyperparathyroidism: role of calcium channels and PTH]. 852 65

Low bone mass, in the asymptomatic patient, predicts future fracture risk as well as high cholesterol or high blood pressure predicts the risk of heart disease or stroke. In patients without fractures, osteoporosis can be diagnosed based on the extent of reduction in bone mass below mean peak bone mass of healthy young individuals. As bone mass decreases, fracture risk increases exponentially. Prevention of the first fracture is a clinical goal. Clinical situations in which an assessment of bone mass and fracture risk affects therapeutic decisions include estrogen deficiency, vertebral abnormalities, radiographic osteopenia, asymptomatic primary hyperparathyroidism, and longterm corticosteroid therapy. Serial measurements can also be used to monitor the effects of osteoporosis treatment in certain situations. The appropriate technique and skeletal site for bone mass measurements should be chosen based on the patient's circumstances. A clinical interpretation can enhance the value of computer-generated bone mass measurement reports and enhance decision making.
 ...
PMID:Consensus of an international panel on the clinical utility of bone mass measurements in the detection of low bone mass in the adult population. 866 48

Over the past 40 years primary hyperparathyroidism (PHP) has changed from a rare, severe disease of the bones and kidneys to a common disease with hypertension, peptic ulcer, pancreatitis, easy fatigue and proximal muscle weakness. We have during these 40 years examined one of the greatest group of patients with PHP. PHP had its maximum incidence in women over the age of 40. The disease is four times frequent in women as in man. The incidence of hypertension and peptic ulcer between patients with PHP is higher as compared with the incidence of these diseases in general populations. The severity of bone changes in individual patients with PHP does not result from the direct action of a single hormone only. Parathyroid hormone (PTH) have hypotensive and vasodilator effects on various vascular beds. The resting blood flow in the limbs of our patients with PHP is increased in comparison with control subjects. PTH increases plasma renin activity in normotensive controls. This effect is partly blocked by beta adrenergic blockers.
 ...
PMID:[Primary hyperparathyroidism]. 871 83

A 14-year-old girl, having mental and growth retardation with end stage renal disease, was affected by a stroke-like attack. The attack was associated with transient low density areas at both sides of the parietal portion on head CT. Lactic acidosis, hypertrophic cardiomyopathy, angina pectoris-like attacks, hypertension and hyperparathyroidism were also observed and they were supposedly due to mitochondrial cytopathy. No morphological or biochemical abnormalities were found on the mitochondrial respiratory chain. However, muscle carnitine palmitoyltransferase (CPT) activity was significantly low, which was restored to a normal level after hyperparathyroidism was controlled by alphacalcidol administration. Furthermore, we also found two more chronic renal failure patients with secondary hyperparathyroidism, as well as the primary hyperparathyroidism patient showing markedly low muscle CPT activity. These findings suggest the possible contribution of parathyroid hormone to lipid metabolism in skeletal muscle and to the myopathic manifestations often seen in hyperparathyroidism.
 ...
PMID:Secondary carnitine palmitoyltransferase deficiency in chronic renal failure and secondary hyperparathyroidism. 872 13

Intracellular calcium has been reported to be increased in essential hypertension, and thought to play a role in its genesis through facilitation of vascular smooth muscle contraction. Since hypertension is more prevalent in primary hyperparathyroidism, intracellular calcium may also be increased in this condition. To investigate whether the hyperparathyroid condition, i.e., hypercalcemia and increased PTH per se, could be associated with high intracellular calcium, we measured intracellular calcium in platelets with the Quin-2 AM fluorometric method in 11 normotensive patients with primary hyperparathyroidism, 15 patients with essential hypertension, and 18 normal controls, all matched for age and sex. We repeated the measurements in 9 of the hyperparathyroid patients after successful surgery. We found that intracellular calcium was higher in normotensive patients with primary hyperparathyroidism than in normal controls (198 +/- 24 vs 113 +/- 11 nM, p < 0.05), but lower than in patients with essential hypertension (198 +/- 24 vs 286 +/- 38 nM, p < 0.05). Successful removal of a parathyroid adenoma decreased intracellular calcium from 215 +/- 22 to 116 +/- 19 nM, (p < 0.01). In the patients with primary hyperparathyroidism, intracellular calcium was strongly correlated with the levels of PTH (r = 0.87, p < 0.01), but not with the total serum calcium levels (r = 0.04, NS). The decrease in intracellular calcium after parathyroidectomy was also strongly correlated with the decrease in PTH (r = 0.84, P < 0.01), but not with the decrease in total serum calcium (r = 0.16, NS). In the patients with essential hypertension, intracellular calcium correlated well with systolic (r = 0.69, p < 0.01), diastolic (r = 0.76, p < 0.01) and especially mean arterial pressure (r = 0.86, P < 0.01). There was no correlation between blood pressure and intracellular calcium in the patients with primary hyperparathyroidism. We conclude that normotensive patients with primary hyperparathyroidism, as well as patients with essential hypertension, can have increased concentrations of intracellular calcium in platelets. The correction of the hyperparathyroid condition normalizes intracellular calcium concentration. The close correlation between PTH and intracellular calcium suggests that PTH may act as a ionophore for calcium entry into cells. Whether the increased levels of intracellular calcium may reflect a pre-hypertensive condition in normotensive patients with primary hyperparathyroidism remains to be determined.
 ...
PMID:Intracellular calcium and blood pressure: comparison between primary hyperparathyroidism and essential hypertension. 877 53


<< Previous 1 2 3 4 5 6 7 8 9 10 Next >>