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Query: UMLS:C0020538 (hypertension)
 170,190 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Low bone mass predicts future fracture risk as well as high cholesterol or high blood pressure can predict the risk of heart disease or stroke. Prevention of the first fracture should be a clinical goal. In patients without fractures, osteopenia and osteoporosis can be diagnosed based on the extent of reduction in bone mass below mean peak bone mass of young healthy individuals. As bone mass decreases, fracture risk increases exponentially. 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 long-term corticosteroid therapy. Serial measurements can also be used to monitor the effects of osteoporosis treatments. The appropriate technique and skeletal site for bone mass measurements should be chosen based on the patient's circumstances and the precision of measurement. A clinical interpretation can enhance the value of computer-generated bone mass measurement reports and improve decision making.
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PMID:Clinical utility of bone mass measurements in adults: consensus of an international panel. The Society for Clinical Densitometry. 879 8

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

Patients with primary hyperparathyroidism (PHPT) show a high incidence of left ventricular hypertrophy, cardiac calcific deposits in the myocardium, and/or aortic and mitral valve calcification and thus may carry an increased risk of death from circulatory diseases. This prospective study was designed to assess an effect of parathyroidectomy on cardiac abnormalities of patients with PHPT. Echocardiography was used to evaluate the mechanical performance of the heart muscle, the thickness of the left ventricular wall, myocardial calcific deposits, and valvular calcifications within 12 and 41 months after parathyroidectomy. In a blinded fashion, aortic and mitral value calcifications were determined in 46% and 39% of patients with PHPT. Calcific deposits in the myocardium were found in 74% of patients. Follow-up studies after parathyroidectomy disclosed no evidence of progression of these calcifications. Before operation left ventricular hypertrophy was detected in 82%. After parathyroidectomy and 41 months of normocalcemia and normal PTH concentrations, a regression of hypertrophy of the interventricular septum and the posterior wall by -6% and -19% (P < 0.05) was observed. Subgroup analysis disclosed the most impressive long-term reduction of left ventricular hypertrophy in patients without a history of hypertension (-11% and -21%; P < 0.05 and P < 0.005); no changes were determined in 9 patients who developed secondary hyperparathyroidism after operation. The present data show a high incidence of left ventricular hypertrophy and aortic and/or mitral valve calcifications in patients with PHPT. Follow-up at 1 year and at 41 months after successful parathyroidectomy disclose regression of hypertrophy. Our results give evidence that parathyroid hormone per se plays an important role in the maintainance of myocardial hypertrophy. Post-surgical restoration of normocalcemia and normalization of parathyroid hormone valvular sclerosis persists without evidence of progression. We further conclude that patients with PHPT and parathyroidectomy are at low risk for the development of severe aortic and mitral valve stenosis within this period of time.
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PMID:Cardiac abnormalities in patients with primary hyperparathyroidism: implications for follow-up. 898 42

Twentyseven patients admitted for surgery for primary hyperparathyroidism were studied preoperatively. Fifteen were normotensive and 12 were either hypertensive, diastolic blood pressure > 95 mmHg or had a raised serum creatinine measuring 109.7 (55-171) mumol/l. The beta 2 microglobulin (beta 2M) urinary excretion was measured on all patients. The beta 2M levels were raised in all patients preoperatively even in those patients who had normal values for conventional renal function tests. Following curative surgery the values are returned to the normal range. The patients were followed up for a mean of 4.2 (2.8-5.6) years. Six patients who were initially normotensive subsequently developed hypertension and the initial beta 2M ratio was significantly higher 386 (122-680) micrograms/l compared to those who remained normotensive 186 (95-340) micrograms/l (p < 0.05). Even higher preoperative beta 2M excretion was found in the initial hypertensive group 505 (87-1160) micrograms/l compared to those who later developed hypertension 386 (122-680) micrograms/l, p < 0.001. This preliminary study suggests that preoperative beta 2M urinary excretion may be of value in identifying those patients who will subsequently develop hypertension, an identified long term cause of death in patients operated on for primary hyperparathyroidism. Further studies are indicated.
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PMID:Beta-2 microglobulinuria and long-term outcome following curative surgery for primary hyperparathyroidism. 912 3

The purpose of this study was to characterize the changes in noradrenergic blood pressure regulation and the causes of this dysregulation in patients with histologically proven primary hyperparathyroidism before and after parathyroidectomy. In untreated hypertensive patients with primary hyperparathyroidism slightly higher plasma levels of norepinephrine, enhanced cardiovascular reactivity to norepinephrine (p<0.05) and increased cytosolic free calcium concentration in platelets (p<0.05) were found. Parathyroidectomy resulted in the correction of noradrenergic blood pressure dysregulation and in the reduction of cytosolic free calcium and led to normotension. In vitro incubation of platelets from normal subjects with heterologous plasma ultrafiltrates from either hypertensive patients with primary hyperparathyroidism or normotensive uremic patients with secondary hyperparathyroidism led to raised platelet calcium in primary hyperparathyroidism but not in secondary hyperparathyroidism, although in both conditions intact parathormone levels were elevated equally. Furthermore, when platelets of normotensive subjects were preincubated with commercially available parathormone, no effect on resting platelet cytosolic calcium was observed. Our results suggest that hypertension in primary hyperparathyroidism may be caused in part by noradrenergic blood pressure dysregulation and seems to be causally linked to the secretion of a parathyroid hypertensive factor, which increases cytosolic calcium and alters vascular tone and reactivity.
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PMID:Noradrenergic blood pressure dysregulation and cytosolic calcium in primary hyperparathyroidism. 941 43

Primary hyperparathyroidism, characterized by hypersecretion of parathyroid hormone (PTH) leading to hypercalcemia and relative hypophosphatemia, is quite common in the elderly. Most patients with primary hyperparathyroidism have only mild hypercalcemia and are symptomless. But others experience various other organ diseases. Primary hyperparathyroidism is also associated with cardiovascular abnormalities, including QT interval shortening, heart block, cardiac arrhythmias, hypertension, myocardial hypertrophy, myocardial calcification and, though rarely, with valvular heart disease. We described a case of primary hyperparathyroidism associated with cardiac abnormalities. An 82-year-old male presented with the complaints of chest discomfort, fatigue, general weakness, nausea and vomiting over a period of months and was admitted in July 1996. Physical examination with heart auscultation showed a pansystolic murmur over the right sternal border and apex region, and a blowing diastolic murmur over the left sternal border. Biochemistry profiles revealed elevations of serum calcium (14.3 mg/dl) and chloride/phosphate ratio (> 33). Endocrinological studies showed elevations of serum PTH-C (4.8 ng/ml) and PTH-intact (705 pg/ml) concentrations. Kidney ultrasonography revealed a left renal stone. A spine X-ray revealed spondylosis and a compression fracture of the lumbar-spine with osteoporotic change. Thyroid ultrasonography and Thallium (Tl201)-technetium (Tc99m) subtraction scan showed parathyroid adenoma in the low pole of the right thyroid bed. Parathyroid aspiration cytology revealed few and discrete cells. Echocardiogram revealed moderate to severe aortic valvular calcification as well as stenosis with moderate aortic regurgitation, mitral regurgitation and myocardial calcification. The patient received parathyroidectomy one month later. During his postoperative days, he suffered from muscle twitching with positive Trousseau's sign and Chvostek's sign. The patient received calcium carbonate and vitamin D for hypocalcemia, diltiazem and capoten for his heart problems. A repeated echocardiogram two months after surgery showed no improvement of valvular calcification.
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PMID:Primary hyperparathyroidism with cardiac abnormalities: a case report. 950 84

A 39-year-old Chinese man with hypertension being evaluated for elevated serum alkaline phosphatase (SAP) levels was found to have an incidental right adrenal mass. The radiological features were characteristic of a large adrenal myelolipoma. This mass was resected and the diagnosis confirmed pathologically. His blood pressure normalised after removal of the myelolipoma, suggesting that the frequently observed association between myelolipomas and hypertension may not be entirely coincidental. Persistent elevation of the SAP levels and the discovery of hypercalcaemia after surgery led to further investigations which confirmed primary hyperparathyroidism due to a parathyroid adenoma. The patient's serum biochemistry normalised after removal of the adenoma. The association of adrenal myelolipoma with primary hyperparathyroidism has been reported in the literature only once previously. Although unconfirmed by genetic studies this association may possibly represent an unusual variation of the multiple endocrine neoplasia type 1 syndrome.
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PMID:The elevated serum alkaline phosphatase--the chase that led to two endocrinopathies and one possible unifying diagnosis. 1006 58

Anesthesia for surgery of primary hyperparathyroidism (HPT) usually concerns asymptomatic elderly women with moderate hypercalcemia. Cardiovascular repercussions of the endocrine disorder are possible, but they are not frequent except for hypertension. Hyperparathyroid crisis is a life-threatening condition with severe hypercalcemia. Intravenous diphosphonates are very effective drugs to control hypercalcemia. The improvement is transient but allows curative parathyroidectomy to be performed with a minimal risk of cardiac arrhythmias. Anesthesia for surgery of secondary HPT concerns patients with chronic renal failure treated by hemodialysis. Cardiovascular disease is frequent and aggravated by the endocrine disorder. In patients with marked aortic stenosis or severe left ventricular dysfunction, parathyroidectomy should be performed by cervicotomy under local anesthesia. Hyperparathyroidism may persist after renal transplantation (tertiary HPT): in this case cardiovascular disease is minimal and the hypercalcemia is moderate. Parathyroidectomy is usually performed by cervicotomy under general anesthesia. Sternotomy is required in the case of an abnormal mediastinal location of a gland. An interaction between myorelaxants and hyperparathyroidism has been observed. Total blood calcium must be systematically assayed postoperatively because postoperative hypocalcemia is constant. Hypocalcemia is moderate in primary and tertiary HPT, due to transient functional hypoparathyroidism, with lowest observed the 2nd or 3rd postoperative day. Hypocalcemia should not be treated when asymptomatic because it resolutes on the 4th or 5th postoperative day. Intravenous calcium infusion may be necessary for 1 or 2 days, if serum calcium is below 1.9 mmol per liter with symptoms of tetany. Persistent hypocalcemia is due to an hungry bone syndrome or organic hypoparathyroidism that should be treated by oral vitamin D and calcium. In secondary HPT, hypocalcemia is early, marked and asymptomatic. Treatment must often be started on the 6th postoperative hour by intravenous calcium infusion, followed by oral vitamin D and calcium. The absence of postoperative hypocalcemia indicate incomplete removal of all abnormal parathyroid tissue. At the third postoperative day, a second cervicotomy may be performed to complete the neck exploration.
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PMID:[Anesthesia and postoperative recovery for parathyroid gland surgery]. 1008 69

Twenty consecutive unselected patients with proven primary hyperparathyroidism (PH), 26 essential hypertensive (EH) patients, and 13 normotensives were studied. Blood pressure (BP) and, under constant salt intake, plasma renin activity (PRA), parathyroid hormone (PTH), urinary and plasma sodium, potassium, aldosterone (ALD), creatinine, total calcium, and phosphate were measured. Patients with PH were also studied 1 and 6 months after successful surgery. In patients with PH, systolic and diastolic BP was significantly lower (P < .001) than in EH patients and higher (P < .005) than in controls. Eight patients with PH (40%) had BP levels greater than 140/90 mm Hg. PTH and plasma and urinary calcium in patients with PH were significantly (P < .01) higher than in controls, while PRA, ALD, phosphate, potassium, and sodium were superimposable in the three groups. PTH in patients with PH was weakly correlated with PRA (positively) and with plasma potassium (negatively) and was not associated with ALD, calcium, sodium, and BP levels. Surgery was followed by a significant reduction (P < .01) in PTH, calcium, and urinary phosphate and an increase (P < .02) in plasma phosphate, potassium, and sodium, whereas PRA, ALD, urinary potassium and sodium, and BP showed no change. In hypertensive patients with PH, PTH, PRA, and plasma and urinary ALD, calcium, and sodium did not differ from the values in normotensive PH patients, and variations in these humoral parameters after surgery were comparable in the two groups. In conclusion, our results show that hypertension is frequently associated with PH. However, the present data raise doubts about the assumption of a renin-mediated causal relationship between hyperparathyroidism and high BP. Indeed, as a unique finding in favor of the hypothesis of a stimulating role of PTH in renin secretion, we observed only a weak relation between PTH and PRA. Thus, unknown and/or unassessed factors related to parathyroid disease cannot be ruled out to explain the hypertension observed in some patients with PH.
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PMID:Renin-angiotensin-aldosterone system in primary hyperparathyroidism before and after surgery. 1009 3

Lithium is a monovalent cation that influences calcium metabolism in various tissues including the brain, kidney, heart, and parathyroid gland. Mr. A received treatment with lithium for 19 years because this medication proved to be effective in the management of his bipolar illness. However, he developed hypercalcemia, hypertension, and episodes of severe bradyarrhythmia (one of them requiring admission to the medical intensive care unit), with lithium levels within the therapeutic range. An extended endocrine workup showed hyperparathyroidism, with elevated serum parathyroid hormone levels, hypercalcemia, hypocalciuria, and normal serum phosphate levels. These biochemical findings are different from those of primary hyperparathyroidism and are attributed to direct actions of the lithium in the kidney. Discontinuation of the lithium did not result in reversal of the abnormal findings. The patient had surgery, and hyperplasia of the parathyroid gland was found. After parathyroidectomy, the bradyarrhythmia subsided and the patient showed improvement both in his psychiatric condition and hypertension. Preliminary observations in nine other lithium-induced hypercalcemic patients show a high frequency of arrhythmias with bradycardia and conduction defects. These findings suggest that hypercalcemia with lithium increases the risk of cardiac arrhythmia and emphasize the need for regular laboratory and electrocardiographic monitoring of patients on maintenance lithium therapy.
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PMID:Lithium therapy, hypercalcemia, and hyperparathyroidism. 1042 26


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