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

We have investigated the role of the parathyroid gland (PTG) in the long-term development of blood pressure (BP) in stroke prone spontaneously hypertensive rats (SHR/SP) and Wistar Kyoto (WKY) rats. After ablation of their own PTGs, SHR/SP animals received PTGs from WKY rats and vice versa. Transplantation resulted in a normal calcium and parathyroid hormone status without signs of hypoparathyroidism. All animals received a high salt diet (8% NaCl) for 4 weeks after transplantation of PTGs. In SHR/SP, which received PTGs from WKY, development of high BP was clearly attenuated when compared to sham-operated SHR/SP rats. WKY rats with PTGs from SHR/SP rats became hypertensive, while WKY sham-operated animals remained normotensive. PTGs from SHR/SP rats are able to induce hypertension in normotensive WKY rats.
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PMID:Development of hypertension in WKY rats after transplantation of parathyroid glands from SHR/SP. 170 92

We studied long-term morbidity after parathyroid surgery for primary hyperparathyroidism in 100 patients and compared it with the long-term morbidity of medical follow-up from the literature. The surgical treatment of primary hyperparathyroidism was associated with negative results of neck explorations, persistent hypercalcemia, recurrent hypercalcemia, permanent hypoparathyroidism, or recurrent laryngeal nerve damage in 13 (19%) of 68 patients followed up for five years postoperatively. A review of medical follow-up as reported in the literature showed progression of disease in 8% to 22% of patients followed up for five to ten years. There was no convincing evidence that mild primary hyperparathyroidism resulted in progressive osteoporosis or renal failure. Furthermore, no significant improvement in hypertension, peptic ulcer disease, or renal function followed successful parathyroid surgery. Unless future studies demonstrate progressive osteoporosis or renal damage in untreated, mild primary hyperparathyroidism, medical follow-up is a reasonable alternative to surgery in the compliant patient over 50 years of age.
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PMID:Primary hyperparathyroidism. A review of the long-term surgical and nonsurgical morbidities as a basis for a rational approach to treatment. 270 30

We studied Na transport in red blood cells (RBC) from six patients with hypoparathyroidism (HYPO; 3 postsurgical and 3 idiopathic) and 13 normal subjects. In HYPO, the effect of treatment-induced increases in serum Ca2+ on RBC Na transport also was examined. Na efflux mediated by the ouabain-sensitive Na,K pump and furosemide-sensitive Na,K cotransport (CoT) was examined by flux methodology in RBCs Na loaded to 5 levels of intracellular Na (Nai; 5-90 mM/liter cells) by the p-chloromercuribenzene method. The pump-mediated Na efflux was similar in untreated HYPO patients and normal subjects. Correction of hypocalcemia by vitamin D and oral calcium produced a mean increase in serum Ca2+ from 6.62 +/- 0.23 (+/- SEM) to 8.73 +/- 0.32 mg/dl. In HYPO patients treated with vitamin D and oral calcium, an increasing serum Ca2+ level was associated with significant (P less than 0.01) reductions in pump activity. Further, there was an inverse correlation (r = 0.813; P less than 0.001) between serum Ca2+ and pump-mediated Na efflux rate. RBC Na efflux through the CoT pathway was markedly reduced (P less than 0.05-0.01) in HYPO patients compared to normal subjects at all levels of Nai. Treatment-induced increases in serum Ca2+ had no effect on the reduced RBC CoT function in HYPO. Thus, changes in ambient serum Ca2+ can modulate the activity of the RBC Na,K pump in HYPO, with increases in Ca2+ inhibiting pump function. The markedly decreased RBC CoT activity was not related to associated hypertension or altered renal function and may represent a primary phenomenon in HYPO. These alterations in RBC Na transport may account for the higher Na, in RBCs of HYPO patients.
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PMID:Altered red cell sodium transport in hypoparathyroidism: relation to serum calcium. 373 32

Calcium homeostasis is a complex process involving calcium, other involved ions, and three calcitropic hormones, parathyroid hormone, calcitonin, and 1,25-dihydroxyvitamin D3. The principal maternal adjustment during pregnancy is an increasing parathyroid hormone secretion which maintains the serum calcium concentration in the face of a falling albumin level, an expanding extracellular fluid volume, an increasing renal excretion, and placental calcium transfer. The placenta transports calcium ions actively, making the fetus hypercalcemic relative to its mother, which in turn stimulates calcitonin release and perhaps suppresses parathyroid hormone secretion by the fetus. A unique extrarenal system for 1 alpha-hydroxylation of 25-hydroxyvitamin D3 exists in the placenta and/or decidua, providing a source of 1,25-dihydroxyvitamin D3 for the fetus. With the abrupt cessation of the placental source of calcium at birth, the neonate's serum calcium level falls for 24 to 48 hours, then stabilizes and rises slightly. Hyperparathyroidism during pregnancy causes complications in both mother and infant and should usually be treated surgically as soon as diagnosed. Maternal hypoparathyroidism can be treated satisfactorily with high doses of supplemental calcium and vitamin D. Osteopenia accompanying long-term heparin administration may respond to 1,25-dihydroxyvitamin D3 (calcitriol) therapy. Diabetes in pregnancy is associated with disturbed neonatal calcium homeostasis, perhaps due to chronic hypomagnesemia. A possible etiologic role of calcium deficiency in pregnancy-related hypertension has been suggested. Dietary deficiency of calcium and/or vitamin D during gestation may lead to several adverse effects in the newborn infant.
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PMID:Calcium metabolism in pregnancy and the perinatal period: a review. 388 Oct 31

The present documentation of 23 female patients with pseudotumour cerebri seen in Benghazi, North-Eastern Libya, over a period of 2 years constituted 21 cases with idiopathic pseudotumour and 2 patients with associated endocrine diseases. The clinical, laboratory and CT scan findings indicated idiopathic hypoparathyroidism in 1 case. The association of pseudotumour and hypothyroidism in a 40-year-old woman is suggested to be more than coincidental. The patient group was significantly more obese. Moderate to severe visual loss occurred in 9 patients. The incidence and extent of visual impairment did not correlate with the duration of symptoms, degree of obesity, use of contraceptive pills, steroid treatment, the presence of systemic hypertension, menstrual irregularity or empty sella. The incidence of 1.7 per 100,000 for the total and 3.6 per 100,000 for the female population in Benghazi observed in the present study is believed to be more than the frequency (as assessed by the hospital incidence) reported from other regions. A high prevalence of obesity may partly explain the increased occurrence of pseudotumour cerebri in North-Eastern Libya.
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PMID:Pseudotumour cerebri: incidence and pattern in North-Eastern Libya. 394 85

A 37-year-old woman with postoperative hypoparathyroidism had hypertension, and elevated plasma renin activity (PRA) and subsequent hyperaldosteronism during a two-month hypercalcemic period caused by vitamin D and excessive calcium supplements. The hypertension with elevated PRA, however, was resistant to the angiotensin II (AII) analog [Sar1, Ile8] ALL. PRA further increased and plasma aldosterone decreased in response to the [Sar1, Ile8] ALL. When the patient became normocalcemic, normotensive and normoreninemic, calcium gluconate (5 mg calcium/kg/h) was infused for one hour. The calcium infusion reproduced hypercalcemic hypertension mediated by an increase in total peripheral resistance. These observations suggest that the hypertension observed while taking vitamin D and excessive calcium supplements may be caused by a direct effect of calcium on peripheral blood vessels and the renin-angiotensin system may play a negligible role.
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PMID:Reversible hypertension caused by calcium overloading in a patient with postoperative hypoparathyroidism. 676 97

A series of 38 cases of primary hyperparathyroidism seen at a single hospital within a four a half year period is reported. The importance of hypercalcemia in the diagnosis of this syndrome and its screening in cases of arterial hypertension, gout, osteoporosis, and families with type I multiple endocrine neoplasia are underlined. The patients in the present series had a florid clinical history with a mean duration of 14 years. Main symptoms were urolithiasis (52%), arterial hypertension (28.9%), bone involvement and pain (23.7%), and peptic ulcer (18.4%). There were a high proportion of patients with hyperuricemia (26.3%), some with classical symptoms of gout. One patient presented simultaneous pituitary and pancreatic involvement. Surgical therapy was undertaken in 25 patients, of whom 24 (96%) were cured, one of them after reoperation. There were no cases of relapse, hypoparathyroidism, or postoperative death. Surgery is the only rational and definitive form of treatment of hyperparathyroidism; both experienced surgeons and pathologists are necessary to deal with the anatomic and histologic subtleties of this interesting endocrine disorder.
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PMID:[Comments on a series of 38 cases of primary hyperparathyroidism (author's transl)]. 724 69

This article begins with a discussion on changes in the maternal calcium-parathyroid axis in response to pregnancy, followed by calcium disorders that can take place during pregnancy. Hypercalcemia and its subsequent disorders, including hyperparathyroidism, hypocalciuric hypercalcemia, and thyroid disease, are reviewed. Also, hypocalcemia and its subsequent disorders, including hypoparathyroidism, vitamin D deficiency, and hypomagnesemia, are addressed. Concluding the article are discussions on bone status and osteoporosis, calcium metabolism in pregnancy-induced hypertension and preeclampsia, and nephrolithiasis in pregnancy.
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PMID:Calcium disorders of pregnancy. 778 23

In the period 1981-1993, 102 patients underwent surgery for primary hyperparathyroidism (HP). Parathyroid adenoma was found in 81, carcinoma in 4 and hyperplasia in 17 patients. HP was usually diagnosed late with marked skeletal or renal damage, psychiatric symptoms and hypertension. Following the first operation in our institution hypercalcemia was successfully reduced in 100 of 102 patients, in two hypercalcemia persisted after the operation and both were reoperated. Postoperative hypocalcemic syndrome (transitory hypoparathyroidism) due to advanced stage of HP and enormous calcium deficit in bones, occurred in 47% of patients (most frequently with skeletal and hypercalcemic form of the disease).
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PMID:[Results of surgical treatment of primary hyperparathyroidism]. 778 88

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.
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PMID:Cervical exploration for primary hyperparathyroidism. 844 Dec 55


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