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

Tortuous, medially-displaced cavernous carotid arteries may cause sellar enlargement which simulates pituitary adenoma. Systemic hypertension appears to account for this tortuosity in some cases, while a congenital anomaly is probably responsible in others. Medical position of the carotid sulci may be demonstrated on sellar tomography. Cerebral arteriography provides the correct diagnosis. Surgery, particularly transsphenoidal hypophysectomy, should be avoided in such patients.
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PMID:Tortuosity of the cavernous carotid arteries causing sellar expansion simulating pituitary adenoma. 17 82

A freeze-dried human diet, based on linoleic acid-enriched food stuffs derived from ruminants, was evaluated and compared with a similarly-prepared diet based on conventional ruminant-derived foodstuffs, using Porton rats in a whole-of-life study. A cereal-based stock diet was used for comparison. Serum biochemical and histopathological examinations were carried out at 0.25, 1.1 and 2.1 years of age and other rats were left until they died of natural causes. Although some diet-specific biochemical differences were noted, triglyceride and cholesterol levels showed changes which were more age-specific than diet-specific. Longevity did not seem to be influenced by quantity or quality of dietary fat. The most common cause of death was a bronchopneumonia at about 2 years of age. Dietary fat also did not affect incidence of tumors. The most common tumor was a pituitary adenoma which occurred most often in females. Only minor causes of death were specific to diet with waxy intra-cardial plaques occurring in less than 5% of rats fed both of the high-fat diets and severe systemic hypertension occurring in rats fed the low-fat stock diet at the same frequency. No deleterious changes were noted that were unique to the linoleic acid-enriched diet.
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PMID:Effects of life span feeding of ruminant-derived human diets to rats. 44 65

A 57-year-old obese woman with hypertension, diabetes mellitus, osteoporosis, and a 40-year history of secondary amenorrhea was diagnosed with corticotropin-dependent Cushing's syndrome. Dynamic endocrine testing and radiological evaluation did not reveal definitively the source of the excess corticotropin. Bilateral adrenalectomy was performed with resolution of the signs and symptoms of hypercortisolism. Four years later, the patient was noted to have rising serum corticotropin levels and an enlarging pituitary mass; hyperprolactinemia also was documented. A diagnosis of Nelson-Salassa syndrome was made, and she underwent a transsphenoidal adenomectomy. A histological examination of the specimen revealed two distinct, albeit contiguous, adenomas: a corticotroph adenoma and a lactotroph adenoma. Postoperatively, the serum prolactin and corticotropin levels decreased significantly. Although the stalk section effect resulting from compression by a pituitary adenoma can raise serum prolactin levels, a concurrent lactotroph adenoma should be considered in patients with nonfunctional or functional pituitary adenomas of other types associated with significantly elevated prolactin levels. The mechanisms underlying simultaneous adrenocorticotropic hormone and prolactin excess are discussed.
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PMID:Coexisting corticotroph and lactotroph adenomas: case report with reference to the relationship of corticotropin and prolactin excess. 131 62

We used color-Doppler echocardiography in an investigation of cardiac morphology and function to verify the cardiac anatomic and functional changes in acromegalic patients with or without hypertension and hyperlipemic states. Fifteen patients with growth hormone-secreting pituitary adenoma (mean age: 47.9 years) and 15 healthy control subjects were studied. We measured serum growth hormone (GH), somatomedin-C, cholesterol, triglyceride levels and carried out echocardiographic studies of the following cardiac morpho-functional parameters: left ventricular diameter, volume, mass and wall systolic stress. Serum GH and somatomedin-C levels were significantly higher in acromegalic patients than in controls (p < 0.001 and p < 0.001 respectively). Echocardiography evidenced increased left ventricular mass (60% of the acromegalic patients; p < 0.05) and increased wall systolic stress (53.3%; p < 0.05). Color-Doppler analysis evidenced abnormal diastolic function in 8 acromegalic patients (p < 0.001). We thus conclude that the most characteristic feature of acromegalic heart disease is left ventricular involvement, diastolic dysfunction, increased left ventricular mass or wall systolic stress. The pathogenesis is most probably multifactorial: essential hypertension, associated with slow and progressive evolution of heart disease, appears to be a determining factor.
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PMID:[Acromegalic cardiopathy: a morphofunctional study with color-Doppler echocardiography]. 145 53

A case of anaplastic astrocytoma following radiotherapy for growth hormone secreting pituitary adenoma is presented with a review of the literature. A 43 year old female was admitted with the signs of acromegaly and hypertension. An eosinophilic pituitary adenoma was subtotally removed by transsphenoidal approach, and followed by 60 Gy irradiation using a 2 x 2 cm lateral opposed field. Fourteen years later at the age of 57, she suffered from headache, recent-memory disturbance and uncinate fits. CT scan and MRI disclosed ring-like enhanced mass lesion in the left temporal lobe, corresponding to the previous irradiated field. 18F-FDG PET showed hypermetabolism at the lesion. Left frontotemporal craniotomy was performed, and a reddish gray gelatinous tumor containing necrotic center and cyst was partially removed. Histologically, the tumor consisted of hypercellular astrocytic cells with perivascular pseudorosette. Coagulation necrosis at the center of the tumor, and hyalinosis and fibrosis of the blood vessels in and around the tumor, which might have been caused by the antecedent radiotherapy, were recognized. Postoperative radio- and chemotherapy were given, however, she expired 13 months after the operation. Seven cases, including ours, of malignant glioma following radiotherapy for pituitary adenoma were reported in the literature. A total dose of irradiation varies from 45 to 95 Gy with a mean of 50 Gy. The period of latency before tumor occurrence ranges from 5 to 22 years with a mean of 10 years. The differentiation of radiation-induced gliomas from radionecrosis of the brain is also discussed.
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PMID:[Anaplastic astrocytoma 14 years after radiotherapy for pituitary adenoma]. 157 77

Timely diagnosis of hypothyrosis was noted in 34% of patients only. Considerable difficulties in the diagnosis of disease were associated with an atypical course of disease in a number of patients. The authors discuss some problems of a clinical picture of hypothyrosis with arterial hypertension, sympatico-adrenal crises, polyserositis, pituitary adenoma, amenorrhea-lactorrhea, premature puberty in boys; they also discuss pathogenesis of sexual advancement of a number of pubertal features in Van Wyk-Grambooh syndrome. Hennes-Ross syndrome was identified as a separate entity.
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PMID:[Atypical clinical variants of hypothyrosis]. 178 Feb 90

333 consecutive patients with hypopituitarism diagnosed between 1956 and 1987 were retrospectively examined. The patients had been given routine replacement therapy. The overall mortality was higher than in an age and sex matched population. Deaths from vascular disorders were also significantly increased (60 [40 male, 20 female] versus 30.8 expected [23.5, 7.4 female]). The hazard function for vascular death was independent of age at diagnosis, time after diagnosis, calendar year of diagnosis, gender, degree of pituitary insufficiency, hypertension, and diabetes mellitus. Mortality risk was raised irrespective of whether hypopituitarism was due to pituitary adenoma or secondary to other diseases. 7 patients (3 male, 4 female) died from malignant diseases (expected 10.1 and 4.1, respectively). These observations indicate that life expectancy is shortened in patients with hypopituitarism. Growth-hormone deficiency could be a factor in this increased mortality from cardiovascular disease.
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PMID:Premature mortality due to cardiovascular disease in hypopituitarism. 197 79

The empty sella turcica is defined as a sella which, regardless of its size, is completely or partly filled with cerebrospinal fluid. An empty sella of normal size is a frequent and probably normal finding in unselected autopsy series. In clinical series an empty sella usually appears enlarged and is often associated with a variety of clinical disorders, constituting the so-called empty sella syndrome. Several causes of an enlarged empty sella have been suggested: a congenitally missing (deficient) sellar diaphragm with or without altered cerebrospinal fluid dynamics, previous pituitary gland hypertrophy or the outcome of a pituitary tumor necrosis. Increased intracranial pressure will induce a sellar enlargement in some patients and, consequently, also the emptiness. This pathogenesis is, however, applicable only in a minority of patients with an empty enlarged sella. Data from the literature and from own studies suggest that the enlarged empty sellae and the associated findings in the majority of cases are caused by spontaneous necrosis of a previous pituitary adenoma. This theory explains the frequent presence of pituitary insufficiency, pituitary hypersecretion, and visual field defects in patients with an empty sella. Furthermore, it offers an explanation of the finding of an empty enlarged sella in some patients with non-traumatic cerebrospinal fluid rhinorrhea and probably also benign intracranial hypertension. Thus, an empty enlarged sella is a stage in the spontaneous course of some pituitary adenomas and the associated findings constituting the empty sella syndrome are an occasional part of the clinical presentation of pituitary adenomas.
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PMID:The empty sella. A reappraisal of etiology and pathogenesis. 179 61

Progestins counteract the positive effect of the estrogen component in oral contraceptives (OCs) on cholesterol levels thus increasing the risk of atherosclerosis. Low androgenic potency progestins do not have a negative effect, however. Other research indicates that the lower the estrogen dose in OCs the lower the risk of deep vein and superficial thrombosis. OC users, especially low dose OC users, with no other risk factors (e.g. smoking and hypertension) are not at increased risk of cardiovascular disease. Some research demonstrates elevated risk of stroke in OC users, however. Elevated cholesterol, obesity, diabetes and other factors further increases the risk of stroke. Combined OCs protect against endometrial and ovarian cancer and this effect increases with use and continues after use. Moreover OC users are not at increased risk of pituitary adenoma. Results of some studies shows an increased risk of cervical cancer, but other only demonstrates a slight increase. So far research does not indicate the following to increase breast cancer risk among OC users: early age at 1st OC use, formulation, family history, and history of benign breast disease. There is an increased risk for liver tumors in OC users, nevertheless it is rare. OCs do not raise the risk of diabetes or gallbladder disease. High dose formulations increases the risk of high blood pressure, but not so with low dose formulations. OC use does not impair, fertility, but delayed conception often occurs. Most research demonstrates no increase in pelvic inflammatory disease in OC users. OCs do not cause congenital malformations. Combined OC use is contraindicated for breast feeding mothers, but progestin only OCs can be used with no advance effects. Results of 1 study demonstrates an increase in HIV infection in OC users, but another study has opposite results. The article concludes with recommended clinical management practices.
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PMID:Reassessment of the metabolic effects of oral contraceptives. 185 68

A 69-year-old female was treated for hyperthyroidism and hypertension. In August 1984, she suddenly began suffering from polyuria and polydipsia. In October, she exhibited fever, headache, vertigo, and poor appetite, probably due to pituitary apoplexy. Her endocrine function was normal, except for partial diabetes insipidus. A contrast-enhanced CT brain scan revealed a pituitary adenoma with a ring-enhanced outer edge and a central low-density area. The MRI scan also indicated cystic adenoma. A CT scan examination repeated 6 months later showed an empty sella with a markedly decreased pituitary adenoma. This case report demonstrates that some empty sella are the final result of pituitary adenoma bleeding or infarction.
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PMID:Pituitary adenoma results in the empty sella syndrome. 258 92


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