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

A 57-year-old male, who had been suffered from hypertension and diabetes mellitus for 10 years, was admitted to the hospital because of thirst, lassitude and muscle wasting. On admission, his urinary excretion of 17-OHCS and plasma cortisol levels were elevated without diurnal variations. Plasma ACTH levels were found to be very low with repeated determinations. Dexamethasone suppression test, 2 mg 4 times a day orally for 2 days, showed no changes in plasma cortisol levels and only a mild reduction in urinary 17-OHCS excretion. Estimation of urinary catecholamines showed an increase only in norepinephrine. Abdominal computerized tomography and radionuclide scanning of adrenal glands with 131I-adosterol demonstrated a well-defined adrenal mass in the left side without apparent changes in the right side. 131I-metaiodobenzylguanidine scintigraphy was negative. At surgery, his left adrenal medulla was found to be hypertrophic in addition to the cortical tumor. The left adrenal gland was also removed. After surgery, excretion of urinary catecholamines fell to nearly the normal range and he was discharged without insulin and antihypertensive drugs. Microscopically, the cortical tumor is an adenoma consisting of lipid laden cells and eosinophilic compact cells. Medullary cells were distinctly hyperplastic in appearance and many of the cells were extensively vacuolated, suggesting an active functional status. The present report describes a patient with Cushing's syndrome who showed increased urinary catecholamine excretion due to the possible coexistence of adrenal medullary hyperplasia. As far as we know, this is the first case of Cushing's syndrome with this abnormality.
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PMID:A case of Cushing's syndrome associated with possible adrenomedullary hyperplasia. 404 90

In 12 patients with life-threatening neurological deficits from vasospasm refractory to other measures, high dose barbiturate therapy was used in an attempt to prevent permanent changes in the brain. In each case angiography was performed and intracranial pressure was measured. Dexamethasone, a low molecular weight dextran, and mannitol were administered. If intracranial pressure (ICP) was elevated, drainage of cerebrospinal fluid and hyperventilation were used. Arterial pressure was maintained at not less than 140/90 preoperatively and 180/100 postoperatively. Barbiturate therapy was continued until vasospasm decreased angiographically and ICP was normal. Eleven of the 12 patients perished. One had a fatal rebleed. One died of an iatrogenic hemothorax. Four died from uncontrollable intracranial hypertension. One improved slightly and then died from a cardiac arrhythmia. One died of increased ICP when her ventriculostomy malfunctioned. One improved and was responding purposefully to pain, only to die suddenly with a low ICP. Two patients became awake and responsive to verbal commands; 1 of these died from Klebsiella meningitis and the other died from an intracerebral hematoma. In the 3 patients in whom hypothermia was also used, profound alterations in acid-base and fluid electrolyte balance occurred. These discouraging results are most likely a reflection of the severity of the patients' condition at the beginning of therapy. There may be some benefit of barbiturates in the management of vasospasm, and the potential effectiveness of barbiturates may be more obvious if therapy is started at an earlier stage. However, until further evidence of the usefulness of this modality becomes manifest, it should be limited to patients with life-threatening impairments unresponsive to all other measures.
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PMID:Treatment of ischemic deficits from cerebral vasospasm with high dose barbiturate therapy. 616 7

The case of a 58-year-old white man with a history of high blood pressure and chronic obstructive pulmonary disease who developed double vision followed by right-sided facial paralysis is reported. A computerized axial tomogram (CT) scan showed an enhancing lesion in the pontine tegmentum, and the diagnoses of pontine glioma or hemorrhage were considered. Physical findings were limited to the cranial nerves. Conservative management with Decadron for 3 weeks resulted in a prompt clinical improvement, and a CT scan 1 month later showed resolution of the lesion, effectively ruling out a glioma. Total clinical recovery occurred at the end of 6 months. To our knowledge this is the first report of a case of Fisher one-and-a-half syndrome with facial paralysis correlated with computed tomography.
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PMID:Pontine hemorrhage causing Fisher one-and-a-half syndrome with facial paralysis. 622 96

Dexamethasone suppressed urinary aldosterone to less than 1.5 micrograms/day in 1-2 days and lowered blood pressure in a woman and in her 2 1/2-yr-old daughter, both of whom have hypertension and hyporeninemia and are members of a kindred with dexamethasone-suppressible aldosteronism. ACTH given for 7 days produced a sustained increase in aldosterone production and a rise in blood pressure in both patients. The abnormal suppression with dexamethasone and further stimulation with ACTH indicate that the aldosteronism is ACTH-dependent in this disorder. The cause of the ACTH-dependence of aldosterone production in this disorder is unknown but may represent continued stimulation rather than the usual (secondary) inhibition by ACTH of 11-hydroxylation and 18-hydroxylation in zone glomerulosa cells. Blood pressure was normal during treatment with spironolactone and during pregnancy, when the action of aldosterone and other similar steroids was presumably blocked by an increased production of progesterone; this suggests that the hypertension is dependent upon sodium-retaining steroids such as aldosterone. Aminoglutethimide given during treatment with ACTH decreased urinary aldosterone and blood pressure and increased PRA, with minimal effects on plasma cortisol or urinary 17-hydroxycorticosteroids. These results provide additional evidence that aldosterone, acting alone or in conjunction with other steroids synthesized by the zona glomerulosa, mediates the hypertension and hyporeninemia of dexamethasone-suppressible aldosteronism.
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PMID:Overproduction of sodium-retaining steroids by the zona glomerulosa is adrenocorticotropin-dependent and mediates hypertension in dexamethasone-suppressible aldosteronism. 626 87

Two patients with low renin hypertension showing an increased urinary excretion with 17-KS, with normal level of plasma deoxycorticosterone and no signs of virilization were reported. Dexamethasone induced reduction in blood pressure and elevation of serum K, in spite of acceleration of the renin-angiotensin-aldosterone system. Thus, it has been inferred that the hypertension was not associated with adrenogenital syndrome but was due to excessive production of an unknown mineralocorticoid.
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PMID:Two cases of low-renin hypertension thought to be due to excessive secretion of unknown mineralocorticoid. 627 83

A 9 year old Mexican boy presented with severe hypertension, hypokalaemia and features suggesting acute glomerulonephritis. Nephrosclerosis was present on renal biopsy. Aldosterone levels were unresponsive to variations in dietary salt intake and plasma renin activity was suppressed. Following oral dexamethasone therapy (2 mg/day), plasma aldosterone decreased to undetectable levels, serum potassium normalized and plasma renin activity gradually increased. Dexamethasone also restored the normal responsiveness of the renin-aldosterone system to postural stimuli. The patient exhibited a marked response to a single dose of ACTH with a rise in plasma aldosterone. Long-term blood pressure control and normal potassium levels have been achieved with oral prednisone therapy (5 mg/day) for a period of one year. This case of dexamethasone suppressible hyperaldosteronism (DSH) illustrates that the degree of hypertension in this syndrome may produce severe renal microvascular lesions. DSH should be considered in all children who present with low renin hypertension.
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PMID:Dexamethasone suppressible hyperaldosteronism in a child with nephrosclerosis. 627 30

Male and female, young (2 months old) and mature (10 months old), obese and nonobese, spontaneously hypertensive rats (SHR) were treated with dexamethasone, 5 micrograms/rat and 10 micrograms/rat, respectively, subcutaneously (SC) 2 times daily for 5 months. Steroid treatment stilled the voracious appetite of the obese SHR, and the massively obese, mature animals were reduced to almost normal size. The young, steroid-treated, obese SHR did not develop their genetically programmed corpulency. The untreated, young and mature, obese SHR ate voraciously, became massively obese, and developed their characteristic Cushing's disease-like spectrum of degenerative changes, eg, hypertension, hyperlipidemia, hyperglycemia, muscle wasting, kidney stones, thin skin, and accelerated aging. The blood pressure of the steroid-treated animals was lowered concomitant with reduced levels of circulating ACTH, beta endorphin, insulin, triglycerides, and cholesterol. Dexamethasone caused hyperlipidemia, hyperglycemia, and increased BUN levels in young obese and nonobese SHR only. The mature obese SHR had giant-sized thymus glands that were further enlarged with steroid treatment; dexamethasone was thymolytic in young, obese and nonobese SHR. Dexamethasone caused severe reduction of pituitary and adrenal gland size, simulating the condition of hypophysectomy. These findings demonstrate that dexamethasone suppression of the pituitary-adrenal axis palliates and prevents the spontaneous development of Cushingoid degenerative changes in these genetically obese and hypertensive rats.
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PMID:Dexamethasone suppression of cushingoid degenerative changes in obese spontaneously hypertensive rats (SHR). 631 58

We have previously suggested that inhibition of renin release by sodium chloride is related to absorptive chloride transport in the loop of Henle. Infusion of sodium chloride fails to inhibit renin release in the adrenalectomized (Adx) rat, and dexamethasone restores renin responsiveness to sodium chloride. The purpose of the present study was to evaluate the relationship between loop function (urinary diluting and concentration capacity) and plasma renin concentration (PRC) in the Adx rat. After hypotonic sodium chloride infusion, free water clearance (CH2O) of Adx rats (0.56 ml/hr/100 g +/- 0.17 SE) was decreased (p less than 0.01) compared to controls (2.86 ml/hr/100 g +/- 0.29 SE); PRC of Adx rats (61.9 units/ml +/- 11.2 SE) was increased (p less than 0.01) above controls (6.0 units/ml +/- 1.7 SE). These differences persisted after administration of d(CH2)5Tyr(Et)VAVP, a potent ADH antagonist. In separate groups of animals, after water deprivation, urine concentration of Adx rat (1,401 mOsm/kg +/- 45 SE) was less (p less than 0.01) than that of controls (2,117 mOsm/kg +/- 169 SE). Dexamethasone normalized both CH2O and urinary concentrating ability and also decreased PRC in Adx rats. Thus, in the glucocorticoid deficient rat, increased renin release is associated with impaired loop function. The loop defect may account for high PRC that is not suppressed by sodium chloride.
Hypertension
PMID:Mechanism of increased renin release in the adrenalectomized rat. Adrenal insufficiency and renin. 633 60

A modification of the EMIT-Tox qualitative serum barbiturate assay (Syva Company, Palo Alto, CA) was evaluated for measuring pentobarbital concentrations. Pentobarbital calibrator solutions were substituted for the secobarbital calibrators provided with the assay kit, and control solutions of pentobarbital were used to determine the modified assay's precision and accuracy. Specificity for pentobarbital with respect to other barbiturates and assay interference from other drugs were evaluated in vitro. Serum samples obtained from 49 patients receiving intravenous pentobarbital sodium to treat intracranial hypertension were assayed by gas-liquid chromatography (GLC) and by the modified EMIT procedure. Samples from patients who were receiving both phenobarbital and pentobarbital (9 of 49) were assayed for both drugs, interference curves were plotted, and the corrected pentobarbital concentrations were compared with GLC values. The modified assay method provided an accurate measurement of serum pentobarbital concentrations of 1-30 micrograms/ml. Significant cross-reactivity with the pentobarbital assay was present for secobarbital, butabarbital, allobarbital, and phenobarbital. Dexamethasone, dopamine, phenytoin, cimetidine, lidocaine, diazepam, morphine, and several other drugs at concentrations of 1000 micrograms/ml did not interfere with the assay. There was a strong correlation between the GLC reference method and the modified EMIT assay (r = 0.96). Clinically important cross-reactivity with phenobarbital was found; the corrected pentobarbital concentrations for patients who had received phenobarbital strongly correlated with GLC results (r = 0.98). The modified assay appears to be sufficiently reliable for determination of pentobarbital serum concentrations.
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PMID:Evaluation of a rapid immunoassay for monitoring serum pentobarbital concentrations. 639 59

To counter the paucity of documention on thromboembolic disorders caused by oral contraceptives (OC), a case study is presented describing the incidence of occlusion of arteria centralis retinae in a 24-year old woman after prolonged use of an OC, Bisecurin. She had taken Bisecurin for 4.5 years and had gained 20 kg during that time, but stopped usage 1 month before admission. She was hospitalized with severe deterioration of vision in the left eye. An eye examination indicated an edematous condition of the retina and reddening of the macula. Acuity of vision value for the left eye was .01 vs. 1.0 for the right, which was confirmed by fluorescein fundus angiography. Moderately decreased antithrombin III (AT III) activity was also ascertained. Treatment consisted of immediate retrobulbar injection with Tolazolin followed by Rheomacrodex, Cavinton infusions, B1 and B12 injections, Oradexon subconjunctival injection as well as vitamin B complex, Cavinton, and Colfarit tablets and a fat-free diet. Significant improvement of the left eye condition appeared 4 weeks later. Periodic follow-ups showed the healing of the condition around the macula; however, the patient suffered permanent damage to the retina due to the arterial occlusion above and below the macula. The disturbed lipid values of metabolism were also returned to normal, as borne out by normal dextrose loading results 8 months later (glucose tolerance was abnormal during examination at admission). The estrogen and progesterone components of OCs have been shown to reduce AT III levels, shorten heparin-thrombin coagulation time, increase fibrinogen levels, decrease HDL cholesterol levels, and produce excess TXA2 (thromboxan) resulting in vasoconstriction and thrombocyte aggregation. The risk of thrombosis is 6 times higher in OC users than in nonusers, although other susceptibility factors (obesity, diabetes, hypertension) also contribute to thrombosis.
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PMID:[Arterial occlusion in the ocular fundus induced by oral contraceptives]. 651 54


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