Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0020538 (hypertension)
 170,190 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A 51-year-old woman with Sneddon's disease presented with transient right hemifield loss of vision and transient right-sided weakness. Over the preceding decade she had experienced a slow decline in mental function. She also had hypertension, migraine, and a mixed seizure disorder. She had skin changes typical for generalized livedo reticularis but she did not have Raynaud's phenomenon or winter ulcerations. Her disease was not understood until the stroke-related symptoms were associated with the skin abnormalities. We review the neuro-ophthalmic manifestations of Sneddon's disease and add data from our case to the growing body of fact that suggests that Sneddon's disease may be an immunologically mediated vasculopathy.
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PMID:Sneddon's disease presenting with visual loss and dementia. 297 41

Twenty-five patients were identified with non-pituitary, nonadrenal ACTH-secreting tumors (bronchial carcinoid, bronchial small cell carcinoma, pancreatic islet cell carcinoma, medullary thyroid carcinoma, thymic carcinoids, metastatic adenocarcinoma, and pancreatic cystadenoma). Clinical features were weakness, hypertension, cushingoid appearance, peripheral edema, personality disorders, and hyperpigmentation. Biochemical features were a markedly increased urinary free cortisol level (all patients), hypokalemia (71 percent of patients), and an elevated ACTH level (72 percent of patients). Surgical therapy consisted of bilateral total adrenalectomy (56 percent of patients). Twelve percent underwent transsphenoidal hypophysectomy and 36 percent had excision of their tumor. No surgical therapy was undertaken in 28 percent. Bilateral total adrenalectomy in patients with a slow-growing malignancy or an unknown tumor secreting ACTH is beneficial in relieving symptoms and prolonging life. Excision of nonmalignant ACTH-producing tumors yields an excellent long-term prognosis.
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PMID:Ectopic ACTH syndrome. Diagnostic and therapeutic aspects. 298 90

Two siblings, a 14.5-year-old boy and his 11.5-year-old sister, with congenital nemaline myopathy presented with severe respiratory failure and, in the case of the older patient, with cor pulmonale and systemic hypertension. The children were treated initially by continuous mechanical ventilation, but after a few weeks they only required ventilation at night. At the start of treatment, both were found to have a decreased ventilatory response to CO2 which apparently improved during 4 to 5 years of follow-up treatment. It has not been possible to wean them from nocturnal mechanical ventilation, but during the daytime they attend school and function almost normally. It is postulated that respiratory failure in nemaline myopathy may not be related to the severity of the muscle weakness but may result from a disturbance of the feedback required for normal control of breathing.
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PMID:Nemaline myopathy as a cause of sleep hypoventilation. 308 71

A number of symptoms that appear to be associated with high blood pressure (headache, dizziness, epistaxis, tinnitus, weakness, drowsiness), and are usually regarded as secondary to hypertension or to antihypertensive drug therapy, were studied in 3858 elderly patients, 67.8% of whom were hypertensive. Of the hypertensive patients, 71.2% were under treatment. Headaches and dizziness were significantly more prevalent in the hypertensive than in the normotensive subjects (32.5 versus 27.4% and 41.5 versus 35.3%, respectively; P less than 0.05) and in treated compared with untreated hypertensives (33.3 versus 29.4% and 43.3 versus 37.1%; P less than 0.05). These differences disappeared after statistical correction for 'awareness of hypertension'. In multiple logistic analysis, female sex, age and awareness of hypertension were significantly associated with a higher prevalence of symptoms, whereas hypertension and antihypertensive treatment were not. We conclude that the presence of these symptoms does not constitute a reliable criterion for starting antihypertensive treatment or judging its efficacy.
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PMID:Prevalence of symptoms generally attributed to hypertension or its treatment: study on blood pressure in elderly outpatients (SPAA). 321 43

Magnesium is an important element for health and disease. Magnesium, the second most abundant intracellular cation, has been identified as a cofactor in over 300 enzymatic reactions involving energy metabolism and protein and nucleic acid synthesis. Approximately half of the total magnesium in the body is present in soft tissue, and the other half in bone. Less than 1% of the total body magnesium is present in blood. Nonetheless, the majority of our experimental information comes from determination of magnesium in serum and red blood cells. At present, we have little information about equilibrium among and state of magnesium within body pools. Magnesium is absorbed uniformly from the small intestine and the serum concentration controlled by excretion from the kidney. The clinical laboratory evaluation of magnesium status is primarily limited to the serum magnesium concentration, 24-hour urinary excretion, and percent retention following parenteral magnesium. However, results for these tests do not necessarily correlate with intracellular magnesium. Thus, there is no readily available test to determine intracellular/total body magnesium status. Magnesium deficiency may cause weakness, tremors, seizures, cardiac arrhythmias, hypokalemia, and hypocalcemia. The causes of hypomagnesemia are reduced intake (poor nutrition or IV fluids without magnesium), reduced absorption (chronic diarrhea, malabsorption, or bypass/resection of bowel), redistribution (exchange transfusion or acute pancreatitis), and increased excretion (medication, alcoholism, diabetes mellitus, renal tubular disorders, hypercalcemia, hyperthyroidism, aldosteronism, stress, or excessive lactation). A large segment of the U.S. population may have an inadequate intake of magnesium and may have a chronic latent magnesium deficiency that has been linked to atherosclerosis, myocardial infarction, hypertension, cancer, kidney stones, premenstrual syndrome, and psychiatric disorders. Hypermagnesemia is primarily seen in acute and chronic renal failure, and is treated effectively by dialysis.
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PMID:Magnesium metabolism in health and disease. 328 51

The purpose of this study is to provide a thorough and comprehensive description of the late onset manifestations of poliomyelitis (PM). In addition, unusual findings, seen in the post-poliomyelitis period, have been presented to further increase awareness of the potential diversity of the problem. The scope of PM sequelae is broad. Following a description of acute PM, the various sequelae are addressed categorically. These include neurologic, vascular, orthopedic, respiratory, sleep and psychologic problems; as well as less commonly recognized maladies. Different theories for PM sequelae have been proposed. Thorough electrodiagnostic testing can frequently confirm or negate the clinical impression. The pathophysiology of vascular problems, as well as the correlation between respiratory involvement, sleep disorders, and hypertension, is reviewed. Orthopedic problems and spinal deformities are discussed. Since overuse weakness is frequently present in these patients, the role of slowly progressive non-fatiguing exercise in their rehabilitation is emphasized. Of significance are the emotional concerns demonstrated by this group of patients. Further considerations include those sequelae not readily recognized in relation to PM. A brief overview of present epidemiologic trends in the United States, and the immunologic effects of vaccination, is presented.
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PMID:Poliomyelitis: late and unusual sequelae. 332 71

Paroxysmal hypertension associated with diaphoresis and facial flushing occurs after brain injury and after spinal cord lesion above the level of sympathetic outflow. This excessive sympathetic activity is due to the failure of inhibitory impulses from supraspinal vasomotor centers to reach the spinal sympathetic outflow. A case of brainstem stroke, with weakness in all four extremities, is presented. The patient experienced paroxysms of hypertension with bladder spasms, which subsided after treatment of the spasms resulting from bladder infection. Serum levels of dopamine, norepinephrine, and epinephrine were elevated during the episode and were normal after subsidence of the paroxysms.
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PMID:Hypertension after brainstem stroke. 334 93

A statistical association between hypertension and hyperparathyroidism has been repeatedly reported, but the underlying pathogenetic mechanism has not been elucidated. A 51-year-old woman was hospitalized because of increasing motor disability caused by multiple bone and muscle aches with generalized weakness. She was found to have marked hypercalcemia and hypophosphatemia, increased parathyroid hormone secretion, but normal renal function and blood pressure level. After the identification and removal of a single parathyroid adenoma, the calcium/phosphate metabolism normalized in a relatively short time during which, however, hypertension developed in the absence of any other endocrine or renal dysfunction. A positive, highly significant relationship was observed between the progressive rise in blood pressure and the gradual increase in serum phosphate concentration occurring after the operation, suggesting that, in the hyperparathyroid phase, an underlying trend to hypertension could have been masked by the phosphate depletion, probably through its effects on cardiac and vascular smooth muscle function.
Hypertension 1988 Mar
PMID:Development of hypertension after correction of primary hyperparathyroidism. 335 May 90

Based on 28 reported patients, constant features of the syndrome of hypertension and hyperkalaemia are hyperkalaemia, hyperchloraemia, normal renal glomerular function and, in all adult patients, hypertension. Inconstant features include short stature, intellectual impairment and muscle weakness. Levels of renin and aldosterone are low, but respond to dietary salt restriction and diuretic therapy, both of which reverse the hypertension and hyperkalaemia. The basic abnormality is excessive renal sodium retention, leading to chronic suppression of renin and aldosterone; the latter is then hyporesponsive to the hyperkalaemic stimulus. Dietary salt loading or impaired production of any natriuretic or chloriuretic factor (for example atrial natriuretic peptide or renal natriuretic prostaglandins) would predispose to development of the syndrome. With normal GFR, this appears to be a unique mechanism for hypertension and hyperkalaemia.
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PMID:The syndrome of hypertension and hyperkalaemia with normal GFR. A unique pathophysiological mechanism for hypertension? 352 20

Liddle's syndrome was diagnosed in a 72-year-old man who presented clinically with hypertension and muscle weakness. This disorder has been characterized by hyporeninemic hypoaldosteronism, hypertension, hypokalemia and enhanced erythrocyte sodium influx. Administration of spironolactone failed to correct the hypertension and electrolyte abnormality, which subsequently improved with triamterene therapy and a low salt diet. However, suppression of the renin-angiotensin-aldosterone system remained unchanged after this treatment. In addition, an atrophic juxtaglomerular apparatus and hypertensive lesions in the arterioles were confirmed by kidney biopsy after triamterene therapy. Therefore, a process of intrinsic hyperactive distal sodium reabsorption, probably affected by aldosterone-independent sodium transport into erythrocytes, appears to be important in the pathogenesis of this syndrome. Triamterene therapy, which usually is performed in patients with this disease, might not be the ultimate therapy in the future even if electrolyte abnormalities were to be improved temporarily.
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PMID:Liddle's syndrome, an uncommon form of hyporeninemic hypoaldosteronism: functional and histopathological studies. 355 Jan 46


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