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

New insights into the physical chemistry and molecular epidemiology of sickle cell anemia have improved our understanding of the pathophysiology of the associated nephropathy, the predictors of this complication, and genetic and other factors that may modify it. In this article, we analyze the current clinicopathologic knowledge with reference to the predilection to nephropathy and the protection from hypertension, as well as the altered renal physiology of the sickle cell state that underlies both these phenomena. In the early stages of sickle cell anemia, the kidney is characterized by impaired function of the renal medulla, as evidenced by reduced capacity to concentrate, acidify, and excrete potassium into the urine. Meanwhile, the cortex functions supranormally, as evidenced by increased renal plasma flow and glomerular filtration rate, proximal tubular function, and urinary diluting capacity. In addition to the complications of hematuria and papillary necrosis, renal insufficiency supervenes in a subgroup of patients. The morphology of the glomerulopathy generally differs between children and adults; in the latter group there is a particularly poor prognosis and markedly shortened life expectancy. Renal replacement therapy has nonetheless been successful. Although hypertension may be found at this stage, it is extremely rare before the onset of significant renal impairment. The possible mechanism of this protection is discussed, with a focus on the compelling need for further investigation in light of the newly gained basic understanding of this hematorenal syndrome.
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PMID:The kidney in sickle cell anemia. 157 59

Maternal mortality is examined from June 1980 to December 1986 at Mulago, Nsambyo, Old Kampala, Rubaga, and Mengo Hospitals in Kampala, Uganda. Clinical or immediate causes, direct and indirect, were recorded from case summary forms based on ICD9 definitions of obstetric complications. The nonabortion maternal mortality rate (NAMMR) was 2.65/1000 deliveries (580 deaths); the abortion-related maternal mortality rate (ARMMR) was 3.58/1000 abortions. The hospital maternal mortality rate was 2.0/1000 deliveries. 75% of maternal deaths of women of 28 weeks' gestation or more had delivered outside the hospital. NAMMR doubled between 1980-86, a statistically significant increase. ARMMR increases were almost significant. 75% were direct obstetric and 21% were indirect obstetric causes. 38% had clinical anemia, 29% had some sepsis, 18% had substantial bleeding, and 14% had obstructed labor. Other contributing conditions were pneumonia, ruptured uterus, laparotomy, evacuations and curettage, malaria, preeclampsia, sickle cell anemia, pulmonary embolism, malnutrition, tetanus, meningitis, prolonged labor, and hepatitis. At admission, 48% were in poor condition, 30% in good condition, and 22% in fair condition. 27% had sickle cell anemia, high blood pressure, multiple pregnancy, or malaria at admission. 64% were admitted within 24 hours after delivery, 67% 1-7 days after delivery, and 92% 7-42 days after delivery. Those in good condition were all admitted 7 days postdelivery. 41% of deaths were due to lack of drugs, 7% lack of fluids, 20% with theater problems, 14% with doctor-related factors, and 3% with midwife-related factors. Better information is needed on mortality before delivery, mortality in hospitals vs. outside, and mortality from abortion, and ectopic and hydatidiform molar pregnancies. An explanation given for the increase in maternal mortality is the decline in economic conditions. Abortion complications may be due to the concealment practiced. Causes are consistent with trends from the 1950s, 1960s, and 1970s in Uganda and developing countries in general. Availability and accessibility of gynecological and obstetric services needs great improvement. Training traditional birth attendants and obtaining rural ambulance services are also needed. Health workers lack creativity and imagination for developing country conditions; scarce resources are not the only problem.
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PMID:Incidence and causes of maternal mortality in five Kampala hospitals, 1980-1986. 176 15

Between December 15, 1988 and November 30, 1990, the application of Rome and New York criteria enabled the diagnosis of 60 cases of gout among patients with arthritis or hyperuricemia seen as out-patients or hospitalised in the Department of Rheumatology of the Brazzavile T.H.G. There were 57 men and 3 women, with a mean age of 51. Gout is the primary form of inflammatory arthropathy in adults in the Congo. Affecting all socio-professional groups, it is diversely associated with obesity, alcoholism, hypertension and diabetes. Initial involvement affects the big toe. Oligo and polyarticular forms predominate because of the absence or delay in specific treatment. This series included 30 per cent of cases of chronic gout. Evidence of renal impairment was found in one third of patients. However, urate lithiasis was absent. Tophi were found preferentially over the elbows. Sickle cell disease was responsible for one case of tophaceous gout. In contrast with the results of studies undertaken before the 1980s, gout is seen to be a common condition in equatorial Africa.
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PMID:[Epidemiological and clinical aspects of gout in equatorial Africa. Apropos of 60 cases followed in the Department of Rheumatology of the Teaching Hospital Center in Brazzaville]. 178 Jun 67

Epidemiological studies have shown a consistent downward trend in the incidence and mortality of stroke in industrialized communities. There are however no reports on the pattern of stroke in Saudi nationals and expatriates in Saudi Arabia. The types and etiologies in 372 subjects (262 Saudis, 110 non-Saudis) are described. Males outnumbered females in the ratios of 2.2:1 and 8.2:1 for Saudis and non-Saudis, respectively. The frequency of stroke increased steadily with age until the 7th decade in Saudis but dropped sharply after the 6th in expatriates. The frequency of stroke types in Saudis was ischemic (61%), hemorrhagic (17%) and unspecified (22%) as against 46, 47, and 7% respectively in non-Saudis. Intracerebral hemorrhage was more frequent than subarachnoid hemorrhage (SAH) and was encountered more often in Saudis than in non-Saudis; SAH was 3 times more common in expatriates than in Saudis. The major predisposing factors for stroke were hypertension, diabetes mellitus, and cardiac disorders. Abnormal hemoglobinopathies, especially sickle cell anemia, were rare. The differences observed in the age and sex distribution and in the stroke pattern between Saudi nationals and expatriates most likely reflect the demographic structure existing in Saudi Arabia.
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PMID:Stroke in a tertiary hospital in Saudi Arabia: a study of 372 cases. 186 67

Much of the morbidity and mortality in sickle cell disease (SCD) is caused by tissue ischemia and infarction resulting from vascular occlusion. Research in this area has been dominated by the hypothesis that vascular occlusion in SCD is due primarily to microvascular obstruction by sickle erythrocytes (SS RBC), yet there is no direct evidence that microvascular occlusion is responsible for any of the vasocclusive complications of SCD. In this paper an alternate hypothesis is proposed: that thrombotic occlusion of larger arteries and veins is an important factor in many of the vasocclusive complications of SCD. Large-vessel cerebral arterial disease (intimal hyperplasia with superimposed thrombosis) has clearly been established as the most important cause of stroke in SCD, and considerable evidence suggests that pulmonary arterial thrombosis/embolism is a major cause of pulmonary infarction and hypertension. The involvement of large-vessel thrombosis in painful crisis, aseptic necrosis of bone, priapism, leg ulcers, retinopathy, and miscarriage has not been adequately investigated. Large-vessel occlusion in SCD is probably a consequence of the abnormal adhesive and procoagulant properties of SS RBC, which produce endothelial damage, secondary intimal proliferation, and thrombosis. Techniques currently used to treat large-vessel occlusion in other disorders (antiplatelet and anticoagulant agents, thrombolytic therapy, angioplasty, endarterectomy, and vascular bypass surgery) should be considered in sickle cell subjects with large-vessel occlusion, especially in the cerebral vasculature.
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PMID:Large-vessel occlusion in sickle cell disease: pathogenesis, clinical consequences, and therapeutic implications. 189 Sep 82

A review of the literature concerning quality of life aspects on ACE-inhibitors in hypertensive patients is given. In the first part of the eighties two prospective multi-center randomised trials were conducted to determine the effect of captopril in comparison to methyldopa or an unselective beta-blocker on the quality of life in patients with mild to moderate hypertension (Hill et al. and Croog et al.). Both studies revealed slight but significant positive effects on indices of quality of life in captopril treated patients compared to those who had methyldopa or an unselective beta-blocker. Later, another ACE-inhibitor, enalapril, has been compared with a selective beta-blocker (Edmonds et al. and Herrick et al.) with respect to side-effects and the quality of life. The measurements of the quality of life tended to favour enalapril, but the differences were small and the over-all tolerability of the two drugs was similar. In conclusion, comparisons with more long standing forms of antihypertensive therapy suggest a slightly more favourable effect of ACE-inhibitors on the quality of life.
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PMID:ACE-inhibitors and quality of life. 210 Mar 71

Calpain, a calcium-dependent, neutral cysteine-protease was purified from the erythrocyte cytosol of subjects having essential hypertension (HTN), sickle cell anaemia, (SCA), or kwashiorkor (KWA). Identical electrophoretic mobility on SDS-polyacrylamide gradient gel, sensitivity to micromolar amounts of Ca2+, absolute requirement for a reducing environment and a high susceptibility to inhibition by leupeptin and thiol-group modifying reagents confirm that calpain preparations from these erythrocytes are equivalent to calpain I. Whereas the extent of calpain activation of erythrocyte membrane Ca2(+)-pumping ATPase of normal subjects was almost equal to that due to calmodulin, calpain activation of the HTN and SCA pump was greater than activation by calmodulin. Like in normal membranes, exogenous calmodulin protected the Ca2(+)-pumping ATPase of these erythrocytes against calpainization; the degree of protection by calmodulin is least in SCA and HTN. Electrophoretic separation of erythrocyte membranes and the purified Ca2(+)-pumping ATPase of HTN, SCA and KWA subjects does not indicate the presence of fragments resulting from the proteolytic action of calpain.
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PMID:Comparative action of calpain on erythrocyte Ca2(+)-pumping ATPase in sickle cell anaemia, essential hypertension and kwashiorkor. 214 87

From 1982 to 1986, there were 1230 sudden death cases autopsied in Osaka Medical Examiner's Office. Among them, 810 cases were classified cardiac deaths (SCDs) such as coronary heart disease (77%), cardiomyopathy (7%), valvular disease (3%). All SCD cases were dead within 24 hours after the appearance of the fatal symptoms, and most of them (72%) were supposed to be instantaneous death. Many of the fatal symptoms began in bed (31%), at bath (17%), at toilet (8%) or at work (8%). 34% of them were thought to be healthy by themselves or by their family members before their deaths. Hypertension (38%), coronary heart disease (13%) and diabetes mellitus (11%) were their major past histories recorded. Cardiac lesions such as myocardial hypertrophy, fibrosis and atherosclerosis of coronary artery were frequently admitted in SCD. SCD has been vigorously studied for a long time in various fields including legal medicine, and it has also attracted a great deal of public attention recently. To clarify the causes and the mechanisms of SCD, investigations of the actual situation of SCD cases is essential. Therefore, 1230 autopsy cases of SCD in Osaka Medical Examiner's Office for recent five years were statistically investigated.
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PMID:A statistical study of sudden cardiac death for past five years in Osaka medical, investigated at the Osaka Medical Examiner's Office. 252 Jun 96

Patients with sickle cell anemia have considerably less hypertension than the black population in general. Factor(s) offering "protection" from hypertension in these patients remain unknown. Hormonal and hemodynamic parameters involved in blood pressure regulation were evaluated in normotensive, stable sickle cell patients and black nonsickle normotensive controls. There was no difference in systolic, diastolic, or mean arterial blood pressure between the two groups. The characteristic hemodynamic findings of increased cardiac index, renal plasma flow, and plasma volume were observed in the sickle cell patients. Urinary sodium excretion was comparable on an ad libitum, high sodium, and low sodium diet. In contrast, plasma renin activity was greater in sickle cell patients at all levels of sodium intake in both supine and upright positions. These findings suggested possible altered vascular responsiveness to endogenous angiotensin II. Plethysmography revealed that sickle cell patients had greater forearm blood flow than normal controls and black nonsickle chronic anemic controls at rest, during cold stimulation, and during exercise. Forearm vascular resistance was significantly lower in the patients and did not increase with cold-induced, sympathetic-mediated stimulation. To assess these findings more directly, the pressor response to the exogenous administration of graded doses of angiotensin II and norepinephrine was measured. There was a marked decrease in the pressor response to angiotensin II but not to norepinephrine in the sickle cell patients. The findings in these studies indicate fundamental differences in blood pressure control in the sickle cell patient, probably at the vascular level.
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PMID:Altered vascular reactivity in sickle hemoglobinopathy. A possible protective factor from hypertension. 264 68

A case of bipolar and relapsing cerebrovascular hemorrhages with hypertension is reported in a 7 year-old Gabonese girl. These strokes were the first sign of a sickle cell disease. Mechanisms of cerebral hemorrhages in sickle cell disease are reviewed and similarities with the "hypertension, convulsion and cerebral hemorrhage after transfusions "syndrome reported by Wasi et al. in thalassemic patients are underlined.
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PMID:[Post-transfusion cerebrovascular hemorrhagic complications disclosing homozygote sickle cell anemia]. 266 Jul 67


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