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)

Subcutaneous recombinant human erythropoietin (rHuEPO) was given for 12 months twice weekly to 10 patients on continuous ambulatory peritoneal dialysis (CAPD) with anemia (hemoglobin less than 9.0 mg/dl). All patients responded to a median weekly dose of between 37.5 to 100 (mean 55 to 105) units/kg and reached a target hemoglobin of 10-12 mg/dl in a mean of 11.7 weeks (range 5-24). Serum iron, iron saturation and ferritin were significantly lower and serum potassium was significantly higher than the pre-treatment level from 1 month onwards. Five patients without pre-treatment iron overload required oral iron supplement and 3 required oral potassium-binding resin. No significant change in other serum biochemical parameters was observed. Blood pressure remained stable during the treatment period but additional or increased dosage of antihypertensive drugs was required in 5 patients. Peritoneal small solute clearance and ultrafiltration and residual renal clearance did not change significantly after correction of anemia. The incidence of peritonitis and exit site infection was similarly unaffected. One patient developed a severe headache which was not associated with hypertension and responded to withdrawal of rHuEPO treatment. Most of the remaining patients showed improvement in subjective well-being. It was concluded that the subcutaneous route twice a week is a safe, convenient and cost-effective way to administer rHuEPO to patients on CAPD.
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PMID:Correction of anemia in patients on continuous ambulatory peritoneal dialysis with subcutaneous recombinant erythropoietin twice a week: a long-term study. 185 28

Recombinant human erythropoietin (rHu-EPO) was given during 12 to 20 months in 15 long term haemodialysis anaemic (mean Hb: 6.6 +/- 1 g/dl) patients who required no blood transfusion. Patients over 65, or with severe arterial disease or with uncontrolled hypertension were not included in this trial. Correction of anaemia (mean Hb 12.1 +/- 0.6 g/dl) was achieved in all patients and maintained all along the study. An improved sense of wellbeing and increased exercise tolerance were reported by all patients. Appropriate maintenance dosage of rHu-EPO was 74 +/- 6 U/kg i.v. twice weekly. High dose oral and/or intravenous iron therapy was necessary in the absence of previous marked iron overload. One retinal venous thrombosis was the sole severe side-effect encountered. A slight but significant increase of blood pressure was observed with the need of intensifying previous anti-hypertensive therapy in one patient and of starting one in one another. Fine adjustment of the dry weight was necessary to maintain blood pressure in the normal range. Heparin requirements increased in the majority of patients because of hollow fibre clotting but there was no evidence of decreased efficacy of dialysis. In two patients clotting of arteriovenous fistula was not obviously related to the rHu-EPO treatment.
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PMID:[Treatment of anemia in chronic hemodialysis patients with recombinant human erythropoietin: long-term results in 15 patients]. 237 41

The traditional options available for the correction of hemodialysis-related anemia are blood transfusions and androgen therapy to stimulate erythropoiesis. A new therapeutic option, recombinant human erythropoietin (r-HuEPO; EPOGEN, AMGEN Inc, Thousand Oaks, CA), is currently undergoing clinical trials. Each treatment alternative has certain attendant adverse effects. The adverse effects of transfusion include transmission of infections such as hepatitis or acquired immunodeficiency syndrome, iron overload, and sensitization to histocompatibility antigens. Androgen therapy can cause masculinization of women and children and, in some forms, is associated with a high incidence of abnormal liver function. Treatment with r-HuEPO has some potential adverse effects, including hypertension, thrombosis of arteriovenous fistulae, prolonged duration of dialysis, hyperkalemia, and iron deficiency. Gradual and careful introduction of r-HuEPO should prevent hypertension from becoming problematic.
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PMID:Adverse effects of therapy for the correction of anemia in hemodialysis patients. 264 19

18 anemic patients undergoing maintenance hemodialysis were treated with recombinant human erythropoietin (EPO) 1-3 times per week for 10.7 +/- 3 months. 4 patients underwent renal transplantation whereas 14 patients could be followed up during 12 months of EPO treatment. Hemoglobin concentration rose (from 7.0 +/- 0.7 to 11.0 +/- 1.1 g/dl, p less than 0.001) with an EPO maintenance dose of 298 units/kg/week. Blood transfusions were totally eliminated. 12 patients without iron overload required iron supplements. In the course of an infectious episode and notwithstanding an increase in EPO dosage, 2 patients exhibited a fall in hemoglobin which rose again after successful treatment of the infection. The few complications observed in connection with the rise in hemoglobin were: 1. deterioration of arterial hypertension in 7/18 with hypertensive encephalopathy in 3 patients, 2. thrombotic occlusion of the vascular hemodialysis access (a-v fistula) in 3/18, 3. periarticular inflammation with calcified deposits due to an elevated calcium-phosphorus product of 6.8 mmol/l in 4/18, 4. occurrence of hyperkalemia (6.9 +/- 0.3 mmol/l) in 7/18. These complications were more frequent during the first 3 months. They were corrected with close monitoring, drug therapy for hypertension, and intensification of dialysis and of treatment with phosphate binding substances, with the result that no differences were found in 14 patients before and after 12 months of treatment with EPO (blood pressure 133 +/- 25/77 +/- 9 vs 139 +/- 26/79 +/- 13 mm Hg [ns], potassium 5.4 +/- 0.4 vs 5.6 +/- 1.0 mmol/l [ns] and calcium-phosphorus product 4.3 +/- 1.0 vs 4.6 +/- 1.3 [ns]).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Treatment of anemia in hemodialysis patients using recombinant human erythropoietin: advantages and disadvantages]. 271 Nov 61

Dietary phosphorus restriction can prevent the progression of renal failure in subtotally nephrectomized rats or in rats with nephrotoxic serum nephritis, independent of protein and caloric intake. Conversely, diets high in phosphorus content result in a more rapid deterioration of renal function. The results are less compelling in indicating that phosphorus restriction can slow the progression of renal failure in the clinical setting. The toxicity of phosphate appears to be related to induction of calcium phosphate precipitation, resulting in tubulointerstitial disease. Most studies of prevention of renal calcification have addressed a single pathway in the development of nephrocalcinosis. These include inhibitors of calcium phosphate precipitation, calcium channel blockers, or an inhibitor of PTH secretion. All of these studies have shown a beneficial effect in preserving renal function. It is possible that a combination of these agents, started early in the course of CRF, may have an additive effect in preventing the progression to ESRD. The discussion of other factors associated with progression of renal failure is beyond the scope of this review. It is obvious that dietary protein restriction, treatment of systemic and intraglomerular hypertension and lipid abnormalities, and prevention of iron overload, all play roles in the preservation of renal function in CRF.
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PMID:Role of phosphate retention in the progression of renal failure. 832 Apr 87

Patients with end-stage renal disease (ESRD) are at a markedly increased risk for cardiovascular complications compared with the general population. In addition to traditional cardiovascular risk factors such as diabetes mellitus, hypertension, hyperlipidaemia or cigarette smoking, a number of population-specific factors are implicated, such as anaemia, hyperhomocysteinaemia, hyperphosphataemia and vascular calcification, as well as inflammation and oxidative stress. Iron overload has been suggested to increase the cardiovascular risk in the general population. Iron supplementation is a widespread clinical practice in ESRD, especially in patients on maintenance haemodialysis (HD). Iron may therefore contribute to cardiovascular complications through effects on low-density lipoprotein oxidation and endothelial dysfunction. Although the effects of iron stores and iron therapy on cardiovascular risk are not well defined in HD patients, the 'iron hypothesis' deserves attention: serum ferritin is a marker of morbidity and mortality in HD patients, and the administration of high amounts of intravenous iron increases the risks of hospitalization and death. In contrast to intravenous iron therapy, intestinal iron absorption is regulated by body iron stores and is suppressed in the presence of infection and iron overload. Prospective studies are needed to clarify the influence of iron stores and iron therapy on overall and cardiovascular morbidity and mortality in ESRD patients.
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PMID:Iron overload and cardiovascular complications in dialysis patients. 1190 55

Chronic liver disease is a major cause of morbidity and mortality in the United States. Although often used to detect liver disease, the prevalence and etiology of elevated aminotransferases are unknown. We analyzed data on adults ages 17 yr and older (N = 15,676) from the Third National Health and Nutrition Examination Survey (1988-1994). Participants were classified as having elevated aminotransferase levels if either aspartate aminotransferase or alanine aminotransferase was elevated above normal. Aminotransferase elevation was classified as "explained" if there was laboratory evidence of hepatitis B or C infection, iron overload, or if there was a history of alcohol consumption. Analyses were weighted to provide national estimates. The prevalence of aminotransferase elevation in the United States was 7.9%. Aminotransferase elevation was more common in men compared to women (9.3% vs 6.6%, p = 0.002), in Mexican Americans (14.9%) and non-Hispanic blacks (8.1%) compared to non-Hispanic whites (7.1%, p < 0.001). High alcohol consumption, hepatitis B or C infection and high transferrin saturation were found in only 31.0% of cases. Aminotransferase elevation was unexplained in the majority (69.0%). In both men and women, unexplained aminotransferase elevation was significantly associated with higher body mass index, waist circumference, triglycerides, fasting insulin, and lower HDL; and with type 2 diabetes and hypertension in women (all p < 0.05). Aminotransferase elevation was common in the United States, and the majority could not be unexplained by alcohol consumption, viral hepatitis or hemochromatosis. Unexplained aminotransferase elevation was strongly associated with adiposity and other features of the metabolic syndrome, and thus may represent nonalcoholic fatty liver disease.
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PMID:The prevalence and etiology of elevated aminotransferase levels in the United States. 1280 14

Zygomycosis is an uncommon but frequently fatal infection and occurs mostly in immunosuppressed hosts, whereas approximately 50% of zygomycosis occurs in diabetic patients. The current patient initially presented with persistent pulmonary edema secondary to renal failure. This was the last of four admissions within 1 year for this 68-year-old woman, for whom the chief complaints were shortness of breath and chest pain. Her past medical history included insulin-requiring type 2 diabetes and hypertension for 10 years, and chronic heart and renal failure. She was previously admitted to the hospital for what appeared to be pulmonary edema secondary to renal failure. In the last admission the patient developed pulmonary hemorrhage and metabolic acidosis. Transbronchial biopsy was performed, showing irregular fungal hyphae in the blood vessels, morphologically consistent with zygomycosis. Central nervous system computed tomography also revealed a large infarct in the cerebral hemisphere. The patient died on the seventh hospital day. At autopsy three organs were extensively involved by zygomycosis: (i) lungs were diffusely hemorrhagic with acute infarcts; (ii) pericardium had fibrotic inflammation; and (iii) the left cerebral hemisphere, cerebellum and pons had large hemorrhagic infarct by zygomycosis infection. Corticosteroid medication and hemodialysis triggered increasing hyperglycemia, metabolic acidosis and iron overload, which contributed to zygomycosis infection that subsequently spread to the heart and brain as a rare consequence.
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PMID:Zygomycosis involving lungs, heart and brain, superimposed on pulmonary edema. 1582 46

For more than a decade, insulin resistance has been proposed as the key linking factor for the metabolic syndrome disease cluster of glucose intolerance, hypertension, dyslipidemia, obesity, and cardiovascular disease. Although most of the epidemiological, experimental, and clinical evidence still support the role of insulin resistance as an important component of this multifaceted syndrome, there is evidence amassing that a neurohormonal mechanism, including an endocrine role for adipocytes, probably plays a more fundamental role. This is supported by the strong associations between obesity, especially central adiposity, and all components of the metabolic syndrome, in contrast to the inconsistent relationships between blood pressure and markers of insulin resistance. However, much of the effect of visceral fat on cardiovascular risk factors is mediated through the metabolic actions of free fatty acids (FFA) on insulin resistance, thus resolving any obesity versus insulin resistance controversy. In addition to the roles of obesity and FFA in the development of insulin resistance syndrome, the high prevalence rates of this disease cluster among subjects from low socioeconomic groups as well as from developing countries have led to alternative hypotheses to better our understanding of the contributory roles of socioeconomic, in utero, and genetic factors in this syndrome. More recently, the pathogenetic roles of iron overload and liver dysfunction have also been re-examined. In this article, the various hypotheses which have been put forward to explain the diverse clinical manifestations of the metabolic or insulin resistance syndrome are summarized and put into perspective. While there is clinical and experimental evidence to support many of these independent pathways, alternative statistical methods such as factor analysis or structural equation modeling may be needed to unravel the complex nature of these interacting pathways. Finally, these hypotheses, if proven, will add new dimensions to our current strategies and emphasize the need to focus on behavioral and socioeconomic interventions in addition to the use of pharmacological therapy in our attempt to control this epidemic disease of modern societies.
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PMID:The insulin resistance syndrome: mechanisms of clustering of cardiovascular risk. 1622 95

There is increasing evidence that moderately elevated body iron stores, below levels commonly found in genetic hemochromatosis, may be associated with adverse health outcomes. Genetic hemochromatosis, characterized by transferrin saturation (TS) greater than 45%, is most often linked to homozygosity of the HFE C282Y allele. The phenotype is also modulated by mutations of more recently discovered genes (including ferroportin, hemojuvelin, hepcidin, and transferrin receptor) and environmental factors (including alcohol, viruses, diet, blood loss). Iron overload without hemochromatosis is characterized by high levels of serum ferritin and normal TS, as seen in dysmetabolic hepatosiderosis. Elevated serum ferritin levels predict incident type 2 diabetes in prospective studies and have been associated with hypertension, dyslipidemia, glucose tolerance disturbances, central adiposity, and metabolic syndrome. High ferritin levels are not synonymous with iron overload and may in some cases be a simple marker of insulin resistance.
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PMID:[Iron overload and insulin resistance]. 1629 93


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