Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0002871 (anemia)
 52,094 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Recombinant human erythropoietin was administered to 59 patients over 65 years of age receiving maintenance hemodialysis treatment in Kyoto and Shiga district, in order to evaluate its utility on renal anemia. After 6 months of administration, the hematocrit rose from 20.8 +/- 3.5% to 28.0 +/- 3.7% with concomitant improvement of subjective symptoms related to anemia. Twelve patients developed side effects, in 10 of whom elevation of blood pressure was observed. We found no clinically significant abnormalities in the laboratory data. In conclusion, recombinant human erythropoietin is highly useful in the treatment of renal anemia in elderly hemodialysis patients.
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PMID:[Utility of recombinant human erythropoietin on the anemia of elderly hemodialysis patients]. 128 37

For the purpose of obtaining basic data and for establishing a support system for elderly people with various health and social problems, a population survey was performed in 1990 to investigate the health and living conditions of elderly people living alone, elderly couples and the bedridden elderly in the town of Shigaraki, Shiga Prefecture. A total of 275 subjects (103 male, 172 female) 65 years of age and over were surveyed. The participation rate in this survey was 88.1%. Analysis of health conditions (morbidity rate, blood pressure, electrocardiograph and blood examination data) of elderly people living alone, elderly couples and the bedridden elderly produced the following: 1) Stroke was the main cause of being bedridden in men, while in women, bone and joint disease, especially fracture, was the main cause. 2) The combined prevalence of hypertension and borderline hypertension in elderly people living alone, elderly couples and the bedridden elderly was over 50%. The bedridden elderly had a lower prevalence than elderly people living alone and elderly couples. 3) Men in all of the above mentioned life styles, had a higher tendency of showing ECG abnormalities than women. The tendency for major ECG abnormalities was high for bedridden elderly, both male and female, with the tendency for men being higher. 4) In bedridden elderly, a tendency of higher prevalence of anemia, in both male and females, lower total serum cholesterol and triglyceride in males compared to elderly people living alone and in elderly couples, was observed.
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PMID:[A comparative study of the health conditions of elderly people living alone, elderly couples and the bedridden elderly at home in a rural area of Shiga Prefecture: special reference to morbidity rate and blood pressure, electrocardiograph and blood examination data]. 824 35

The baboon response to intravenous infusion of Shiga toxin 1 (Stx-1) varied from acute renal failure, proteinuria, hyperkalemia, and melena with minimal perturbation of host inflammatory and hemostatic systems (high-dose group, 2.0 microg/kg; n = 5) to renal failure with hematuria, proteinuria, thrombocytopenia, schistocytosis, anemia, and melena (low-dose group, 0.05 to 0.2 microg/kg; n = 8). Both groups exhibited renal shutdown and died in 57 hours or less. Both groups produced urine that was positive for tumor necrosis factor and interleukin-6 although neither of these cytokines was detectable (</=5 ng/ml) in the general circulation. Light and electron microscopy showed organelle disintegration and necrosis of the renal proximal tubular epithelium and of the intestinal mucosal epithelium at the tips of the microvilli, both of which were previously shown to bear Gb3 receptors. The renal distal tubular epithelium was spared. The renal proximal tubular epithelial changes were accompanied by swelling of visceral epithelial cells (podocytes) and by swelling and detachment of endothelial cells of the glomerular capillaries. In addition, all of the animals receiving low-dose Stx-1 showed microvascular fibrin deposition and thrombosis in renal glomerular and peritubular capillaries in association with a fall in hematocrit and platelet count and a rise in schistocyte count. The gastrointestinal villous tip lesions were accompanied by varying degrees of mucosal and submucosal congestion, hemorrhage, or necrosis. Electron microscopic images of cerebral cortex and cerebellum showed diffuse unraveling of myelin sheaths with occasional disintegration of neuronal cell bodies. In contrast to the gastrointestinal mucosal and renal proximal tubular epithelium, the Gb3 receptor glycolipid of the renal glomerular and neuronal tissues as determined using toxin overlay thin-layer chromatography plates was below the limit of detection (<13 pM/g wet tissue). We conclude that, depending on the status of the host and amount of toxin infused, Stx-1 can produce a variety of responses ranging from damage to cells carrying the Gb3 receptor (renal proximal tubular epithelial cells and gastrointestinal mucosa) to damage to renal glomerular tissues with microvascular thrombosis as a result of the host's inflammatory response localized to the kidney. We conclude that this thrombotic coagulopathy arises from local changes in the kidney because the appearance of host inflammatory mediators was limited to the urine. This suggests that the initial host response is localized in the kidney, and that the systemic thrombocytopenia, anemia, and schistocytosis may arise secondarily.
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PMID:Characterization of the baboon responses to Shiga-like toxin: descriptive study of a new primate model of toxic responses to Stx-1. 1023 66

Oral infection with enterohemorrhagic Escherichia coli (EHEC) may cause severe enteritis, followed in up to 10% of cases by an extraintestinal complication, the hemolytic uremic syndrome (HUS). HUS is characterized by a triad of symptoms: anemia, thrombocytopenia, and acute renalfailure due to thrombotic microangiopathy. EHEC produces several virulence factors, among which a family of phage-encoded cytotoxins, called Shiga toxin 1 and Shiga toxin 2, seems to be most important. However, since an appropriate animal model is not available, pathogenicity of these emerging enteric pathogens is still poorly understood. Germ-free gnotobiotic piglets infected orally with an O1577:H7 or an O26:H11 EHEC wild-type isolate, both producing Shiga toxin 2, developed intestinal and extraintestinal manifestations of EHEC disease, including thrombotic microangiopathy in the kidneys, the morphologic hallmark of HUS in humans. Thus, gnotobiotic piglets are suitable to further study the pathophysiology of EHEC-induced HUS. It can be expected that data obtainedfrom this animal model will improve our current standard of knowledge about this emerging infectious disease.
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PMID:Gnotobiotic piglets develop thrombotic microangiopathy after oral infection with enterohemorrhagic Escherichia coli. 1221 73

A child with a history of diarrhea presented with transient anemia, reticolucytosis, and red blood cell fragmentation. Blood pressure and levels of blood platelets, creatinine, and urea were normal, as were results of urinalysis. Escherichia coli harboring genes for Shiga toxin were detected in stool specimens. It is concluded that extraintestinal diseases caused by Shiga toxin-producing bacteria sometimes present without any renal involvement.
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PMID:Microangiopathic anemia without thrombocytopenia and kidney disease in a child with diarrhea caused by Shiga toxin-producing Escherichia coli. 1472 32

Hemolytic uremic syndrome is caused primarily by Shiga toxin-producing Escherichia coli O157:H7. The most common cause of acute renal failure in children, hemolytic uremic syndrome also can occur in adults. Characteristic features of the syndrome are microangiopathic anemia, thrombotic thrombocytopenia, and renal failure. Although the presentation of this syndrome is diverse, the classic prodromal illness is bloody diarrhea following ingestion of hamburger meat contaminated with E. coli O157:H7, the most common mode of infection in the United States. Children with hemolytic uremic syndrome generally present with gastroenteritis complaints (e.g., abdominal pain or tenderness, nausea or vomiting, fever, anemia); affected adults may be asymptomatic. Complications from hemolytic uremic syndrome can include intussusception, chronic renal failure, and seizures in severe cases. Because an incubation period of approximately one week occurs between the start of diarrhea and the onset of hemolytic uremic syndrome, physicians should maintain a high index of suspicion; early laboratory testing is important to diagnose and manage this syndrome. Obtaining a complete blood count and stool culture and performing Shiga toxin testing are the first of a series of tests that may help diagnose hemolytic uremic syndrome.
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PMID:Hemolytic uremic syndrome: an emerging health risk. 1700 34

The non-toxic enzymic A subunit of Shiga toxin 1 (StxA1) reduces expression and replication of the bovine retroviruses, bovine leukemia virus and bovine immunodeficiency virus (BIV). Here, the impact of StxA1 on representative positive and negative stranded RNA viruses was compared. BIV and equine infectious anemia virus were sensitive to picomolar concentrations of StxA1 while poliovirus, rhinovirus, and vesicular stomatitis virus were only marginally sensitive to nanomolar concentrations of toxin. Thus, the length of the reproductive cycle and/or other factors, but not viral encapsulation may play a role in determining sensitivity to StxA1. The effects of StxA1 at concentrations from 0.01 to 10 microg/ml on the most sensitive virus (BIV-infected cultures of fetal bovine lung cells) were analyzed by electron microscopy 48 h post challenge. Cells treated with 0.1 microg StxA1/ml or higher toxin concentrations were similar in appearance and showed progressively fewer viral factories with increasing toxin concentration. However, cells treated with 0.01 microg/ml StxA1 had a radically different appearance, exhibiting smooth cell membranes and high vacuolization. These results showed that complex retroviruses were more sensitive to StxA1 than single-stranded RNA viruses and that StxA1 interfered with retroviral replication in a concentration-dependent manner.
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PMID:Differential sensitivity of viruses to the antiviral activity of Shiga toxin 1 A subunit. 1719 49

Hemolytic uremic syndrome is the clinical triad of thrombocytopenia, microangiopathic hemolytic anaemia and acute renal failure. Cases not associated with a preceding Shiga-like toxin producing Escherichia coli are described as atypical HUS (aHUS). Approximately 50% of patients with aHUS have mutations in one of three complement regulatory proteins, Factor H (CFH), membrane cofactor protein (MCP;CD46) or factor I (IF). A common feature of these three proteins is that they regulate complement by cofactor activity. Decay accelerating factor (DAF; CD55) regulates the complement system by disassociating the alternative and classical pathway convertases. Like CFH and MCP, the gene for DAF lies within the regulators of complement activation (RCA) gene cluster at 1q32. In 1998, we described linkage to this region in families with aHUS which led to the discovery of mutations in CFH and MCP. We therefore genotyped DAF in a panel of 46 aHUS patients including families with linkage to the RCA cluster. A mutation, I197V, was identified in one patient with familial HUS which was not found in 100 healthy controls. Molecular modelling of this mutation shows that the I197V mutation does not reside in an area which would be predicted to be important in decay accelerating activity. The expression of I197V on EBV-transformed B lymphocytes was equivalent to that of wild type controls. There was no significant decrease in decay acceleration activity of the recombinantly produced I197V mutant compared with wild type, as measured by a complement-mediated lytic assay. In conclusion, this study, identifies only one mutation in DAF in 46 patients with aHUS. This mutation, I197V, does not impair complement regulation and cannot be implicated in the pathogenesis of aHUS in this patient. This suggests that the complement regulatory abnormality in aHUS is principally one of deficient cofactor activity rather than of decay acceleration activity.
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PMID:The decay accelerating factor mutation I197V found in hemolytic uraemic syndrome does not impair complement regulation. 1736 71

Escherichia coli strains producing Shiga toxins (Stxs) colonize the lower gastrointestinal tract and cause watery diarrhea, hemorrhagic colitis, and hemolytic-uremic syndrome (HUS). HUS is characterized by hemolytic anemia, thrombocytopenia, and acute renal failure. Oliguria associated with acute tubular necrosis and microangiopathic thrombosis has been reported as the most common cause of renal failure in Argentinean children. Our study was undertaken to obtain a model of HUS in rats that was similar to the clinical and renal histopathology findings described in humans. Rats were intraperitoneally inoculated with culture supernatant from recombinant E. coli expressing Stx2. Glomerular filtrate volume evaluated from clearance of creatinine resulted in a progressive reduction (from 53% at 24 h to 90% at 48 h). Urine volume increased significantly at 24 h but returned to normal levels at 48 h. Evidence of thrombocytopenia, anemia and leukocytosis was documented. Macroscopic analysis revealed a hyperemic peritoneal face with intestinal water accumulation. The kidneys were friable and congestive. Histopathological analysis showed glomerular and tubular necrosis as well as microangiopathic thrombosis. Our findings indicated vascular damage and kidney lesions similar to those described in humans with HUS.
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PMID:Development of an experimental hemolytic uremic syndrome in rats. 1825 62

Shiga toxin-producing Escherichia coli is a principal source of regional outbreaks of bloody diarrhea and hemolytic-uremic syndrome in the United States and worldwide. Primary bacterial virulence factors are Shiga toxin types 1 and 2 (Stx1 and Stx2), and we performed parallel analyses of the pathophysiologies elicited by the toxins in nonhuman primate models to identify shared and unique consequences of the toxemias. After a single intravenous challenge with purified Stx1 or Stx2, baboons (Papio) developed thrombocytopenia, anemia, and acute renal failure with loss of glomerular function, in a dose-dependent manner. Differences in the timing and magnitude of physiologic responses were observed between the toxins. The animals were more sensitive to Stx2, with mortality at lower doses, but Stx2-induced renal injury and mortality were delayed 2 to 3 days compared to those after Stx1 challenge. Multiplex analyses of plasma inflammatory cytokines revealed similarities (macrophage chemoattractant protein 1 [MCP-1] and tumor necrosis factor alpha [TNF-alpha]) and differences (interleukin-6 [IL-6] and granulocyte colony-stimulating factor [G-CSF]) elicited by the toxins with respect to the mediator induced and timing of the responses. Neither toxin induced detectable levels of plasma TNF-alpha. To our knowledge, this is the first time that the in vivo consequences of the toxins have been compared in a parallel and reproducible manner in nonhuman primates, and the data show similarities to patient observations. The availability of experimental nonhuman primate models for Stx toxemias provides a reproducible platform for testing antitoxin compounds and immunotherapeutics with outcome criteria that have clinical meaning.
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PMID:Distinct physiologic and inflammatory responses elicited in baboons after challenge with Shiga toxin type 1 or 2 from enterohemorrhagic Escherichia coli. 2030 1


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