Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0002878 (hemolytic anemia)
 7,530 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The hemolytic-uremic syndrome (HUS) is an acute disorder, characterized by the triad of microangiopathic hemolytic anemia, nephropathy and thrombocytopenia. The great majority of patients are children, usually under 4 years of age, although adults can be affected. The onset is abrupt and usually follows gastroenteritis or upper respiratory infection. Later, clinical manifestations based on the triad, such as pallor, jaundice, edema, hypertension and purpura soon develop. The urinary output is reduced and the urine may appear dark yellow or tea-colored. Laboratory tests of peripheral blood show severe hemolytic anemia associated with fragmented red blood cells and thrombocytopenia, usually below 50,000/microliters. The blood urea nitrogen, serum creatinine and lactate dehydrogenase concentrations are elevated. Proteinuria and microscopic hematuria, which are indicative of active glomerular damage are also seen. Profound understanding of these manifestations is sufficient to permit an early diagnosis of HUS.
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PMID:[Diagnosis and clinical features of hemolytic uremic syndrome]. 843 21

The effects of cisplatin on erythropoietin (EPO) production were investigated in comparison with the effects of phenylhydrazine in rats. Cisplatin (4.5 mg/kg i.p. bolus) decreased red blood cell count (RBC), hematocrit (Hct) and hemoglobin concentration (Hgb) for 14 days after dosing. These decreases were accompanied with increases of blood urea nitrogen (BUN) and serum creatinine (s-CRE). Both serum EPO concentration and kidney EPO mRNA content were significantly decreased in cisplatin-treated rats. On the other hand, phenylhydrazine (10 mg/kg p.o. once a day for 8 days) decreased RBC, Hct and Hgb, and increased serum EPO concentration and kidney EPO mRNA content. Phenylhydrazine had little effect on BUN or s-CRE. These results suggest that a suppression of EPO production is involved in the pathophysiology of cisplatin-induced renal anemia and that measurement of serum EPO concentration and kidney EPO mRNA content is available for distinguishing renal anemia from hemolytic anemia.
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PMID:Effects of cisplatin on erythropoietin production in rats. 888 84

We reported a case of a 3-year-old girl with hemolytic uremic syndrome (HUS), which showed hemolytic anemia (Hemoglobin 8.2 g/dl, lactate dehydrogenase 1277 IU/l and total bilirubin 0.6 mg/dl), small purpura on the skin (platelet 7.3 x 10(4)/microliter) and slightly decreased output of urine (creatinine 0.4 mg/dl and blood urea nitrogen 27.2 mg/dl). Verotoxin producing Escherichia coli (E. coli) O157 was not isolated, but Salmonella agona and E. coli O125, which is one of the enteropathogenic E. coli, were detected from her stool culture. However, the IgM antibody against verotoxin producing E. coli (VTEC) O157 lipopolysaccharide was detected in both serum of the acute and convalescent phase by immunoblot assay. In addition verotoxin DNA was demonstrated in the stool by PCR method. Therefore, we think this HUS might be due to VTEC O157, which must have been co-infected with Salmonella agona and E. coli O125. There have been four cases including the present case of co-infection with VTEC O157 so far, and the other three cases were of the Salmonella species. Although the reason of co-infection was unknown, we may infer that food might be contaminated with some pathogens including Salmonella species or that these patients might be already infected with Salmonella species prior to VTEC infection. Even when some other pathogens were detected by a stool culture from a patient with HUS, we should pay attention to demonstrate associated of VTEC and HUS by the specific antibodies and PCR for verotoxin DNA.
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PMID:[A case of hemolytic uremic syndrome documented co-infection of vertoxin producing Escherichia coli O157 and other pathogens]. 933 32

Two ewes died after being fed rabbit ration and mineral salts designated for cows. This food is known to contain copper levels above that indicated for sheep. Blood counts revealed anemia, and serological tests showed high blood urea nitrogen, glutamic pyruvic transaminase and glutamic oxalacetic transaminase values. At necropsy, the animals had hepatopathy and nephropathy. Hepatic copper levels were 414 ppm. Histological examination revealed chronic active hepatitis with bile casts and tubular nephrosis. The liver, spleen and kidneys had hemosiderosis. This was attributed to the massive hemolysis caused by the copper. The liver failure and hemolytic anemia caused death in these sheep.
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PMID:Copper toxicosis in sheep: a case report. 955 65

An increased incidence of TTP has been noted among patients receiving intravascular stents to improve patency in diseased coronary, renal, and peripheral arteries. Placement of transjugular intrahepatic porto-systemic shunt stents is often associated with subsequent development of severe hemolysis. We have prospectively studied the development of microangiopathic hemolysis or TTP in patients undergoing intravascular stent placement for peripheral vascular or renal artery disease. Hemolysis was evaluated both before and after stent placement by measuring complete blood count, total bilirubin, lactate dehydrogenase (LDH), haptoglobin and reticulocyte count, and examining peripheral blood films of all patients. Coagulation parameters, blood urea nitrogen and creatinine were measured to exclude disseminated intravascular coagulation or thrombotic thrombocytopenic purpura as a potential cause of hemolysis. Seventeen patients (median age 69 years) were evaluated. One patient was on ticlopidine. Mean hematocrit fell from 41.8% pre-stenting to 35.5% post-stenting (P = 0.003) but without significant change in reticulocyte count (1.7 vs. 1.6%, P = 0.605), LDH (546 vs. 560 IU/l; P = 0.836), bilirubin (0.62 vs. 0.63 mg/dl; P = 1.0), or haptoglobin (183 vs. 158 mg/dl; P = 0.083). Thus, this drop in hematocrit could not be attributed to hemolysis. Peripheral blood films revealed fewer than 1% schistocytes before and after stent placement in all cases. Absence of significant changes in mean platelet count (240 vs. 210 x 10(9)/L; P = 0.088), fibrinogen (385 vs. 378 mg/dl; P = 0.789), BUN (24.5 vs. 16.8; P = 0.079), and creatinine (1.38 vs. 1.24; P = 0.757) argue against development of TTP or DIC resulting from stent placement. No patient developed new renal impairment, a neurological syndrome, or unexplained fever after stent placement. At a mean of 6 weeks follow-up after stent placement, patients have not developed signs of hemolytic anemia or worsening renal function. Our findings argue against a primary risk of microangiopathic hemolytic anemia or TTP due to intravascular stents in patients not receiving ticlopidine.
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PMID:Intravascular stents do not cause microangiopathic hemolysis or thrombotic microangiopathy. 1054 Mar 68

Categories of undesirable effects of drugs are described. Recent experiments on the production of hypersensitization (1) by the use of ECT solution to enhance skin sensitization to penicillin, (2) through the activity of common metabolites of different drugs, and (3) to a non-sensitizing drug by pretreatment with a sensitizing agent are reviewed. The mechanism of hemolytic anemia due to an inherited enzymatic defect and that of drug-induced purpura and the agranulocytic agents is discussed. The three groups of drugs-(1) rarely toxic, e.g. quinine; (2) always toxic in sufficient amounts, e.g. nitrogen mustard; (3) intermediate, e.g. chloramphenicol-are presented, with special consideration of chloramphenicol. It is the responsibility of the pharmacologist to develop and adopt newer methods for toxicity detection, and of the clinician to practise caution in prescribing drugs and to attempt the early recognition of any disorder they may induce. The incidence, diagnosis, prevention, treatment and prognosis of the drug-induced dyscrasias are discussed.
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PMID:Drug-induced blood dyscrasias. 1400 57

A 47-year-old white woman with a history of stage III squamous cell carcinoma of the anus was transferred to Johns Hopkins Hospital for further evaluation of renal failure, hemolytic anemia, and thrombocytopenia. The patient was first diagnosed with squamous cell carcinoma of the anus 1 year before admission. She was treated with external beam radiation of the pelvis and two cycles of mitomycin C-based chemotherapy (a cumulative dose, 34 mg/m(2)). Her clinical course was complicated by Clostridium difficile colitis and myositis successfully treated with prednisone. Three months before admission, the patient developed dysuria. Her creatinine increased from normal to 1.7 mg/dL, and microscopic hematuria was present. A renal ultrasound and an abdominal computed tomographic scan showed no abnormalities or obstruction. One month before admission, she underwent a cystoscopy, which showed only radiation-induced changes in the bladder. Two weeks before admission, the patient became delirious and was taken to a hospital, where she was found to be anemic, with a hematocrit level of 23.7%, and thrombocytopenic with a platelet count of 110,000/mm(3). Her creatinine level was 5.9 mg/dL. Previous values of hematocrit, platelet count, and serum creatinine were normal. On admission at Johns Hopkins Hospital the patient had no complaints. She was afebrile on physical examination and had normal vital signs. Head, neck, chest, cardiovascular, and abdominal examinations were normal. There was skin pallor, but no echymoses or petechiae. She was alert and oriented with normal mental status. Her neurologic examination was normal. Laboratory data showed a white blood cell count of 6390/mm(3), a hematocrit level of 26.5%, and a platelet count of 26,000/mm(3). Her blood urea nitrogen level was 57 mg/dL, creatinine level was 4.0 mg/dL, and lactate dehydrogenase was 550 U/L (reference, 115 to 275 U/L). Urinalysis showed innumerable red blood cells and large protein. A peripheral blood smear showed fragmented red blood cells, schistocytes, no abnormal white blood cells, and few platelets. There was no radiographic or clinical evidence of relapse of her squamous cell carcinoma. What is the diagnosis?
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PMID:Cases from the Osler Medical Service at Johns Hopkins University. 1474 66

Brown spider (Loxosceles genus) venom can induce dermonecrotic lesions at the bite site and systemic manifestations including fever, vomiting, convulsions, disseminated intravascular coagulation, hemolytic anemia and acute renal failure. The venom is composed of a mixture of proteins with several molecules biochemically and biologically well characterized. The mechanism by which the venom induces renal damage is unknown. By using mice exposed to Loxosceles intermedia recombinant dermonecrotic toxin (LiRecDT), we showed direct induction of renal injuries. Microscopic analysis of renal biopsies from dermonecrotic toxin-treated mice showed histological alterations including glomerular edema and tubular necrosis. Hyalinization of tubules with deposition of proteinaceous material in the tubule lumen, tubule epithelial cell vacuoles, tubular edema and epithelial cell lysis was also observed. Leukocytic infiltration was neither observed in the glomerulus nor the tubules. Renal vessels showed no sign of inflammatory response. Additionally, biochemical analyses showed such toxin-induced changes in renal function as urine alkalinization, hematuria and azotemia with elevation of blood urea nitrogen levels. Immunofluorescence with dermonecrotic toxin antibodies and confocal microscopy analysis showed deposition and direct binding of this toxin to renal intrinsic structures. By immunoblotting with a hyperimmune dermonecrotic toxin antiserum on renal lysates from toxin-treated mice, we detected a positive signal at the region of 33-35 kDa, which strengthens the idea that renal failure is directly induced by dermonecrotic toxin. Immunofluorescence reaction with dermonecrotic toxin antibodies revealed deposition and binding of this toxin directly in MDCK epithelial cells in culture. Similarly, dermonecrotic toxin treatment caused morphological alterations of MDCK cells including cytoplasmic vacuoles, blebs, evoked impaired spreading and detached cells from each other and from culture substratum. In addition, dermonecrotic toxin treatment of MDCK cells changed their viability evaluated by XTT and Neutral-Red Uptake methodologies. The present results point to brown spider dermonecrotic toxin cytotoxicity upon renal structures in vivo and renal cells in vitro and provide experimental evidence that this brown spider toxin is directly involved in nephrotoxicity evoked during Loxosceles spider venom accidents.
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PMID:Brown spider dermonecrotic toxin directly induces nephrotoxicity. 1600 84

Phenothiazine is an aromatic tricyclic compound that first emerged from the furtive chemical activity surrounding the aniline dye industry at the latter half of the 19th century. It contains both nitrogen and sulphur atoms and is the parent molecule of a multitude of drugs that have enjoyed varied and extensive use throughout medical and veterinary practice. The compound itself is not without biological activity and has been shown to possess insecticidal, antifungal, antibacterial and anthelmintic properties. It was this latter vermifugal application that has earned the molecule a place alongside penicillin and DDT for its colossal impact on mankind. Following its extensive usage over many years, unwanted reactions including neuromuscular incoordination, photosensitization and haemolytic anaemia have been reported and these have limited its use in the present climate. Investigations into the mode of action of phenothiazine and its underlying biochemical properties have been undertaken but the molecule has yet to reveal its secrets and still poses problems of understanding at the molecular level. This article reviews the literature, both established and current, and presents a contemporary view on phenothiazine and its interaction with biological systems.
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PMID:Phenothiazine: the parent molecule. 1701 93

Hemolytic uremic syndrome (HUS), which is caused by Shiga toxin-producing Escherichia coli infection, is the leading cause of acute renal failure in children. At present, there is no complete small animal model of this disease. This study investigated a mouse model using intraperitoneal co-injection of purified Shiga toxin 2 (Stx2) plus LPS. Through microarray, biochemical, and histologic analysis, it was found to be a valid model of the human disease. Biochemical and microarray analysis of mouse kidneys revealed the Stx2 plus LPS challenge to be distinct from the effects of either agent alone. Microarrays identified differentially expressed genes that were demonstrated previously to play a role in this disease. Blood and serum analysis of these mice showed neutrophilia, thrombocytopenia, red cell hemolysis, and increased serum creatinine and blood urea nitrogen. In addition, histologic analysis and electron microscopy of mouse kidneys demonstrated glomerular fibrin deposition, red cell congestion, microthrombi formation, and glomerular ultrastructural changes. It was established that this C57BL/6 mouse is a complete model of HUS that includes the thrombocytopenia, hemolytic anemia, and renal failure that define the human disease. In addition, a time course of HUS disease progression that will be useful for identification of therapeutic targets and development of new treatments for HUS is described.
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PMID:A murine model of HUS: Shiga toxin with lipopolysaccharide mimics the renal damage and physiologic response of human disease. 1708 44


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