ascorbic-acid has been researched along with Anemia--Hemolytic* in 32 studies
2 review(s) available for ascorbic-acid and Anemia--Hemolytic
Article | Year |
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The anemia of scurvy.
Topics: Adult; Anemia, Hemolytic; Anemia, Macrocytic; Ascorbic Acid; Ascorbic Acid Deficiency; Blood Cell Count; Bone Marrow Cells; Erythrocytes; Erythropoiesis; FIGLU Test; Folic Acid; Folic Acid Deficiency; Hemolysis; Hemorrhagic Disorders; Humans; Iron; Leukocytes; Liver; Reticulocytes; Scurvy; Tissue Extracts; Vitamin B 12; Vitamin B 12 Deficiency | 1968 |
[AUTOALLERGY IN CLINICAL INTERNAL MEDICINE].
Topics: Adrenal Cortex Hormones; Adrenocorticotropic Hormone; Agranulocytosis; Anemia, Hemolytic; Anemia, Hemolytic, Autoimmune; Ascorbic Acid; Autoantibodies; Autoimmune Diseases; Blood Transfusion; Chloroquine; Colitis; Colitis, Ulcerative; Drug Hypersensitivity; Drug Therapy; Hemoglobinuria; Hemoglobinuria, Paroxysmal; Humans; Internal Medicine; Leukopenia; Lupus Erythematosus, Systemic; Neutrophils; Purpura; Purpura, Thrombocytopenic; Purpura, Thrombotic Thrombocytopenic; Splenectomy; Thrombocytopenia; Thyroiditis; Toxicology; Vitamins | 1964 |
1 trial(s) available for ascorbic-acid and Anemia--Hemolytic
Article | Year |
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Does vitamin C cause hemolysis in premature newborn infants? Results of a multicenter double-blind, randomized, controlled trial.
We tested the hypothesis that vitamin C supplementation of premature neonates is associated with hemolysis.. A double-blind, randomized, controlled trial of vitamin C supplementation (50 mg/day) was undertaken in premature neonates (birth weight, 1000 to 1500 gm). Infants were randomly assigned to receive vitamin C (Ce-Vi-Sol) (n = 32) or placebo (n = 24) for 14 days. Twenty-three subjects per group were required to detect a difference of 1 SD in corrected carboxyhemoglobin values (alpha = 0.05, beta = 0.10).. Day 14 vitamin C levels were lower in control subjects than in supplemented neonates (62 +/- 24 vs 125 +/- 62 micromol/L, p = 0.005). There was no difference in corrected blood carboxyhemoglogin concentrations (0.72 +/- 0.44 vs 0.72 +/- 0.23%; p = 0.95), other parameters of hemolysis, weight gain, blood sampled, presumed septic episodes, necrotizing enterocolitis, feeding intolerance, or transfusion. On day 14, bilirubin values were higher in control subjects than in the supplemented group (77 +/- 37 vs 55 +/- 33 micromol/L; p = 0.04). When a distant outlier in the nonsupplemented group was excluded (163 micromol/L), statistical significance was lost (73 +/- 32 vs 55 +/- 33 micromol/L; p = 0.09).. Oral supplementation of premature infants with vitamin C is not associated with evidence of increased erythrocyte destruction, hyperbilirubinemia, or other morbidity. Topics: Anemia, Hemolytic; Ascorbic Acid; Double-Blind Method; Female; Hemolysis; Humans; Hyperbilirubinemia; Infant, Newborn; Infant, Premature; Infant, Premature, Diseases; Male | 1997 |
29 other study(ies) available for ascorbic-acid and Anemia--Hemolytic
Article | Year |
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High dose vitamin C induced methemoglobinemia and hemolytic anemia in glucose-6-phosphate dehydrogenase deficiency.
Investigational use of intravenous vitamin C has been on the rise, but its side effects may be underreported. A 75-year-old woman presented with acute onset of jaundice, dark urine and shortness of breath after receiving 30 g of vitamin C infusion as an unconventional therapy for her hemifacial spasm. Diagnosis of methemoglobinemia and hemolytic anemia was made clinically and confirmed on laboratory tests. She recovered with supportive treatment and packed cell transfusion. Her previously unrecognised underlying condition of glucose-6-phosphate dehydrogenase (G6PD) deficiency was confirmed months after the initial presentation. This is the first reported case of methemoglobinemia and hemolytic anemia induced by high dose vitamin C in a female patient with G6PD deficiency. The dosage of vitamin C administered was also relatively low compared with previous adult reports. When administered at physiological dose, vitamin C can be used as an alternative to methylene blue in treatment of methemoglobinemia in patients with G6PD deficiency. However at supraphysiological dose vitamin C can paradoxically lead to hemolytic anemia in the same group of patients. Physicians should be alert of these potential complications of high dose vitamin C. Topics: Aged; Anemia, Hemolytic; Ascorbic Acid; Female; Glucosephosphate Dehydrogenase Deficiency; Hemifacial Spasm; Humans; Methemoglobinemia; Vitamins | 2020 |
Vitamin C deficiency: rare cause of severe anemia with hemolysis.
Historically known to be a disease of sailors and soldiers in the seventeenth and eighteenth century, scurvy is a rare nutritional deficiency in the developed world, but it can still be seen among the alcoholics and the malnourished. We present a case of a 39-year-old alcoholic male who presented with progressive fatigue and diffuse purpuric rash with scattered ecchymosis for 2 months. Blood work was remarkable for hemoglobin of 9.1 g/dl, which further dropped to 7 g/dl over the next few days. He was then found to have hemolysis on lab work. After an extensive workup, the common causes of hemolytic anemia were ruled out, vitamin C level was checked, which interestingly resulted as 0 mg/dl. Supplementation with oral vitamin C resulted in the gradual resolution of hemolytic anemia and rash. Hemoglobin improved to 15 g/dl in 4 weeks, with normalization of vitamin C level. The clinical features of scurvy can easily be confused with conditions such as vasculitis, deep venous thrombosis, and systemic bleeding disorders. Therefore, comprehensive workup up is required prior to the diagnosis. Although rare, being a reversible condition, early diagnosis and treatment of scurvy in high-risk populations cannot be stressed enough. Topics: Administration, Oral; Adult; Alcoholism; Anemia, Hemolytic; Ascorbic Acid; Ascorbic Acid Deficiency; Humans; Male | 2019 |
Telferia Occidentalis and Vitamin C Attenuate Phenylhydrazine-Induced Haemolytic Anaemia and Associated Cardio-renal Dysfunctions via Inhibition of Oxidative Stress and Proapoptotic -Protein (Bax) Expressions.
The study investigated the modulatory roles of the aqueous leaf extract of Telferia occidentalis, a traditional haematinic, and vitamin C on cardiovascular dysfunction associated with subchronic Phenylhydrazine exposure.. Fifty adult male rats were randomly selected and divided into one of five groups of ten animals each: Control; 40 mgkg. Oral exposure of rats to PHZ, without T. occidentalis or vitamin C treatment, resulted in a significant (p<0.05) decrease in the haematological parameters, but increased the blood pressure parameters of rats However, treatment with vitamin C and T. occidentalis leaf extract significantly (p<0.05) ameliorated the aforementioned PHZ-induced alterations of rats haemogram, and blood pressure. Biochemical analysis revealed significant (p<0.05) reduction in the activities of superoxide dismutase and catalase of untreated PHZ-exposed rats, but the levels of malondialdehyde, hydrogen peroxide and myeloperoxidase of the rats were significantly (p<0.05) increased compared with those of the extract treated rats. Immunohistochemical analysis revealed a greater expression of Bax-protein in the cardiac and renal tissues of the untreated PHZ exposed rats, compared with the extract and vitamin C treated groups.. The mitigation of oxidative stress and inhibition of Bax-protein expression are probable mechanisms of action of T. occidentalis in the amelioration of haemolytic anaemia, and its use as adjunct medication in the management of some diseases is justifiable. Topics: Anemia, Hemolytic; Animals; Ascorbic Acid; bcl-2-Associated X Protein; Catalase; Cucurbitaceae; Hemodynamics; Hydrogen Peroxide; Kidney; Male; Malondialdehyde; Myocardium; Oxidative Stress; Peroxidase; Phenylhydrazines; Phytotherapy; Plant Extracts; Plant Leaves; Rats; Superoxide Dismutase | 2018 |
Severe acute haemolytic anaemia associated with severe methaemoglobinaemia in a G6PD-deficient man.
Methaemoglobin is a form of haemoglobin in which the ferrous (Fe Topics: Acute Disease; Adult; Anemia, Hemolytic; Antioxidants; Ascorbic Acid; Blood Transfusion; Diagnosis, Differential; Glucosephosphate Dehydrogenase Deficiency; Humans; Male; Methemoglobinemia; Nepal; Severity of Illness Index | 2018 |
Modulatory effects of melatonin and vitamin C on oxidative stress-mediated haemolytic anaemia and associated cardiovascular dysfunctions in rats.
Background Phenylhydrazine (PHE) in experimental animal models has been widely reported to cause haemolytic anaemia, via the induction of oxidative stress and thus causing deleterious cardiovascular complications. Hence, this study was designed to evaluate the possible modulatory role of melatonin (MLT) or vitamin C when co-administered with PHE. Methods Anaemia was established with PHE administration. MLT or vitamin C was co-administered with PHE. Haematological parameters, markers of oxidative stress, enzymic and non-enzymic antioxidants, blood pressure and electrocardiograms were assessed. Results PHE administration led to a significant (p<0.05) increase in malondialdehyde (MDA), and hydrogen peroxide (H2O2) generated in cardiac, renal and red blood cell (RBC) lysates. PHE also significantly reduced the activity of glutathione peroxidase (GPx), superoxide dismutase (SOD) and reduced glutathione (GSH) contents, respectively. The RBC counts, haemoglobin (Hb) concentration and packed cell volume (PCV) were also significantly reduced following the administration of PHE. Furthermore, the systolic blood pressure (SBP), diastolic blood pressure (DBP) and mean arterial blood pressure (MABP) increased significantly in rats administered PHE alone. Similarly, PHE administration led to a significant drop in heart rate but prolonged QRS, QT and QTc interval. Pathology of the heart and kidney was also observed in PHE treated group. However, treatment with MLT and vitamin C improved enzymic and non-enzymic antioxidant system together with the restoration of SBP, DBP and MABP to near normal. The architectural anarchy observed in the heart and kidney of PHE administered rats was reversed to some extent. Conclusions Hence, MLT and vitamin C could be employed as therapeutic targets in various cardiovascular diseases and its complications. Topics: Anemia, Hemolytic; Animals; Antioxidants; Ascorbic Acid; Blood Pressure; Catalase; Erythrocytes; Glutathione; Glutathione Peroxidase; Heart; Hemoglobins; Hydrogen Peroxide; Hypertension; Kidney; Male; Malondialdehyde; Melatonin; Myocardium; Oxidative Stress; Phenylhydrazines; Rats, Wistar; Superoxide Dismutase; Vitamins | 2017 |
Iron-rich drinking water and ascorbic acid supplementation improved hemolytic anemia in experimental Wistar rats.
Anemia is a frequent problem in both the primary and secondary health care programs. In contrast, most areas of northeast India are vulnerable to iron toxicity. In the present study, we documented the effect of administration of iron rich water on hemolytic anemia in a Wistar rats' animal model. Hemolytic anemia was induced by phenyl hydrazine through intraperitoneal route and diagnosed by the lowering of blood hemoglobin. After inducing the hemolytic anemia, 24 Wistar rats (n = 6 in four groups) were randomly assigned to 1 mg/l, 5 mg/l, and 10 mg/l ferric oxide iron along with 1 mg/ml ascorbic acid administered through drinking water; a control group was treated with iron-free water. The hematological and biochemical parameters, iron levels in liver, spleen, and kidney were estimated after 30 d of treatment. In the group treated with 5 mg/l iron and ascorbic acid, a significant increase of serum iron and ferritin, and a decrease of TIBC (total iron binding capacity) were observed without changes in other biochemical parameters and histopathological findings. However, in the group treated with 10 mg/l iron and ascorbic acid, hematological changes with significantly higher values for white blood cell count, serum glutamic phospho transaminase, serum glutamic oxaloacetic transaminase, alkaline phosphatase, glucose, splenic, and liver iron content, indicate potential toxicity at this supplementation level. Data suggest that the optimum concentration of iron (5 mg/l) and ascorbic acid solution may improve anemic conditions and may be therapeutically beneficial in the treatment of iron deficiency anemia without any negative impact, while 10 mg/l in drinking water seems to be the threshold for the initiation of toxicity. Topics: Anemia, Hemolytic; Animals; Ascorbic Acid; Dietary Supplements; Drinking Water; Iron; Male; Phenylhydrazines; Rats; Rats, Wistar | 2014 |
Methemoglobinemia and hemolysis in a patient with G6PD deficiency treated with rasburicase.
Topics: Anemia, Hemolytic; Antioxidants; Ascorbic Acid; Cyclophosphamide; Glucosephosphate Dehydrogenase Deficiency; Hemolysis; Humans; Male; Methemoglobinemia; Middle Aged; Multiple Myeloma; Myeloablative Agonists; Treatment Outcome; Tumor Lysis Syndrome; Urate Oxidase | 2013 |
Severe haemolytic anaemia due to ingestion of naphthalene (mothball) containing coconut oil.
Naphthalene, a widely used industrial and household chemical, has rarely been an agent of poisoning worldwide. Severe haemolysis from naphthalene poisoning is rare and can be a challenge to clinicians. We report a 22-year-old female, who accidentally ingested naphthalene mixed coconut oil and got admitted with recurrent vomiting, headache and passage of dark urine. Severe intravascular haemolysis with hypotension and neutrophilic leukocytosis was detected. She was treated with red blood cell transfusions, intravenous saline infusion and ascorbic acid. Topics: Administration, Oral; Anemia, Hemolytic; Ascorbic Acid; Coconut Oil; Erythrocyte Transfusion; Female; Glucose; Hemoglobinuria; Hemolysis; Humans; Hypotension; Infusions, Intravenous; Methemoglobinemia; Naphthalenes; Plant Oils; Poisoning; Severity of Illness Index; Treatment Outcome; Young Adult | 2012 |
Acute naphthalene poisoning following the non-accidental ingestion of mothballs.
Ingestional naphthalene mothball poisoning leading to prolonged haemolysis and methaemoglobinaemia can present with diagnostic and therapeutic challenges. A 19-year-old woman ingested 12 mothballs, and presented two days later with haemolysis and methaemoglobinaemia. She was treated with red blood cell transfusions, intravenous methylene blue, N-acetylcysteine and ascorbic acid. Continuous venovenous haemofiltration was conducted for 45 hours. Haemolysis with anaemia and methaemoglobinaemia persisted even after five days post-ingestion. Clinical and biochemical parameters improved. We describe a case of ingestional naphthalene poisoning with a good outcome after treatment. Topics: Acetylcysteine; Adult; Anemia, Hemolytic; Ascorbic Acid; Erythrocyte Transfusion; Female; Hemolysis; Humans; Methemoglobinemia; Methylene Blue; Naphthalenes; Poisoning; Suicide, Attempted; Time Factors; Treatment Outcome | 2009 |
Antioxidant prevention of Heinz body formation and oxidative injury in cats.
To determine the effectiveness of 3 antioxidants in preventing Heinz body anemia in cats.. Prospective study.. 44 specific-pathogen-free healthy cats.. Cats were housed individually, divided randomly into 4 groups, and given the following orally every 12 hours: empty gelcaps (control cats), N-acetylcysteine (NAC, 100 mg/kg of body weight), vitamin E (d,l-alpha-tocopherol; 400 IU), or ascorbate (250 mg). After 2 weeks, Heinz bodies were induced by dietary onion powder (OP; 1% or 3% of dry matter) or propylene glycol (PG, 8% wt/vol in drinking water) for an additional 3 weeks. Intake of treated water or food was recorded daily. Body weight, PCV, Heinz body and reticulocyte percentages, reduced glutathione concentration, and total antioxidant status were measured twice weekly in all cats.. Heinz body percentage and degree of anemia did not differ significantly among cats receiving antioxidants and control cats except in cats that ingested water containing PG, in which antioxidant supplementation was associated with a decrease in water intake. Of cats that were fed a diet that contained OP, cats that received NAC had significantly higher reduced glutathione concentrations, compared with other cats in the experiment. Total antioxidant status did not consistently correlate with antioxidant supplementation or type of oxidant administered (ie, OP or PG).. Although the effect of antioxidant supplementation on Heinz body anemia in cats was minimal, antioxidants may have subclinical biochemical effects such as GSH sparing that may be important against milder forms of oxidative stress. Topics: Acetylcysteine; Anemia, Hemolytic; Animals; Antioxidants; Ascorbic Acid; Cat Diseases; Cats; Eating; Female; Free Radical Scavengers; Glutathione; Heinz Bodies; Hematocrit; Male; Propylene Glycol; Prospective Studies; Random Allocation; Specific Pathogen-Free Organisms; Vitamin E | 2001 |
Long-term clinical outcome in patients with glutathione synthetase deficiency.
The objective was to determine the long-term clinical outcome and the effects of treatment of patients with glutathione synthetase (GS) deficiency (n = 28).. The diagnosis was based on demonstration of a marked decrease in GS activity in erythrocytes or cultured fibroblasts in all patients and was supported by finding a decrease in erythrocyte or fibroblast glutathione, presence of 5-oxoprolinuria, or both. The treatment varied but usually included correction of acidosis and supplementation with vitamins C and/or E.. Sixteen patients were severely affected with neurologic symptoms such as seizures and psychomotor retardation; 7 had died at the time of the study. None of the severely affected patients had been treated with both vitamins C and E from the neonatal period. No significant difference was found in GS activity between patients with or without neurologic symptoms or in erythrocyte or fibroblast glutathione levels. Five patients had recurrent bacterial infections.. On the basis of clinical symptoms, patients with GS deficiency can be classified into 3 phenotypes: mild, moderate, and severe. Our results indicate that early supplementation with vitamins C and E may improve the long-term clinical outcome. Topics: Acidosis; Adult; Anemia, Hemolytic; Ascorbic Acid; Child; Child, Preschool; Erythrocytes; Female; Fibroblasts; Genes, Recessive; Glutathione Synthase; Humans; Infant; Infant, Newborn; Male; Mutation; Nervous System Diseases; Psychomotor Disorders; Time Factors; Vitamin E | 2001 |
Haemolysis induced by ascorbic acid in paroxysmal nocturnal haemoglobinuria.
Topics: Adult; Anemia, Hemolytic; Ascorbic Acid; Carbonated Beverages; Erythrocytes; Hemoglobinuria, Paroxysmal; Hemolysis; Humans; Male | 1994 |
Bioavailability and the mechanisms of intestinal absorption of iron from ferrous ascorbate and ferric polymaltose in experimental animals.
The comparative bioavailability from matching quantities of iron in the form of ferrous ascorbate or ferric polymaltose was defined in rats. Studies were carried out in the intact animals under basal conditions and also when requirements for this metal were either increased or decreased by manipulating stores or erythropoietic activity. No significant difference was found in the total quantity of iron absorbed from either salt or complex under any of these circumstances, suggesting that the mucosal mechanism regulating the overall process was common to both. However, the rate of transfer from the lumen into portal blood was distinctive, reaching a maximum with salt at 30 min compared to 24 h for the complex. To explore the possibility that iron from the two sources was initially handled by different subcellular pathways, the radiolabeled compounds were instilled into loops of bowel that had been isolated between ligatures in vivo. Enterocytes were harvested and fractionated, and incorporation into ferritin and transferrin was determined using RIA. From salt, iron appeared rapidly in duodenal but not ileal ferritin, whereas mucosal transferrin increased under conditions of stimulated absorption, suggesting that this protein may act as a shuttle for the metal. In contrast, iron from polymaltose showed a cumulative incorporation into duodenal ferritin over time that correlated with iron absorption, defined by the appearance of radiolabel in the serum and in the carcass; a similar pattern was demonstrable in ileal mucosal cells. Conversely, binding of iron to transferrin was minimal. No iron polymaltose was found within the mucosal cells. It is suggested that the low rate of iron transfer from this ferric complex may reflect its extracellular breakdown in the lumen of the gastrointestinal tract. Topics: Anemia, Hemolytic; Animals; Ascorbic Acid; Biological Availability; Blood Transfusion; Bloodletting; Cell Fractionation; Centrifugation, Density Gradient; Erythropoiesis; Ferric Compounds; Intestinal Absorption; Intestinal Mucosa; Iron; Iron Radioisotopes; Male; Rats; Transferrin | 1990 |
Vitamin C-induced erythrocyte damage in premature infants.
This study was undertaken after the observation in a premature infant of a hemolytic anemia with Heinz bodies that appeared to result from administration of a multivitamin preparation. In vitro incubation of erythrocytes of premature infants with sodium ascorbate (0.1 mg/ml) for 3 hours significantly raised the number of Heinz body-containing cells from 17.6 +/- 5.7% to 27.2 +/- 8.2% (mean +/- SE). Erythrocytes of term infants and those of adults developed Heinz bodies after exposure to higher sodium ascorbate concentrations (1.0 mg/ml). Erythrocytes of adult and newborn guinea pigs were similarly affected by sodium ascorbate. Daily intraperitoneal injections of 500 mg of sodium ascorbate, given for 7 days to four adult guinea pigs, caused significant Heinz body formation. These studies indicate that the erythrocytes of premature infants are uniquely sensitive to the development of Heinz bodies after exposure to sodium ascorbate. The levels required to produce Heinz bodies in vitro are in the range of those found in vivo after routine administration of vitamin C to premature infants. The significance of these observations in the development of hyperbilirubinemia in premature infants and in the safety of vitamin C remains to be determined. Topics: Adult; Anemia, Hemolytic; Animals; Ascorbic Acid; Erythrocytes; Erythrocytes, Abnormal; Female; Guinea Pigs; Heinz Bodies; Humans; Infant, Low Birth Weight; Infant, Newborn; Infant, Premature, Diseases | 1988 |
[Hemolytic anemia in chronically dialyzed patients induced by free chlorine in tap water (author's transl)].
Topics: Adult; Anemia, Hemolytic; Ascorbic Acid; Female; Hemolysis; Humans; Hypochlorous Acid; Japan; Kidney Failure, Chronic; Male; Renal Dialysis; Water Supply | 1979 |
Hemolysis in dialized patients caused by chloramines.
Topics: Anemia, Hemolytic; Ascorbic Acid; Cell Survival; Charcoal; Chloramines; Chromium Radioisotopes; Erythrocytes; Filtration; Hemolysis; Hexosephosphates; Humans; Methemoglobin; Osmosis; Renal Dialysis; Uremia; Water Pollution, Chemical; Water Supply; Water-Electrolyte Balance | 1974 |
Familial spinocerebellar degeneration, hemolytic anemia, and glutathione deficiency.
Topics: Adult; Amino Acids; Anemia, Hemolytic; Ascorbic Acid; Cerebellar Diseases; Cyanides; Electroencephalography; Electromyography; Erythrocytes; Female; Glutathione; Humans; Leukocytes; Male; Metabolism, Inborn Errors; Muscles; Neural Conduction; Peptide Synthases; Potassium; Renal Aminoacidurias; Spinal Cord Diseases; Syndrome | 1974 |
Hemolysis in dialyzed patients: tap water-induced red blood cell metabolic deficiency.
Topics: Anemia, Hemolytic; Ascorbic Acid; Carbon Radioisotopes; Cell Survival; Chromium Radioisotopes; Erythrocytes; Glucose; Glucosephosphate Dehydrogenase Deficiency; Heinz Bodies; Hemolysis; Hexosephosphates; Humans; Metabolism, Inborn Errors; Primaquine; Renal Dialysis; Sulfonamides; Uremia; Water | 1972 |
[Variation of blood catalase in different human pathological conditions].
Topics: Anemia, Hemolytic; Anemia, Hypochromic; Ascorbic Acid; Bilirubin; Blood Transfusion; Catalase; Chronic Disease; Glomerulonephritis; Gout; Hemoglobinometry; Humans; Iron; Kidney Diseases; Liver Diseases; Nephritis; Nitrogen; Rheumatic Fever; Surgical Procedures, Operative | 1972 |
Iron absorption and distribution in normal and scorbutic guinea pigs.
Topics: Anemia, Hemolytic; Animals; Ascorbic Acid; Guinea Pigs; Hemoglobinometry; Intestinal Absorption; Iron; Male; Scurvy; Spleen | 1972 |
Red cell hexosemonophosphate shunt deficiency in uremia.
Topics: Anemia, Hemolytic; Antimalarials; Ascorbic Acid; Carbon Isotopes; Cell Survival; Chromium Isotopes; Erythrocytes; Glucose; Heinz Bodies; Hexosephosphates; Humans; Renal Dialysis; Sulfhemoglobin; Sulfonamides; Uremia | 1972 |
Effects of dietary modifications on cholesterol-induced anemia in guinea pigs.
Topics: Adipose Tissue; Anemia, Hemolytic; Animals; Ascorbic Acid; Body Weight; Cholesterol; Choline; Cottonseed Oil; Creatine; Creatinine; Dietary Fats; Dietary Proteins; Erythrocytes; Fatty Acids; Guinea Pigs; Intestinal Absorption; Lipid Metabolism; Lipids; Liver; Male; Metabolism; Muscles; Phospholipids; Tartrates; Time Factors; Vitamin E; Vitamin E Deficiency | 1971 |
A case of hemolytic anemia and methemoglobinemia.
Topics: Adult; Anemia, Hemolytic; Ascorbic Acid; Female; Heinz Bodies; Humans; Methemoglobinemia | 1971 |
[Therapy of anemias].
Topics: Adrenal Cortex Hormones; Androstanes; Anemia, Aplastic; Anemia, Hemolytic; Anemia, Hypochromic; Anemia, Macrocytic; Anemia, Pernicious; Ascorbic Acid; Blood Transfusion; Humans; Iron; Iron-Dextran Complex; Ketones; Splenectomy; Vitamin B 12 | 1970 |
Hydrogen peroxide generation in the erythrocytes of newborn infants.
Topics: Anemia, Hemolytic; Ascorbic Acid; Azoles; Catalase; Culture Techniques; Erythrocytes; Humans; Hydrogen Peroxide; Infant, Newborn; Infant, Premature | 1970 |
OXIDATIVE HEMOLYSIS AND ERYTHROCYTE METABOLISM IN HEREDITARY ACATALASIA.
Topics: Acatalasia; Anemia; Anemia, Hemolytic; Ascorbic Acid; Azides; Catalase; Cyanides; Erythrocyte Aging; Erythrocytes; Ethylmaleimide; Genetics, Medical; Glucose; Glucosephosphate Dehydrogenase Deficiency; Glucosephosphates; Glutathione; Hemoglobins; Hemolysis; Hexosephosphates; Humans; Metabolism, Inborn Errors; Methemoglobin; Peroxides; Pharmacology; Phenylhydrazines; Primaquine; Sulfhemoglobin; Sulfhydryl Compounds | 1965 |
SULFONAMIDE METHEMOGLOBINEMIA AND HEMOLYTIC ANEMIA DURING RENAL FAILURE.
Topics: Adenosine Triphosphate; Anemia; Anemia, Hemolytic; Ascorbic Acid; Blood Chemical Analysis; Blood Glucose; Carbon Dioxide; Erythrocyte Count; Erythrocytes; Geriatrics; Glucosephosphate Dehydrogenase; Glutathione; Hemoglobinometry; Hemolysis; Kidney Diseases; Metabolism; Methemoglobinemia; Nucleosides; Pyelonephritis; Renal Insufficiency; Sulfamethizole; Sulfathiazoles; Sulfonamides; Toxicology; Urinary Catheterization | 1964 |
[LEDERER-BRILL SYNDROME AND ITS ETIOPATHOLOGY].
Topics: Aminosalicylic Acid; Aminosalicylic Acids; Anemia; Anemia, Hemolytic; Ascorbic Acid; Drug Therapy; Favism; Glucosephosphate Dehydrogenase Deficiency; Glucosephosphates; Metabolism; Pharmacology; Toxicology; Tuberculosis; Tuberculosis, Cutaneous | 1964 |
[Acute hemolytic anemia following ingestion of a PAS-ascorbate solution].
Topics: Aminosalicylic Acid; Anemia; Anemia, Hemolytic; Ascorbic Acid; Pharmaceutical Solutions | 1953 |