vitamin-k-semiquinone-radical and Anemia--Hemolytic

Topics: Anemia, Hemolytic; Aniline Compounds; Animals; Antimalarials; Catalase; Dihydroxyphenylalanine; Erythrocytes; Female; Genes; Glucosephosphate Dehydrogenase Deficiency; Glutathione; Heterozygote; Humans; Hydrogen Peroxide; Mice; Peroxidases; Phenylhydrazines; Primaquine; Quinolines; Radiation Effects; Sex Chromosomes; Triazoles; Ultraviolet Rays; Vitamin K

The clinical presentation of acute hepatitis B virus (HBV) infection is usually related to the onset of liver failure and damage. Anaemia may occur, but it is only rarely attributed to haemolysis. The authors report about the case of a 41-year-old woman with the diagnosis of acute HBV infection and coagulopathy (without encephalopathy) who developed non-immune haemolytic anaemia. Total recovery of the analytical liver profile, coagulopathy and anaemia was achieved through treatment targeting HBV.This case shows that, although rare, non-immune haemolytic anaemia may occur in association with acute HBV infection and that HBV suppression seems to lead to progressive anaemia resolution.

Topics: Acetylcysteine; Acute Disease; Adult; Anemia, Hemolytic; Antiviral Agents; Female; Folic Acid; Guanine; Hepatitis B; Humans; Treatment Outcome; Vitamin B Complex; Vitamin K; Vitamins

A Somali cat was presented with recurrent anorexia, lethargy, vomiting and icterus. A macrocytic-hypochromic, regenerative haemolytic anaemia was identified and hereditary pyruvate kinase deficiency was confirmed by means of breed-specific DNA mutation analysis. The case was complicated by the presence of markedly elevated serum liver enzyme activities, hyperbilirubinaemia, coagulopathy and ultrasonographic evidence of gall bladder choleliths and extrahepatic bile duct obstruction. The choleliths consisted of 100 per cent bilirubin, likely because of chronic haemolysis and haeme degradation. In conclusion, haemosiderosis and bilirubin cholelithiasis can be a consequence of chronic haemolysis in pyruvate kinase-deficient cats, as seen in human beings with a variety of chronic haemolytic disorders.

Topics: Anemia, Hemolytic; Animals; Belgium; Bilirubin; Cat Diseases; Cats; Cholelithiasis; Euthanasia, Animal; Female; Hemosiderosis; Pyruvate Kinase; Radiography; Splenomegaly; Vitamin K

The enzyme DT-diaphorase catalyses the 2-electron reduction of quinones. This reaction may facilitate the detoxification of such compounds, since the hydroquinone so formed can be converted into non-toxic conjugates. There is evidence for the involvement of DT-diaphorase in the detoxification of menadione (2-methyl-1,4-naphthoquinone) in a wide range of cells and tissues in vitro, but no information is available on the possible influence of this enzyme on the harmful effects of menadione in vivo. In animals, menadione is selectively toxic to erythrocytes, causing haemolytic anaemia. In the present study, rats were treated with dicoumarol, an inhibitor of DT-diaphorase, or butylated hydroxyanisole (BHA), a substance that increases the activity of this enzyme in vivo. They were then challenged with a toxic dose of menadione. Dicoumarol increased the severity of menadione-induced haemolytic anaemia while BHA decreased it, consistent with a role for DT-diaphorase in the detoxification of menadione in vivo, as previously described in vitro.

Topics: Anemia, Hemolytic; Animals; Antioxidants; Butylated Hydroxyanisole; Dicumarol; Dihydrolipoamide Dehydrogenase; Enzyme Inhibitors; Erythrocytes; Female; Heinz Bodies; Hemolysis; Hemostatics; Liver; NAD(P)H Dehydrogenase (Quinone); Organ Size; Rats; Rats, Sprague-Dawley; Spleen; Vitamin K

The present study describes the effect of high doses of vitamin K3 (8-30 mg/kg) administered daily by intramuscular injection during seven days; on blood smear, red blood cells (RBC) and concentration of hemoglobin (Hb) counts, value of hematocrit (Ht), mean corpuscular hemoglobin concentration (MCHC), reticulocyte and erythroblast counts, total and differential counting of leukocytes (WBC) and total and fractionated serum bilirubin concentration of albino male rats. Results were then compared with findings in normal rats treated with the same doses of sodium bisulfite. In animals treated with vitamin K3 a statistically significant decrease in the number of erythrocytes and in the concentration of Hb, Ht and MCHC was found together with a concomitant increase of erythroblast and reticulocyte counting. In regard to the blood smear, it was observed that erythrocytes vary in their hemoglobin content, size, shape and in their staining properties (polychromatophilia) where as the leukocytes were found to be morphologically normal, but in an increased number. Lymphocytes occasionally showed azurophil granules. Platelets assumed irregular shape and in normal amounts. The leukocytes count showed leukocytosis with marked neutrophilia, eosinophilia, lymphocytosis and monocytosis. Also, the presence of clinical jaundice with an increase of the serum "indirectly-reacting" bilirubin was also observed. These findings indicate that hypervitaminosis K3 induces a marked hemolytic microcytic hypochromic anemia and changes in the white blood cells count. Further studies will be pursued in order to obtain a better understanding of the causes and/or the mechanisms that induce these alterations in the blood cells.

Topics: Analysis of Variance; Anemia, Hemolytic; Animals; Bilirubin; Body Weight; Epidemiologic Methods; Erythrocyte Indices; Hematocrit; Hemoglobins; Injections, Intramuscular; Leukocyte Count; Male; Rats; Rats, Inbred Strains; Venezuela; Vitamin K

Human erythrocytes were treated with menadione to oxidatively denature hemoglobin and release ferriprotoporphyrin IX (ferriheme, FP) intracellularly. The high affinity of FP for chloroquine was used to detect its release. After incubation for 1 hr at 37 degrees C and pH 7.4 with 0.5 mM menadione, erythrocytes bound 14C-chloroquine with an apparent dissociation constant of 10(-6)M. Untreated erythrocytes did not bind chloroquine with high affinity. At a chloroquine concentration in the medium of 2 microM, for example, menadione-treated erythrocytes bound 70 mumole chloroquine/kg and untreated erythrocytes bound 13.4 mumole/kg. The intracellular location of FP released by menadione was verified by finding that Tween 80 did not prevent chloroquine binding. By contrast, Tween 80 inhibited the binding of chloroquine to erythrocytes treated with extracellular FP. The hemolytic response to menadione was characteristic of the hemolytic response to FP. Thus, 5 microM chloroquine caused hemolysis to increase to 60% from baseline values of 5% in experiments using erythrocytes treated either with 0.5 mM menadione or with 5 microM FP; and, in both cases, the potentiating effect of chloroquine was inhibited by 1 microM mefloquine or 10 microM quinine. Higher concentrations of menadione caused hemolysis in the absence of chloroquine. We conclude that FP released by menadione exists intracellularly in a form that is accessible to bind chloroquine and to express its lytic activity.

Topics: Anemia, Hemolytic; Animals; Erythrocytes; Female; Heme; Hemin; Hemolysis; Humans; Kinetics; Male; Mice; Rats; Receptors, Drug; Vitamin K

Topics: Anemia, Hemolytic; Animals; Blood Transfusion; Erythrocytes; Heinz Bodies; Humans; Infant, Newborn; Infant, Premature, Diseases; Rabbits; Spleen; Vitamin K

Topics: Anemia, Hemolytic; Cytoplasm; Erythrocytes; Heinz Bodies; Humans; In Vitro Techniques; Infant, Newborn; Infant, Newborn, Diseases; Vitamin K

Topics: Anemia; Anemia, Hemolytic; Erythrocytes; Glucosephosphate Dehydrogenase Deficiency; Glucosephosphates; Humans; Infant; Infant, Newborn; Infant, Newborn, Diseases; Naphthalenes; Poisoning; Toxicology; Vitamin K

Topics: Analgesics; Analgesics, Non-Narcotic; Anemia; Anemia, Hemolytic; Antimalarials; Antipyretics; Erythroblastosis, Fetal; Female; Fetal Diseases; Glucosephosphate Dehydrogenase Deficiency; Glucosephosphates; Humans; Hyperbilirubinemia; Infant; Infant, Newborn; Infant, Newborn, Diseases; Jaundice; Jaundice, Neonatal; Maternal-Fetal Exchange; North Carolina; Novobiocin; Pregnancy; Salicylates; Sulfisoxazole; Toxicology; Vitamin K

Topics: Anemia; Anemia, Hemolytic; Blood Chemical Analysis; Drug Therapy; Exchange Transfusion, Whole Blood; Genetics, Medical; Glucose; Glucosephosphate Dehydrogenase Deficiency; Glucosephosphates; Hemoglobinometry; Humans; Infant Mortality; Infant, Newborn; Jaundice; Jaundice, Neonatal; Kernicterus; Naphthalenes; Oxidoreductases; Phosphates; Toxicology; Vitamin K

Topics: Anemia, Hemolytic; Antimalarials; Brain Diseases; Cerebral Palsy; Chloramphenicol; Genetics, Medical; Glucosephosphate Dehydrogenase; Glucosephosphate Dehydrogenase Deficiency; Glucosephosphates; Humans; Hyperbilirubinemia; Infant; Infant, Newborn; Jaundice; Jaundice, Neonatal; Naphthalenes; Nitrofurantoin; Phenylhydrazines; Pregnancy; Quinidine; Sulfonamides; Thailand; Toxicology; Vitamin K

Topics: Anemia; Anemia, Hemolytic; Anemia, Neonatal; Child; Humans; Infant; Infant, Newborn; Infant, Newborn, Diseases; Kernicterus; North Carolina; Vitamin K; Vitamins

Topics: Anemia; Anemia, Hemolytic; Child; Diagnosis, Differential; Erythroblastosis, Fetal; Hematologic Diseases; Infant; Virus Diseases; Vitamin K

Topics: Anemia; Anemia, Hemolytic; Child; Humans; Infant; Infant, Newborn; Infant, Newborn, Diseases; Jaundice; Vitamin K

Topics: Anemia; Anemia, Hemolytic; Child; Humans; Infant; Infant, Newborn; Infant, Premature; Infant, Premature, Diseases; Vitamin K

Topics: Anemia; Anemia, Hemolytic; Child; Humans; Inclusion Bodies; Infant; Infant, Newborn; Infant, Premature; Infant, Premature, Diseases; Vitamin K; Vitamins

Topics: Anemia; Anemia, Hemolytic; Child; Humans; Infant; Infant, Premature, Diseases; Vitamin K