ascorbic-acid and Jaundice

Topics: Abdomen; Abdominal Muscles; Ascorbic Acid; Female; Hernia; Humans; Jaundice; Laparotomy; Male; Methods; Microscopy, Electron, Scanning; Middle Aged; Postoperative Complications; Pressure; Risk; Surgical Wound Dehiscence; Surgical Wound Infection; Suture Techniques; Sutures; Uremia; Wound Healing

Hemolysis induced by high dose ascorbic acid (AA) in patients with G6PD deficiency has been reported, but is rare. To our knowledge, this is the first reported case of a male with G6PD deficiency, coexpressed with cholecystolithiasis and cholecystitis, who developed extreme hemolysis and hyperbilirubinemia after receiving pharmacological doses ascorbic acid infusion.. A 27-year-old man history with glucose-6-phosphate dehydrogenase deficiency was admitted to our hospital because of cholecystolithiasis and cholecystitis. He appeared with scleral jaundice and very deep colored urine after receiving pharmacological doses ascorbic acid infusion.. Clinical findings when combined with his medical history and various laboratory results confirmed the diagnosis as hemolysis and hyperbilirubinemia induced by ascorbic acid.. The patient was treated with steroids, hepatoprotective drugs, and folic acid in addition avoidance of agents with known hemolysis risk (such as vitamin C).. As a result, the patient's symptoms from hemolytic jaundice improved, hemoglobin remained stable, and the patient was discharged 11 days later.. Clinicians should bear in mind the possibility that vitamin C exposure may result in hemolysis in patients with G6PD deficiency, especially in those with known severe disease.

Topics: Adult; Ascorbic Acid; Cholecystitis; Cholecystolithiasis; Glucosephosphate Dehydrogenase Deficiency; Humans; Hyperbilirubinemia; Jaundice; Male

Topics: Abdominal Pain; Anemia; Antioxidants; Ascorbic Acid; Child, Preschool; Cough; Cytochrome-B(5) Reductase; Diagnosis, Differential; Emergency Service, Hospital; Glucosephosphate Dehydrogenase Deficiency; Headache; Humans; Hypoxia; Intensive Care Units; Jaundice; Male; Methemoglobinemia; Methylene Blue; Morocco; Oxygen Inhalation Therapy; United States; Vicia faba

Topics: Aged; Aged, 80 and over; Aging; Antioxidants; Ascorbic Acid; beta Carotene; Humans; Jaundice; Lung Neoplasms; Macular Degeneration; Middle Aged; Randomized Controlled Trials as Topic; Smoke Inhalation Injury; Vitamin E; Zinc

The production of radicals was examined in vitro in liver supernatant prepared from LEC rats of different ages before and after the onset of jaundice. Each liver supernatant was subjected to heat-treatment at 90 degrees C for 10 min to remove heat-labile proteins, and then the production of radicals in the resultant supernatant in the presence of hydrogen peroxide and 5,5'-dimethyl-1-pyrroline oxide (DMPO) was studied by ESR. Two sharp ESR signals that completely decayed with time within 5 min after the addition of hydrogen peroxide were observed for the sample prepared from LEC rats before the onset of jaundice, followed by the appearance of four signals of a hydroxyl radical-DMPO adduct after 5 min. On the other hand, in the supernatant prepared from LEC rats after the onset of jaundice, the former two signals were not observed or observed only marginally, and the signals of the hydroxyl radical-DMPO adduct showed a different pattern of decay from that for the supernatant prepared from LEC rats before the onset of jaundice. With the addition of ascorbic acid to the liver supernatant prepared from LEC rats after the onset of jaundice, the former signals of the ascorbate and hydroxyl radicals reappeared. The present results suggest that ascorbate and hydroxyl radicals are produced in the liver of LEC rats with the onset of jaundice, depending on the relative ratio of ascorbic acid and cuprous ions.

Topics: Animals; Ascorbic Acid; Copper; Female; Free Radicals; Hydrogen Peroxide; Hydroxyl Radical; Jaundice; Liver; Rats; Zinc

It has been previously established that the attenuation of hepatic lipid peroxidation by a fat-free diet is accompanied by a marked rise in plasma bilirubin in Gunn rats. Present in vitro studies confirmed that microsomal lipid peroxidation caused the concurrent degradation of added bilirubin but failed to show that microsomal superoxide, hydroxyl radical or hydrogen peroxide would degrade bilirubin. Moreover, although injection of vitamin E completely inhibited microsomal lipid peroxidation and bilirubin degradation it had no effect on plasma bilirubin. No evidence has therefore been obtained that in Gunn rats, in the absence of bilirubin glucuronidation, that reactive oxygen species provide a significant physiological pathway of bilirubin disposal.

Topics: Animals; Ascorbic Acid; Bilirubin; Dietary Fats; Hydrogen Peroxide; Hydroxyl Radical; Jaundice; Lipid Peroxidation; Microsomes, Liver; Rats; Rats, Gunn; Reactive Oxygen Species; Vitamin E

The Long Evans Cinnamon (LEC) rat spontaneously develops fulminant hepatitis, which is usually lethal due to excess copper accumulation in the liver and is considered an animal model of Wilson's disease. LEC rats show a strong appetite for proline solution. Daily oral (p.o.) administration of proline resulted in significant delay of mortality. Feeding a copper-deficient diet greatly delayed the onset of jaundice and mortality and voluntary consumption or p.o. administration of proline further delayed jaundice and prevented mortality. LEC rats also consume ascorbic acid solutions, and p.o. administration of ascorbate also results in a significant delay in the appearance of jaundice and mortality. Combined treatment with ascorbic acid and proline is additive to delay further jaundice and mortality. An endogenous antioxidant protein, thioredoxin, when infused by minipump IP, could also inhibit the incidence of jaundice. These results indicate that antioxidant treatment combined with proline may be of benefit in Wilson's disease and possibly other forms of hepatic dysfunction.

Topics: Aging; Animals; Antioxidants; Ascorbic Acid; Copper; Diet; Infusion Pumps, Implantable; Jaundice; Male; Proline; Rats; Rats, Inbred Strains; Thioredoxins

A new colorimetric method for the assay of biliverdin in biological fluids is described. The method, based upon the reaction of biliverdin with barbituric acid, offers improved sensitivity and selectivity when compared to direct spectrophotometric measurements. Using this method biliverdinaemia was observed in two patients with obstructive jaundice of malignant origin.

Topics: Ascorbic Acid; Barbiturates; Bilirubin; Biliverdine; Colorimetry; Edetic Acid; Humans; Jaundice; Methods; Time Factors

Topics: Alkaptonuria; Ascorbic Acid; Bilirubin; Biphenyl Compounds; Clinical Laboratory Techniques; Cyanates; Enzymes; Epinephrine; Fructose; Glucose Oxidase; Glucose Tolerance Test; Glycosuria; Humans; Hydrazones; Hydroquinones; Indicators and Reagents; Iron; Jaundice; Melanins; Metabolic Diseases; Peroxidases; Phenylacetates; Silver Nitrate

Topics: Ascorbic Acid; Child, Preschool; Hepatitis; Humans; Hyperbilirubinemia; In Vitro Techniques; Indicators and Reagents; Infant; Infant, Newborn; Jaundice; Spectrophotometry; Urine

Topics: Ascorbic Acid; Blood Chemical Analysis; Child; Gastroenteritis; Jaundice; Liver Diseases; Liver Function Tests; Nutrition Disorders; Respiratory Tract Diseases; Rickets

Topics: Ascorbic Acid; Erythroblastosis, Fetal; Flavonoids; gamma-Globulins; Humans; Infant; Infant, Newborn; Jaundice; Jaundice, Neonatal; Pathology; Rh-Hr Blood-Group System; Rutin

Topics: Ascorbic Acid; Child; Female; Humans; Infant; Infant, Newborn; Jaundice; Pregnancy; Vitamins

Topics: Adrenal Cortex; Adrenal Cortex Hormones; Anemia, Hemolytic, Congenital; Ascorbic Acid; Bilirubin; Capillary Permeability; Capillary Resistance; Folic Acid; Humans; Infant, Newborn; Jaundice; Jaundice, Neonatal; Vitamin B Complex