allopurinol and Anemia

Topics: Acute Disease; Adrenal Cortex Hormones; Allopurinol; Anemia; Autoimmune Diseases; Blood Coagulation Disorders; Blood Platelets; Blood Transfusion; Chronic Disease; Granulocytes; Humans; Infection Control; Leukemia; Uric Acid

Topics: Allopurinol; Aluminum; Anemia; Antihypertensive Agents; Blood Transfusion; Bone Diseases; Diet Therapy; Diet, Sodium-Restricted; Diuretics; Humans; Hydroxides; Hypertension; Kidney Failure, Chronic; Palliative Care; Parathyroid Glands; Uric Acid; Vitamin D

The emergence of chloroquine resistance, and a world-wide scarcity of quinine, have resulted in a search for newer antimalarial drugs directed against falciparum malaria. Allopurinol causes virtually complete inhibition of purine biosynthesis of malaria parasites, which may prove lethal to the parasites. This study was designed to examine if allopurinol is additive to quinine in the treatment of acute falciparum malaria. Forty-seven Asian-Indian adults with acute complicated falciparum malaria were assigned to a treatment period of five days. They were randomly assigned to receive either oral allopurinol (12 mg/kg in three divided doses for five days) plus quinine (600 mg intravenously every 8 hr for two days, followed by 600 mg orally every 8 hr for three days ) (n = 24), or quinine alone (600 mg intravenously every 8 hr for two days, followed by 600 mg orally every 8 hr for three days) (n = 23). The responses were assessed by parasite clearance time, defervescence time, splenomegaly disappearance time, and cure rate. In the allopurinol-quinine (ALLQUIN)-treated group, all the durations were significantly shorter than those in the quinine alone (QUIN)-treated group. They were ALLQUIN versus QUIN (mean +/- SD = 65.33 +/- 11.47 hr versus 76.78 +/- 18.20 hr; P = 0.0214; 57.66 +/- 13.01 hr versus 82.52 +/- 23.55 hr, P = 0.0002; 10 +/- 1.64 days versus 14.65 +/- 2.4 days; P = 0.0002), respectively. The cure rate was higher in the ALLQUIN group (91.7%) than in the QUIN group (87%). However, this difference was not statistically significant. Therefore, this study indicates that allopurinol can be an additive to quinine to bring about both faster eradication of Plasmodium falciparum and clinical remission than with quinine alone.

Topics: Acute Disease; Acute Kidney Injury; Adolescent; Adult; Aged; Allopurinol; Anemia; Antimalarials; Antimetabolites; Drug Therapy, Combination; Female; Follow-Up Studies; Humans; Malaria, Cerebral; Malaria, Falciparum; Male; Middle Aged; Parasitemia; Quinine; Splenomegaly

Severe anemia is an important contributor to mortality in children with severe malaria. Anemia in malaria is a multi-factorial complication, since dyserythropoiesis, hemolysis and phagocytic clearance of uninfected red blood cells (RBCs) can contribute to this syndrome. High levels of oxidative stress and immune dysregulation have been proposed to contribute to severe malarial anemia, facilitating the clearance of uninfected RBCs. In a cohort of 552 Ugandan children with severe malaria, we measured the levels of xanthine oxidase (XO), an oxidative enzyme that is elevated in the plasma of malaria patients. The levels of XO in children with severe anemia were significantly higher compared to children with severe malaria not suffering from severe anemia. Levels of XO were inversely associated with RBC hemoglobin (ρ =  - 0.25, p < 0.0001), indicating a relation between this enzyme and severe anemia. When compared with the levels of immune complexes and of autoimmune antibodies to phosphatidylserine, factors previously associated with severe anemia in malaria patients, we observed that XO is not associated with them, suggesting that XO is associated with severe anemia through an independent mechanism. XO was associated with prostration, acidosis, jaundice, respiratory distress, and kidney injury, which may reflect a broader relation of this enzyme with severe malaria pathology. Since inhibitors of XO are inexpensive and well-tolerated drugs already approved for use in humans, the validation of XO as a contributor to severe malarial anemia and other malaria complications may open new possibilities for much needed adjunctive therapy in malaria.

Topics: Anemia; Antigen-Antibody Complex; Child; Erythrocytes; Humans; Malaria, Falciparum; Xanthine Oxidase

The prevalence of chronic kidney disease (CKD) is increasing worldwide; black patients have an increased risk of developing CKD and end stage kidney disease (ESKD) at significantly higher rates than other races.. A cross sectional study was carried out on black patients with CKD attending the kidney outpatient clinic at Charlotte Maxeke Johannesburg Academic Hospital (CMJAH) in South Africa, between September 2019 to March 2020. Demographic and clinical data were extracted from the ongoing kidney outpatient clinic records and interviews, and were filled in a questionnaire. Patients provided blood and urine for laboratory investigations as standard of care, and data were descriptively and inferentially entered into REDcap and analysed using STATA version 17. Multivariable logistic regression analysis was used to identify demographic and clinical variables associated with advanced CKD.. A total of 312 black patients with CKD were enrolled in the study with a median age of 58 (IQR 46-67) years; 58% patients had advanced CKD, 31.5% of whom had grossly increased proteinuria, 96.7% had hypertension, 38.7% had diabetes mellitus and 38.1% had both hypertension and diabetes mellitus. In patients with advanced CKD, the median age was 61 (IQR 51-69) years, eGFR 33 (30-39) mL/min/1.73 m2, serum bicarbonate 22 (IQR 20-24), haemoglobin 12.9 (IQR 11.5-14.0) g/dl and serum uric acid 0.43 (IQR 0.37-0.53). The prevalence of metabolic acidosis was 62.4%, anemia 46.4% and gout 30.9% among those with advanced CKD, while the prevalence of metabolic acidosis and anaemia was 46.6% and 25.9% respectively in those with early CKD. Variables with higher odds for advanced CKD after multivariable logistic regression analysis were hypertension (OR 3.3, 95% CI 1.2-9.2, P = 0.020), diabetes mellitus (OR 1.8, 95% CI 1.1-3.3, P = 0.024), severe proteinuria (OR 3.5, 95% CI 1.9-6.5, P = 0.001), angina (OR 2.5, 95% CI 1.2-5.1, P = 0.008), anaemia (OR 2.9, 95% CI 1.7-4.9, P = 0.001), hyperuricemia (OR 2.4, 95% CI 1.4-4.1, P = 0.001), and metabolic acidosis (OR 2.0, 95% CI 1.2-3.1, P = 0.005). Other associations with advanced CKD were loss of spouse (widow/widower) (OR 3.2, 95% CI 1.4-7.4, P = 0.006), low transferrin (OR 2.4, 95% CI 1.1-5.1, P = 0.028), hyperkalemia (OR 5.4, 95% CI 1.2-24.1, P = 0.029), use of allopurinol (OR 2.4, 95% CI 1.4-4.3, P = 0.005) and doxazosin (OR 1.9, 95% CI 1.2-3.1, P = 0.006).. Hypertension and diabetes mellitus were strongly associated with advanced CKD, suggesting a need for primary and secondary population-based prevention measures. Metabolic acidosis, anemia with low transferrin levels, hyperuricemia and hyperkalemia were highly prevalent in our patients, including those with early CKD, and they were strongly associated with advanced CKD, requiring clinicians and dietitians to be proactive in supporting the needs of CKD patients in meeting their daily dietary requirements towards preventing and slowing the progression of CKD.

Topics: Acidosis; Aged; Allopurinol; Anemia; Bicarbonates; Cross-Sectional Studies; Diabetes Mellitus; Doxazosin; Hemoglobins; Humans; Hyperkalemia; Hypertension; Hyperuricemia; Middle Aged; Prevalence; Proteinuria; Renal Insufficiency, Chronic; South Africa; Tertiary Care Centers; Transferrins; Uric Acid

Reactive oxygen species (ROS) metabolism is regulated by the oxygen-mediated enzyme reaction and antioxidant mechanism within cells under physiological conditions. Xanthine oxidoreductase (XOR) exhibits two inter-convertible forms (xanthine oxidase (XO) and xanthine dehydrogenase (XDH)), depending on the substrates. XO uses oxygen as a substrate and generates superoxide (O

Topics: Acetophenones; Aging; Allopurinol; Anemia; Animals; Fatty Liver; Mice, Mutant Strains; Muscular Atrophy; NADPH Oxidases; Superoxide Dismutase-1; Superoxides; Xanthine Dehydrogenase

Acquired ichthyosis is a rare condition that can reveal an unsuspected haematological malignancy, thus allowing early diagnosis and management. If ichthyosis regresses under treatment for the haematological disorder, its recurrence reflects a turning point in the course of the disease and implies worsening of the prognosis.. The patients were examined at a joint dermatology/haematology consultation. The diagnosis of ichthyosis was based on clinical examination alone with no patients undergoing skin biopsy.. Our series included three men and two women aged 38 to 65 years consulting for a variety of reasons including asthenia, anaemia and adenopathy. Ichthyosis occurred 2 to 9 months after the initial symptoms of the blood disease. Lesions consisted of diffuse brown scales. The disease was associated with lymphadenopathy and biological inflammatory syndrome. Two patients were presenting non-Hodgkin lymphoma, one had Hodgkin's disease, one had chronic myeloid leukaemia in progression and one had an undifferentiated lymphomatous process. Treatment was based on chemotherapy and emollients. The ichthyosis progressed in step with the underlying malignancy in all cases, with regression being complete in three cases, partial in one case and absent in one case.. In rare cases, acquired ichthyosis reveals systemic disease, and may be of infectious, endocrine or drug origin; it may also be idiopathic. However, it is most often a paraneoplastic syndrome with cutaneous expression encountered during haematological malignancies. Because of the variety of causative blood dyscrasias, ichthyosis cannot be used to guide their diagnosis, although it remains a reliable monitoring tool.. Acquired ichthyosis should prompt the clinician to search for a neoplastic condition, primarily a haematological disorder, guided by other associated signs, given that in our study, skin lesions generally appear to precede signs of the blood disease.

Topics: Adult; Aged; Allopurinol; Anemia; Antibodies, Monoclonal, Murine-Derived; Antineoplastic Agents; Antineoplastic Combined Chemotherapy Protocols; Benzamides; Bleomycin; Cyclophosphamide; Doxorubicin; Etoposide; Female; Hematologic Neoplasms; Hodgkin Disease; Humans; Ichthyosis; Imatinib Mesylate; Leukemia, Myeloid, Accelerated Phase; Lung Neoplasms; Lymphoma, B-Cell; Male; Middle Aged; Paraneoplastic Syndromes; Parotid Neoplasms; Piperazines; Platelet Aggregation Inhibitors; Prednisone; Procarbazine; Pyrimidines; Retrospective Studies; Rituximab; Schizophrenia; Stomach Neoplasms; Vincristine

Mutations in the UMOD gene encoding uromodulin (Tamm-Horsfall glycoprotein) result in the autosomal dominant transmission of progressive renal insufficiency and hypo-uricosuric hyperuricemia leading to gout at an early age. The clinical appearance is characterized by renal insufficiency and gout occurring in the late teenage years, with end-stage kidney disease characteristically developing between 40 and 70 years of age. This report provides a long-term characterization of renal functional decline in three children from one family with a novel UMOD mutation (c.891T>G, p.C297W) who received allopurinol and a low protein diet. While renal functional decline is slow in individuals with UMOD mutations, it may appear early in life and be associated with marked hyperuricemia. Anemia was also noted in this family.

Topics: Adult; Allopurinol; Anemia; Antimetabolites; Child; Child, Preschool; Combined Modality Therapy; Diet, Protein-Restricted; Family Health; Female; Genetic Predisposition to Disease; Glomerular Filtration Rate; Humans; Hyperuricemia; Infant; Kidney Failure, Chronic; Kidney Function Tests; Male; Mucoproteins; Mutation; Uromodulin

Topics: alpha-Amino-3-hydroxy-5-methyl-4-isoxazolepropionic Acid; Analgesics; Anemia; Animals; Antipsychotic Agents; Bone Marrow Cells; Drug Evaluation, Preclinical; Humans; Pharmaceutical Preparations; Receptors, Epoprostenol; Xanthine Oxidase

Topics: Aged; Allopurinol; Anemia; Captopril; Drug Interactions; Drug Resistance; Erythropoietin; Female; Humans; Kidney Failure, Chronic; Male; Middle Aged; Piperidines; Recombinant Proteins

Hyperuricemia is present in 20-40% of pediatric and adult patients with essential hypertension. This metabolic abnormality may represent an additional risk factor for the development of cardiovascular disease. Therefore, we performed the following studies to determine 1) whether hyperuricemia is more prevalent in the spontaneously hypertensive rat (SHR) and 2) whether allopurinol treatment has a beneficial effect on the development of hypertension in this strain, based on its capacity to lower the serum uric acid concentration and to act as an antioxidant agent. SHR and control Wistar-Kyoto (WKY) rats were assigned to two groups, one given tap water to drink and the other provided water containing allopurinol (400 mg/l) to furnish an approximate daily dose equal to 100 mg/kg body wt. This treatment was maintained for 15 weeks. The serum uric acid levels were similar in untreated SHR and WKY rats (1.85 +/- 0.10 versus 1.66 +/- 0.14 mg/dl; p = 0.28). In the control WKY rat strain, allopurinol therapy did not adversely affect weight gain or hematocrit and did not cause an increase in mortality. It resulted in a moderate decrement in kidney function (creatinine clearance: allopurinol-treated group 0.32 +/- 0.09 versus control group 0.46 +/- 0.04 ml/min/100 g body wt, in conjunction with mild-to-moderate tubulointerstitial inflammation (allopurinol-treated group 0.9 +/- 0.4 versus control group 0).(ABSTRACT TRUNCATED AT 250 WORDS)

Topics: Allopurinol; Anemia; Animals; Drinking; Hypertension; Kidney; Male; Osmolar Concentration; Rats; Rats, Inbred SHR; Rats, Inbred WKY; Uric Acid

The effect of dietary iron on the development of copper-deficiency anemia in the growing rat was investigated. For up to 80 d, female rats (75 g) were fed purified diets containing adequate, marginal or low levels of iron, and either 0.7 or 10 ppm copper. Hemoglobin levels and factors postulated to affect liver iron mobilization, including ferroxidase (Fox) I and II, ascorbate and liver xanthine dehydrogenase (XDH) were assayed. By d 7, Fox I activity in the copper-deficient groups was 10% that of the copper-sufficient groups; thereafter, Fox I activity remained low, and was not affected by dietary iron. Fox II activity in the copper-deficient groups after d 28 was 50-75% of values from rats adequate in copper. On d 49, hemoglobin levels in the copper-deficient groups were lower than in the copper-sufficient groups fed low and marginal levels of iron, but were similar to those fed adequate iron. Liver iron was similar in both groups fed adequate iron, but was higher in the copper-deficient than in the copper-sufficient rats fed low or marginal levels of iron. Copper deficiency tended to result in slightly lower ascorbate levels on d 80 at all levels of iron. Liver XDH activity tended to be lower in the copper-deficient groups than in the copper-sufficient groups on d 28 and 49. These results show that copper deficiency may impair liver iron mobilization in the growing rat if dietary iron is low. Possible mechanisms include decreased Fox activity and/or decreased iron reduction by ascorbate or XDH.

Topics: Anemia; Animal Nutritional Physiological Phenomena; Animals; Ascorbic Acid; Body Weight; Ceruloplasmin; Copper; Diet; Drug Interactions; Female; Hematocrit; Hemoglobins; Iron; Kidney; Liver; Myocardium; Organ Size; Oxidoreductases; Rats; Rats, Inbred Strains; Spleen; Xanthine Dehydrogenase; Xanthine Oxidase; Zinc

Purine nucleotide degradation refers to a regulated series of reactions by which human purine ribonucleotides and deoxyribonucleotides are degraded to uric acid in humans. Two major types of disorders occur in this pathway. A block of degradation occurs with syndromes involving immune deficiency, myopathy or renal calculi. Increased degradation of nucleotides occurs with syndromes characterized by hyperuricemia and gout, renal calculi, anemia or acute hypoxia. Management of disorders of purine nucleotide degradation is dependent upon modifying the specific molecular pathology underlying each disease state.

Topics: Adenosine Deaminase; Adenosine Monophosphate; Adenosine Triphosphate; AMP Deaminase; Anemia; Animals; Deoxyribonucleotides; Female; Gout; Humans; Hypoxia; Male; Nucleotidases; Phosphorylation; Purine Nucleotides; Purine-Nucleoside Phosphorylase; Purine-Pyrimidine Metabolism, Inborn Errors; Purines; Ribonucleotides; Uric Acid; Urinary Calculi; Xanthine Oxidase

Topics: Allopurinol; Anaphylaxis; Anemia; Antibiotics, Antineoplastic; Bicarbonates; Blood Transfusion; Child; Child, Preschool; Cystitis; Disseminated Intravascular Coagulation; Erythrocytes; Female; Furosemide; Heart Arrest; Heparin; Humans; Hydrogen-Ion Concentration; Kidney; Leukemia; Lung Diseases; Male; Mercaptopurine; Mutation; Neoplasms; Phospholipids; Renal Dialysis; Thrombocytopenia; Uric Acid

Immunoblastic lymphadenopathy is a recently described lymphoproliferative disorder, presumably of B-cell origin. It is characterized by regional or generalized lymphadenopathy, usually associated with hypergammaglobulinemia or dysproteinemia. Other findings may be hepatosplenomegaly, dermatitis, fever, malaise, weight loss, and various altered immunologic reactions. Histologically, the involved lymph nodes show immunoblast, plasmacytoid, and plasma cell proliferation. This may be extranodal as well. The case reported here is one of the few followed up prospectively. The patient's purpuric eruption was an apparent manifestation of a type II mixed cryoglobulinemia. Differing from what has usually been reported, we noted hypogammaglobulinemia and findings in part of altered cell-mediated immunity. Despite leukopenia and anemia there were no infectious episodes. Although a satisfactory treatment regimen has not been established, there was beneficial response to prednisone and short courses of melphalan.

Topics: Allopurinol; Anemia; B-Lymphocytes; Cryoglobulins; Female; Humans; Leukopenia; Lymphatic Diseases; Melphalan; Middle Aged; Paraproteinemias; Prednisone; Purpura, Hyperglobulinemic

Topics: Adult; Allopurinol; Anemia; Arthritis; Benzofurans; Gout; Humans; Hyperlipidemias; Hypothyroidism; Hypoxanthines; Kidney Calculi; Male; Metabolism, Inborn Errors; Pedigree; Pentosyltransferases; Uric Acid; Uricosuric Agents

Topics: Anemia; Animals; Chickens; Liver; Liver Neoplasms; Lymphoma; Neoplasm Transplantation; Poultry Diseases; Transplantation, Homologous; Uric Acid; Xanthine Oxidase

Topics: Allopurinol; Anemia; Anti-Bacterial Agents; Humans; Infant; Intellectual Disability; Lesch-Nyhan Syndrome; Neurologic Manifestations; Uric Acid; Urinary Calculi; Urinary Tract Infections

Topics: Aged; Allopurinol; Ampicillin; Anemia; Bone Marrow Cells; Bone Marrow Diseases; Bone Marrow Examination; Drug Hypersensitivity; Eosinophils; Female; Fibroblasts; Histiocytes; Humans; Lymphoid Tissue; Male; Mast Cells; Middle Aged; Plasma Cells; Procainamide

Topics: Anemia; Animals; Buffers; Chromatography, Gel; Cold Temperature; Drug Stability; Liver; Male; Methylene Blue; NAD; Rabbits; Time Factors; Vitamin E; Vitamin E Deficiency; Xanthine Oxidase

Topics: Adenosine Triphosphate; Allopurinol; Anemia; Brain Diseases; Carbon Isotopes; Child, Preschool; Erythrocytes; Fibroblasts; Humans; Infant; Intellectual Disability; Kidney Diseases; Male; Metabolism, Inborn Errors; Purines; Self Mutilation; Transferases; Uric Acid

Topics: Adult; Aged; Allopurinol; Anemia; Arthritis; Bicarbonates; Blood Sedimentation; Chronic Disease; Female; Gout; Humans; Joint Diseases; Male; Middle Aged; Phenylbutazone; Physical Exertion; Probenecid; Uric Acid

Topics: Anemia; Anemia, Pernicious; Folic Acid; Hematopoiesis; Oxidoreductases; Xanthine Oxidase