Lead Poisoning Induced Severe Hemolytic Anemia, Basophilic Stippling,Mimicking Erythrocyte Pyrimidine 5'-nucleotidase Deficiency in BetaThalassemia Minor
{"title":"Lead Poisoning Induced Severe Hemolytic Anemia, Basophilic Stippling,Mimicking Erythrocyte Pyrimidine 5'-nucleotidase Deficiency in BetaThalassemia Minor","authors":"P. Warang, R. Colah, P. Kedar","doi":"10.4172/2161-0495.1000346","DOIUrl":null,"url":null,"abstract":"Lead is a highly toxic metal and a very strong poison. Lead poisoning usually occurs over a period of months or years. The poisoning can cause severe mental and physical impairment. Young children are most vulnerable to lead poisoning [1-2]. Lead poisoning is accompanied by an acquired deficiency of erythrocyte pyrimidine 5'nucleotidase (P5’N). Genetically determined deficiency of P5’N enzyme was associated with chronic hemolysis, marked basophilic stippling of erythrocytes on peripheral blood smear and accumulations of intra-erythrocyte pyrimidine-containing nucleotides [3-4]. Pyrimidine-containing nucleotides are almost absent in the normal erythrocytes but it was reported that in lead poisoning, 12% of erythrocyte showed accumulation of pyrimidine nucleotides in the blood of a patient and P5’N activity was suppressed to 50% that in normal erythrocytes in lead poisoning [2]. In most of βthalassemia carriers and other hemoglobin variant (Hb-E) showed marginally reduced Purine/Pyrimidine nucleotide ratios but normal P5’N-1 activity [5]. This report describes the clinical severity of leadinduced hemolytic anemia in two Indian patients with basophilic stippling associated with intra-erythrocyte accumulations of pyrimidine-containing nucleotides which mimicking hereditary P5’N deficiency.","PeriodicalId":15433,"journal":{"name":"Journal of Clinical Toxicology","volume":"13 1","pages":"1-3"},"PeriodicalIF":0.0000,"publicationDate":"2017-04-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"5","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Journal of Clinical Toxicology","FirstCategoryId":"1085","ListUrlMain":"https://doi.org/10.4172/2161-0495.1000346","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"","JCRName":"","Score":null,"Total":0}
引用次数: 5
Abstract
Lead is a highly toxic metal and a very strong poison. Lead poisoning usually occurs over a period of months or years. The poisoning can cause severe mental and physical impairment. Young children are most vulnerable to lead poisoning [1-2]. Lead poisoning is accompanied by an acquired deficiency of erythrocyte pyrimidine 5'nucleotidase (P5’N). Genetically determined deficiency of P5’N enzyme was associated with chronic hemolysis, marked basophilic stippling of erythrocytes on peripheral blood smear and accumulations of intra-erythrocyte pyrimidine-containing nucleotides [3-4]. Pyrimidine-containing nucleotides are almost absent in the normal erythrocytes but it was reported that in lead poisoning, 12% of erythrocyte showed accumulation of pyrimidine nucleotides in the blood of a patient and P5’N activity was suppressed to 50% that in normal erythrocytes in lead poisoning [2]. In most of βthalassemia carriers and other hemoglobin variant (Hb-E) showed marginally reduced Purine/Pyrimidine nucleotide ratios but normal P5’N-1 activity [5]. This report describes the clinical severity of leadinduced hemolytic anemia in two Indian patients with basophilic stippling associated with intra-erythrocyte accumulations of pyrimidine-containing nucleotides which mimicking hereditary P5’N deficiency.