RBC’s appear to have bite of cytoplasm (“Bite cells”) in
Correct Answer: G-6-P deficiency
Description: Ans. d (G-6PD deficiency) (Ref. Harrison's medicine 18th/ch. 106)The most typical feature is the presence of bizarre poikilocytes with red cells that appear to have unevenly distributed hemoglobin (hemighosts) and red cells that appear to have had parts of them bitten away (bite cells or blister cells).G6PD deficiency# In G6PD deficient individuals, acute HA can develop as a result of three types of triggers:(1) Fava beans,(2) Infections, and(3) Drugs.# Typically, a hemolytic attack starts with malaise, weakness, and abdominal or lumbar pain.# After an interval of several hours to 2-3 days, the patient develops jaundice and dark urine, due to hemoglobinuria.# The anemia is moderate to extremely severe, usually normocytic and normochromic, and due partly to intravascular hemolysis; hence, it is associated with hemoglobinemia, hemoglobinuria, and low or absent plasma haptoglobin.# The blood film shows anisocytosis, polychromasia, and spherocytes with typical bite cells.# A classic test, now rarely carried out, is supravital staining with methyl violet, which, if done promptly, reveals the Heinz bodies, consisting of precipitates of denatured Hb and regarded as a signature of oxidative damage to RBCs.# LDH is high and so is the unconjugated bilirubin, indicating that there is also extravascular hemolysis.# The most serious threat from acute HA in adults is the development of ARF (exceedingly rare in children).# Once threat of acute anemia is over, and with no comorbidity, full recovery from acute HA asso with G6PD is the rule.Peripheral SmearAssociated DiseaseBiconcaveNormal1Ring sideroblastsMyelodysplasia2NormoblastsIDA, hemolytic anemia, anemia of chronic disease like CRF3MicrocytesIDA, Thalassemia4MacrocytesMegaloblastic anemia5Burr cellsAplastic anemia, azotemia6Spur cellsSevere hemolytic anemia with cirrhosis7ElliptocytesHereditary elliptocytosis, hereditary hemorrhagic telangiectasia, thalassemia, SCA8EchinoctesSevere renal disease9StomatocytesHereditary stomatocytes, ethanol abuse10Target cellsThalassemia, HbC disease, liver disease11Howell Jolly bodiesPernicious anemia, hemolytic anemia, sprue, leukemia, after splenectomy12Cabot's ringSevere megaloblastic anemia13Heinz bodiesDrug-induced hemolytic anemia, splenectomy, HMP deficiency14Dohle bodiesSevere infections, thermal burns, cytotoxic drugs15Auer rods in myeloblastsAML type 316Punctate basophiliaLead poisoning,megaloblastic anemia, thalassemia17Rod like, spectacle likePelger Huet anomaly of granulocytes18Alder Reilly anomalyGorgoylism19SpherocytesHereditary spherocytosis, autoimmune hemolysis20Macro-ovalocyteMegaloblastic anemia (also hypersegmented PMNs), marrow failure21Helmet cell, schistocyteDIC, traumatic hemolysis22Bite cellG6PD deficiency23Teardrop cellMyeloid metaplasia with myelofibrosis24AcanthocyteSpiny appearance in abetalipoproteinemia25Target cellHbC diseaseAspleniaLiver diseaseThalassemia26PoikilocytesNonuniform shapes in TTP/HUS, microvascular damage, DIC27Burr cellTTP/HUS28Basophilic stipplingThalassemiasAnemia of chronic diseaseIron deficiencyLead poisoningEducational Points:Drugs that Carry Risk of clinical Hemolysis in Persons with G6PD Deficiency Definite RiskPossible RiskDoubtful RiskAntimalarialsPrimaquineChloroquineQuinine Dapsone/ chlorproguanil SuiphamethoxazoleSulfasalazineSulfisoxazole DapsoneSulfadimidineSulfadiazineAntibacterial antibioticsCotrimoxazoleNiridazoleCiprofloxacinChloramphenicolNalidixic acidNitrofurantoinNorfloxacinp-Aminosalicylic acidAntipyreticsAcetanilidePhenazopyridine (Pyridium)Acety Isa 1 icy lie acid high dose (<3 g/d)Acetylsalicylic acid<3 g/dAcetaminophen,PhenacetinOthersNaphthaleneMethylene blueVitamin K analoguesAscorbic acid >1 gRasburicaseDoxorubicinProbenecid
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