Volume. 35, No. 2 july. 2011 - The Chest and Heart Association of ...

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Chest & Heart Journal Vol. 35, No.-2, July 2011tubercular drugs is in 59(59.0%) cases and the rest41(41.0%) cases have taken irregular basis. Thedistribution of adverse effects among the studypopulation is recorded. Nausea, vomiting and highcolored urine are complained by 94(94.0%) cases,71(71.0%) cases and 22(22.0%) cases respectively 19 .The distribution of study population according toblood grouping is recorded in this study. Amongthe 100 cases the most common blood group is Ogroup which is 37(37.0%) cases followed by B groupand A group which are 28(28.0%) cases and26(26.0%) cases respectively. The AB group is foundin only 9(9.0%) cases. Similar result was reportedby Dean 24 and mentioned that the blood group Ois common and blood group AB is the least common.The distribution of Rh typing of blood grouping isrecorded in this study. Among the 100 cases mostlyare positive Rh blood group which is 97(97.0%) andthe rest 3(3.0%) cases are Rh negative blood group.The finding of chest X-ray among the studypopulation is recorded. Positive chest X-ray findinglike cavity, patchy opacity etc are found in85(85.0%) cases and the rest 15(15.0%) cases showsnormal findings. Barnes et al 20 reported a similarresult and mentioned that almost 88% patientsshows such positivity of chest x-ray. From thesefindings it may be established that routine CXRsare useful in hospitals serving populations and theprobability of detecting AFB on sputum smear isgreatly influenced by the roentgen graphicfindings 21 .Among 100 cases DAT is positive in only 5(5.0%)cases and the rest 95(95.0%) cases are negative.Lawrence et al 1 reported four mechanisms bywhich drugs induce a positive DAT. Many drugscan cause a positive DAT however, only some ofthese will cause hemolytic anaemia 22 . As such theserologic data must be correlated with the patient’sclinical history and drug history. The clinicalevidence like fever, anaemia, jaundice that wouldsupport the diagnosis of drug induced immunehemolytic anaemia includes the association ofhemolysis with the initiation of drug therapy andresolution with discontinuation of the drug 25 .Worlledge 24 also reported that Rifampicindependent antibodies have been found in the Seraof 1 to 50% patients on Rifampicin, dependingprimarily on the schedule of administration of drug.Also antirifampicin antibodies were reported in33% of those receiving once weekly dosingcompared to 0.8% on daily therapy.Martinez J. et el 25 also reported Streptomycininduced antibodies which cause positive DAT andimmune haemolytic anaemia by immune complexmechanism.Ahren et el 27 reported that the DAT were stronglypositive for IgG and C3d and tests for rifampicindependent antibodies. This shows that rifampicinmay stimulate the production of autoantibodiesand/or drug dependent antibodies.In this study, DAT in positive in 5% cases and 95%cases are DAT negative.Among DAT positive cases, 03(3%) are blood groupO, followed by A & B blood group which are 01(1%)& 01(1%) respectively 2 .Many other toxicities are reported byantitubercular drugs. Isoniazid (INH) may causeneurotoxic & hepatotoxic effects. Haemolysis hasoccurred in patients with glucose-6-phosphatedeficiency. Rifampicin may cause skin rash,thrombocytopania, nephritis & liver dysfunction 28 .If given less often than twice weekly, it may causea flu-like syndrome & anaemia. Ethambutal maycause dose dependant visual disturbances 29 .Pyrazinamide may cause non-gouty polyarthralgia.Streptomycin may cause ototoxicities,nephrotoxicities, neuromuscular blockade & skinrashes 30 .Conclusion:In this study drug induced antibody is detected bydirect antiglobulin test. The finding of the studypermit to identify the patients who developedantibody which may coat on red cell surface.This study suggests that positive DAT may behelpful in further management of tuberculouspatients who may be at risk of developing anaemiawhich will cause discontinuation of drug.The overall goal of tuberculosis control to reducemorbidity, mortality and transmission oftuberculosis is no longer a public health problem.In conclusion, during treatment with antituberculardrug prompt identification of anaemiaand close monitoring of patient will be done to findout the cause of anaemia by DAT to establishwhether the drug is responsible for anaemia ordue to any other cause.92
Study of Direct Antiglobulin Test among the Patients ReceivingIt is also important to identify the blood group fortransfusion to the patient due to anaemia and forexclusion of cause of anaemia which may be dueto drug or other antibodies produced bytransfusion.Recommendations:Further study is recommendation with followingproposals:• The study will help the physicians & healthworkers who are working on tuberculouspatients to reduce morbidity &use of appropriatedose of drug which will prevent discontinuationof therapy.• A large scale national epidemiological studyshould be done.• DAT should be performed in all patients receivinganti TB drug after 4weeks & subsequently afterinitiation of treatment.• Close monitoring and follow up of the patientsshould be done to avoid drug inducedautoimmune haemolytic anaemia.• S.bilirubin will be done in every patient after4weeks of initiation of treatment.• DOTs corner of Primary Health care Centre(Upazilla Health Complex) should be closelymonitored for the evidence of drug inducedhaemolytic anaemia.• A further study will be done for the detection ofspecific antitubercular drug which causehaemolytic anaemia frequently.• Multicentered study will be included.• Study period will be prolonged.References:1. Lawrence LW, Harmening DM, Green R:Haemdytic Anaemias: Extra corpuscularDefects and Acquired Intra corpuscularDefects. In Clinical Hematology andFundamentals of Hemostasis, 4 th edition.Philadelphia, FA Davis Company, 2002, 2122. Jefferies LC, Elder AF: Transfusion Therapyin Autoimmune Hemolytic Anaemia. In MintzPD(ed): Transfusion Therapy: ClinicalPrinciples & Practice,Bethesda, AmericanAssociation of Blood Banks Press,1999, 43Farhana Islam et al.3. Harmening DM, Prihoda LA, Green R:Autoimmune Hemolytic Anaemia. InHarmening DM,(ed): Modern Blood Bankingand Transfusion Practices, 4 th edition.Philadelphia, FA Davis Company, 1999, 455-456.4. Arndt PA, Garratty G. The changing spectrumof drug induced immune hemolytic anemia.Semin Hematol. 2005;42:137-144.5. World Health Organization. Tuberculosis factsheet. Available from URL: http://www.who.int/gtb/ publications/factsheet/index.htm. Accessed on 1 July 20036. National Tuberculosis Control Programme(NTCP). National Guidelines and OperationalManual for Tuberculosis Control. FourthEdition. Directorate General of HealthServices. Ministry of Health and FamilyWelfare. Dhaka, Bangladesh 2004, 17.7. Yee D, Valiquette C, Pelletier M, Parisien I,Rocher I, Menzies D. Incidence of SeriousSide Effects from First-Line AntituberculosisDrugs among Patients Treated for ActiveTuberculosis. American Journal ofRespiratory and Critical Care Medicine 2003;Vol 167: 1472-14778. Gehrs BC, Friedberg RC. AutoimmuneHemolytic Anemia American Journal ofHematology 2002; 69: 258-2719. Ahrens N, Genth R, Salama A.. Belateddiagnosis in three patients with rifampicininducedimmune haemolytic anaemia. BritishJournal of Haematology. 2002;117(2): 441–44310. Krönig B., Fiegel P., Weihrauch Th., HöfflerD., Jahnecke J., Arndt-Hanser A. A case ofsevere repeated immunological reactions tointermittent rifampicin treatment. EuropeanJ Clin Pharma. 1972; 5(1): 53-57, DOI: 10.1007/BF0056089611. Guzzini F, Angiolini F, Cazzaniga L, GaspariniP, Milvio E, Mosconi L. Immune hemolyticanemia and acute kidney failure due torifampicin. Recenti Prog Med. 1994;85(3):182-512. Garratty G. Drug-ind, Fiegel P.,Weihrauchuced immune hemolytic anemia.American Society of Hematology, Hematology2009:73-7993
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