ABSTRACT
Introduction: Chronic lymphoproliferative disorderrepresent clonal proliferation of morphologically andimmunophenotypically mature B or T cells characterized by alow proliferation rate and prolonged cell survival. Study aimedto assess the correlation between bone marrow morphologyand immunophenotypic findings in patients of ChronicLymphoproliferative Disorders (CLPD’s) and to assess therole of flowcytometric immunophenotyping in diagnosis andsubclassification of CLPD’s.Material and Methods: 48 newly diagnosed cases ofCLPD were included. After complete clinical evaluation theyunderwent marrow aspiration, biopsy and immunophenotypingby flowcytometry with selected panel of monoclonalantibodies.Results: On morphology 47.9% cases were CLL. In 52.1%non CLL cases , 4.2% were PLL , 2% case as LPL and45.8% cases were CLPD-unclassifiable. Commonest patternof marrow infiltration noted on trephine biopsy was diffuse inCLL, HCL-V, B-PLL and T-CLPD. On immunophenotyping95.8% cases were B-CLPD and 4.25% T-CLPD. CD5, CD22,CD23, FMC7 and SmIg were used as first line markersfollowed by CD 10, CD 25, CD103, CD38, CD138 andCyclin D1 (on biopsy sections) as second line markers. Finalimmunophenotypic diagnosis was CLL (54.2%), B-CLPDunclassified (29.2%), 4.1% each of LPL, MCL, T-CLPD and2% each of B-PLLand HCL-V.Conclusion: Concordance rate between morphologicaldiagnosis and immunophenotypic diagnosis was 79.17%.Hence, Flowcytometry is necessary for confirmationof diagnosis and to classify the CLPD cases which areunclassifiable by morphology
ABSTRACT
Introduction: Human immunodeficiency virus (HIV) may result in variable haematological manifestations. Thrombotic events are more common among HIV-infected persons than the general population, possibly due to the increased inflammatory/hypercoagulable state and presence of concurrent comorbidities. Aims and Objectives: (1) Screen for coagulation abnormalities in HIV-infected patients. (2) Detect certain prothrombotic factors such as deficiency of protein C and protein S and elevation of homocysteine as possible precursors of coagulation defects in HIV patients. (3) Correlation of coagulation abnormalities with CD4 counts. Methods: A pilot study of 1-year duration conducted in the Department of Pathology in collaboration with ART centre, KGMU Lucknow. All diagnosed HIV-seropositive patients (n = 30) who were not taking Vitamin K, antithrombotic and antiplatelet drugs including aspirin, oral contraceptives and not having known protein C/S deficiency were included in the present study as cases. Apart from this, 30 age- and sex-matched healthy individuals were also included in the present study. Assessment of the bleeding time, prothrombin time and activated partial thromboplastin time, complete blood count was done. Protein C and S were measured by calorimetric assay. Serum homocysteine was measured by the semi-automated method. CD4 count was done by flow cytometry. Results: The findings of the present study suggest a relationship between HIV, its complications and thrombosis. The HIV-seropositive patients have reduced levels of haemoglobin, CD4 counts, platelet counts, mean platelet volume, protein C and S activity as compared to the healthy individuals. Thrombophilic abnormality in the form of hyperhomocysteinaemia is more frequent in HIV-infected patients. All these parameters have a definite correlation with CD4 count.