Evaluation of Thrombocytopenia in Megaloblastic Anemia by Platelet Indices and Megakaryocytes- Comparison with Hypoproduction and Hyperdestruction

• Main Authors: Rajalakshmi Birur Rajashekar, Asha Mahadevappa, Sapna Patel
• Format: Article
• Language: English
• Published: JCDR Research and Publications Pvt. Ltd. 2017-01-01
• Series: National Journal of Laboratory Medicine
• Subjects: ineffective thrombopoiesis; mean platelet volume; platelet distribution width; platelet large cell ratio
• Online Access: http://www.njlm.net/articles/PDF/2196/25525_CE[VSU]_F(GH)_PF1(VsuGH)_PFA(GH)_PF2(VsuGH).pdf

Introduction: Thrombocytopenia may result from many mechanisms such as: marrow hypoplasia (decreased megakaryocytes), ineffective thrombopoiesis (normal to increased megakaryocytes) and increased destruction of platelets (increased megakaryocytes). The cause of thrombocytopenia in megaloblastic anemia has been postulated as hypoproduction in some studies, whereas ineffective thrombopoiesis has been proposed as the mechanism in others. Aim: This study was taken up to study the platelet indices in thrombocytopenia secondary to megaloblastic anemia, hypoproduction and hyperdestruction. And also aimed to evaluate the discriminative function of platelet indices in megaloblastic anemia in comparison with hypoproductive and hyperdestructive causes of thrombocytopenia and to correlate platelet indices with bone marrow megakaryocyte cellularity. Materials and Methods: Platelet indices in 32 cases of thrombocytopenias of megaloblastic etiology were compared with platelet indices of 31 cases of marrow proven hypoproductive thrombocytopenias (aplastic anemia, hypoplastic anemia, acute leukemia) and 32 cases of hyperdestructive thrombocytopenias (Immune thrombocytopenia). Descriptive analysis was used and comparison among means of platelet indices in all the groups was done with one way ANOVA using Scheffe’s test. Categorical data was analyzed using Chi-square test. Platelet indices and bone marrow megakaryocytes were analyzed and correlated in each group. A p-value of less than 0.05 was considered statistically significant. Results: The mean values platelet indices were significantly higher (p<0.05) in the hyperdestructive group [PDW(16.6fL), MPV(12.1fL), P-LCR(42.3%)] compared to the hypoproductive group [PDW(11.8fL), MPV(10.9fL), P-LCR(31.5%)]. Whereas, mean values of PDW (14.7fL) and MPV (11.6fL) in the megaloblastic group showed a significantly higher value (p-value<0.05) than hypoproductive group but no statistical significant difference was seen compared to hyperdestructive group (p-value>0.05). The mean P-LCR (37.4%) in megaloblastic group was intermediate between both the other groups with a significant statistical difference (p-value<0.05). Conclusion: Both hypoproduction and ineffective thrombopoiesis are the underlying pathomechanisms in megaloblastic thrombocytopenia as evidenced by the marrow findings and platelet indices. Platelet indices are of significant discriminative value in differentiating the various causes of thrombocytopenias. We hereby infer that megaloblastic thrombocytopenia is to be included as a separate category apart from hypoproliferative and hyperdestructive groups.