Letters to the Editor
Indian Pediatrics 2006; 43:1010-1011
Persistent Thrombocytopenia after Dengue Hemorrhagic Fever
A 9-month-old boy presented with history of high grade fever for five days, hypotension, soft hepatomegaly and malena. Investigations revealed a hematocrit of 53.4% and platelet count of 58,000 per cubic mm. DHF was confirmed serologically by dengue specific IgM and IgG antibodies by ELISA test. The child recovered in 10 days; however, thrombocytopenia persisted (platelet count: 12,000/mm3). A bone marrow aspirate, performed on 26th day of illness, suggested adequate megakaryocytes.
A 9-year-old girl presented with history of high grade fever for four days, myalgia, hypotension, epistaxis and petechiae. Investigations revealed a platelet count of 40,000 per cubic mm, and a hematocrit of 48.6%. DHF was confirmed serologically by ELISA for IgG and IgM antibodies. She had persistent thrombocytopenia of 13,000 per cubic mm of blood at 30 days. A bone marrow aspirate revealed adequate megakaryocytes.
Persistent thrombocytopenia in both cases responded to intravenous methylprednisolone. Thrombocytopenia is known to occur in DHF, which promptly recovers by 9-10 days of illness(2). The pathogenesis of persistent thrombocytopenia in these two cases is not clearly understood. Following are possible mechanisms that have been postulated for thrombocytopenia in DHF;
(a) Dengue virus induces bone marrow suppression(2);
(b) Dengue virus can bind to human platelets in presence of virus specific antibody and immune mediated clearance of platelets(3);
(c) Spontaneous aggregation of platelets to vascular endothelial cell pre-infected by virus inducing aggregation, lysis and platelet destruction(4).
(d) Anti-platelet antibodies generated after dengue virus infection causes destruction of platelets(5).
In the two patients that we are reporting, the presence of adequate megakaryocytes, confirmed by bone marrow aspirate, with co-existent thrombocytopenia at a time when the virus was normally expected to have been cleared and prompt response to methyl prednisolone suggests immune mediated platelet destruction. Persistent thrombocytopenia can cause intracranial or vulnerable deeper site bleeds and intravenous methylprednisolone rapidly increase platelet count to safer levels to reduce mortality and morbidity.