​Pathology - Aplastic Anemia

​Pathology - Aplastic Anemia
Aplastic anemia may occur after carbamazepine medication and subsequently developed invasive aspergillosis. Aplastic anemia originates from defective or inadequate multipotent myeloid stem cells (acquired or hereditary), or antigen receptor change causing T-cell activated stem cell suppression (caused by medications, infection, or other factors). The result is decreased erythrocytes, leukocytes, and platelets, known as pancytopenia.
Bone marrow is hypocellular with fatty infiltration. Aplastic anemia is more typically idiopathic, and myelotoxic medicines (alkylating agents, antimetabolites) most commonly employed for cancer therapy generate doserelated suppression. However, certain drugs might result in aplastic anemia in an unanticipated form, including carbamazepine (first-line treatment of TN), chloram-phenicol, streptomycin, hydralazine, and indomethacin to mention a few. Medication side effects might be overwhelming, but it is most important to concentrate on the most prevalent and the most serious. Aplastic anemia can result in significant infection (by opportunistic organisms as in this case) from neutropenia and bleeding from thrombocytopenia. Other causes include certain viruses (parvovirus B19, EBV, HIV) and Fanconi’s anemia.