Hematological abnormalities in HIV infected patients include anemia, thrombocytopenia and granulocytopenia. Anemia and neutropenia are generally caused by inadequate production due to suppression of bone marrow by HIV infection through abnormal cytokine expression and alteration of the bone marrow microenvironment. Thrombocytopenia is due to immune mediated destruction of platelets in addition to inadequate production. Other etiologies include drugs, secondary opportunistic infections, malignancies and nutritional deficiencies.
HIV and anemia
Anemia is a frequent hematological manifestation of human immunodeficiency virus (HIV) infection. The causes of HIV related anemia are multifactorial. There is increased production of cytokines especially in advanced disease which may block marrow production of red cells, decreased erythropoietin production, opportunistic infections such as Mycobacterium avium complex and Parvovirus B-19, administration of drugs such as Zidovudine, ganciclovir and trimethoprim – sulfamethoxazole and myelophthisis caused by malignancies such as lymphoma. Other uncommon mechanisms for HIV associated anemia postulated are autoimmune destruction of red blood cells, Vitamin B12 deficiency and direct infection of marrow precursor cells.
The prevalence of anemia in patients with acquired immunodeficiency syndrome (AIDS) has been estimated to be 63-95%. Treatment of HIV related anemia requires correction of nutritional deficiencies, blood transfusion, recombinant human erythropoietin and modification of offending medications.
HIV and Neutropenia
Neutropenia in ART naïve HIV infected children is most commonly seen as drug-related toxicity and due to opportunistic infections. Treatment of neutropenia includes granulocyte-colony stimulating factor (G-CSF).
HIV and Thrombocytopenia
Thrombocytopenia is a known complication in patients infected with HIV-1. However, the exact immune mechanism leading to platelet destruction is unclear. Elevated levels of antiplatelet IgG antibodies and non-specific deposition of circulating immune complexes and complements have been suggested as the cause of increased clearance of platelet. However studies have depicted that increased levels of anti-platelet IgG antibodies are not causally related to the development of thrombocytopenia in children. With evidence of viral RNA present in megakaryocytes, a direct role of HIV in the pathophysiology of thrombocytopenia may be present.
Though HIV associated idiopathic thrombocytopenic purpura (ITP) clinically resembles classic ITP, it rarely leads to bleeding and splenomegaly as well as lymphadenopathy is quite rare.
Treatment consists of ART, intravenous immunoglobulins, steroids, anti-rhesus immunoglobulin, danazol or vincristine in a symptomatic patient. Other drugs that have been tried are Alpha interferon, Danazol, Specific Anti-D immunoglobulins and thrombopoietin but results are conflicting. Zidovudine (AZT) has been found to have a good rise in platelet count in large number of patients.
HIV and thrombosis
Though thromboembolic phenomenon in HIV infected patients have been described, the incidence ranges from 0.26% to 7.6%. Higher incidence has been found in patients with active opportunistic infections, Malignancy, patients with AIDS or patients on highly active antiretroviral therapy especially on protease inhibitors. Mechanisms including presence of antiphospholipid antibodies, anticardiolipin antibodies, decreased activity of natural anticoagulants (especially proteins) and increased platelet activation have been proposed. It appears that CD4 counts < 200/mm3, presence of opportunistic infections, AIDS related neoplasms or autoimmune disorder associated with HIV such as autoimmune hemolytic anemia (AIHA) may predispose to thrombosis.
The mechanism proposed for high prevalence of different antiphospholipid antibodies is B-cell polyclonal activation.
Treatment of thrombosis in association with HIV consists of low dose aspirin as a prophylactic agent to prevent further thrombosis. For patients with acute thrombosis, full anticoagulation with intravenous or subcutaneous heparin followed by warfarin therapy is the treatment of choice.
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