haemopoiesis, altered coagulation, and immune-mediated cytopenias with bone marrow cellularity and dysplasia.Haematological abnormalities may be direct effect of HIV itself or 2° to concurrent infection, malignancy, or therapeutic agents. Common findings are haemopoiesis, altered coagulation, and immune-mediated cytopenias with bone marrow cellularity and dysplasia.
Most common form of cytopenia and an independent prognostic factor; 8% of all PLWH and 50–75% of patients with AIDS. Usually due to erythropoiesis, but other mechanisms (e.g. infection, drug toxicity, malignancy, dietary deficiencies, alcohol abuse, blood loss) may contribute. Chronic anaemia causes fatigue, exertional dyspnoea, and a hyperdynamic state that, if severe, may lead to angina, congestive cardiac failure, and confusion.
Examine and test for iron, vitamin B12, and folate deficiencies, haemolysis, and blood loss according to red cell indices. Eliminate possible causes by excluding infection and malignancy, and reviewing drug therapy. Bone marrow examination may be required, particularly if pancytopaenia and common causes excluded.
• HIV-related: normocytic normochromic anaemia 
in frequency and severity as HIV progresses. May be a direct effect of HIV on bone marrow progenitor cells, erythropoietin production, and cytokines (inhibit haemopoiesis). Improves or normalizes with ART provided that drug effects do not supervene.
• Macrocytosis and normal haemoglobin—typical with AZT.
• Macrocytic anaemia—caused by AZT. AZT exerts broader myelosuppressive effects, more frequent in patients receiving higher doses (in 
1% receiving 500 mg/day) and those with advanced disease. Improves following discontinuation. Anaemia may require blood transfusion following discontinuation of AZT.
• Normocytic normochromic anaemia—associated with normal or reticulocyte count, 2° to bone marrow suppression. Causes include anaemia of chronic infection and drugs (e.g. ganciclovir, co-trimoxazole, amphotericin, and interferons).
• Haemolytic anaemia—features are macrocytosis, haptoglobin, and lactic dehydrogenase, indirect bilirubin, and reticulocyte count. Common causes include drugs, e.g. dapsone (with methaemoglobinaemia), ribavirin, and primaquine. Glucose-6-phosphate dehydrogenase (G6PD) deficiency predisposes to dapsone and primaquine haemolysis. Autoimmune haemolytic anaemia (AIHA) with positive Coombs’ test also occurs.
• Bone marrow infiltration (usually causes pancytopenia):
• OI—most commonly MAC (also TB and CMV).
• Tumours—lymphoma and rarely KS.
• Parvovirus B19 infects erythroid precursors. In immune deficiency, persistent infection may result in severe chronic normocytic normochromic anaemia. Diagnosed by detecting B19 parvovirus antibodies and PCR for B19 in serum and/or bone marrow. Responds well to high-dose IV immunoglobulins (0.4 g/kg/day), which contain parvovirus antibodies, but may require repeated blood transfusions.
Occurs in around 6–9%. HIV-related immune thrombocytopenia is a frequent early finding, tending to deteriorate as HIV progresses. Commonly an isolated haematological abnormality. Results from clearance of immunoglobulin-coated platelets by reticulo-endothelial system. with levels of antiplatelet immunoglobulin. May be result of drug toxicity, immune and non- immune destruction, or defective platelet production.
Exclude underlying causes, e.g. drug toxicity, liver disease, alcoholism, and lymphoma. Further investigation not usually necessary, presence of normal or megakaryocytes on bone marrow examination is sufficient to diagnose HIV-induced thrombocytopenia.
• Mild and asymptomatic: ART, switch/discontinue implicated drugs.
• Symptomatic or before surgical procedures: IV immunoglobulins, steroids, and ART.
• Substantial bleeding: packed red cells and platelet transfusion.
Rare, of unknown aetiology, usually seen in early stages of HIV infection. Characterized by hyaline microvascular deposits on biopsy. Clinical features include fever, renal impairment, neurological deficit, and microangiopathic haemolytic anaemia. Mortality rate 65% without treatment. There may be response to plasmapheresis, steroids, ART, and antiplatelets (e.g. aspirin).
HIV directly implicated, especially in advanced stages. More commonly due to drug toxicity, associated infection, and bone marrow infiltration. Risk of bacterial infection significantly when absolute neutrophil count <500 cells/µL. Drugs causing neutropenia include AZT, ganciclovir, co-trimoxazole, pentamidine, interferon alfa α, and chemotherapeutic agents.
Careful review of medication. Withdraw offending drug(s) if absolute neutrophil count <500 cells/µL. If cause uncertain, consider bone marrow examination.
• Granulocyte colony stimulating factor:
• drug-induced (if implicated drug cannot be reduced or stopped).
Risk of thrombotic disease associated with low CD4 counts, OIs, neoplasms, and HIV-associated autoimmune disorders.
• High inflammatory state: D-dimer and cytokines are found in advanced disease.
• Lupus anticoagulant may be detected with thrombo-embolic disease.
• Levels of active protein S frequently found, not associated with immune suppression.
• Contributing prothrombotic factors include plasminogen activator inhibitor level, abnormal platelet aggregation, and von Willebrand factor.
• ART does not fully reverse pro-coagulant effect of HIV.
Generalized lymphadenopathy involving two extra-inguinal sites persisting for more than 3 months. Of no prognostic significance, but other causes of generalized lymphadenopathy should be excluded (see box). Occurs in up to 70% of patients within 1 year of seroconversion, but may co-exist with other manifestations of HIV infection. Lymph nodes usually symmetrical, >1 cm in size, rubbery, and non-tender. May be accompanied by hepatosplenomegaly. Biopsy for histology and culture should be done in those with systemic symptoms of fever, weight loss or if inflammatory markers are raised or large lymph nodes that increase in size overtime. Mediastinal lymphadenopathy usually has other causes and should be investigated.