Hepatitis C virus (HCV) infection, severe liver damage and uncontrolled HIV replication are all associated with a greater risk for low platelets in people with HIV, according to a study published online September 3 in the Journal of Acquired Immune Deficiency Syndromes.
Thrombocytopenia, the technical term for too few platelets, was once quite common in people living with HIV. Having a low platelet count means that the blood has a harder time forming clots, which amplifies the chance of bruising and excessive bleeding—increasing the risk of stroke in severe cases. The incidence of thrombocytopenia since the introduction of potent three-drug combination HIV therapy is not well known, though it has dropped.
To determine the likelihood of developing thrombocytopenia, Kristen Marks, MD, MS, and her colleagues from Weill Cornell Medical College in New York City, compared 73 people with HIV who were diagnosed with thrombocytopenia with 73 people with HIV who did not have the condition. The two groups were matched based on age, sex and other health factors, such as using drugs that can cause low platelet counts. The average age was 41; about half of the participants were female; and just over half had a CD4 count greater than 200.
Marks and her colleagues found that HCV infection—particularly uncontrolled HCV infection and advanced liver disease—made someone far more likely to have thrombocytopenia. Interestingly, uncontrolled HIV infection was also highly associated with low platelets, regardless of a person’s CD4 count or previous AIDS diagnosis.
The authors conclude that people with HCV and HIV coinfection should be monitored carefully for low platelets, as even mild thrombocytopenia can result in internal bleeding. Thrombocytopenia should also be carefully considered when deciding whether to start interferon-based HCV treatment because that drug can contribute to low platelet counts. Marks’s team also comments that the majority of thrombocytopenia cases in people without HCV or liver damage are likely a result of uncontrolled HIV replication; the authors note that further research will be necessary to understand why this is the case.