NEW YORK (Reuters Health) – In HIV-infected patients, risk factors for thrombocytopenia include interruptions in antiretroviral therapy, high HIV RNA levels, hepatitis C virus (HCV) infection, and cirrhosis, according to two papers in the Journal of Acquired Immune Deficiency Syndromes for December 15.

In the first paper, Dr. Marie-Anne Bouldouyre, from Hopital Saint Louis, Paris, and colleagues report that one in four patients who interrupted their highly active antiretroviral therapy (HAART) developed thrombocytopenia (<150,000 platelets/microliter) over the 96-week study period.

In the second study, Dr. Kristen M. Marks and colleagues at Weill Cornell Medical College, New York, and associates showed that the odds of thrombocytopenia (here defined as 3 months) were increased by 5.3-fold with an HIV RNA level >400 copies/mL, by 6.1-fold with HCV infection, and by 24.0-fold with cirrhosis.

A number of studies have examined antiretroviral treatment interruptions as a way of making therapy more manageable, Dr. Bouldouyre and colleagues note. Even though the results indicate that such an approach yields “unacceptable” increases in morbidity and mortality, some patients still stop their medications for periods of time.

To examine the impact of interrupted antiretroviral therapy on platelet counts, the authors analyzed data from 391 “well-suppressed” patients who had been randomized to receive HAART either intermittently (8 weeks off, 8 weeks on) or continuously for 96 weeks as part of an earlier trial.

At 96 weeks, the thrombocytopenia rate was much higher in the intermittent therapy group than in the continuous treatment group: 25.4% vs. 9.8% (p < 0.001). Moreover, the median time to thrombocytopenia in the former group was just 9 weeks compared with 40 weeks in the latter.

On multivariate analysis, intermittent therapy upped the odds of thrombocytopenia by 4.1-fold (p < 0.0001). Other risk factors included a history of thrombocytopenia (OR, 11.9) and a low baseline platelet count (OR, 3.4). Moreover, the authors found that as platelet counts fell, so did CD4+ cell counts, while HIV RNA levels rose.

In the paper from the New York-based group, the authors note that thrombocytopenia was a common finding in HIV patients during the 1980s and early 1990s, but little has been reported since the introduction of potent antiretroviral therapy in the mid 1990s.

Their case-control study included 146 HIV-infected patients with and without thrombocytopenia who were seen at two HIV clinics at New York Presbyterian Hospital-Weill Cornell Center in the last few years. Cases and controls were matched by age, gender, and first clinic visit.

Fifty-eight percent of case patients had platelet counts of 50,000/microliter or lower and 38% had levels of 30,000/microliter or lower. As noted, uncontrolled HIV replication, HCV infection, and cirrhosis were all risk factors for thrombocytopenia.

Major bleeding events (gastrointestinal, intracranial, or requiring hospitalization) were 6.5-times more common in case patients than in controls (p = 0.014).

J Acquir Immune Defic Syndr 2009;52:531-537,595-599.