Abnormalities in the blood clotting process develop as HIV disease gets worse say US doctors, putting patients at increased risk of potentially fatal clots.
Researchers first noted eight years ago that HIV-infected people appear to be at increased risk of a blood clot in the veins, or venous thromboembolism (VTE).
The blood clots cause most problems when they develop in a vein far below the surface of the skin, forming a deep vein thrombosis (DVT).
Sometimes the clot which forms a DVT can break off and travel in the bloodstream to become lodged in the lungs - forming a pulmonary embolism - and can be fatal.
People are at increased risk of a VTE if they are older and immobile but until now researchers were unclear about why people with HIV were at greater risk.
This study looked at blood samples from 94 women who took part in the Women’s Interagency HIV Study, an ongoing HIV trial carried out in six US cities.
Thirty-four of the women had a history of clinical AIDS, 11 had CD4 counts of less than 200 but no AIDS symptoms and 49 were HIV-infected but asymptomatic. Fifty uninfected women were used as a comparison group.
None of the women had other risk factors for VTE such as cancer, pregnancy or acute infection.
The researchers studied the levels of two components of the blood that are associated with clotting: protein S and factor VIII. Clots are more likely to form when protein S levels are low but factor VIII levels are high.
They found that the protein S levels were highest in the healthiest women and lowest in the most ill. So HIV-negative women had the highest levels, with lower levels in those with asymptomatic HIV infection, lower still in those HIV-infected women with low CD4 counts but no AIDS symptoms and lowest in those with clinical AIDS. Exactly the opposite relationship with was seen with factor VIII.
This is the first study to show a clear relationship between advancing HIV disease and changes in the blood that can lead to clots.
The researchers point out that women with known risk factors for VTE were excluded from the study and there is no reason to think that the results would be different in men.
They hypothesise that the inflammation caused by HIV infection could be leading to these abnormalities in the coagulation system.
Further studies are now being carried out to look at these clotting factors in more detail and at the effect of HAART on coagulation markers.
The 2056 HIV infected woman taking part in the Women’s Interagency HIV Study as a whole are also being monitored for the development of a VTE.
Levine AM et al. Progressive prothrombotic state in women with advancing HIV disease. Journal of Acquired Immune Deficiency Syndrome 2006;42(5):572-577.