HIV patients with declining platelet counts appear to be at increased risk for HIV–associated dementia, according to a report in the September issue of Archives of Neurology, one of the JAMA/Archives journals.
“Human immunodeficiency virus–associated dementia (HIV-D) is a syndrome encompassing a spectrum of cognitive, behavioral and motor deficits that usually has an insidious onset and a chronic progressive course,” the authors write as background information in the article. Therapies leading to longer life for HIV patients have paradoxically increased the prevalence of this condition. Identifying biological markers for the development of HIV–associated dementia is critical both for diagnosing the disorder and for understanding its underlying mechanisms.
Lynn M. Wachtman, D.V.M., M.P.H., of Bloomberg School of Public Health, The Johns Hopkins University School of Medicine, Baltimore, and colleagues studied 396 patients with advanced HIV who were recruited for this prospective study between 1998 and 2003. Participants were examined every six months and completed mental and physical evaluations. Blood samples were also collected and assessed for platelet count (the number of clotting cells in the blood), hemoglobin levels, CD4 lymphocyte count (a measure of certain types of white blood cells, which reflects the state of the immune system) and plasma HIV RNA levels (which indicate the amount of “viral load,” and predict HIV progression).
After a median (midpoint) follow-up of 31.1 months, 40 participants developed HIV–associated dementia. A decline in platelet count from baseline was associated with the development of dementia within six to 12 months. “Those HIV-infected individuals with a decline in platelets from baseline values at this lagged time point had a two-fold increased risk of dementia” in several different analyses, the authors write. The specific timing of the association indicates that the levels of circulating platelets fluctuate as HIV–associated dementia develops, they note.
“Further analyses indicated that decline from baseline platelet levels was associated with a five- to six-fold increased risk of dementia during the first two years of follow-up, but it was not associated with an increased risk of dementia after two years,” the authors continue. “It is possible that individuals who do not progress rapidly to neurologic compromise differ in respect to immune activation, treatment adherence or virologic control relative to those who develop dementia more rapidly.”
“Because CD4 cell counts and HIV RNA levels have proven not to be predictive of HIV–associated dementia, it is important to investigate alternative serum and hematologic markers,” the authors conclude. “Should these markers be routinely measured in a clinical setting, such as platelet counts, they may prove useful for patient management. This study identifies a significant association between platelet decline and incident HIV–associated dementia.” Further study of platelet levels during HIV–associated dementia may lead both to a specific marker for the development of HIV–associated dementia and a better understanding of how the disease develops.
(Arch Neurol. 2007;64(9):1264-1272. Available pre-embargo to the media at www.jamamedia.org.)
Editor’s Note: Please see the article for additional information, including other authors, author contributions and affiliations, financial disclosures, funding and support, etc.
Archives of Neurology