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Prostaglandin inhibiting therapies reduced cancer risk in HIV-infected women
Fitzgerald DW. Cancer Prev Res. 2012;5:34-40.
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Therapies that inhibit the synthesis of prostaglandin may reduce the risk for cervical cancer and systemic inflammation in HIV-infected women, new findings published in Cancer Prevention Research suggest.
Compared with women without HIV, women with HIV had higher urinary prostaglandin E-M levels (6.8 ng/mg creatinine vs. 11.2 ng/mg creatinine; P=.02), which directly correlated with HIV-1 viral load (P=.003).
“Complications of chronic inflammation, including cancer and cardiovascular disease are an increasing cause of illness and mortality in HIV-infected people,” Daniel W. Fitzgerald, MD,of the division of infectious diseases at Weill Cornell Medical College, told Infectious Disease News. “This study suggests that the prostaglandin pathway plays an important role in this inflammation. Drugs that inhibit prostaglandin E2 (PGE2) synthesis — such as aspirin, [nonsteroidal anti-inflammatory drugs] or selective cyclooxygenase-2 (Cox-2) inhibitors — exist and could be especially attractive in people living with HIV/AIDS who are at increased risk for cancer.”
From November 2008 to June 2009, participants were recruited from the GHESKIO clinical and research center in Port-au-Prince, Haiti. Levels of cervical Cox-2 mRNA and urinary PGE-M, a biomarker of systemic PGE2 levels, were assessed among HIV-negative women with a negative cervical human papillomavirus test (n=17), HIV-infected women with a negative HPV test (n=18) and HIV-infected women with cervical HPV and high-grade squamous intraepithelial lesions (n=13).
The researchers found that cervical Cox-2 levels were significantly associated with HIV (P=.006) and HPV status (P=.002), and positively correlated with urinary PGE-M levels (P=.005).
“Further studies are warranted to elucidate the mechanism(s) by which HIV-1 infection induces Cox-2 in cervical cells and enhances systemic PGE2 synthesis,” the researchers wrote. “Although a strong correlation was found between levels of cervical Cox-2 and urinary PGE-M, it is highly unlikely that cervical inflammation is responsible for increased systemic PGE2 levels. It is much more likely that the findings in the cervix reflect a systemic inflammatory process. The correlation between Cox-2 expression and systemic PGE2 levels suggests that elevated PGE2 results from increased Cox-2 activity, likely in systemic lymphocytes and macrophages, but this needs to be verified.”
Disclosure: This research was supported by grants CA142422 from the NCI, TW00018 and TW007988 from the Fogarty International Center, and the Flight Attendant Medical Research Institute.
A growing consensus holds that HIV-associated inflammation is responsible for much of the morbidity of even well treated HIV infection. This article suggests that this might be true for the combination of HIV with HPV infection, noting higher levels of COX-2 associated inflammatory markers in cervical secretions in HIV-infected women. The authors speculate that COX-2 inhibitors may have a therapeutic role in this situation. The study is quite small and of course anti-inflammatory drugs can have adverse effects in long-term use. Thus, this should be seen as an interesting, but not yet clinically applicable report.
- Paul A. Volberding, MD
Infectious Disease News Chief Medical Editor
Disclosure: Dr. Volberding reports no relevant financial disclosures.
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