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  These 2 studies were reported at ICAAC (Dec 2001). The first study from Nunez in Spain reports that non-hodgkin (NHL) and Hodgkin lymphoma were associated with lower CD4 counts even if people were on HAART. In the 2nd study discussed below, researchers looked at HIV+ patients in the Veteran's Administration system. They found HIV+ patients were more likely to have cancers than HIV-negative patients in the VA. The authors of the second study suggest lifestyle may play a contributing factor. For example, HIV+ patients may be more likely to be former IVDUs, etc.
I don't know of any studies exploring the possibility that taking many drugs for HIV and related complicaions may play a contributing role in increasing risk for developing a cancer. So I don't think we have any research data on that possibility. This is purely speculative on my part. Persons with HIV tend to be more sedentary, perhaps smoke cigarettes more, is diet worse in terms of fats?, do they take more adjunctive drug therapy & does this contribute to perhaps increasing cancer risk?.....Or, is HIV and/or a low CD4 count a contributing factor......How does the risk for cancer in HIV relate to "when to begin HIV therapy". In addition to the many real considerations discussed at length relating to the question of when to begin therapy, is delaying initiation of HAART until CD4s are low, perhaps <350, or perhaps when viral load is >50,000, contribute to the risk for developing cancer. We do not have answers to these questions.
Trends in the Occurrence of Cancer in HIV-Infected Patients in the Era of Highly Active Antiretroviral Therapy (HAART). Abstract I-248
Instituto de Salud Carlos III, Madrid, Spain
Background: The introduction of HAART has led to dramatic reductions in the incidence of some AIDS-related tumors, while the incidence of other malignancies seems to remain unchanged or to be on the rise.
Methods: Patients with a diagnosis of cancer were retrospectively identified among all HIV+ subjects seen at a reference HIV-Hospital between 1996 and 2000. The cumulated incidence of malignancies was calculated for every year: number of tumors diagnosed/number of HIV+ subjects attended in a certain year. Age, HIV risk factor, CD4+ and use of HAART were recorded.
Results: 75 malignancies were identified. The HIV factor of patients was as follows: IVDU 27 (40%), homosex. 28 (41%), heterosex. 13 (19%). The male/female ratio was 48/21. Mean (range) age and CD4 counts were 39 (23-64) and 323 (7-1111) respectively. Table shows the number of cases and cumulate incidence (in brackets) by year of diagnosis and type of tumor. Non-Hodgkin (NHL) and Hodgkin (HL) lymphomas were significantly associated with lower CD4 counts regardless the use of HAART (p=0.02). Age was higher for subjects with hepatocarcinoma (HCC) (p=0.01).
  Conclusions: Malignancies are gaining importance over opportunistic infections among the HIV+ population during the HAART era. Most tumors were diagnosed in patients with relatively preserved immunity and predominantly in prior IVDU or homosexual men. While the incidence of KS and NLH is decreasing, HCC and other non-AIDS defining tumors are expected to become more frequent with the increase in life span of HIV+ patients.
Total Cancer Incidence Among HIV+ Veterans Relative to the General Population. Abstract: I-249
VA Pittsburgh Center for Health Services Research, Pittsburgh, PA
Background: As people with HIV are living longer on treatment, there has been growing concern that they may be at substantially increased risk for cancer. To examine current cancer patterns in HIV+ persons, we compared cancer incidence among a cohort of HIV+ veterans enrolled in the Veterans with HIV/AIDS Cohort Study (VACS) to cancer incidence in the general population using the Surveillance, Epidemiology, and End Results (SEER) Cancer Incidence Public-Use Database, 1973-1997.
Methods: The 868 HIV+ male veterans were used in this initial analysis. Using ICD-9 diagnosis codes assigned in the Veterans Affairs electronic medical records we calculated observed cancer incidence rates (IRs) for these HIV+ veterans from January 1998 to December 1999. Using 1996 and 1997 SEER data, the most recent two-year interval available, age-adjusted cancer IRS were calculated for males ages 25-84. Poisson regression was used to calculate age-adjusted VACS to SEER rate ratios for specific and total cancers with 95% confidence intervals.
Results: Oral cavity and pharnyx (oral), digestive system, respiratory system, skin, male genital system, ill-defined, and total cancers were compared. Each of these age-adjusted cancer IRS occurred among HIV+ veterans in statistically significant excess over the general population: oral (RR = 9.41; CI = 3.5-25.1; p-value <.001), digestive (RR = 2.63; CI = 1.1-6.3; p-value = 0.030), respiratory (RR = 3.1; CI = 1.3-7.5; p-value = 0.011), skin (RR = 13.2; CI = 7.3-23.9; p-value < 0.001), male genital (RR = 2.9; CI = 1.5-5.8; p-value = 0.002), ill-defined (RR = 30.8; CI = 13.8-68.6; p-value <.001), and total (RR = 4.8; CI = 3.6-6.4; p-value <0.001).
Conclusions: For all categories compared age-adjusted cancer rates were elevated among HIV+ veterans compared to the general population. While some of this may be explained by differences in lifestyle and other exposures, the magnitude of risk suggests that HIV or its treatment may put individuals at greater risk for subsequent cancer.
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