The primary lung cancer patients identified in the HIV-AIDS cohort were characterized by early age at diagnosis. The median age at the time of primary lung cancer diagnosis was 49 years. This is in contrast to the general U S population, where the median age at lung cancer diagnosis is 68 years. Most primary lung cancers were identified in young white (66.7%) and African-American men (27.8%). The occurrence of lung cancer in primarily young men is consistent with the observations of multiple other investigators. However, we share the concern of Sridhar et al that as the incidence of both lung cancer and HIV continue to rise in women, more cases of HIV-associated lung cancer will be observed in young women over the next several years.
Homosexual-bisexual men and IV drug users comprised the mode of HIV transmission in approximately 80.5% of the primary lung carcinoma patients in the cohort. Similar demography has been observed by other investigators.
In accord with many other studies, all of the major histologic cell types of primary lung carcinoma were observed (Table 6). Likewise, adenocarcinoma was the most frequently observed histology (11.8%). However, nine cases (11.8%) were non-small cell carcinomas, not otherwise specified. Thus, the frequency of histologic subgroups may actually be slightly different than illustrated in Table 6 based on the true cellularity of these nine cases.
Fishman et al reported that 60% of the 30 HIV-positive patients with proven bronchogenic carcinoma in their series had a history of pulmonary tuberculosis, PCP, or both. OIs were seen in a smaller percentage of our primary lung cancer patients (47.2%). Not unexpectedly, PCP was the most frequently observed infection (27.7%). None of the OIs in our study were diagnosed in statistically higher numbers in the primary lung carcinoma group as compared to the total cohort.
This study clearly indicates that HIV-AIDS patients have a statistically increased risk of primary lung cancer. The underlying biological mechanism responsible remains to be elucidated. Many theories have been proposed. It is well known that normal pulmonary immunologic surveillance is impaired in HIV-infected patients. Rook et al have documented depressed natural killer cell activity in HIV-positive patients. Alteration in natural killer cell activity may allow unchecked proliferation of spontaneously developing tumor cells. Others advocate the HIV virus may stimulate the release of aberrant growth factors resulting in oncogenesis. CD4 counts were inconsistently available in our HIV-AIDS cohort. However, other investigators have reported counts ranging between 13 and 500 cells per cubic millimeter in infected lung cancer patients and no direct correlation has been made conclusively 21,28-30,39 Interestingly, HIV causes hyperplasia of epidermal cells. This has been postulated as a possible cause for the increased incidence of invasive cervical carcinoma, and possibly that of the oral cavity and anorectum. However, this does not help to explain the increased incidence of adenocarcinoma.
Table 6—Reported Cases of Lung Cancer in HIV-AIDS Patients

Source, yr Lung Cancer Cell Type
Irwin et al, 1984 1
Moser et al, 1985 1
Nusbaum, 1985 1
Tirelli et al, 1988 1
Monfardini et al, 1989 4 1 2 1
Braun et al, 1990 4 1 1
Nguyen et al, 1991 1
Gachupin-Garcia and Selwyn, 1991 2
Sridhar et al, 1992 8 6 1 2 1 1
Karp et al, 1993 7
Vaccher et al, 1993 11 2 1 1 3 2
Tenholder and Jackson, 1993 1 1
Toi and Myers, 1993 2
Aaron et al, 1994 1 2
Gruden et al, 1995 4 4 1 2 1 1
Cone et al, 1995 3
Mady, 1995 1
White et al, 1995f 20 3
Fishman et al, 1995* 13 9 2 2 1 2 1
Barchielli et al, 1995 4*
Ferrozzi et al, 1996 2
Present study, 1996 7 7 2 3 9 3 1 4