Human T Lymphotropic Virus Type 1 Infection. Part 3
The cumulative incidence of gastric cancer was 1.1% during the first 5 years of follow‐up (1994–1998) and 3.0% during the entire (i.e., 10‐year) follow‐up period (1999–2003) in the HTLV‐1–positive group, compared with 2.7% and 8.0%, respectively, in the HTLV‐1–negative group. The incidence of gastric cancer in the HTLV‐1–positive group was lower than that in the HTLV‐1–negative group. Among men, the cumulative incidence of gastric cancer was 1.8% during the first 5 years of follow‐up and 4.8% during the overall follow‐up period in the HTLV‐1–positive group, compared with 4.6% and 11.1%, respectively, in the HTLV‐1–negative group. Among women, the cumulative incidence of gastric cancer was 0.7% for the 5‐year period and 1.9% for the 10‐year period in the HTLV‐1–positive group, compared with 1.7% and 6.1%, respectively, in the HTLV‐1–negative group.
The cumulative survival rate during the first 5 years of follow‐up among the 49 patients with gastric cancer was 28.6% (4 of 14 patients) in the HTLV‐1–positive group, compared with 34.3% (12 of 35 patients) in the HTLV‐1–negative group.
We found that the incidence of gastric cancer in the HTLV‐1–positive group was lower than that in the HTLV‐1–negative group. Iwata et al. reported that the hazard ratio associated with HTLV‐1 infection for death from all causes, excluding ATL, was 1.77 (95% CI, 0.93–3.37) for males and 1.87 (95% CI, 1.12–3.12) for females, although analysis of cause‐specific mortality revealed a significantly increased risk for nonneoplastic disease in each group. Arisawa et al. reported that HTLV‐1‐seropositivity was associated with increased mortality from all causes, excluding ATL (risk ratio [RR], 1.3; 95% CI, 1.0–1.7), and that HTLV‐1 infection was not associated with an increased risk of any cancer other than ATL, colorectal cancer, liver cancer, and lung cancer but was associated with a reduced risk of gastric cancer (RR, 0.42; 95% CI, 0.17–0.99). In addition, Asou et al. and Kozuru et al. reported that HTLV‐1 infection was associated with an increased risk of various cancers.
There is increasing evidence to suggest that gastric infection with H. pylori is a risk factor for gastric cancer. Stored serum samples collected from individuals without gastric cancer were tested for IgG antibodies to H. pylori by ELISA. The mean time between serum collection and diagnosis of gastric carcinoma was 14.2 years. Of the 109 patients with confirmed gastric cancer, 84% had been infected previously with H. pylori, compared with 61% of matched control subjects (OR, 3.6; 95% CI, 1.8–7.3). The Eurogast Study Group demonstrated a significant correlation between the gastric cancer mortality rate and the prevalence of H. pylori seropositivity. It can be predicted that mortality from gastric cancer in a population with a 100% prevalence of H. pylori infection would be 6 times that in a population with a 0% prevalence. The World Health Organization and the International Agency for Research on Cancer consensus group stated in 1994 that there was sufficient epidemiologic and histologic evidence to classify H. pylori as a definite carcinogen. In 1998 Huang et al. reported results of a meta‐analysis of the relationship between H. pylori seropositivity and gastric cancer, Asaka et al. and Kikuchi et al. reported an association between H. pylori infection and the development of gastric cancer, and in 2001 Uemura et al. reported that gastric cancer developed in 4.7% of persons infected with H. pylori but in no uninfected persons during a mean follow‐up duration of 7.8 years. It has thus become clear that H. pylori infection is associated with the development of gastric cancer.