RESEARCH Table 4. Univariate analysis of risk factors for resistance to >1 antimicrobial agent among Helicobacter pylori isolates submitted to HARP, 1998–2002a Proportion of patients harboring resistant H. pylori isolate Risk factor Exposed, no. (%) Unexposed, no. (%) Odds ratio (95% CI) Zantac use 12 mo before EGD 25 (48) 89 (32) 2.0 (1.1–3.6)b Tums use 12 mo before EGD 19 (51) 95 (32) 2.2 (1.1–4.4)b Tums use 30 d before EGD 12 (55) 102 (33) 2.4 (>1.0–5.8)b Mylanta use 12 mo before EGD 4 (15) 110 (36) 0.3 (0.1–1.0) Took antibiotic 12 mo before EGD 29 (43) 68 (34) 1.5 (0.9–2.6) Past treatment of H. pylori infection with PPI 5 (71) 109 (34) 4.9 (1.0–26) Clarithromycin 5 (83) 109 (33) 9.9 (1.1–86) Treatment for H. pylori a second time in the past 5 years 11 (65) 107 (32) 3.8 (1.4–11) Treatment of H. pylori infection more than once with PPI 8 (80) 106 (33) 8.1 (1.7–39) Clarithromycin 8 (80) 106 (33) 8.1 (1.7–39) Age >57 years 50 (31) 68 (37) 0.8 (0.5–1.2) Race/ethnicity Black 67 (39) 51 (29) 1.6 (1.0–2.4) Hispanic 2 (11) 116 (35) 0.2 (0.1–1.0) Male sex 65 (31) 47 (42) 0.6 (0.4–1.0) HARP site New York, NY 3 (14) 115 (35) 0.3 (0.1–1.0) Palo Alto, CA 4 (17) 114 (35) 0.4 (0.1–1.1) Atlanta, GA 8 (22) 110 (36) 0.5 (0.2–1.1) Nashville, TN 11 (24) 107 (35) 0.6 (0.3–1.2) aN = 347; HARP, Helicobacter pylori Antimicrobial Resistance Monitoring Project; EGD, esophagogastro -duodenal endoscopy; PPI, proton pump inhibitor; CI, confidence interval. bThese risk factors were not considered for multiv ariate analysis because of small cell -size differences between subjects with a resistant H. pylori infection and those without. variate analysis. In the first-phase, multivariate model, antimicrobial resistance was significantly associated with previous antimicrobial treatment for H. pylori, and antacid use was protective. However, in this model, geographic location was highly collinear with race, which necessitated the second-phase multivariate model, in which the contri- bution of race was assessed by conditioning on geographic location, previous antimicrobial treatment for H. pylori infection, and antacid use. This model clearly demonstrated an association between black race and infection with an antimicrobial-resistant H. pylori. This association may indi- cate persistent transmission of resistant strains or in vivo induction of resistance. The association between H. pylori infection and blacks in the United States has been amply documented (2,3). However, the association between inci- dence of H. pylori resistance and black race is new. The biologically plausible association between previous antimi- crobial use and resistance approached significance in the second-phase model; however, many study participants could not recall whether they were previously treated. This model does not rule out an independent association between geographic location and resistance. Enrollment of additional participants in HARP may sufficiently enhance the statistical power of the study to show such an associa- tion, while enrollment in sites serving a more racially diverse population may help clarify the contributions of geographic location as a risk factor for resistant infection. This study has several limitations. While drawn from various regions in the continental United States, the 11 HARP sites represent a convenience sample of academic medical centers that is not truly representative of the U.S. population. Some participating sites enrolled more patients per month than others, so that cumulative data are biased towards individual study sites. Most of the participating hospital sites serve adult populations, and thus the results largely reflect resistance incidence towards adult patients. Patients undergoing endoscopy for H. pylori-related illness constitute a minority of infected persons, whose clinical condition and H. pylori-resistance status may not be repre- sentative of the total population with underlying H. pylori infection. Although this trend has not been documented, Table 5. Phase I multivariate analysis of risk factors for resistance to >1 antimicrobial agent among H. pylori isolates submitted to HARP, 1998–2002a Exposure Odds ratio (95% CI) Patient treated another time for infection 6.0 (2.0–20) Took Mylanta in last 12 mo 0.3 (0.1–0.8) HARP site New York, NY 0.2 (0.1–0.7) Palo Alto, CA 0.2 (0.1–0.7) Atlanta, GA 0.2 (0.1–0.6) Nashville, TN 0.4 (0.2–0.9) aN = 347; HARP, Helicobacter pylori Antimicrobial Resistance Monitoring Project; CI, confidence interval. 1092 Emerging Infectious Diseases • www.cdc.gov/eid • Vol. 10, No. 6, June 2004