Violet Kayamba Tropical Gastroenterology & Nutrition group, Department of Internal Medicine, PO Box 50398, Nationalist Road, Lusaka, Zambia. Julia Butt Infection and Cancer Epidemiology Group, German Cancer Research Center (DKFZ), Heidelberg, Germany Matthew Gordon Varga Department of Epidemiology, UNC Gillings School of Global Public Health and the Lineberger Comprehensive Cancer Center, 3207B Michael Hooker Research Center, Chapel Hill, NC 27599 USA. Aaron Shibemba University Teaching Hospital, Department of Pathology, Private Bag RW IX, Nationalist Road, Lusaka, Zambia Maria Blanca Piazuelo Department of Medicine, Division of Gastroenterology, Hepatology and Nutrition, Vanderbilt University Medical Center, Nashville, 37232, Tennessee, USA Keith Turker Wilson Veterans Affairs Tennessee Valley Healthcare System, Nashville, 37212, Tennessee, USA Kanekwa Zyambo Tropical Gastroenterology & Nutrition group, Department of Internal Medicine, PO Box 50398, Nationalist Road, Lusaka, Zambia Simutanyi Mwakamui Tropical Gastroenterology & Nutrition group, Department of Internal Medicine, PO Box 50398, Nationalist Road, Lusaka, Zambia Chola Mulenga Tropical Gastroenterology & Nutrition group, Department of Internal Medicine, PO Box 50398, Nationalist Road, Lusaka, Zambia Tim Waterboer Infection and Cancer Epidemiology Group, German Cancer Research Center (DKFZ), Heidelberg, Germany Meira Epplein Cancer Risk, Detection, and Interception Program, Duke Cancer Institute, and Department of Population Health Sciences, Duke University, Durham, North Carolina, USA Douglas Corbett Heimburger Vanderbilt Institute of Global Health, Vanderbilt Medical Center, 2525 West End Avenue, Suite 750, Nashville, 37203, Tennessee, USA. Masharip Atadzhanov Vanderbilt Institute of Global Health, Vanderbilt Medical Center, 2525 West End Avenue, Suite 750, Nashville, 37203, Tennessee, USA Paul Kelly Tropical Gastroenterology & Nutrition group, Department of Internal Medicine, PO Box 50398, Nationalist Road, Lusaka, Zambia

Keywords: Gastric cancer; Helicobacter pylori; Zambia

Abstract

Introduction
Little is known about specific bacterial characteristics of Helicobacter pylori (H. pylori) infection influencing gastric carcinogenesis in Zambia. The aim of this study was to evaluate the associations between pre-selected H. pylori antibodies with gastric cancer, premalignant lesions and active gastritis.
Methods
This was cross-sectional study with multiple comparisons of patients with gastric cancer (GC), gastric premalignant (GP) lesions and active or chronic gastritis. A fluorescent bead-based antibody multiplex serology assay was used to quantify antibodies to thirteen immunogenic H. pylori antigens. Logistic regression models were used to examine the associations.
Results
Included were 295 patients with: 59 GC, 27 GP lesions, 48 active and 161 chronic gastritis. Overall, 257/295 (87%) were H. pylori positive. H. pylori seropositivity was not associated with sex, age, body mass index, socio-economic status, HIV infection, alcohol consumption or cigarette smoking (p-values all above 0.05). When compared to the patients with chronic gastritis, the presence of catalase and cinnamyl alcohol dehydrogenase (Cad) antibodies was positively associated with GP lesions (OR 3.53; 95% CI 1.52-8.17 and OR 2.47; 95% CI 1.08-5.67 respectively). However, seropositivity to Cad antibodies was significantly lower in GC patients (OR 0.28; 95% CI 0.09-0.83). Compared to chronic, active gastritis was significantly associated with (p<0.05) H. pylori sero-positivity (OR 9.46; 95% CI 1.25-71.52) and specific antibodies including cytotoxin-associated gene A, vacuolating cytotoxin A, Helicobacter cysteine-rich protein C, hypothetical protein HP0305 and outer membrane protein HP1564.
Conclusions
Among Zambian patients seen at a single center, antibodies to H. pylori (CagA, VacA, Omp, HcpC, HP0305 and HpaA) were associated
with active gastritis.

Section

Original Research

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