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Oesophagus, stomach, duodenum II
PWE-189 Helicobacter Pylori, HIV and Gastric Hypochlorhydria in the malawian population
  1. J Geraghty1,
  2. A Thumbs2,
  3. A Kankwatira3,
  4. T Andrews4,
  5. A Moore5,
  6. R Malamba6,
  7. N Mtunthama6,
  8. K Hellberg2,
  9. L Kalongolera2,
  10. S Sarkar5,
  11. P O’Toole5,
  12. A Varro7,
  13. DM Pritchard5,8,
  14. M Gordon5,6,9
  1. 1Gastroenterology, Manchester Royal Infirmary, Manchester, UK
  2. 2Surgery
  3. 3Medicine, Queen Elizabeth Central Hospital, Blantyre, Malawi
  4. 4Pathology, Royal Liverpool University Hospital, Liverpool
  5. 5Gastroenterology, Royal Liverpool University Hospital, Liverpool, UK
  6. 6Malawi-Liverpool-Wellcome Trust Clinical Research Programme, Queen Elizabeth Central Hospital, Blantyre, Malawi
  7. 7Cellular and Molecular Physiology
  8. 8Gastroenterology, Institute of Translational Medicine
  9. 9Department of Clinical Infection, Microbiology and Immunology, Institute of Infection and Global Health, University of Liverpool, Liverpool, UK

Abstract

Introduction HIV and Helicobacter pylori are common chronic infections in sub-Saharan Africa. Both conditions can predispose to gastric hypochlorhydria that may be a risk factor for enteric infections and reduced drug absorption. We have investigated to what extent HIV and H. pylori infections are associated with hypochlorhydria in a Malawian cohort of patients undergoing endoscopy.

Method 104 sequential symptomatic adults referred for gastroscopy at Queen Elizabeth Central Hospital, Blantyre, Malawi, had blood taken for rapid HIV testing and fasting serum gastrin analysis. Gastric fluid was aspirated for pH testing, and gastric biopsies were taken.

Results After 9/104 HIV-infected patients who were already established on antiretroviral therapy were excluded, 17/95 (25.0%) were seropositive for untreated HIV, and 68/95 (71.6%) patients were H. pylori positive by histology. Hypochlorhydria (fasting gastric pH >4.0) was present in 55.8% (53/95) of patients. H. pylori infection was significantly associated with hypochlorhydria (OR 2.91, [1.02–7.75], p = 0.046). While single infection with HIV was not significantly independently associated with hypochlorhydria. H. pylori and HIV co-infection was more strongly associated with hypochlorhydria (OR 6.25, [1.33–29.43], p = 0.020) than either infection alone, suggesting an additive effect of co-infection. HIV infection was associated with higher serum gastrin levels (91.3pM vs. 53.1pM, p = 0.040), while H. pylori infection was not (63.1pM vs. 55.1pM, p = 0.610). Irrespective of H. pylori and HIV status, most patients (>90%) exhibited pangastritis. Only three patients had histological evidence of gastric atrophy, of which only one was HIV-infected.

Conclusion H. pylori infection was associated with fasting hypochlorhydria, while HIV was not independently associated. HIV and H. pylori co-infection, however, was more strongly associated with hypochlorhydria than H. pylori infection alone. The mechanism of this apparent additive effect between HIV and H. pylori remains unclear, but appears to be related to chronic pangastritis rather than gastric atrophy, and associated with hypergastrinaemia in HIV-infected individuals.

Disclosure of interest None Declared.

https://doi.org/10.1136/gutjnl-2015-309861.636

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