African Enigma Research Articles

African enigma: key player in human immunodeficiency virus pathogenesis in developing countries?

Recent data ([10][1]) show that enteric helminthic infections result in the secretion of type 2 cytokines (interleukin-4 [IL-4], IL-5, IL-6, IL-10) and a type 1-to-type 2 shift in cytokine profiles. The predominant production of type 2 cytokines is associated with a reduced incidence of gastritis

Reply to "The 'African enigma' - another explanation"

Reply to "The 'African enigma' - another explanation"

Solving the African enigma: Parasites may have their place

GASTROENTEROLOGY 2000;119:611

Helicobacter pylori gastritis in Africa.

* Helicobacter pylori gastritis progresses to gland loss and intestinal metaplasia in a considerable proportion of colonized subjects. * The progression to atrophic gastritis is a slow process, occurring with an incidence of 1-2% per year. * The progression of chronic H. pylori gastritis is the same in Africa as in Europe and South America. * This supports the concept of H. pylori as a causative factor of pre-neoplastic conditions of the gastric mucosa; other factors must play a modulating role in the progression to cancer. H. pylori gastritis may progress to atrophic gastritis and lead to the development of intestinal metaplasia, dysplasia and eventually gastric cancer in a minority of subjects. The available data on the kinetics of H. pylori gastritis are limited, but nevertheless very consistent. They suggest that the progression to gland loss or atrophic gastritis among H. pylori-positive subjects occurs at a rate of 1-2% per year. As H. pylori gastritis usually persists for life, a considerable proportion of H. pylori-positive subjects thus eventually show signs of gastric gland loss. The majority of these subjects progress to intestinal metaplasia. Despite these consistent findings in different areas of the world, the incidence of gastric cancer is only moderately related to the prevalence of H. pylori. An example is the so-called African enigma, referring to a low incidence of gastric cancer in certain countries of Africa, despite a high prevalence of H. pylori in all age groups. This is not due to differences in progression to atrophic gastritis; other yet unidentified factors therefore must play a role.

The African Pipit enigma

The African Pipit enigma

THE AFRICAN ENIGMA: ANALYSIS OF THE HOST RESPONSE TOHELICOBACTER PYLORI INFECTION

121 Despite the almost ubiquitous nature of H.pylori infection in Africa there is surprisingly little peptic ulcer disease and gastric carcinoma, diseases now thought to be closely linked to such infection in the West and Far East. It is not known whether such geographical variations are due to infection with organisms of different pathogenicity or to dissimilarities in the host response. The aim of this study was to provide more detail on the gastric mucosal and serological response toH.pylori infection in the Gambia. Children with diarrhoea and malnutrition (n=24; age range 3mo-11yrs [mean age 20 mo]) and adults with dyspesia (n=11; age range 18-70 yrs [mean age 37yrs]) were eligible for entry into the study. Subjects underwent multiple gastric mucosal biopsy for histological and microbiological analysis. Western blotting was used to identify antibodies to the cytotoxin-Associated Gene A (CagA) and anti-H.pylori IgG antibodies. Gastric infection with H.pylori was common with 54% (13/24) of the children and 64% (7/11) of adults positive on either histology or culture. Using the Houston Classification of gastritis, 19/20 infected cases were suitable for analysis. A striking finding was the complete absence of an acute inflammatory response in 74% (14/19) cases and only a mild response in 3/19 and moderate response in 2/19 cases. There were no cases of severe acute inflammation and no instances of intestinal metaplasia. Similarily, gastric atrophy was observed less commonly that is reported in cases of H.pylori infection in the West and was seen in only 15% (3/19) cases. Despite the relatively mild histological responses toH.pylori infection all those with proven infection had evidence of exposure to virulent CagA-positive strains of the bacterium. This study suggests that it is differences in the host response to H.pylori rather than infection with less virulent organisms that account for the African enigma.