Successful H. pylori treatment requires the knowledge of local antimicrobial resistance. Data on the efficacy of H. pylori eradication regimens available in sub-Saharan Africa are scant, hence the optimal treatment is unknown. Our goals were to determine the efficacy of available regimens in Rwanda as well as evaluate the effect of treatment on health-related quality of life (HRQoL) in patients undergoing esophagogastroduodenoscopy.

This is a randomized controlled trial conducted from November 2015 to October 2016 at a tertiary hospital in Rwanda. Enrollees were 299 patients (35% male, age 42 ± 16 years (mean ± SD)) who had a positive modified rapid urease test on endoscopic biopsies. After a fecal antigen test (FAT) and HRQoL assessment by the Short Form Nepean Dyspepsia Index (SF-NDI) questionnaire, patients were randomized 1:1:1:1 to either a triple therapy combining omeprazole, amoxicillin and one of clarithromycin/ciprofloxacin/metronidazole or a quadruple therapy combining omeprazole, amoxicillin, ciprofloxacin and doxycycline. All therapies were given for a duration of 10 days. The outcome measures were the persistence of positive FAT (treatment failure) 4 to 6 weeks after treatment and change in HRQoL scores.

The treatment success rate was 80% in the total population and 78% in patients with a history of prior triple therapy. Significant improvement in HRQoL in the total group (HRQoL mean scores before and after treatment respectively: 76 ± 11 and 32 ± 11, p < 0.001) and the group with functional dyspepsia (HRQoL mean scores before and after treatment respectively: 73 ± 11 and 30 ± 9, P < 0.001) was observed across all treatment groups. Using clarithromycin based triple therapy (standard of care) as a reference, the group treated with metronidazole had worse HRQoL (p = 0.012) and had a trend towards worse treatment outcome (p = 0.086) compared to the ciprofloxacin based combination therapies.

Clarithromycin and ciprofloxacin based combination therapies are effective and safe to use alternatively for H. pylori eradication and improve HRQoL. Among the regimens studied, metronidazole based triple therapy is likely to be clinically inferior.

The clinical trial was retrospectively registered ( PACTR201804003257400 ) with the Pan African Clinical Trial Registry database, on April 6th, 2018 in South Africa.

The probiotic Lactobacillus rhamnosus GG (LGG) can play a role in establishing a harmless relationship with Helicobacter pylori and reduce gastric pathology in East African populations. H. pylori has the ability to inhabit the surface of the mucous layer of the human stomach and duodenum. In the developing world, an estimated 51% of the population is carrier of H. pylori, while in some Western countries these numbers dropped below 20%, which is probably associated with improved sanitation and smaller family sizes. Colonization by H. pylori can be followed by inflammation of the gastric mucus layer, and is a risk factor in the development of atrophic gastritis, peptic ulcers and gastric cancer. Notwithstanding the higher prevalence of H. pylori carriers in developing countries, no equal overall increase in gastric pathology is found. This has been attributed to a less pro-inflammatory immune response to H. pylori in African compared to Caucasian populations. In addition, a relatively low exposure to other risk factors in certain African populations may play a role, including the use of non-steroidal anti-inflammatory drugs, smoking, and diets without certain protective factors. A novel approach to the reduction of H. pylori associated gastric pathology is found in the administration of the probiotic bacterium Lactobacillus rhamnosus yoba 2012 (LRY), the generic variant of LGG. This gastro-intestinal isolate inhibits H. pylori by competition for substrate and binding sites as well as production of antimicrobial compounds such as lactic acid. In addition, it attenuates the host's H. pylori-induced apoptosis and inflammation responses and stimulates angiogenesis in the gastric and duodenal epithelium. The probiotic LRY is not able to eradicate H. pylori completely, but its co-supplementation in antibiotic eradication therapy has been shown to relieve side effects of this therapy. In Uganda, unlike other African countries, gastric pathology is relatively common, presumably resulting from the lack of dietary protective factors in the traditional diet. Supplementation with LRY through local production of probiotic yogurt, could be a solution to establish a harmless relationship with H. pylori and reduce gastric pathology and subsequent eradication therapy treatment.

The study was undertaken to document the prevalence of Helicobacter pylori and endoscopic diagnoses in Rwandans presenting for gastroscopy.

We studied an endoscopic database containing 961 consecutive gastroscopy patients at the University Teaching Hospital, Butare, over 12 months. Patient characteristics, endoscopic diagnoses and H. pylori status (by modified rapid urease testing) were analysed.

The overall H. pylori positivity rate was 75% (n=825), similar to that found elsewhere in sub-Saharan Africa. Common endoscopic diagnoses included duodenal ulceration (20%), duodenitis (9%), benign gastric outlet obstruction (6%) and malignancy (5%). Duodenal ulceration was strongly associated with H. pylori infection (OR 6.2 [3.1-12.6]; p<0.001).

The facts that H pylori infection is commoner in duodenal ulcer (DU) patients than in the normal population, and that eradication results in most cases being cured, have led to the belief that it causes DU. However, early cases of DU are less likely than established ones to be infected. H pylori-negative cases are usually ascribed to specific associated factors such as non-steroidal anti-inflammatory drugs (NSAIDs), Crohn's disease, and hypergastrinaemia, but even after excluding these, several H pylori-negative cases remain and are particularly common in areas of low prevalence of H pylori infection. Moreover, this incidence of H pylori negative DU is not associated with a fall in overall DU prevalence when compared with countries with a higher H pylori prevalence. In countries with a high H pylori prevalence there are regional differences in DU prevalence, but no evidence of an overall higher prevalence of DU than in countries with a low H pylori prevalence. There is no evidence that virulence factors are predictive of clinical outcome. After healing following eradication of H pylori infection DU can still recur. Medical or surgical measures to reduce acid output can lead to long-term healing despite persistence of H pylori infection. Up to half of cases of acute DU perforation are H pylori negative. These findings lead to the conclusion that H pylori infection does not itself cause DU, but leads to resistance to healing, i.e., chronicity. This conclusion is shown not to be incompatible with the universally high prevalence of DU compared with controls.

Study the pathological changes in gastric mucosa of Nyarwanda, Nkole (both with high prevalence of stomach cancer) and Ganda (with low prevalence of this cancer) ethnic groups in the presence of Helicobacter pylori (H. pylori) infection.

Do pathological changes accompanying H. pylori infection explain the varying prevalence of stomach cancer in these populations?

Retrospective cross sectional study.

A total of 114 patients of the above ethnic groups with upper gastrointestinal symptoms who underwent endoscopic biopsy examination between January 1996 and June 2002 formed the basis of this study.

The severity of gastritis correlated with the presence of H. Pylori in Ganda and Nyarwanda but not in Nkole. Intestinal metaplasia (IM) was observed in Nyarwanda and Nkole and in some of these cases there was H. pylori. Gastric atrophy (GA) was also commonly observed in Nkole and Nyarwanda and H. pylori was detected more in the severe form of GA. Lymphoid follicle formation was not associated with H. pylori infection in all study groups.

The major histological features relating stomach cancer to H. pylori in this study were presence of the infection in IM and GA that was observed mainly in Nyarwanda and Nkole. The lack of association between presence of lymphoid follicle and H. pylori infection probably explains the rarity of MALT lymphoma in Africa as these tumours are said to arise from H. pylori associated lymphoid follicles.

The African enigma describes the dissociation between the prevalence of Helicobacter pylori infection and H. pylori-related diseases. The aim of this study was to use an evidence-based review of endoscopic data from African countries to test whether there are data to support the concept of an African enigma.

A Medline search was carried out to identify prospective endoscopic studies in African populations. Data collected included: the number of endoscopies, age range (or mean age if available), indications for endoscopy, country, years during which data were collected, male to female ratio, and specific outcome of duodenal ulcer, gastric ulcer, or gastric cancer.

Forty prospective endoscopic studies from 17 African countries were identified (20,531 patients) and evaluated between 1972 and 2001. Mean ages ranged from 31 to 53.1 years and male to female ratios from 0.67:1 to 4.64:1. H. pylori-related clinical outcomes were common; duodenal ulcers in 4326 patients (21.1%), gastric ulcers in 691 patients (3.4%), and gastric cancers in 503 patients (2.4%).

Prospective upper endoscopic trials suggest that the clinical outcomes associated with H. pylori infection in Africa are similar to those seen in industrialized countries. No dissociation between the prevalence of H. pylori infection and H. pylori-related diseases existed; the African enigma as such does not exist and the continued study of the mechanism of a non-existent phenomenon is a misuse of resources. The myth resulted from reliance on anecdotal data and selection bias in populations with extremely limited access to health care and a relatively short life expectancy.

We conducted a retrospective literature review of all the data published on Helicobacter pylori in Africa in order to test whether the prevalence of diseases associated with this organism differs from that in developed nations.

Both sero-epidemiological (n = 8) as well as prospective endoscopic studies in subjects with either dyspepsia or epigastric pain (n = 23) and one retrospective study were available for analysis.

Sero-epidemiology confirmed both the early age of acquisition in children (50% by 10 years) as well as the high prevalence of the organism (61%) in adult asymptomatic individuals. Endoscopic studies in dyspeptic individuals revealed the presence of the organism in 72%. Duodenal ulceration was noted in 26% of 3473 cases and in these, H. pylori was present in 90%. An association of gastric metaplasia with duodenal ulceration was identified in the one study in which it was investigated. Gastric ulceration occurred approximately four-fold less frequently (7% of 2286 cases) than duodenal ulceration and the organism was evident in 75% of the gastric ulceration cases. Findings of intestinal metaplasia (14%) and gastric cancer (3.4%) were not infrequent, but the paucity of accurate epidemiological data made it difficult to establish a correlation between the two.

It would appear that prospective endoscopic-based studies in African subjects may question the standard dogma of a low prevalence of H. pylori-associated diseases in Africa. Further research is clearly required.

Helicobacter pylori is the aetiological agent of chronic gastritis and a major causative factor in duodenal and gastric peptic ulcer disease; a strong association also exists with gastric cancer and primary gastric lymphoma. The prevalence of infection in adults ranges from less than 15% in developed countries to virtually 100% in less developed areas. If H. pylori infection alone was responsible for the development of gastritis, peptic ulcer disease, gastric carcinoma and primary gastric lymphoma, one would expect the frequency of all these conditions to parallel closely the prevalence of H. pylori infection. This is clearly not the case: therefore, genetic, environmental and cultural factors must act in concert with H. pylori to induce different outcomes of the infection. This paper outlines the geographic approach to the study of disease and discusses the possible application of this methodology to the inquiry into the relationship between H. pylori, atrophic gastritis and gastric cancer. Preliminary results of a study showing great variation in the prevalence of intestinal metaplasia in duodenal ulcer patients from different geographic origin are presented and briefly discussed.

The decision to treat a patient should in general always be based on potential risk and advantage. Widespread and uncontrolled use of all kinds of anti-H. pylori regimens may promote development of antimicrobial resistant strains. In particular, antimicrobial monotherapy is associated with failure to eradicate H. pylori and induction of resistant strains. Polychemotherapy is much more effective and has a lower risk for development of antimicrobial resistant H. pylori strains but carries the risk of significant drug-related side effects. If the prescribed anti-H. pylori regimen is not effective in at least 80%, or if the patient is not compliant, this type of therapy should not be considered. Also if reinfection is to be expected, the risk may outweigh potential benefits (Graham, 1993). Guidelines published in 1990 by an international working party during the World Congress of Gastroenterology recommended H. pylori eradication only in patients where duodenal ulcer was a serious management problem requiring lifelong maintenance therapy, and in whom complications (bleeding, perforation) had occurred or surgery was considered (Tytgat et al, 1990). Recently less stringent guidelines were recommended. A National Institutes of Health (NIH) Consensus Development Conference has recommended that all patients with gastric or duodenal ulcer who are H. pylori infected should be treated with antimicrobials including patients presenting with an ulcer for the first time. In addition, patients on maintenance antisecretory medication should also be contacted and treated for H. pylori infection (Anonymous, 1994). The ulcer relapse rate during prolonged follow-up after H. pylori eradication is very low. Despite this, it is advised that antisecretory medication is continued after successful H. pylori eradication in patients with previous ulcer complications. In all other patients maintenance antisecretory medication can be stopped after successful eradication. It is not known whether H. pylori eradication lowers the risk of NSAID-induced ulceration or whether the risk of ulcer complications is reduced.

Gastric Helicobacter pylori infection is common throughout the tropics yet does not always correlate with the incidence of serious upper gastrointestinal pathology. In a consecutive series of 213 patients examined by gastroscopy for dyspepsia in northern Nigeria, 176 (92%) of 193 with acceptable biopsies had gastritis. Only 16 (8%) had a histologically normal gastric mucosa. H. pylori was present in 161 of 192 patients (84%); 31/41 (75%) with chronic gastritis and 130/135 (96%) with active gastritis. Serious pathology, ulcer and gastric cancer were present in only 29 (14%).

The spiral organism Helicobacter pylori has been causally implicated in the genesis of various gastroduodenal diseases. Since these diseases are common in southern India, this study was undertaken to determine the prevalence of H. pylori in the gastric mucosa of asymptomatic adults and patients with various gastroduodenal diseases. H. pylori was detected in the gastric mucosa of 25 of 30 (83.3%) normal volunteers. Prevalence rates in the disease groups were also high, and included 38 of 41 patients with duodenal ulcer (92.6%), 13/16 with gastric ulcer (81.3%), and 85/119 subjects (71.4%) with non-ulcer dyspepsia. Light microscopic examination of the gastric mucosa provided the best method of detecting H. pylori. H. pylori colonization was significantly associated with histological abnormalities, mainly chronic atrophic gastritis (147) and superficial gastritis (11), while only three of 161 H. pylori positive patients had histologically normal antral mucosa. Ultrastructural examination revealed changes in the apical complex of the gastric mucosal cells in response to bacterial adhesion, with mucus depletion and cellular damage. Bacteria were also noted disrupting the tight junctions and entering the intercellular spaces. The high prevalence of H. pylori infection may explain the high incidence of gastritis, duodenal ulceration and gastric carcinoma in this population. However, in this population, the prevalence of infection in asymptomatic individuals was nearly as high as that in duodenal ulcer, underlining the need for further study to identify the differences in host response or bacterial pathogenicity that lead to the development of ulcer in only some individuals.

The frequency of Helicobacter pylori (HP) infection in 208 patients with upper gastrointestinal tract symptoms from the Southern Province of Saudi Arabia was studied prospectively. The occurrence of HP was documented histologically and using a rapid urease test in antral endoscopic biopsies. Our results showed that 82.2% of the 208 patients included were positive for HP with a male:female ratio of approximately 1:1 (88:83). The age range was 14 to 80 years and the median age was 38.2 years. The frequencies of HP infection among Saudi and non-Saudi patients were 86% and 71%, respectively. Frequencies of HP infection were 88%, 77.5%, and 93% during the second, third, and fourth decades of life. Among the 140 patients with histologically proven antral gastritis, 128 cases (91%) were positive for HP whereas 29 cases (17%) of the 171 patients positive for HP did not show histologic evidence of antral gastritis. Our data showed that HP was present in 92.5% of patients with endoscopic diagnosis of duodenal ulceration, 81% of patients with duodenitis, 80% of patients with both duodenitis and gastritis, 69% of patients with gastric antral erythema, and 81% of patients with non-ulcer dyspepsia (normal upper gastrointestinal endoscopy). Histologically proven antral gastritis was seen in 80% of patients with endoscopic diagnosis of duodenal ulceration, 76% of patients with antral erythema, 70% of patients with both duodenitis and gastritis, 33% of patients with duodenitis only, and 66% of patients with non-ulcer dyspepsia. Among the 208 patients included in the study, gastric ulcerationw as only seen in two cases, both positive for HP.

Helicobacter pylori infection is common in northern Nigeria, but the age of acquisition is unknown. In a prospective study, immunoglobulin G antibodies to H. pylori were measured in 143 children under the age of 20 years. Ninety-one percent of 43 randomly chosen subjects over 10 years had antibodies to H. pylori. A further 100 children under 10 years presenting to the University of Maiduguri Teaching Hospital were also tested. Sixty-nine percent had antibodies, including 58% of those aged under 1 year. H. pylori infection is acquired at an early age, and in this study was not associated with any other pathology. This study was carried out in an area where peptic ulceration and gastric cancer are uncommon. The early acquisition of H. pylori infection may be important in relation to its apparent lack of pathogenicity.

A total of 160 adult Malawians with epigastric pain for longer than 2 weeks was investigated by endoscopy and serologically for evidence of infection with Helicobacter pylori. The organism was demonstrated histologically and/or by culture in 141 (88%) patients. With histological means and/or culture as the 'gold standard', the histological technique was 100% sensitive while culture was only 81% sensitive. All isolates tested were sensitive to amoxycillin and tetracycline; 74% were resistant to metronidazole. Endoscopic findings were normal in 104 (65%) patients (86.5% H. pylori positive). Evidence of duodenal ulcer was found in 41 (25%) patients (95% H. pylori positive). Histologically, gastritis was common, severe gastritis being associated with increased colonisation by H. pylori. Two kinds of urease test were found to be 100% specific for the presence of H. pylori. The sensitivity of the serological test (Helico-G test) was 98% but its specificity was only 27%. These results provide important background information for planned therapeutic studies in patients with upper gastro-intestinal disease in Malawi.

One hundred and thirty north Nigerian patients with non-ulcer dyspepsia were treated with tripotassium dicitrato bismuthate and amoxycillin, or antacid. Symptoms resolved in 28 (33%) of bismuth and amoxycillin recipients completing the trial compared with 1 (4%) of the antacid recipients. Symptomatic improvement did not relate to clearance of Helicobacter pylori.

Helicobacter pylori (HP) in the gastric antrum has been strongly associated with both duodenal ulcer (DU) and chronic active gastritis (CAG). The relationship between HP and DU has been interpreted as causal by many observers. An alternate hypothesis is that HP coincidently colonizes CAG, which is independently associated with DU by some yet-unknown mechanism.

To assess the extent to which a causal relationship between HP and DU has been demonstrated, we performed a methodologic critique of published clinical studies. We carried out a literature search to identify clinical studies that included at least 25 subjects. Of the eight studies we identified, six used a cross-sectional design and two used a prospective cohort design. We applied methodologic criteria to assess causation: strength of association, biologic gradient, temporality, and experiment.

A strong association between HP and DU was demonstrated in all eight studies. Biologic gradient and temporality were not assessed in any study. In the two experimental studies of therapy, loss of antral HP was associated with a decreased rate of DU relapse; however, we did not interpret this as sufficient to support causality because the effect may have been due to a direct mucosal action rather than eradication of HP.

We conclude that published evidence does not establish HP as a cause of DU. One approach to address causality would be an observational cohort study of ulcer relapse to assess the temporal relationships between HP, CAG, and DU.

This investigation was aimed at assessing whether the Yemeni habit of chewing Qat on a regular basis had a significant effect on the upper alimentary tract. Seventy patients with dyspepsia attending Al-Thawra Hospital in Taiz, Yemen Republic were examined by endoscopy. Biopsies were taken from the oesophagus, stomach and duodenum. The patients included 28 who gave a history of daily Qat intake, 21 with less frequent intake and 21 who took none. The only statistically significant finding associated with daily Qat intake was a higher prevalence of duodenal ulcer, particularly in females. However, a strong association was also found between heavy smoking and ulcer, with most ulcer patients who chewed Qat daily being heavy smokers. Chewing Qat was not associated with a higher prevalence of oesophageal dysplasia, making it unlikely to be the cause of the perceived high incidence of oesophageal carcinoma in Yemen. There was a high prevalence of gastric H. pylori colonization (93%) and columnar-lined lower end of oesophagus (18%), as well as low prevalence of intestinal metaplasia of stomach (4%); this was not, however, related to chewing Qat. Further epidemiological and histological studies are needed to assess the significance of these findings in relation to the incidence of oesophageal and gastric carcinoma in Yemen.

The prevalence of Helicobacter pylori in patients with upper gastrointestinal symptoms in the north of Jordan was studied prospectively. The occurrence of H. pylori was documented histologically and bacteriologically in 169 patients attending endoscopy for upper gastrointestinal symptoms. Our results showed that H. pylori was present in 70% of patients with acute gastritis, 73% of patients with chronic gastritis, 68% of patients with acute on chronic gastritis, 83% of patients with duodenal ulceration, 75% of the patients with gastric ulceration, 64% of patients with no pathology, and 68% of patients regardless of the pathology found. There was a sharp rise in the prevalence of H. pylori with age, up to the age of 40 years with an annual increase in the prevalence of 2%. This study shows that the prevalence of H. pylori in Jordan is similar to that seen in other developing countries with infections occurring at a lower age and with the annual infection rate being double that seen in developed countries.

The role of Helicobacter pylori infection in causing chronic dyspepsia is in need of further clarification. More well-designed prospective studies are necessary to ascertain whether and to what extent H. pylori-related chronic inflammation in the stomach and the duodenum causes dyspeptic symptoms; whether and to what extent there is a symptom cluster characteristic for H. pylori-related gastroduodenitis; whether and to what extent H. pylori infection is demonstrable in the chronic dyspeptic population; and whether and to what extent H. pylori infection interferes with gastrin homoeostasis and acid secretion or induces motor disturbances. Well-designed prospective H. pylori-eradication studies may further contribute in unravelling its role in chronic dyspepsia, especially in patients with active polymorphonuclear gastroduodenitis and hyperacidity.

Epigastric pain is a common complaint throughout Africa, mostly in the form of non-ulcer dyspepsia. It has recently been suggested that Helicobacter (= Campylobacter) pylori, a bacterium that colonizes the gastric mucosa and causes type B gastritis, may be the cause of this epigastric pain. This paper reports the endoscopic, histological and bacteriological findings in 57 patients presenting with epigastric pain to the University of Maiduguri teaching hospital during one year, together with a review of the African literature. Of 57 patients, 49 had non-ulcer dyspepsia, 7 peptic ulceration and 1 carcinoma of the stomach. 93% of the patients had histological gastritis, and of these 87% were colonized with H. pylori. The bacterium was cultured from 13 patients. This high prevalence of gastritis and H. pylori has been found throughout Africa. The figures support a causative role for H. pylori in histological gastritis. At present the evidence in support of a causative role in non-ulcer dyspepsia is not strong enough to be able to recommend the routine use of anti-H. pylori therapy in patients with epigastric pain.

Campylobacter pylori is a newly described, spiral-shaped, gram-negative bacillus that is oxidase positive, catalase positive, and urease positive and grows slowly in culture. Although observed in human tissue at the beginning of the century, it was not cultured until 1982. Because there are significant morphological and genetic differences between this organism and other species of Campylobacter, it will probably be reclassified in a new genus. Current information indicates that the organism primarily resides in the stomach tissue of humans and nonhuman primates and may occasionally spread to the esophagus or other parts of the alimentary tract under appropriate conditions. Significant evidence has accumulated in the last several years to show that it causes gastritis, and there is mounting evidence that it may participate in the development of duodenal ulcers. It may also be associated with gastric ulcers and nonulcer dyspepsia. It can be detected in patients by culture of biopsy specimens or histological staining of biopsy tissue. Indirect evidence for the presence of the organism can be obtained by detection of urease in a tissue biopsy specimen, by urea breath tests, or by detection of specific antibody. It may not be necessary to implement these procedures for routine use, however, until the role of the organism can be defined better. Ultimately, the discovery of this organism may lead to radical changes in the diagnosis and treatment of gastric disease.

Campylobacter pylori infection has been recognized as being strongly associated with chronic gastritis and duodenal ulceration, but the prevalence of C. pylori infection in a normal population is not known. A serological survey was conducted in four countries with different geographical and socioeconomic status, in a randomly chosen population as representative as possible, by using an enzyme-linked immunosorbent assay (ELISA) with a sonic extract of two strains as the antigen. The test had a specificity of 94% when 600 ELISA units was used as the threshold. In France, few children were infected before the age of 10 years. The prevalence then increased gradually to 36.7% in the sixth decade of life. This increasing prevalence of infection with age was also observed in Algeria, Vietnam, and the Ivory Coast but at a higher rate (80 to 90%). In Vietnam, as in France, few children were infected, whereas in Africa, C. pylori infection occurred earlier. The prevalence of infection did not differ with sex for a particular age group; it also did not differ with respect to gastric symptoms, smoking and drinking habits, or urban or rural residence when these potential risk factors were studied. The epidemiological data available on peptic ulcer disease in developing countries compared with developed countries led to the speculation that infection with C. pylori is not a sufficient condition to develop this disease.

A strong positive correlation has been demonstrated between the (antral mucosal) presence of Campylobacter pylori and active duodenal and gastric ulceration. Moreover, both duodenal and gastric ulcers heal, and remain in remission, as a consequence of therapeutic measures which eradicate C. pylori. However, the Henle-Koch postulates have not been fulfilled, because C. pylori has not been shown to produce ulcers. As for the claim that ulcer disease represents an infection with C. pylori because therapeutic eradication heals ulcers, it has been shown that antibiotics and metronidazole, as well as bismuth subcitrate, exert antiulcer actions by mechanisms which do not involve their antibacterial effects. The association between C. pylori and ulcer disease, which was noted half a century ago, remains unexplained now as it did then.

In a consecutive prospective series of 208 Swedish primary peptic ulcer patients, 146 gastric, 55 duodenal and 7 in both sites, gastroduodenitis was found in 97.6% of the cases. The mucosal inflammation was associated with CP in 87% and 91% of the gastric and duodenal ulcer cases respectively. No significant correlation was found between CP colonisation and the type or severity of mucosal inflammation. Gastric metaplasia was present in only 8% of 48 bulbar ulcer cases. Ulcer healing and eradication of CP was achieved in 52% of patients treated with bismuth subnitrate in combination with erythromycin or according to the triple approach.