Background:Helicobacter pylori (H. pylori) infection is the most prevalent type of bacterial infection. Current guidelines from different regions of the world neglect specific African conditions and requirements. The African Helicobacter and Microbiota Study Group (AHMSG), founded in 2022, aimed to create an Africa-specific consensus report reflecting Africa-specific issues. Summary: Eighteen experts from nine African countries and two European delegates supported by nine African collaborators from eight other countries prepared statements on the most important African issues in four working groups: (1) epidemiology, (2) diagnosis, (3) indications and prevention, and (4) treatment. Limited resources, restricted access to medical systems, and underdeveloped diagnostic facilities differ from those of other regions. The results of the individual working groups were presented for the final consensus voting, which included all board members. Key Messages: There is a need for further studies on H. pylori prevalence in Africa, with diagnosis hinged on specific African situation. Treatment of H. pylori in the African setting should be based on accessibility and reimbursement, while indication and prevention should be defined in specific African countries.

Helicobacter pylori (H. pylori) was first assigned to the family of campylobacters before being renamed H. pylori. The obligate pathogen was first identified in 1982 and infects more than half of the world’s population [1]. Depending on the socioeconomic conditions, regions, and ethnicities, a broadly varying prevalence can be found. H. pylori infection is the most widespread bacterial infection all over the world [2] triggering chronic active gastritis in a subgroup of patients with more severe manifestations, such as gastroduodenal ulcers, mucosa-associated lymphoma, and gastric cancer. More than 90% of gastric cancers are associated with H. pylori infection [3] which led to its classification as class 1 carcinogen by the International Agency for Research on Cancer (IARC) in 1994 [4‒6].

During the last 4 decades, significant progress has been made in the management of H. pylori infection [7‒11]. Several international and national guidelines have established diagnostic and therapeutic algorithms based primarily on studies mostly from developed regions. As in previous guidelines, eradication therapy is recommended in all H. pylori-infected subjects, but the ability to screen for infection is limited in Africa [10, 12]. Resistance rates and the achievement of eradication regimes in developed parts of the world have not been sufficiently documented for Africa [12].

H. pylori is an obligate pathogen of African origin [13, 14]. Africa shows one of the highest H. pylori prevalence rates worldwide. The main focus of infectious disease research in Africa in past decades was linked to the human immunodeficiency virus, tuberculosis, hemorrhagic viruses, and Ebola [15‒18]. Funding of H. pylori research is underdeveloped and needs urgent improvement. In addition, international guidelines have neglected the specificity of the African health system, which complicates its implementation in African countries [8].

Based on different resources in African healthcare systems and the different availabilities of primary care physicians and diagnostic facilities, the African Helicobacter and Microbiota Study Group (AHMSG) was founded in June 2022. During the founding meeting held in Lagos, Nigeria, experts from nine African countries, as well as two delegates of the European Helicobacter and Microbiota Study Group, discussed the most relevant issues in implementing guidelines for the management of H. pylori infection in Africa. A review of the latest knowledge was conducted, and different working groups were formed, as listed below. Successively, the identification of areas of importance, systematic literature reviews to identify best evidence to support each statement, the draft of statements, and discussions with the group were performed.

  • WG 1: epidemiology

  • WG 2: diagnosis

  • WG 3: indications and prevention

  • WG 4: treatment

Each working group presented several statements, which were discussed for adjustment in the plenum. After the agreement, a Delphi vote was initiated to summarize the agreement between group members and delegates.

Two rounds of voting were conducted. Each delegate was asked to select one of the following ratings.

  • Agree strongly

  • Agree with reservation

  • Undecided

  • Disagree

  • Disagree strongly

In each case, if the vote did not reach 80% for “agree strongly” and “agree with reservations,” the statement was rephrased with repeated votes. Consensus was defined by >80% votes with “agree strongly” and added “agree with reservations.”

The definition of the level of evidence and strength of the recommendations was completed after voting was completed. Based on the characteristics of the studies, the evidence levels and grade of recommendation were based on the Grades of Recommendations, Assessment, Development and Evaluation system [19‒21] (GRADE), which takes into account the quality of evidence and strength of recommendations as listed as follows.

Quality of Evidence

High Quality (A)

Further research is very unlikely to change our confidence in the estimate of effect.

Moderate Quality (B)

Further research is very unlikely to have an important impact on our confidence in the estimate of the effect and may change the estimate.

Low Quality (C)

Further research is very likely to have an important impact on our confidence in the estimate of the effect and is likely to change the estimate.

Very Low Quality (D)

Any estimate of effect is very uncertain.

Strength of Recommendation

Strong Recommendation (1)

It includes strong recommendation for using an intervention and strong recommendation against using an intervention.

Weak Recommendation (2)

It includes weak recommendation for using an intervention and weak recommendation against using an intervention. The final meeting was done virtually on October 21, 2022, including 12 delegates.

Statement 1: With increasing life expectancy (LE) in Africa, H. pylori has the potential to become a relevant burden on the health system.

Agreement: 100%; level of evidence: C; level of recommendation: 2.

However, the actual prevalence of H. pylori infection in Africa has not yet been determined. However, existing literature from countries with data suggests a high burden of infection on the continent. Prevalence data published between 2014 and 2020 in Burundi, Rwanda, Congo-Brazzaville, and Cameroon have been reported to be 70.8%, 75%, 93.1%, and 73.2%, respectively [22‒25]. Regions in West Africa, including Nigeria, Ghana, Togo, and the Republic of Benin, have reported prevalence of 87.8%, 88%, 70.41%, and 71.5%, respectively [26‒29]. Prevalence as high as 71.43% has been reported in Algeria, 63.8% in Morocco, and 64.6% in Egypt, all located in the northern part of Africa [30‒32]. Diet, level of literacy, and age among other factors have been highlighted as influencing variations in prevalence from one region to another [12]. Between 1995 and 2025, LE and healthy LE increased in most regions worldwide. Most African countries have demonstrated improved LE and healthy LE based on economic development and investment in medical systems [33]. Because relevant complications of H. pylori infection reach their peak in older age, an increase in H. pylori-related complications, such as gastric cancer, may occur in the future [33].

Statement 2: Quality data on H. pylori prevalence of asymptomatic carriage of the infection are rare in several African countries.

Agreement: 100%; level of evidence: C; level of recommendation: 1.

H. pylori is a successful bacterial colonizer in humans [14] and often infects the host for a lifetime. It is estimated that 50% of the world’s population is infected with H. pylori. However, this prevalence varies greatly, ranging from <10% to >90%, with large differences between countries and between communities in the same country [2, 34].

In Africa, the risk factors for H. pylori infection including socioeconomic conditions, poor hygiene, and promiscuity are high [12]. Consequently, the prevalence of H. pylori infection is believed to be approximately 80% [12]. However, reports of H. pylori prevalence on the continent vary greatly among regions, with several countries reporting rare to no data. Additionally, most reports are related to individuals with clinical symptoms that were included in investigations aiming for a diagnosis. Data on H. pylori carriage in healthy individuals and early detection of this bacterium are scarce.

H. pylori infection is often asymptomatic. In a small proportion of individuals, it leads to different diseases, including peptic ulcers, chronic atrophic gastritis, gastric cancer, and gut lymphoma [35]. The study of H. pylori biology since its discovery by Warren and Marshall in 1982 [1] was associated with enigmas [36, 37]. In Africa, as in some other low-income countries of the world, one enigma, which is still partly persistent, is the association between high H. pylori prevalence and low incidence of gastric cancer [36, 38].

Knowledge of asymptomatic carriage of H. pylori is important given that besides the diseases it directly causes, it might promote or aggravate other diseases, such as diabetes and heart diseases [39]. However, some studies have suggested that H. pylori could protect against diseases such as asthma [40‒45] and inflammatory bowel diseases [46]. The high prevalence of H. pylori carriage in Africa provides an opportunity to conduct studies to decipher the negative and positive effects of H. pylori carriage.

Statement 3: Data on virulence factors of circulating H. pylori clones are rare in several African countries.

Agreement: 96.6%; level of evidence: C; level of recommendation: 1.

Despite the high prevalence of H. pylori carriage [12], information on the genotypes of circulating strains is missing in most African countries. Many published studies have focused only on individuals who have developed clinical symptoms based on H. pylori infection. Additionally, most microbiology laboratories in Africa lack equipment and expertise to isolate and characterize H. pylori strains phenotypically or genotypically.

Several virulence factors contribute to H. pylori phenotypes [35]. It is well established that H. pylori-causing gastric cancer depends on the presence of cytotoxin-associated gene (cag) pathogenicity island that encodes CagA, which is classified as a primary carcinogen [47, 48]. Currently, there are only few data published about H. pylori virulence factors in Africa [49].

H. pylori strains can be classified into two groups based on their virulence factors. Virulent strains, called type I, possess the cag pathogenicity island and express an active form (s1/m1) of the vacuolating cytotoxin, whereas avirulent type II strains lack cag PAI and express a benign form (s2/m2) of vacuolating cytotoxin [50]. Although H. pylori is now formally classified as a carcinogen, the association of cag-negative, non-carcinogenic type II strains with possible benefits is still debated [51]. In the era of high-throughput sequencing and genomics, there is a need to investigate the genotypes of H. pylori strains carried by both clinically ill and asymptomatic carriers of H. pylori. This investigation has to be undertaken in both cross-sectional and longitudinal studies throughout Africa to generate data that will be of public health benefit, including the early phases of disease development, contribution of environmental and host factors, and possible benefits conferred by H. pylori carriage [2].

Statement 4: Significant differences of H. pylori prevalence are reported for different African countries. Next to regional differences, other factors such as socioeconomic status, education, and water sources might influence the prevalence rates in Africa.

Agreement: 90%; level of evidence: C; level of recommendation: 1.

Africa has an average reported H. pylori prevalence of 70.1% [52], but there are striking differences within and between countries. For instance, the prevalence in the northern regions of Nigeria is as high as 87.8% [53], whereas it is a mean of 42.8% in the southern regions. Another West African region with high prevalence is Ghana at 88% [27]. In Kenya, the prevalence is 73.3% [54] and in South Africa, 77.6% [2], 67.7% in Zimbabwe [55], and 84% in Zambia [56]. However, many of these were not determined at the population level.

Risk factors for H. pylori infection are largely unknown. It has been traditionally reported that these are directly linked to low socioeconomic status; however, the data are conflicting. While some studies report an association with low socioeconomic status [53], others refute this [57]. Similarly, factors such as poor access to clean water and overcrowding have also showed conflicting data [53, 58]. Other risk factors for H. pylori acquisition, such as alcohol consumption and smoking, might be important [53]; however, the data are limited. Infection is mostly acquired in childhood through oral, fecal, or oral-oral transmission [59].

Statement 5: In Western countries, the majority of H. pylori infections occur during childhood. There is paucity of data regarding the age when H. pylori transmission occurs in Africa.

Agreement: 90%; level of evidence: C; level of recommendation: 1.

H. pylori has its only ecological niche in the gastric mucosa, where infection lasts for a lifetime if not treated. Epidemiological data of H. pylori infection in high-income countries show prevalence of 10–20% with early acquisition of the bacterium during childhood [34, 60]. In low-income countries, prevalence of H. pylori infection is much higher, with several investigations reporting as high as 90% or above [2, 61]. This high prevalence could be explained by several factors. First, similar to high-income country, family transmission, especially mother-to-child transmission, is the primary and earliest source of H. pylori acquisition [62, 63]. Second, poor hygiene and weak socioeconomic conditions promote horizontal transmission of H. pylori [63]. Third, although poorly investigated in Africa, domestic animals may acquire H. pylori from humans and serve as vehicles for transmission [61]. Lastly, H. pylori infections are rarely diagnosed and treated in African settings. Most data available for children in Africa are from studies reporting seroprevalence. These studies might have underestimated the actual carriage of H. pylori because of the yet-to-develop gastric acid secretion in newborns and infants, the immune escape abilities of the bacterium, and differences in the sites of gastric colonization [64]. Despite these limitations, the high prevalence of H. pylori carriage, evidence of mother-to-child and horizontal transmission, and the large size of households in African settings suggest early acquisition in childhood, as indicated by several studies that reported H. pylori infection in children under 1 year of age [65‒67]. Additional well-designed investigations are needed to accurately estimate the age of H. pylori infections in African children.

Statement 1: Endoscopic diagnosis with standardized biopsies is indicated in patients with dyspeptic symptoms older than 45 years or in patients with alarm symptoms.

Agreement: 93.7%; level of evidence: A; level of recommendation: 1.

Current guidelines recommend taking two biopsies from the corpus and antrum of the stomach for histological investigation [68‒70], but the gold standard is the updated Sydney classification system [68], which advises collecting specimens from five or more sites, including the incisura angularis. Histology enables visualization of gastric morphology. It allows for the detection of gastric preneoplastic conditions [7, 8, 10]. The sensitivity and specificity of histology for detection of H. pylori vary between 53% and 90%, depending on the pathologist’s experience, quality of biopsies, and density of colonization for the detection of H. pylori [71]. Many factors have the potential to affect the diagnostic accuracy of H. pylori detection, such as staining techniques used, medications (proton pump inhibitors [PPIs], antibiotics), and acute peptic ulcer bleeding [8, 72]. However, the accuracy of histological diagnosis can be improved using special staining techniques, immunopathology, or digital pathology [73]. A recent study reported a high percentage (94%) of H. pylori detection with the standard hematoxylin-eosin staining compared to special staining [74].

However, the high sensitivity and specificity of histopathological diagnosis of H. pylori using multiple gastric biopsies have been reported in Egypt [75]. A cross-sectional case-control study in South Africa, Kgomo and Ks [76], reported a 100% correlation between histology and rapid urease test for the diagnosis of H. pylori in patients with acute bleeding and non-bleeding gastric ulcers.

Statement 2: Urea breath test (UBT) is useful for epidemiological studies and for assessing the effectiveness of eradication therapy.

Agreement: 90.6%; level of evidence: A; level of recommendation: 1.

The UBT is regarded as the gold standard for noninvasive methods of H. pylori diagnosis [77]. Two different UBTs were available. Both 13C and 14C tests provided comparable results. 14C uses radioactive isotopes, with some restrictions when used in children or pregnant women [75]. Both UBTs have advantages of being noninvasive, safe, accurate, and with a sensitivity of 95.9% and a specificity of 95.7%. UBT is useful for noninvasive diagnosis when endoscopy is not indicated and for follow-up examinations after eradication. 13C UBT can even be used in children for the diagnosis of H. pylori, and variable levels of accuracy have been reported [78].

Although UBT is considered a noninvasive diagnostic method, its use in Africa is not widespread. A review report on the use of UBT for the diagnosis of H. pylori infection was only found in North Africa (Algeria and Egypt) and West Africa (Nigeria) and one report from South Africa [12, 79‒81]. However, 13C is less frequently used. The limited use of UBT in Africa is a result of the cost and availability of facilities, among other factors [12]. An expansion of its use through the nationwide availability of 13C-UBT facilities in health institutions across Africa has been advocated. Therefore, there is a need to implement modern 13C-UBT facilities nationwide in each African country.

Statement 3: Monoclonal stool antigen test (SAT) if validated can be used for diagnosis and assessment of the effectiveness of H. pylori eradication.

Agreement: 90.6%; level of evidence: A; level of recommendation: 1.

Stool ELISA using a monoclonal antibody is an efficient noninvasive test for the diagnosis of H. pylori infection [8, 78]. SAT is a fast, simple, and inexpensive test and a useful tool for epidemiological studies and screening programs [82, 83]. The sensitivity and specificity of SAT are 94% and 97%, respectively [7, 72, 82].

SAT has the potential to distinguish actively infected patients from successfully treated ones. However, to confirm definitive eradication, it is advisable to screen 30–60 days posttreatment [83]. The test should be performed at least 2 weeks after discontinuation of PPI and 4 weeks for antibiotic and bismuth compounds to avoid false-negative results due to inhibition of growth of bacteria [7, 8, 72, 84].

Statement 4: H. pylori susceptibility testing (culture or PCR) should be performed in cases of multiple treatment failure (more than 3 attempts) to eradicate H. pylori.

Agreement: 93.7%; level of evidence: B; level of recommendation: 1.

Increased antibiotic resistance also affects the treatment of H. pylori. The WHO (2018) defined H. pylori as a high-priority pathogen for antibiotic research and development for successful eradication [85]. Knowledge of local resistance rates is needed to choose an appropriate treatment strategy [8, 86‒88].

PCR is a simple, accurate, fast, and highly efficient method for H. pylori detection [89‒91]. This method offers high sensitivity and specificity (95%) [92]. In comparison with other tests, PCR can be performed on specimens collected from both invasive and noninvasive procedures. Gastric biopsy samples obtained for rapid urease testing can be used for accurate PCR diagnosis [93]. Accurate primer design and gene selection are critical for successful PCR reaction [94]. H. pylori genes, such as vacA, cagA, ureA, glmM, Hsp60, 16SrRNA, 23SrRNA, and ureC, can be used to amplify the H. pylori genome [95]. Two or more target genes are amplified to increase the specificity of diagnosis and reduce false-positive rates [92].

Stool PCR and direct detection of H. pylori in biopsies using real-time PCR have been demonstrated in Nigeria [96]. Droplet digital PCR (ddPCR) is more sensitive than other PCR methods. One study evaluated the ability of ddPCR to detect H. pylori infection in patients initially diagnosed as negative by conventional tests. Surprisingly, ddPCR targeting three H. pylori-specific genes detected H. pylori in a significant proportion (36%) of dyspeptic patients initially diagnosed as negative [97], although its biological relevance remains unclear.

As discussed in the Maastricht/Florence VI report, there is no consensus about the use of molecular-based detection in routine clinical practice in Africa. The recovery and PCR amplification of H. pylori DNA from formalin-fixed paraffin-embedded (FFPE) gastric tissues for the detection of H. pylori have also been demonstrated. PCR amplification of the 16SrDNA gene in H. pylori DNA isolated from FFPE gastric tissues has been previously shown [98]. DNA extracted from FFPE gastric tissues has also been reported to be suitable for the amplification of H. pylori 23S rRNA with the potential to reveal point mutations that mediate clarithromycin resistance [99].

There is a need to improve susceptibility testing of H. pylori, especially in cases of treatment failures [100]. In Africa, there has been a surge in the rate of antibiotic resistance in H. pylori to antibiotics [52]. Although the use of culture methods in susceptibility testing has been reported in some institutions in Africa, their availability is limited [12]. Recently, more efficient molecular approaches have been developed. Susceptibility-based therapy, as a result of the wide availability of molecular antibiotic susceptibility testing (AST) methods (using H. pylori DNA isolated from biopsy or stool), is under debate [87].

The major disadvantages of PCR-based diagnostics are that the costs of the method are not covered and molecular-based detection is not universally available in Africa [90]. In addition to susceptibility-based eradication treatment, AST plays a crucial role for surveillance of local resistance rates. Therefore, there is an urgent need to improve the availability and reimbursement of AST in Africa.

Statement 1a: H. pylori is classified as an infectious disease, and eradication therapy should be offered to all infected patients because of its subsequent effects on health, unless there are compelling contraindications.

Agreement: 100%; level of evidence: A; level of recommendation: 1.

As established in several international guidelines, H. pylori infection is defined as an infectious disease, irrespective of symptoms or complications related to H. pylori infection [10]. Eradication therapy must be the treatment of choice in infected patients whenever detected [8, 10]. H. pylori is the most common human pathogen. It persists for life, except when it is treated with antibiotics or auto-eradicates gastric mucosal atrophy and metaplasia with achlorhydria [72]. It is a major cause of morbidity and mortality due to PUD, gastric cancer, gastric atrophy, MALT lymphoma, idiopathic thrombocytopenic purpura, and gastrointestinal bleeding [11, 51, 101‒105]. The advantages of eradication include reducing the reservoir of infected individuals, preventing transmission, reducing costs from management of the disease and complications, halting the progression of mucosal damage, curing H. pylori-related PUD, and reducing the risk of gastric cancer and gastrointestinal bleeding [106]. Thus, all H. pylori-infected individuals should receive eradication therapy even in Africa.

Statement 1b: H. pylori testing is strongly recommended in patients with present or past peptic ulcer disease, gastric mucosa atrophy and/or intestinal metaplasia, first-degree relatives of patients with gastric cancers, following gastric cancer resection or in cases of MALT lymphoma.

Agreement: 96.8%; level of evidence: A; level of recommendation: 1.

H. pylori infection leads to chronic active gastritis and preneoplastic conditions, such as gastric mucosal atrophy and metaplasia with achlorhydria [107]. The pathogen is the main cause of morbidity and mortality from complications, such as PUD, gastric cancer, MALT lymphoma, idiopathic thrombocytopenic purpura, and gastrointestinal bleeding [8.10–11, 106]. Eradication therapy reduces costs from management of the disease and complications, halting the progression of mucosal damage, curing H. pylori-related PUD, and reducing the risk of gastric cancer in high-prevalence regions as well as gastrointestinal bleeding [7, 108]. Eradication has the potential to improve the grades of gastric atrophy and intestinal metaplasia [109].

Statement 1c: Other indications for H. pylori testing include long-term PPI use, functional dyspepsia, prevention of PUD and gastrointestinal bleeding prior to long-term NSAID, aspirin or other antithrombotic therapy as well as patients’ preference to be eradicated.

Agreement: 100%; level of evidence: B; level of recommendation: 1.

Functional dyspepsia, prevention of PUD, and gastrointestinal bleeding prior to long-term NSAID or aspirin therapy or low-dose aspirin use in patients at high risk for ulcers are indications for testing of H. pylori [8, 11, 107, 110, 111], as well as patients’ preference to be tested and eradicated, but these have not been validated in Africa. Current data also demonstrate the effects of H. pylori eradication before the initiation of long-term aspirin treatment in the general population [112]. H. pylori infection and GERD are known to be negatively associated [113]; however, eradication of H. pylori does not exacerbate GERD [114, 115]. Patients with functional dyspepsia show improvement in symptoms following the eradication of H. pylori [103, 116, 117]. H. pylori infection and NSAIDS use are independent risk factors for PUD and bleeding. Eradicating H. pylori infection in naïve users has been shown to be useful [112, 118, 119].

Statement 2: Serological tests (pepsinogen I, II and H. pylori antibody) are useful for gastric cancer risk stratification; nevertheless, the value for these parameters in Africa still has to be researched.

Agreement: 93.7%; level of evidence: C; level of recommendation: 1.

For over 2 decades, serological tests have been used to diagnose H. pylori infection and gastric atrophy [10]. These tests include H. pylori serology and serum pepsinogen I, II, and gastrin levels for hypoacidity [120]. Hypoacidity occurs in patients with glandular atrophy and can progress to metaplasia, dysplasia, and gastric carcinoma. Thus, assaying serum pepsinogen (and additional gastrin) levels can be useful in assessing the risk of gastric cancer. Studies have reported a higher level of progression to gastric cancer in individuals with low serum pepsinogen levels and H. pylori serology, consistent with atrophic gastritis [121‒123]. Data from screening strategies in African cohorts were lacking.

Statement 3: The widespread implementation of programs focused on personal hygiene, environmental hygiene, and improved living conditions has the potential to prevent the transmission of H. pylori and reduce the prevalence in Africa.

Agreement: 95.2%; level of evidence: C; level of recommendation: 1.

The prevalence of H. pylori infection is high in regions with slow improvement in standards of living [2, 124‒126]. Socioeconomic status in childhood is a major determinant of prevalence, and it is reflective of hygiene, sanitation, living conditions, risk of cross-infection, and level of education [107]. Although the precise mode of transmission of H. pylori is unknown, there is evidence of person-to-person transmission from epidemiological and genetic studies [63, 127‒129]. The burden of disease caused by H. pylori is high in Africa, and the greatest impact on reducing this burden of disease from H. pylori will emerge from improved socioeconomic status which will interrupt transmission [12, 107].

Statement 4: H. pylori testing is indicated in conditions as listed in statements 1b and 1c, 30–60 days following the completion of eradication therapy to assess the effectiveness of therapy, and a positive family history of gastric cancer.

Agreement: 96.4%; level of evidence: A; level of recommendation: 1.

H. pylori is a Gram-negative bacterium identified as the cause of chronic active gastritis in each infected subject. In a subgroup of patients, peptic ulcer disease, mucosa-associated lymphoid tumor [8, 130, 131], and gastric cancer can develop. Dyspepsia [10, 101, 103, 116] is considered to be the main symptom of infection. Testing for H. pylori in these patients helps in diagnosis and treatment, which may lead to the cure of the disease and prevention of complications. Some patients may not clear the infection after treatment; thus, follow-up tests must confirm therapeutic success. Indeed, the indications for H. pylori testing include patients with PUD, mucosal-associated lymphoid tumor, dyspepsia, after completion of treatment for established H. pylori infection, and a positive family history of H. pylori infection [8, 11].

Statement 5: The role of H. pylori should be further evaluated in unexplained iron deficiency anemia, idiopathic thrombocytopenic purpura, and vitamin B12 deficiency in African communities.

Agreement: 92.8%; level of evidence: B; level of recommendation: 1.

Iron deficiency anemia, idiopathic thrombocytopenic purpura, and vitamin B12 deficiency are associated with H. pylori [8, 107, 110] and are indications for H. pylori infection eradication [8, 132, 133], but they have not been studied in Africa. Thus, there is a need for African studies to evaluate the role of H. pylori in these conditions.

Statement 6: The reinfection with H. pylori after successful eradication should be studied in Africa to judge the effectiveness in reducing the re-transmission rates with regard to socioeconomic restrictions.

Agreement: 90.6%; level of evidence: B; level of recommendation: 1.

Eradication of H. pylori as a means of preventing transmission has been documented [8, 11, 91, 107], but has not been studied in Africa. Eradication reduces the reservoir of infected individuals and prevents transmission. However, reinfection with H. pylori after successful eradication has not been studied specifically under African conditions. Such a study could help judge the effectiveness of reducing transmission rates with regard to socioeconomic restrictions.

Statement 1: Evidence regarding H. pylori resistance rates to antibiotics in Africa is scarce, and more studies are needed to guide choice of appropriate first-line therapy and subsequent therapies.

Agreement: 93.5%; level of evidence: C; level of recommendation: 1.

Resistance of H. pylori to antibiotics determines the efficacy of current eradication therapy world [8, 85, 134‒137]. The antibiotics recommended for eradication treatment of H. pylori in Africa are amoxicillin, clarithromycin, metronidazole, and tetracycline.

According to current EHMSG guidelines, the first-line therapy should consist of amoxicillin, clarithromycin, and a PPI when local clarithromycin resistance rates are <15% [8]. An alternative first-line therapy is quadruple therapy with amoxicillin, clarithromycin, metronidazole, and PPI [8]. The recommended second-line or salvage therapeutic regimens can include levofloxacin-based triple therapy, sequential non-bismuth quadruple therapy, or bismuth-based quadruple therapy. In the choice of a regimen for second-line therapy, all possible attempts should be made to avoid previously used antibiotics and consistent with local conditions such as reimbursement, availability of drugs, and resistance rates.

Antibiotic resistance studies of H. pylori have been reported in Africa [79, 137‒145] with widespread results. However, these reports come from less than one-third of the countries on the continent. Although there are wide variations in the antibiotic resistance rates, there are uniform local resistances to metronidazole of over 90% throughout Africa. In the few studies available, amoxicillin resistance was reported to a range from 30% to 85%, whereas resistance to clarithromycin was generally higher than the acceptable rate of 15% [79, 146]. Methodological differences should be excluded in future studies to align the tests used for international comparability. Therefore, the traditional first-line triple therapy may no longer be effective in many African countries. Further studies are required to draw firm conclusions and recommendations for effective H. pylori antibiotic eradication regimens for H. pylori in Africa. Currently, there are not enough data to refute clarithromycin-based triple therapy as first-line treatment in Africa.

Statement 2: All patients requiring H. pylori eradication should be asked about any antibiotic allergy to avoid prescribing any of them in the current or future eradication regimens.

Agreement: 100%; level of evidence: B; level of recommendation: 1.

Eradication of H. pylori infection often requires an acid suppressant, and a combination of antibiotics such as amoxicillin will be used. However, available reports indicate a substantial percentage (up to 10%) of patients has reported allergy to penicillin class of antibiotics. This phenomenon is more frequently described in the USA, especially among African Americans, females, and older people, but less frequently in Asians [147]. Such allergy labels, however, result in the substitution of antibiotics for second-line drugs, which may have less efficacy or be more expensive [148].

When properly evaluated, nearly 90% of these patients did not have allergies and tolerated the penicillin, hence the campaign by the American Board of Internal Medicine (ABIM) foundation [149]. However, the manifestation of penicillin allergy varies from skin rash and urticaria to severe anaphylaxis, which can be life threatening [8, 150, 151]. Considering this severe complication, it is important to ask for a history of penicillin allergy and properly evaluate it before deciding on the choice of antibiotics.

Statement 3: All patients requiring H. pylori eradication should be asked about antibiotics given in previous failed eradication attempts to avoid them in subsequent H. pylori eradication regimens as this may increase resistance.

Agreement: 93.5%; level of evidence: A; level of recommendation: 1.

Most international treatment guidelines have recommended first-line and second-line therapies taking into account resistance rates to clarithromycin, possible allergies, and side effects such as QTc. prolongation, among others [8, 9, 11, 152, 153]. Although molecular testing methods are currently available for the characterization of H. pylori antibiotic susceptibility, these tests are not widely available, particularly in African settings [3].

Knowledge of previous antibiotic treatment can guide the choice of future antibiotics to minimize the risk of resistance development [12, 85, 87, 136, 153]. One drawback is that some patients may not remember the previous drugs or use them appropriately for the prescribed duration or for other indications [134, 154]. When molecular techniques become available, genotypic tailoring of eradication treatment has to be evaluated in Africa.

Statement 4: Locally effective regimens (achieving more than 90% eradication rates) should be considered as the first-line regimens for H. pylori eradication.

Agreement: 100%; level of evidence: A; level of recommendation: 1.

The current recommended first-line therapy for the eradication of H. pylori infection is a combination of amoxicillin, clarithromycin, and a PPI. International guidelines emphasize prolonging this standard triple therapy to 14 days [7, 8]. Metronidazole is a substitute for amoxicillin, but current guidelines do not recommend its use based on a dramatic increase in resistance to more than 40%. In the USA, the preferred first-line therapy is a combination of bismuth, metronidazole, tetracycline, or amoxicillin and a PPI (bismuth quadruple therapy) [152]. Current European guidelines stratify by the local clarithromycin resistance rates: less than 15% clarithromycin-based triple therapy will be recommended, and higher than 15% or unknown bismuth-based quadruple therapy will be recommended [8]. Overall, however, H. pylori eradication with the standard triple therapy should be employed only in areas where local eradication rates exceed 85%. The obvious contradiction between published resistance rates and the first-line recommendation is based on the lack of availability both from nationwide AST facilities and bismuth-based treatment options.

A few African studies on H. pylori susceptibility have reported divergent antibiotic resistance rates. Resistance to metronidazole is almost 100% in most reports, whereas resistance to amoxicillin ranges from 30% to 85% [79, 146]. The significant difference in susceptibility reports from other regions worldwide underlines the need to verify these data. The lowest antibiotic resistance rates have been reported for the quinolones (≤12%) [137]. In Senegal, resistance to levofloxacin and amoxicillin was reported to be 0% each. Even more difficult to obtain are reports of H. pylori eradication rates after therapy, as many patients fail to return for posttreatment H. pylori testing because of the high cost of the recommended simple UBT or even a lack of availability [12, 53, 155, 156].

It is obvious that local eradication rates should determine the choice of first-line therapy, but metronidazole must be avoided in Africa [136]. The lack of consistent resistance data from Africa and the lack of confirmation of eradication success emphasize the need for further studies.

Statement 5: All regimens should be used for 14 days unless there is locally available evidence to support the efficacy of 10-day regimens.

Agreement: 100%; level of evidence: A; level of recommendation: 1.

The duration of H. pylori eradication therapy has increased over the years. Fourteen days of therapy is recommended by European and American guidelines [8, 152]. Increasing evidence suggests that better eradication rates could be achieved with a longer duration of therapy, especially in the presence of a high percentage of clarithromycin resistance among the community [157, 158]. Therefore, updated guidelines from both European and North American societies recommend 14-day therapy to achieve better outcomes with H. pylori eradication therapies [8, 9]. A long-term registry of H. pylori treatment in European countries reported a gradual increase in the duration of H. pylori eradication prescriptions from 7 to 14 days, reflecting a change in practice among physicians in Europe, which was associated with a similar increase in the effectiveness of the treatment prescribed [159]. Although 7-day regimens can eradicate H. pylori in some populations, this was achievable in the absence of H. pylori resistance mutations. Recent studies have reported similar H. pylori eradication rates with 7-day potassium-competitive acid blocker (P-CAB)-containing regimens in comparison with 14-day PPI-containing regimens [160]. Some guidelines recommend shorter treatment courses (less than 14 days) when using bismuth quadruple and concomitant therapy when local evidence is given [8, 161]. Although shortening the treatment duration can increase compliance, more local evidence from Africa is needed before considering shortening the treatment duration to avoid the emergence of drug resistance.

Statement 6: All patients receiving H. pylori eradication therapy should be offered a test to confirm the success of eradication 30–60 days after completion of treatment. For reliable test results, antibiotics should not be used 4 weeks prior to the test, and PPIs (or P-CABs) should be avoided for least 2 weeks prior to the test. Serology should not be used to assess the effectiveness of eradication.

Agreement: 93.5%; level of evidence: A; level of recommendation: 1.

Patients receiving H. pylori eradication therapy should be offered a test to confirm eradication. It is important to determine treatment outcomes to distinguish between successful eradication and recrudescence to prevent the risk of underdiagnosis of treatment failure. Noninvasive tests are recommended, such as UBT and SAT [8, 152, 162‒165]. Treatment outcomes should be performed not less than 4 weeks after the completion of eradication therapy. This is due to the prolonged antibacterial activity of antibiotics and bismuth compounds [8, 162], and PPI should be withheld preferably 2 weeks prior to retesting [166] because PPIs tend to interfere with the sensitivity of the SAT and urease breath test [84, 166]. An early SAT of less than 4 weeks to confirm eradication would identify patients who have treatment failure and allow early initiation of second-line treatment. In Africa, there are few data to fully support the European recommendations concerning the duration of treatment, selection of treatment regimen, and testing for eradication success. This must be addressed in future [167‒169].

Statement 7: Second-line and subsequent regimens for H. pylori eradication should be based on local evidence and best clinical practice recommendations. After multiple failures (3 or more), it is recommended to perform AST to antibiotics, most importantly to clarithromycin (genotypic or phenotypic AST) following local circumstances, and base the subsequent regimens on the obtained results.

In contrast to the current European guidelines and the ongoing debate [8, 87] concerning initial AST before initiating antibiotic treatment, African conditions do not allow the recommendation of widespread and frequent AST. Facilities must be established, and culture-based or molecular testing must be trained and standardized [12] as mentioned above.

Statement 8: Best eradication rates will be achieved with optimized doses of acid suppressants (PPIs or P-CAB if available). It is recommended to use twice daily high dose of any of them.

Agreement: 96.8%; level of evidence: A; level of recommendation: 1.

PPIs have shown bactericidal effects in vitro, possibly through the inhibition of bacterial H+/K+-ATPase and bacterial urease. This effect was not shown to be relevant in vivo. Raising gastric pH with dual doses of PPIs (rather than once daily) increases the susceptibility of H. pylori to antibiotics [170, 171]. Therefore, combining PPIs with antibiotics is considered an established treatment for H. pylori infection [7, 8]. Optimization of H. pylori eradication regimens (providing the maximum dose of antibiotics, maximum duration of therapy, and highest dose of acid suppression) can achieve the highest eradication rates depending on the regimen used and population studied [172]. New agents include the P-CAB drugs which have a more potent gastric antisecretory effect than the PPIs when prescribed in combination with two antibiotics and these drugs can increase eradication rates. They are currently being investigated in possible dual therapies [173‒177].

Statement 9: Recommended treatment doses and durations are listed inTable 1 . After failure of three eradication therapies, further treatment should be guided with AST.

Table 1.

Recommended therapies for H. pylori infection

DrugFrequencyDuration
A. First-line therapies (provided there was no previous exposure to macrolides and local resistance to clarithromycin is <15%) 
 Clarithromycin triplea 
  PPIb (standard or double dose) BID 14 days 
  Clarithromycin 500 mg BID 
  Amoxicillin 1 g BID 
B. Salvage therapies 
 Concomitant clarithromycina 
  PPIb (standard dose) BID 14 days 
  Clarithromycin 500 mg BID 
  Amoxicillin 1,000 mg BID 
  Nitroimidazole 500 mg BID 
 Levofloxacin triplea 
  PPIb (standard dose) BID 14 days 
  Levofloxacin 500 mg QD 
  Amoxicillin 1,000 mg BID 
 Bismuth quadruple 
  PPIb (standard dose) BID 10–14 days 
  Bismuth subcitrate (120–300 mg) or subsalicylate (300 mg) QID 
  Tetracycline (500 mg) QID 
  Metronidazole (250–500 mg) QID 
DrugFrequencyDuration
A. First-line therapies (provided there was no previous exposure to macrolides and local resistance to clarithromycin is <15%) 
 Clarithromycin triplea 
  PPIb (standard or double dose) BID 14 days 
  Clarithromycin 500 mg BID 
  Amoxicillin 1 g BID 
B. Salvage therapies 
 Concomitant clarithromycina 
  PPIb (standard dose) BID 14 days 
  Clarithromycin 500 mg BID 
  Amoxicillin 1,000 mg BID 
  Nitroimidazole 500 mg BID 
 Levofloxacin triplea 
  PPIb (standard dose) BID 14 days 
  Levofloxacin 500 mg QD 
  Amoxicillin 1,000 mg BID 
 Bismuth quadruple 
  PPIb (standard dose) BID 10–14 days 
  Bismuth subcitrate (120–300 mg) or subsalicylate (300 mg) QID 
  Tetracycline (500 mg) QID 
  Metronidazole (250–500 mg) QID 

aBismuth compounds can be added to these regimens to increase their efficacy.

bPPI can be replaced with P-CABs when available, as evidence supports the superiority of this drug over PPIs for the eradication of H. pylori.

Agreement: 90.3%; level of evidence: B; level of recommendation: 1.

The treatment of H. pylori should be based on local experience with the efficacy of different anti-infective therapies [12]. Different eradication regimens have been tried in distinct African countries (Egypt, Kenya, Nigeria, Rwanda, and South Africa) with variable eradication rates ranging from 56% to 94.5% based on the used regimen and studied population [146, 178‒181]. Given the lack of solid evidence derived from systematic reviews and meta-analyses from different African countries, treatment should be based on the best available international evidence. Several first- and second-line options for the treatment of H. pylori have been proposed by the European, American, and Canadian guidelines [7‒9, 152].

These options can be used temporarily, guided by current and evolving local evidence, and must be regularly updated. A recently published report from Egypt recommended that all patients receiving H. pylori treatment regimens should be tested for successful eradication at least 1 month posttreatment [75]. It is also recommended that failure of three attempts to eradicate H. pylori warrants further treatment guided by susceptibility testing.

The current situation of H. pylori infection in Africa is dominated by a high prevalence and underdeveloped facilities and access to diagnostic and treatment compared to more developed regions. Therefore, the AHMSG formed four working groups to address the most relevant issues for the specific African situation.

  • WG 1 “epidemiology” collected current African prevalence data and defined needs for further studies.

  • WG 2 “diagnosis” established recommendations based on the specific African situation with underdeveloped facilities and low access to endoscopy and molecular-based diagnostics.

  • WG 3 “indications and prevention” defined African-specific recommendations for testing and treatment of H. pylori infection.

  • WG 4 “treatment” based the treatment recommendation of accessibility and re-imbursement on different African healthcare systems.

Look into the Future

The founding of the AHMSG in June 2022 marked the beginning of a new era of H. pylori infection in Africa. Clinicians, microbiologists, and scientists from different African countries have merged to become more effective.

Various problems with H. pylori diagnosis and treatment are specific to Africa and differ significantly from those in other regions. In the near future, the list of goals with high priority will be as follows:

  • 1.

    More detailed information on the actual prevalence and resistance to provide a complete map of H. pylori infection in Africa.

  • 2.

    Networking scientists, politicians, industry, and international societies to improve the equipping of hospitals and laboratories.

  • 3.

    Standardization of processes and algorithms to achieve comparability of diagnosis and therapeutic results.

  • 4.

    Argument for the implementation of nationwide cancer registries to underline the need for interventions against infection-associated cancers.

  • 5.

    Organizing national meetings, multinational conferences, web-based educational offers, and national and continental guidelines to increase awareness of H. pylori infection in Africa.

The first Lagos consensus report created by a group of enthusiastic experts was the first step toward improving H. pylori management in Africa.

An ethics statement was not required for this study type, and no human or animal subjects or materials were used.

S.S.I.: Richen Group for supporting attendances at the EHMSG conference. C.S. received honoraria for advice from Sanofi and Lilly; honoraria for talks from Luvos, Juvisé, Sanofi, and Tillots; and funding for scientific projects from Luvos, DZIF, and Bavarian Ministry of Health. R.U., R.N., Y.D., M.L., C.O., D.N., A.A., J.T., J.H., M.S., G.R., J.O., N.A., A.A., V.K., and R.N. reported no conflict.

This document was developed from the AHMSG scientific meeting held in Lagos, Nigeria, which was funded by the Richen Group. However, the Richen Group had no role in the design, data collection, data analysis, and reporting of this study.

The following are the collaborators: P. Ocama, D. Asrat, K. Tachi, A. Rajula, Y.A. Awuku, A.M. Moussa, A.R. Kpossou, A.-N. Adwoa, and N. Oudou. Stella Smith organized and coordinated the consensus process and contributed in the WG 2 comments and the main document draft and reviewing of the manuscript. Christian Schulz contributed to the main document draft comments and reviewing of the manuscript and took care of reference management. Rose Ugiagbe coordinated WG 3 and wrote questions/statements and writing of WG 3. Roland Ndip coordinated WG 2 and wrote some questions/statements of WG 2. Yakhya Dieye coordinated WG 1 and wrote some questions/statements of WG 1. Marcis Leja contributed to some statements in WG 3 and 4. Charles Onyekwere contributed to some questions/statements of WG 4. Dennis Ndububa contributed to some questions/statements in WG 4. Abraham Ajayi contributed to question/statement in WG 2. Tolulope Jolaiya contributed questions/statement of WG 2. Hyasinta Jaka contributed to question/statement in WG 2 and WG 3. Mashiko Setshedi contributed to question in WG 1. Revathi Gunturu contributed to comments in WG 3. Jesse Otegbayo, Naima Amrani, Anthony Arigbabu, Violet Kayamba, and Pueya Nashidengo contributed to elaborate on the statements for which all delegates voted upon.

All data generated or analyzed during this study are included in this article. Further inquiries can be directed to the corresponding author.

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