1
|
Archampong TN, Asmah RH, Richards CJ, Martin VJ, Bayliss CD, Botão E, David L, Beleza S, Carrilho C. Gastro-duodenal disease in Africa: Literature review and clinical data from Accra, Ghana. World J Gastroenterol 2019; 25:3344-3358. [PMID: 31341360 PMCID: PMC6639557 DOI: 10.3748/wjg.v25.i26.3344] [Citation(s) in RCA: 8] [Impact Index Per Article: 1.3] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Grants] [Track Full Text] [Download PDF] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Received: 03/15/2019] [Revised: 05/14/2019] [Accepted: 05/31/2019] [Indexed: 02/06/2023] Open
Abstract
Gastroduodenal disease (GDD) was initially thought to be uncommon in Africa. Amongst others, lack of access to optimal health infrastructure and suspicion of conventional medicine resulted in the reported prevalence of GDD being significantly lower than that in other areas of the world. Following the increasing availability of flexible upper gastro-intestinal endoscopy, it has now become apparent that GDD, especially peptic ulcer disease (PUD), is prevalent across the continent of Africa. Recognised risk factors for gastric cancer (GCA) include Helicobater pylori (H. pylori), diet, Epstein-Barr virus infection and industrial chemical exposure, while those for PUD are H. pylori, non-steroidal anti-inflammatory drug (NSAID)-use, smoking and alcohol consumption. Of these, H. pylori is generally accepted to be causally related to the development of atrophic gastritis (AG), intestinal metaplasia (IM), PUD and distal GCA. Here, we perform a systematic review of the patterns of GDD across Africa obtained with endoscopy, and complement the analysis with new data obtained on pre-malignant gastric his-topathological lesions in Accra, Ghana which was compared with previous data from Maputo, Mozambique. As there is a general lack of structured cohort studies in Africa, we also considered endoscopy-based hospital or tertiary centre studies of symptomatic individuals. In Africa, there is considerable heterogeneity in the prevalence of PUD with no clear geographical patterns. Furthermore, there are differences in PUD within-country despite universally endemic H. pylori infection. PUD is not uncommon in Africa. Most of the African tertiary-centre studies had higher prevalence of PUD when compared with similar studies in western countries. An additional intriguing observation is a recent, ongoing decline in PUD in some African countries where H. pylori infection is still high. One possible reason for the high, sustained prevalence of PUD may be the significant use of NSAIDs in local or over-the-counter preparations. The prevalence of AG and IM, were similar or modestly higher over rates in western countries but lower than those seen in Asia. . In our new data, sampling of 136 patients in Accra detected evidence of pre-malignant lesions (AG and/or IM) in 20 individuals (14.7%). Likewise, the prevalence of pre-malignant lesions, in a sample of 109 patients from Maputo, were 8.3% AG and 8.3% IM. While H. pylori is endemic in Africa, the observed prevalence for GCA is rather low. However, cancer data is drawn from country cancer registries that are not comprehensive due to considerable variation in the availability of efficient local cancer reporting systems, diagnostic health facilities and expertise. Validation of cases and their source as well as specificity of outcome definitions are not explicit in most studies further contributing to uncertainty about the precise incidence rates of GCA on the continent. We conclude that evidence is still lacking to support (or not) the African enigma theory due to inconsistencies in the data that indicate a particularly low incidence of GDD in African countries.
Collapse
Affiliation(s)
- Timothy N Archampong
- Department of Medicine and Therapeutics, School of Medicine and Dentistry, University of Ghana, Accra Box 4236, Ghana
- Department of Genetics and Genome Biology, University of Leicester, Leicester LE1 7RH, United Kingdom
| | - Richard H Asmah
- Department of Medical Laboratory Sciences, School of Biomedical and Allied Health Sciences, University of Ghana, Accra Box 4236, Ghana
| | - Cathy J Richards
- Department of Histopathology, Leicester Royal Infirmary, Leicester LE1 5WW, United Kingdom
| | - Vicki J Martin
- Department of Histopathology, Leicester Royal Infirmary, Leicester LE1 5WW, United Kingdom
| | - Christopher D Bayliss
- Department of Genetics and Genome Biology, University of Leicester, Leicester LE1 7RH, United Kingdom
| | - Edília Botão
- Department of Pathology, Maputo Central Hospital, Maputo POBox 1164, Mozambique
| | - Leonor David
- Department of Pathology, Medical Faculty of the University of Porto, Porto 4200-465, Portugal
- Institute of Molecular Pathology and Immunology at the University of Porto (Ipatimup), Porto 4200-465, Portugal
- Instituto de Investigação e Inovação em Saúde (i3S), University of Porto, Porto 4200-465, Portugal
| | - Sandra Beleza
- Department of Genetics and Genome Biology, University of Leicester, Leicester LE1 7RH, United Kingdom
| | - Carla Carrilho
- Department of Pathology, Faculty of Medicine, Eduardo Mondlane University, Maputo POBox 257, Mozambique
- Department of Pathology, Maputo Central Hospital, Maputo POBox 1164, Mozambique
| |
Collapse
|
2
|
Westerik N, Reid G, Sybesma W, Kort R. The Probiotic Lactobacillus rhamnosus for Alleviation of Helicobacter pylori-Associated Gastric Pathology in East Africa. Front Microbiol 2018; 9:1873. [PMID: 30154777 PMCID: PMC6102400 DOI: 10.3389/fmicb.2018.01873] [Citation(s) in RCA: 19] [Impact Index Per Article: 2.7] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Download PDF] [Figures] [Journal Information] [Subscribe] [Scholar Register] [Received: 05/30/2018] [Accepted: 07/25/2018] [Indexed: 12/16/2022] Open
Abstract
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.
Collapse
Affiliation(s)
- Nieke Westerik
- Department of Molecular Cell Biology, VU University Amsterdam, Amsterdam, Netherlands
- Yoba for Life Foundation, Amsterdam, Netherlands
| | - Gregor Reid
- Canadian R&D Centre for Human Microbiome and Probiotics, Lawson Health Research Institute, London, ON, Canada
- Department of Microbiology and Immunology, and Surgery, Western University, London, ON, Canada
| | | | - Remco Kort
- Department of Molecular Cell Biology, VU University Amsterdam, Amsterdam, Netherlands
- Yoba for Life Foundation, Amsterdam, Netherlands
- Department of Microbiology and Systems Biology, Netherlands Organization for Applied Scientific Research, Zeist, Netherlands
- ARTIS-Micropia, Amsterdam, Netherlands
| |
Collapse
|
3
|
Archampong TNA, Asmah RH, Wiredu EK, Gyasi RK, Nkrumah KN. Factors associated with gastro-duodenal disease in patients undergoing upper GI endoscopy at the Korle-Bu Teaching Hospital, Accra, Ghana. Afr Health Sci 2016; 16:611-9. [PMID: 27605979 DOI: 10.4314/ahs.v16i2.32] [Citation(s) in RCA: 7] [Impact Index Per Article: 0.8] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 12/12/2022] Open
Abstract
BACKGROUND There is a high prevalence of gastro-duodenal disease in sub-Saharan Africa. Peptic ulcer disease in dyspeptic patients, 24.5%, was comparable to prevalence of gastro-duodenal disease among symptomatic individuals in developed countries (12 - 25%). Limited data exists regarding its associated risk factors despite accumulating evidence indicating that gastroduodenal disease is common in Ghana. OBJECTIVES This study investigates risk factors associated with gastro-duodenal disease at the Korle-Bu Teaching Hospital, Accra, Ghana. METHODS This study utilized a cross-sectional design to consecutively recruit patients referred with upper gastro-intestinal symptoms for endoscopy. The study questionnaire was administered to study participants. Helicobacter pylori infection was confirmed by rapid-urease examination at endoscopy. RESULTS Of 242 patients sampled; 64 had duodenal ulcer, 66 gastric ulcer, 27gastric cancer and 64 non-ulcer dyspepsia. Nineteen (19) had duodenal and gastric ulcer while 2 had gastric ulcer and cancer. A third (32.6%) of patients had history of NSAID-use. H. pyloriwas associated with gastric ulcer (p=0.033) and duodenal ulcer (p=0.001). There was an increased prevalence of duodenal ulcer in H. pylori-infected patients taking NSAIDs, P=0.003. CONCLUSION H. pylori was a major risk factor for peptic ulcer disease. However, NSAID-related gastro-duodenal injury has been shown to be common in H. pylori infected patients. It highlights the need for awareness of the adverse gastro-intestinal effects in a H. pylori endemic area.
Collapse
|
4
|
Tovey FI. Role of dietary phospholipids and phytosterols in protection against peptic ulceration as shown by experiments on rats. World J Gastroenterol 2015; 21:1377-1384. [PMID: 25663757 PMCID: PMC4316080 DOI: 10.3748/wjg.v21.i5.1377] [Citation(s) in RCA: 13] [Impact Index Per Article: 1.3] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Track Full Text] [Download PDF] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Received: 11/04/2014] [Accepted: 12/22/2014] [Indexed: 02/06/2023] Open
Abstract
Geographically the prevalence of duodenal ulceration is related to the staple foods in the diet in regions of developing countries where the diet is stable. It is higher in regions where the diet is based on milled rice, refined wheat or maize, yams, cassava, sweet potato, or green bananas, and is lower in regions where the staple diet is based on unrefined wheat or maize, soya, certain millets or certain pulses. Experiments on rat gastric and duodenal ulcer models showed that it was the lipid fraction in staple foods from low prevalence areas that was protective against both gastric and duodenal ulceration, including ulceration due to non-steroidal anti-inflammatory drugs (NSAIDs). It also promoted ulcer healing. The lipid from the pulse, Dolichos biflorus, horse gram which was highly protective was used to identify the fractions with protective activity in the lipid. The protective activity lay in the phospholipid, sterol and sterol ester fractions. In the phospholipid fraction phosphatidyl choline (lethicin) and phosphatidyl ethanolamine (cephalin) were predominant. In the sterol fraction the sub-fractions showing protective activity contained β-sitosterol, stigmasterol, and an unidentified isomer of β-sitosterol. The evidence from animal models shows that certain dietary phospholipids and phytosterols have a protective action against gastroduodenal ulceration, both singly and in combination. This supports the protective role of staple diets in areas of low duodenal ulcer prevalence and may prove to be of importance in the prevention and treatment of duodenal ulceration and management of recurrent ulcers. A combination of phospholipids and phytosterols could also play an important role in protection against ulceration due to NSAIDs.
Collapse
|
5
|
Abstract
The prevalence of duodenal ulceration in India, Africa, China and other developing countries is high in some regions and low in others, despite a high prevalence of Helicobacter pylori infection throughout the areas. This variation is related to the staple diet of the regions involved. In regions where, because of the climate, the staple food is milled white rice, wheat or maize, or cassava, yams,sweet potato and green bananas the prevalence of duodenal ulcer is higher than in regions where the staple diet is based on unrefined wheat or maize, soya, certain millets or pulses. These differences have been reproduced in animal peptic ulcer models. Using these models it has been shown that the protective factor against ulceration lies in the lipid fraction present in staple foods from the low prevalence areas. The lipid fraction not only gave protection in the experimental models against ulceration but also promoted healing. The pulse Dolichos biflorus (horse gram) gave the greatest yield of the lipid and this was used for further investigations. It was found that the ulceroprotective activity of the lipid lay in its phospholipid and sterols fractions. The presence or absence of protective lipid in the diet would account for the regional differences in duodenal ulcer prevalence.
Collapse
|
6
|
Kate V, Ananthakrishnan N, Tovey FI. Is Helicobacter pylori Infection the Primary Cause of Duodenal Ulceration or a Secondary Factor? A Review of the Evidence. Gastroenterol Res Pract 2013; 2013:425840. [PMID: 23606834 PMCID: PMC3623110 DOI: 10.1155/2013/425840] [Citation(s) in RCA: 12] [Impact Index Per Article: 1.0] [Reference Citation Analysis] [Abstract] [Track Full Text] [Download PDF] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Received: 01/27/2013] [Accepted: 03/07/2013] [Indexed: 02/06/2023] Open
Abstract
Helicobacter pylori (H. pylori) has a role in the multifactorial etiology of peptic ulcer disease. A link between H. pylori infection and duodenal ulcer disease is now established. Other contributing factors and their interaction with the organism may initiate the ulcerative process. The fact that eradication of H. pylori infection leads to a long-term cure in the majority of duodenal ulcer patients and the fact that the prevalence of infection is higher in ulcer patients than in the normal population are cogent arguments in favor of it being the primary cause of the ulceration. Against this concept there are issues that need explanation such as the reason why only a minority of infected persons develop duodenal ulceration when infection with H. pylori is widespread. There is evidence that H. pylori infection has been prevalent for several centuries, yet duodenal ulceration became common at the beginning of the twentieth century. The prevalence of duodenal ulceration is not higher in countries with a high prevalence of H. pylori infection. This paper debate puts forth the point of view of two groups of workers in this field whether H. pylori infection is the primary cause of duodenal ulcer disease or a secondary factor.
Collapse
Affiliation(s)
- Vikram Kate
- Department of General and Gastrointestinal Surgery, Jawaharlal Institute of Postgraduate Medical Education and Research, Pondicherry 605006, India
| | - N. Ananthakrishnan
- Mahatma Gandhi Medical College & Research Institute, Pondicherry 607402, India
| | - Frank I. Tovey
- Division of Surgery and Interventional Science, University College London, London W1W 7ET, UK
| |
Collapse
|
7
|
Tovey FI, Bardhan KD, Hobsley M. Dietary phosphilipids and sterols protective against peptic ulceration. Phytother Res 2012; 27:1265-9. [PMID: 23097339 DOI: 10.1002/ptr.4865] [Citation(s) in RCA: 11] [Impact Index Per Article: 0.8] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 07/28/2012] [Revised: 09/23/2012] [Accepted: 09/27/2012] [Indexed: 12/16/2022]
Abstract
The prevalence of duodenal ulceration in regions of developing countries with a stable diet is related to the staple food(s) in that diet. A higher prevalence occurs in areas where the diet is principally milled rice, refined wheat or maize, yams, cassava, sweet potato or green bananas, and a lower prevalence in areas where the staple diet is based on unrefined wheat or maize, soya, certain millets or certain pulses. Experiments using animal peptic ulcer models showed that the lipid fraction in foods from the staple diets of low prevalence areas gave protection against both gastric and duodenal ulceration, including ulceration due to non-steroidal anti-inflammatory drugs (NSAIDs), and also promoted healing of ulceration. The protective activity was found to lie in the phospholipid, sterol and sterol ester fractions of the lipid. Amongst individual phospholipids present in the phospholipid fraction, phosphatidyl ethanolamine (cephalin) and phosphatidyl choline (Lecithin) predominated. The sterol fraction showing activity contained β-sitosterol, stigmasterol and an unidentified isomer of β-sitosterol. The evidence shows that dietary phytosterols and phospholipids, both individually and in combination, have a protective effect on gastroduodenal mucosa. These findings may prove to be important in the prevention and management of duodenal and gastric ulceration including ulceration due to NSAIDs.
Collapse
Affiliation(s)
- F I Tovey
- Division of Surgery and Interventional Science, University College, London, UK.
| | | | | |
Collapse
|
8
|
Raji Y, Oloyede GK. Antiulcerogenic effects and possible mechanism of action of Quassia amara (L. Simaroubaceae) extract and its bioactive principles in rats. AFRICAN JOURNAL OF TRADITIONAL, COMPLEMENTARY, AND ALTERNATIVE MEDICINES : AJTCAM 2011; 9:112-9. [PMID: 23983328 PMCID: PMC3746530 DOI: 10.4314/ajtcam.v9i1.16] [Citation(s) in RCA: 5] [Impact Index Per Article: 0.4] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Track Full Text] [Subscribe] [Scholar Register] [Indexed: 11/17/2022]
Abstract
The effects of Quassia amara extract (Q. amara) and its bioactive principles-quassin and 2-methoxycanthin-6-one on gastric ulceration were studied in albino rats. Q. amara (200-800 mg/kg p.o.; 5-20 mg/kg i.p) and 2-methoxycanthin-6-one (12.5, 25.0 and 50.0 mg/kg p.o; 1, 2 and 4 mg/kg i.p) but not quassin (12.5, 25.0 and 50 mg/kg p.o; 1, 2 and 4 mg/kg i.p) significantly inhibited gastric ulceration induced by indomethacin (40mg/kg). Administration of Q. amara (800 mg/kg p.o and 20 mg/kg i.p) and 2-methoxycanthin-6-one (12.5 mg/kg p.o; 4 mg/kg i.p) caused between 77%-85% cytoprotection against indomethacin (40 mg/kg, i.p) - induced gastric ulceration. Quassin did not cause any significant change in indomethacin-induced gastric ulceration. The inhibition of gastric ulceration produced by Q. amara and 2-methoxycanthin-6 one was accompanied by significant dose-dependent decreases (P< 0.01) in total gastric acidity. To investigate the probable mechanism of action, the individual effects of the extract and its principles alone and in combination with histamine (1 mg/kg) or cimetidine (0.12 mg/kg) on gastric acid secretion in situ were studied. Q. amara (20 mg/kg) and 2-methoxycanthin-6-one (4 mg/kg) but not quassin significantly (P< 0.01) inhibited the basal and histamine-induced gastric acid secretion. Inhibition of gastric acid secretion by Q. amara and 2-methoxycanthin-6-one was accentuated by cimetidine. The results suggest that Q. amara and its bioactive principle, 2-methoxycanthin-6-one possess antiulcer activity probably acting via histamine H2 receptor. This could be a potential source of potent and effective antiulcer agents.
Collapse
Affiliation(s)
- Yinusa Raji
- Department of Physiology University of Ibadan Ibadan, Nigeria.
| | | |
Collapse
|
9
|
Ma LS. A tribute to Dr. Frank I Tovey on his 90th birthday. World J Gastroenterol 2011; 17:3565-6. [PMID: 21987600 PMCID: PMC3180010 DOI: 10.3748/wjg.v17.i31.3565] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Download PDF] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Received: 08/09/2011] [Revised: 08/11/2011] [Accepted: 08/14/2011] [Indexed: 02/06/2023] Open
Abstract
This paper pays a tribute to Dr. Frank I Tovey on his 90th birthday which happens on September 1, 2011, and briefly describes the major findings in his research career and contributions as follows. The geographical prevalence of duodenal ulceration is related to staple diets. Unrefined wheat and maize, soya, certain pulses and millets are associated with a low prevalence while refined wheat, maize and rice, yams, cassava and green banana with a high prevalence. Predominant foodstuffs from low prevalence areas are ulceroprotective in rat peptic ulcer models. The protective activity lies in the lipid fraction present in these foodstuffs. The lipid fraction also promotes ulcer healing, is active both orally and intramuscularly and is ulceroprotective against non-steroidal anti-inflammatory drugs (NSAIDs). The phospholipids and phytosterols present in the lipid have been identified to be responsible for this protective activity. The combination of phospholipids and phytosterols may be of value in the prevention and treatment of duodenal ulceration and protection against the ulcerogenic effect of NSAIDs.
Collapse
|
10
|
Tovey FI, Capanoglu D, Langley GJ, Herniman JM, Bor S, Ozutemiz O, Hobsley M, Bardhan KD, Linclau B. Dietary Phytosterols Protective Against Peptic Ulceration. Gastroenterology Res 2011; 4:149-156. [PMID: 27942332 PMCID: PMC5139726 DOI: 10.4021/gr328w] [Citation(s) in RCA: 5] [Impact Index Per Article: 0.4] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Download PDF] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Accepted: 07/04/2011] [Indexed: 12/24/2022] Open
Abstract
BACKGROUND In developing countries the prevalence of duodenal ulceration is related to the staple diet and not to the prevalence of Helicobacter pylori. Experiments using animal peptic ulcer models show that the lipid fraction in foods from the staple diets of low prevalence areas gives protection against ulceration, including ulceration due to non-steroidal anti-inflammatory drugs (NSAIDs), and also promotes healing of ulceration. The lipid from the pulse Dolichos biflorus (Horse gram) was highly active and used for further investigations. Further experiments showed the phospholipids, sterol esters and sterols present in Horse gram lipid were gastroprotective. Dietary phospholipids are known to be protective, but the nature of protective sterols in staple diets is not known. The present research investigates the nature of the protective phytosterols. METHODS Sterol fractions were extracted from the lipid in Dolichos biflorus and tested for gastroprotection using the rat ethanol model. The fractions showing protective activity were isolated and identification of the components was investigated by Gas Chromatography-Mass Spectrometry (GC-MS). RESULTS The protective phytosterol fraction was shown to consist of stigmasterol, β-sitosterol and a third as yet unidentified sterol, isomeric with β-sitosterol. CONCLUSIONS Dietary changes, affecting the intake of protective phospholipids and phytosterols, may reduce the prevalence of duodenal ulceration in areas of high prevalence and may reduce the incidence of recurrent duodenal ulceration after healing and elimination of Helicobacter pylori infection. A combination of phospholipids and phytosterols, such as found in the lipid fraction of ulceroprotecive foods, may be of value in giving protection against the ulcerogenic effect of NSAIDs.
Collapse
Affiliation(s)
- Frank I Tovey
- Division of Surgery and Interventional Science, University College, London, UK
| | - Doga Capanoglu
- Department of Gastroenterology, Ege University, Bornova, Turkey
| | | | | | - Serhat Bor
- Department of Gastroenterology, Ege University, Bornova, Turkey
| | - Omer Ozutemiz
- Department of Gastroenterology, Ege University, Bornova, Turkey
| | - Michael Hobsley
- Division of Surgery and Interventional Science, University College, London, UK
| | | | | |
Collapse
|
11
|
|
12
|
Controversies in the Helicobacter pylori/duodenal ulcer story. Trans R Soc Trop Med Hyg 2008; 102:1171-5. [PMID: 18589464 DOI: 10.1016/j.trstmh.2008.04.035] [Citation(s) in RCA: 13] [Impact Index Per Article: 0.8] [Reference Citation Analysis] [Abstract] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 04/21/2008] [Revised: 04/24/2008] [Accepted: 04/24/2008] [Indexed: 12/12/2022] Open
Abstract
In patients with Helicobacter pylori-positive duodenal ulcer (DU), the organism must be eradicated to achieve rapid, stable healing. However, evidence is against much else that is commonly accepted. (1) Does H. pylori cause the ulcer? Evidence against includes archaeopathology, geographical prevalence, temporal relationships and H. pylori-negative DU patients. DU can recur after eradication of H. pylori infection, and DUs may remain healed after reduction of acid secretion despite persistent infection. The faster healing of ulcers when H. pylori has been eradicated is due to the organism's interference with neoangiogenesis and the healing of wounded epithelial cells. (2) Does H. pylori infection persist until pharmacologically eradicated? Studies based on current infection show that H. pylori infection is a labile state that can change in 3 months. High rates of gastric acid secretion result in spontaneous cure, whereas low rates permit re-infection. Hydrochloric acid, necessary for producing a DU, is strongly associated with the likelihood of an ulcer. At the start, patients owe their ulcer to gastric hypersecretion of hydrochloric acid; approximately 60% may be H. pylori-negative. If acid is suppressed, the less acid milieu encourages invasion by H. pylori, especially if the strain is virulent.
Collapse
|
13
|
Lawal OO, Rotimi O, Okeke I. Helicobacter pylori in gastroduodenal diseases. J Natl Med Assoc 2007; 99:31-4. [PMID: 17304966 PMCID: PMC2569589] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Abstract] [MESH Headings] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 05/14/2023]
Abstract
OBJECTIVE To determine the prevalence and disease association of Helicobacter pylori (H. pylori) in dyspeptic patients in southwest Nigeria. SETTING Obafemi Awolowo University Teaching Hospitals Complex, Ile-lfe, Nigeria. METHODS Consecutive dyspeptic patients for upper gastrointestinal endoscopy from January 1996 to March 1997 were investigated for H. pylori in gastric biopsy by histopathology and culture. Patients without gastroduodenal ulcerations or neoplastic lesions constituted the nonulcer dyspeptic (NUD) group. RESULTS 138 (92 males, 46 females) patients aged 4.5-85 years [mean (7) = 45+/-SD 17.8 years] who had upper gastrointestinal endoscopy were analyzed for presence of H. pylori. Eighty-three had histopathology alone, while 55 others had both histology and culture. Endoscopic diagnosis included duodenal ulcer (DU) (n=35, 23%); gastric ulcer (n=4, 3%); gastric cancer (n=14, 9%); NUD, including gastritis (n=49, 32%); duodenitis (n=47, 31%); and normal (n=16, 11%). Overall, H. pylori was positive in 107 of 138 (77.5%) patients. There was a significant association of H. pylori with DU and NUD (p<0.000). Three-quarters of cases of normal endoscopy harbored H. pylori. The finding of 80% and 85% H. pylori in gastritis and duodenitis, respectively, was of interest. CONCLUSIONS These findings suggest that DU and NUD were the main clinical expressions of H. pylori infection in southwest Nigerian dyspeptic patients similar to what is found in developed nations. Of note is the high incidence of H. pylori in endoscopically normal patients.
Collapse
Affiliation(s)
- Oladejo O Lawal
- Department of Surgery, College of Health Sciences, Obafemi Awolowo University, 220005 Ile-Ife, Osun State, Nigeria.
| | | | | |
Collapse
|
14
|
Abstract
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.
Collapse
Affiliation(s)
- Michael Hobsley
- Department of Surgery, Royal Free and University College Medical School, London, United Kingdom.
| | | | | |
Collapse
|
15
|
Sonnenberg A. Causes underlying the birth-cohort phenomenon of peptic ulcer: analysis of mortality data 1911–2000, England and Wales. Int J Epidemiol 2006; 35:1090-7. [PMID: 16709617 DOI: 10.1093/ije/dyl093] [Citation(s) in RCA: 29] [Impact Index Per Article: 1.5] [Reference Citation Analysis] [Abstract] [MESH Headings] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 01/28/2023] Open
Abstract
BACKGROUND Since humans have been infected with Helicobacter pylori for millennia, it has remained an enigma why the occurrence of gastric and duodenal ulcer rose suddenly during 19th century. The study aim is to present a mathematical model of H. pylori epidemiology that explains the peculiar long-term trends of ulcer disease. METHODS Gastric and duodenal ulcer mortality data from England and Wales between 1911 and 2000 were used to validate a model based on two simple and straightforward assumptions about H. pylori infection. First, the infection rate fell in the general population between 1,800 and 2,000. Second, gastric ulcer was caused by H. pylori infection contracted between the ages 5 and 15 and duodenal ulcer was caused by H. pylori infection contracted after the age of 15. As the infection receded in the general population, the two fractions of subjects who became infected between the ages 5 and 15 or after the age of 15 increased among consecutive birth cohorts. RESULTS The analysis of the actual long-term mortality from gastric and duodenal ulcer indicates an underlying birth-cohort pattern. These birth-cohort patterns of gastric and duodenal ulcer could be simulated by the interaction of two opposing time trends, namely a declining infection rate and a rising fraction of individuals acquiring their infection at increasingly older ages. The superimposition of a declining and a rising trend resulted in a bell-shaped curve of ulcer occurrence affecting consecutive birth-cohorts born between 1830 and 1970. Similar to the real data, the modelled cohort pattern of gastric ulcer preceded that of duodenal ulcer by 20 years. CONCLUSION The birth-cohort phenomenon of ulcer disease can be explained by a receding H. pylori infection accompanied by a simultaneous shift in its age of acquisition.
Collapse
Affiliation(s)
- Amnon Sonnenberg
- Portland VA Medical Center P3-GI, 3710 SW US Veterans Hospital Road, OR 97239, USA.
| |
Collapse
|
16
|
Abstract
BACKGROUND In South Africa there is suggestive evidence that home-pounded maize protects against duodenal ulceration. Therefore the purpose of the present paper was to test, in an animal model, whether oil from home-pounded maize gives protection against ulceration and whether this effect is present in commercially prepared maize oil. METHODS Gastric ulceration was induced in rats with topical ethanol 1 h after giving oil prepared either from fresh-pounded or from commercially treated maize. The lengths of the linear ulcers produced were measured with a planimeter and summed in each rat. Control observations were made using arachis oil (which is known not to be ulceroprotective) and horse gram lipid (which is known to be strongly ulceroprotective). Statistical comparisons were performed mainly with the Mann-Whitney U-test, but also with reference to the normal distribution. Thin-layer chromatography (TLC) was performed on the oil from fresh maize, and the fractions similarly investigated for ulceroprotective activity. RESULTS Fresh maize oil was strongly ulceroprotective (P = 0.0039), commercial maize oil was not (P = 0.2864). The active ingredient in the fresh maize oil was located in the fraction near the solvent front. CONCLUSION These findings support the hypothesis that home-pounded maize protects against duodenal ulceration.
Collapse
Affiliation(s)
- Frank I Tovey
- Department of Surgery, University College London, London, UK.
| | | | | | | |
Collapse
|
17
|
Agha A, Graham DY. Evidence-based examination of the African enigma in relation to Helicobacter pylori infection. Scand J Gastroenterol 2005; 40:523-9. [PMID: 16036504 DOI: 10.1080/00365520510012280] [Citation(s) in RCA: 48] [Impact Index Per Article: 2.4] [Reference Citation Analysis] [Abstract] [MESH Headings] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Indexed: 02/04/2023]
Abstract
OBJECTIVE 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. MATERIAL AND METHODS 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. RESULTS 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%). CONCLUSIONS 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.
Collapse
Affiliation(s)
- Aamer Agha
- Department of Medicine, VA Medical Center and Baylor College of Medicine, Houston, TX, USA
| | | |
Collapse
|
18
|
|
19
|
Ryan-Harshman M, Aldoori W. How diet and lifestyle affect duodenal ulcers. Review of the evidence. CANADIAN FAMILY PHYSICIAN MEDECIN DE FAMILLE CANADIEN 2004; 50:727-32. [PMID: 15171675 PMCID: PMC2214597] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Abstract] [MESH Headings] [Subscribe] [Scholar Register] [Indexed: 04/29/2023]
Abstract
OBJECTIVE To demonstrate the role of diet in reducing or aggravating risk of duodenal ulcer (DU). QUALITY OF EVIDENCE MEDLINE was searched from January 1966 to December 2001 for articles on the relationship between diet and lifestyle and DU using the key words duodenal ulcer and diet, fibre, or lifestyle. Evidence that these factors are associated with DU arose mainly from three case-control and three prospective studies (level II evidence) and from expert opinion (level III evidence). MAIN MESSAGE A high-fibre diet appears to reduce risk of DU; soluble fibre might be associated with reduced risk also. Vitamin A intake is associated with lower risk of DU. Little evidence indicates that fat, type of fat, protein intake, or consumption of alcohol or caffeine affect the etiology of DU. CONCLUSION A high-fibre diet, particularly if the fibre comes from fruit and vegetables, could reduce risk of DU; vitamin A might also be beneficial.
Collapse
|
20
|
Neuhann HF, Swai B, Carpenter CF, Shao O. Efficacy of different antibiotic regimens for eradication treatment of Helicobacter pylori infection in peptic ulcer disease in Tanzanian patients. Trop Doct 2003; 33:225-8. [PMID: 14620428 DOI: 10.1177/004947550303300413] [Citation(s) in RCA: 1] [Impact Index Per Article: 0.0] [Reference Citation Analysis] [MESH Headings] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 11/15/2022]
Affiliation(s)
- H F Neuhann
- Kilimanjaro Christian Medical Centre and College, Department of Internal Medicine, Moshi, Tanzania.
| | | | | | | |
Collapse
|
21
|
Rocha AM, Rocha GA, de Magalhães Queiroz DM, Ani AE, Okeke EN, Bello CS, Malu AO. Anti-CagA antibodies in Helicobacter pylori-positive patients and blood donors from Nigeria. Trop Doct 2001; 31:147-9. [PMID: 11444335 DOI: 10.1177/004947550103100310] [Citation(s) in RCA: 5] [Impact Index Per Article: 0.2] [Reference Citation Analysis] [Abstract] [MESH Headings] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 11/16/2022]
Abstract
The prevalence of antibodies to CagA protein was evaluated in 174 Helicobacter pylori-positive. subjects: 110 patients submitted to upper gastrointestinal endoscopy and 64 male blood donors. The patients were from different regions of Nigeria: Jos, North, Benue,West and East and the blood donors were from Jos. Sera were assayed for anti-CagA antibodies using Helicobacter p120, CagA ELISA (Viva Diagnostika, Hürth, Germany). Anti-CagA antibodies were detected in 104 (94.5%) patients and in 61 (95.3%) blood donors (P=1.0). Patients from the Benue region presented a lower frequency of anti-CagA antibodies than patients from the other regions (P=0.0004). When the subjects were stratified by age, a significant increase in IgG concentration was observed among the men (P=0.03) but not among the women (P=0.57) or among the blood donors (P=0.83). In conclusion, similarly toAsian countries, CagA-positive H. pylori infection is highly frequent in Nigeria.
Collapse
Affiliation(s)
- A M Rocha
- Laboratory of Research in Bacteriology, Faculdade de Medicina, Universidade Federal de Minas Gerais, Belo Horizonte, Brazil
| | | | | | | | | | | | | |
Collapse
|
22
|
|
23
|
Fernando N, Holton J, Zulu I, Vaira D, Mwaba P, Kelly P. Helicobacter pylori infection in an urban African population. J Clin Microbiol 2001; 39:1323-7. [PMID: 11283050 PMCID: PMC87933 DOI: 10.1128/jcm.39.4.1323-1327.2001] [Citation(s) in RCA: 35] [Impact Index Per Article: 1.5] [Reference Citation Analysis] [Abstract] [MESH Headings] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 12/04/2000] [Accepted: 01/23/2001] [Indexed: 01/03/2023] Open
Abstract
We have studied 221 adults drawn from an impoverished urban population with high human immunodeficiency virus (HIV) seroprevalence (35%) to determine the prevalence of gastroduodenal pathology and its relationship to serological markers of Helicobacter pylori virulence proteins and other potential environmental and immunological determinants of disease including HIV infection. Eighty-one percent were H. pylori seropositive, and 35% were HIV seropositive. Urban upbringing and low CD4 count were associated with a reduced likelihood of H. pylori seropositivity, as was current Ascaris infection, in keeping with recent evidence from an animal model. One hundred ninety-one adults underwent gastroduodenoscopy, and 14 had gastroduodenal pathology. Mucosal lesions were a major cause of abdominal pain in this population. While the majority of patients with gastroduodenal pathology (12 of 14) were seropositive for H. pylori, none were seropositive for HIV. Smoking was associated with increased risk of macroscopic pathology, and a history of Mycobacterium bovis BCG immunization was associated with reduced risk. Antibodies to H. pylori lipopolysaccharide were associated with pathology. HIV infection was associated with protection against mucosal lesions, suggesting that fully functional CD4 lymphocytes may be required for the genesis of gastroduodenal pathology.
Collapse
Affiliation(s)
- N Fernando
- Department of Bacteriology, Royal Free and University College London Medical School, London, United Kingdom.
| | | | | | | | | | | |
Collapse
|
24
|
Jayaraj AP, Tovey FI, Lewin MR, Clark CG. Duodenal ulcer prevalence: experimental evidence for the possible role of dietary lipids. J Gastroenterol Hepatol 2000; 15:610-6. [PMID: 10921413 DOI: 10.1046/j.1440-1746.2000.02214.x] [Citation(s) in RCA: 26] [Impact Index Per Article: 1.0] [Reference Citation Analysis] [Abstract] [MESH Headings] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Indexed: 12/11/2022]
Abstract
BACKGROUND AND AIMS Mapping the geographical distribution of duodenal ulcer in relation to staple diets, and experiments on animal peptic ulcer models suggested that the lipid fraction in certain foodstuffs had a protective effect which was most marked in the lipid obtained from Horse gram (Dolichos biflorus). Lipid obtained from stored polished rice or rice bran was ulcerogenic. Further animal experiments were designed to investigate the protective and healing effects of Horse gram lipid (HGL) against peptic ulceration. METHODS Three effects were investigated in rats: (i) the protective effect of HGL on peptic ulceration produced by using pyloric ligation in combination with South Indian diet or rice bran oil, or by cysteamine, alcohol or aspirin; (ii) the effect of HGL on mast cell degranulation in response to pyloric ligation and rice bran oil; and (iii) the healing effect of HGL on acute gastric ulceration produced by alcohol, on chronic gastric ulceration produced by topical acetic acid or on chronic duodenal ulcer following cysteamine. RESULTS Horse gram lipid was shown to be protective and to promote ulcer healing in all the models used. Mast cell degranulation was inhibited. CONCLUSION The experiments confirm the presence of a lipid in certain staple foods that have protective and healing properties in experimental peptic ulcer animal models. The differences in the prevalence of duodenal ulceration between different regions in some developing countries with a high prevalence of Helicobacter pylori infection might be explained by the presence or absence of protective lipids or ulcerogenic factors in the staple diet.
Collapse
Affiliation(s)
- A P Jayaraj
- Department of Surgery, Royal Free and University College Medical School, London, United Kingdom
| | | | | | | |
Collapse
|
25
|
Abstract
In general, peptic ulcer occurs at equal rates in the East and the West but with marked regional differences in both, even within the same country. In the West, the incidence of peptic ulcer, particularly duodenal ulcer, rose sharply at the turn of the century and has shown a rapid decline in the past three decades. In the East, the rise was equally impressive, but the decline appears to have been delayed, only starting in the past decade. Asians present their ulcer symptoms a decade earlier than Caucasians, and it has been suggested that this early presentation may be attributable to Helicobacter pylori (H. pylori) infection at a younger age. Interestingly, the male-to-female ratio is much higher in the East than in the West, and the duodenal-to-gastric ulcer ratio manifests a much wider variation in Asians than in Caucasians. As in Western countries, peptic ulcer occurrence in the East shows a cyclical trend, with a peak frequency in the winter months. In the West, the placebo healing rate varies widely up to 78%, whereas in the East it is rather consistent at around one-third. These variations in geographical distribution, time trends, sex and ulcer ratios, seasonal rates and behavioral response to placebo treatment indicate that while H. pylori is a major cause of peptic ulceration, other environmental and genetic factors contribute to ulcer formation. The parietal cell mass and acid secretory capacity of Asian patients with duodenal ulcer are only slightly more than half of those of Caucasian patients, which may explain why Asian patients respond equally well to half the standard dose of anti-secretory agents used in Caucasians. H. pylori infection is generally more prevalent in the East than in the West and is more resistant to metronidazole. The response to standard triple therapies for eradication, however, appears to be as effective in the East as in the West.
Collapse
Affiliation(s)
- S K Lam
- Department of Medicine, University of Hong Kong, Queen Mary Hospital
| |
Collapse
|
26
|
Abstract
Helicobacter pylori infection may not be the primary cause of duodenal ulceration in cases not associated with non-steroidal anti-inflammatory drugs, but may be a secondary complication. In developing countries with a uniformly high prevalence of H. pylori infection there are marked regional differences in the prevalence of duodenal ulcer (DU). In some countries, especially those with a low prevalence of H. pylori, 30-40% or more patients with DU may be H. pylori negative. The absence of H. pylori infection in early cases of DU is also reported. In DU patients with antral H. pylori infection, duodenal colonization by H. pylori may often be absent. After complete H. pylori eradication, recurrence of DU within 6 months in some reports is as high as 20%. The evidence suggests that high acidity and reduced duodenal mucosal resistance remain the primary causes of DU and that H. pylori infection, when present, results in chronicity. Reduced mucosal resistance results in duodenal gastric metaplasia which permits colonization of the duodenum with H. pylori from the antrum. Therefore, whatever causes reduced mucosal resistance may be the primary factor and evidence suggests that this cause may be diet related. This would explain the enigma of regional variations in DU prevalence unrelated to H. pylori prevalence.
Collapse
Affiliation(s)
- F I Tovey
- Department of Surgery, Royal Free and University College Medical School, London, United Kingdom.
| | | |
Collapse
|
27
|
Ani AE, Malu AO, Onah JA, Queiroz DM, Kirschner G, Rocha GA. Antimicrobial susceptibility test of Helicobacter pylori isolated from Jos, Nigeria. Trans R Soc Trop Med Hyg 1999; 93:659-61. [PMID: 10717760 DOI: 10.1016/s0035-9203(99)90089-5] [Citation(s) in RCA: 25] [Impact Index Per Article: 1.0] [Reference Citation Analysis] [Abstract] [MESH Headings] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 01/16/2023] Open
Abstract
Fifty-five strains of Helicobacter pylori isolated from November 1997 until October 1998 from 33 female and 22 male adults attending for endoscopy at the Evangel Hospital, Jos, Nigeria were assayed for antibiotic susceptibility to amoxycillin, clarithromycin, metronidazole and tetracycline by the E-test strip method. Minimum inhibitory concentration (MIC) within the attainable peak serum concentrations for each drug was used as the parameter to determine the susceptibility of H. pylori. The results showed 100% susceptibility for amoxycillin, 89.0% for tetracycline, 87.3% for clarithromycin and 60% for metronidazole. The MIC50 and MIC90 values were: 0.016 microgram/mL and 0.75 microgram/mL for amoxycillin, 0.016 microgram/mL and 2 micrograms/mL for clarithromycin, 0.094 microgram/mL and 12 micrograms/mL for tetracycline, and 2 micrograms/mL and > 48 micrograms/mL for metronidazole. The MIC90 values for metronidazole (> 48 micrograms/mL) and tetracycline (12 micrograms/mL) were in each case higher than the break-point value (peak serum concentrations) of 8 micrograms/mL for metronidazole and 3 micrograms/mL for tetracycline. This pattern of resistance to metronidazole and tetracycline has to be considered when therapeutic regimens against H. pylori contain either or both drugs.
Collapse
Affiliation(s)
- A E Ani
- Department of Medical Microbiology, Faculty of Medical Sciences, University of Jos, Nigeria.
| | | | | | | | | | | |
Collapse
|
28
|
Abstract
BACKGROUND 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. METHODS 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. RESULTS 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. CONCLUSION 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.
Collapse
Affiliation(s)
- M Kidd
- Department of Medicine, University of Cape Town and Groote Schuur Hospital Observatory, South Africa
| | | | | |
Collapse
|
29
|
Wong BC, Ching CK, Lam SK, Li ZL, Chen BW, Li YN, Liu HJ, Liu JB, Wang BE, Yuan SZ, Xu CP, Hou XH, Zhang AT, Zheng ZT. Differential north to south gastric cancer-duodenal ulcer gradient in China. China Ulcer Study Group. J Gastroenterol Hepatol 1998; 13:1050-7. [PMID: 9835323 DOI: 10.1111/j.1440-1746.1998.tb00569.x] [Citation(s) in RCA: 35] [Impact Index Per Article: 1.3] [Reference Citation Analysis] [Abstract] [MESH Headings] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Indexed: 02/06/2023]
Abstract
There are suggestions that duodenal ulcer protects individuals from gastric cancer and that rice is ulcerogenic while wheat is gastro-protective. We aimed to examine the relationship of gastric cancer, duodenal and gastric ulcers in different geographical regions in China and identified dietary risk factors for duodenal ulcer and gastric cancer. The prevalence of peptic ulcer and gastric cancer among symptomatic patients in eight major cities, four each from the north and the south representing all the six defined regions of China were studied. Endoscopy and case records over a 10 year period were reviewed and cases of confirmed duodenal and gastric ulcer and gastric cancer, together with the total number of endoscopies performed per year, were recorded. Rates were expressed as cases/1000 endoscopies. Results were compared to another epidemiological study on diet and mortality in the same regions in China conducted at the same time. Duodenal ulcer rates were 2.4-fold higher in southern China than northern China, whereas gastric cancer rates were 1.6-fold higher in the north than in the south. Correlation studies showed for the first time an inverse linear relationship between the gastric cancer rates and the duodenal ulcer rates (r=-0.8076, P=0.015), as well as the duodenal ulcer: gastric ulcer ratios (r=-0.9133, P=0.002). Gastric ulcer rates were higher in southern China but did not correlate with the gastric cancer rates (r=0.1455, P=0.731). Duodenal ulcer rates were found to be related to daily rice intake (r=0.8554, P=0.029) and inversely related to daily wheat flour intake (r=-0.8472, P=0.033). Gastric cancer rates were not related to any dietary risk factors tested. We concluded there was an inverse relationship between gastric cancer rates and duodenal ulcer rates. Although duodenal ulceration and gastric cancer are both linked to Helicobacter pylori infection, the findings of this study indicate independent additional aetiological factors for the pathogenesis of these conditions. Dietary factors such as rice or wheat intake may play a role.
Collapse
Affiliation(s)
- B C Wong
- Department of Medicine, Queen Mary Hospital, University of Hong Kong, China
| | | | | | | | | | | | | | | | | | | | | | | | | | | |
Collapse
|
30
|
Boucher BJ. Intestinal absorption of beta-carotene, lycopene and lutein in men and women following a standard meal. Br J Nutr 1998; 80:115. [PMID: 9797651 DOI: 10.1017/s0007114598001846] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [MESH Headings] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 11/06/2022]
|
31
|
Rauws EJ, Tytgat GN. Helicobacter pylori in duodenal and gastric ulcer disease. BAILLIERE'S CLINICAL GASTROENTEROLOGY 1995; 9:529-47. [PMID: 8563052 DOI: 10.1016/0950-3528(95)90047-0] [Citation(s) in RCA: 17] [Impact Index Per Article: 0.6] [Reference Citation Analysis] [Abstract] [MESH Headings] [Track Full Text] [Subscribe] [Scholar Register] [Indexed: 01/31/2023]
Abstract
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.
Collapse
Affiliation(s)
- E J Rauws
- Department of Gastroenterology and Hepatology, Academic Medical Centre, Amsterdam, The Netherlands
| | | |
Collapse
|
32
|
Alam MM. Incidence of duodenal ulcer and its surgical management in a teaching hospital in Bangladesh. Trop Doct 1995; 25:67-8. [PMID: 7778197 DOI: 10.1177/004947559502500206] [Citation(s) in RCA: 5] [Impact Index Per Article: 0.2] [Reference Citation Analysis] [Abstract] [MESH Headings] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 01/27/2023]
Abstract
Duodenal ulcer patients with or without complications admitted in the surgical departments of Rajshahi Medical College Hospital (RMCH) during the period of 13 years from 1980-1992 were studied retrospectively. Duodenal ulcer accounted for 10/1000 admission and five operations per week. Of the 1623 patients with uncomplicated ulcer, only 623 needed surgical treatment. However, all of the 1599 who presented with pyloric stenosis, 1047 with peritonitis due to perforation, and 13 with hematemesis were operated upon. This study confirms previously published reports of high incidence of duodenal ulcer admissions in the hospital but shows a diminishing number in the uncomplicated cases requiring surgery.
Collapse
Affiliation(s)
- M M Alam
- Department of Surgery, Rajshahi Medical College, Bangladesh
| |
Collapse
|
33
|
Thompson L, Cockayne A, Spiller RC. Inhibitory effect of polyunsaturated fatty acids on the growth of Helicobacter pylori: a possible explanation of the effect of diet on peptic ulceration. Gut 1994; 35:1557-61. [PMID: 7828972 PMCID: PMC1375611 DOI: 10.1136/gut.35.11.1557] [Citation(s) in RCA: 86] [Impact Index Per Article: 2.8] [Reference Citation Analysis] [Abstract] [MESH Headings] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Indexed: 01/27/2023]
Abstract
Diets high in polyunsaturated fatty acids may protect against duodenal ulcer, possibly through inhibiting the growth of Helicobacter pylori. This hypothesis was tested in vitro by incubating H pylori microaerophilically with a range of polyunsaturated fatty acids. omega-3 Linolenic acid significantly, but reversibly, inhibited growth at 1.8, 2.5, and 5 x 10(-4) M (p < 0.01), while concentrations of 10(-3) M killed virtually all organisms, with cell lysis observed by electron microscopy. Similar inhibitory effects were seen with other polyunsaturated fatty acids, at concentrations of 2.5 x 10(-4) M the relative inhibitory potencies were oleic (C18:1) < linoleic (C18:2) < arachidonic (C20:4) < omega-3 linolenic (C18:3) = omega-6 linolenic (C18:3) = eicosapentanoic (C20:5) acid. Cell fractionation studies with 14C labelled linolenic acid showed that the linolenic acid was associated with the membrane fraction. Commonly ingested dietary polyunsaturated fatty acids inhibit the growth of H pylori in vitro, an effect which deserves further in vivo study.
Collapse
Affiliation(s)
- L Thompson
- Department of Therapeutics, University Hospital, Nottingham
| | | | | |
Collapse
|
34
|
Holcombe C, Umar H, Lucas SB, Kaluba J. Low incidence of clinically significant gastroduodenal pathology despite a high incidence of Helicobacter pylori infection. Trans R Soc Trop Med Hyg 1994; 88:569-71. [PMID: 7992342 DOI: 10.1016/0035-9203(94)90166-x] [Citation(s) in RCA: 8] [Impact Index Per Article: 0.3] [Reference Citation Analysis] [Abstract] [MESH Headings] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 02/08/2023] Open
Abstract
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%).
Collapse
Affiliation(s)
- C Holcombe
- Department of Surgery, University of Maiduguri, Nigeria
| | | | | | | |
Collapse
|
35
|
Abstract
Two hundred and forty-three Nigerian patients referred for endoscopy at the Jos University Teaching Hospital in Nigeria were studied. Their overall mean age was 37.7 years (SD 12.7), among those with ulcers it was 38.4 years. The male:female ratio was equal in general, but among those with ulcers it was 2:1. Duodenal and gastric ulcers were found in 42(17.3%) and 12(4.9%) patients respectively, ratio of 3.5:1. There were 3 patients each with oesophageal and gastric carcinoma. Our findings do not support the belief that the savannah region of West Africa is an area of low prevalence of peptic ulcer disease. In the light of the importance of Helicobacter pylori infection in the pathogenesis of gastroduodenal diseases and the apparent discrepancy between its prevalence and that of associated diseases in the developing countries, there is a need to reappraise our traditional beliefs about the epidemiology of these diseases, using similar methods to those used in developed countries.
Collapse
Affiliation(s)
- A O Malu
- Department of Medicine, Jos University Teaching Hospital, Nigeria
| | | | | |
Collapse
|
36
|
Holcombe C, Kaluba J, Lucas SB. Helicobacter pylori infection and gastritis in healthy Nigerians. Eur J Epidemiol 1994; 10:223-5. [PMID: 7813703 DOI: 10.1007/bf01730375] [Citation(s) in RCA: 7] [Impact Index Per Article: 0.2] [Reference Citation Analysis] [Abstract] [MESH Headings] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 01/27/2023]
Abstract
In a study of forty asymptomatic volunteers from northern Nigeria; 35 (87.5%) had histological gastritis and 32 (80%) were infected by Helicobacter pylori. All but one of the patients infected by Helicobacter Pylori had histological gastritis. This high prevalence of H. Pylori infection in young, asymptomatic subjects, occurs in an area with a low prevalence of duodenal ulcer. The possible reasons for this are discussed.
Collapse
Affiliation(s)
- C Holcombe
- Academic Department of Surgery, University of Maiduguri, Nigeria
| | | | | |
Collapse
|
37
|
Affiliation(s)
- F I Tovey
- Department of Surgery, University College London, UK
| |
Collapse
|
38
|
Abstract
There are five known environmental, causative factors for peptic ulcer, namely, non-steroidal anti-inflammatory drugs (NSAID), Helicobacter pylori infection, cigarette smoking, environmental stress and dietary habit. There have been six factual, epidemiological observations on peptic ulcer this century: the rise and fall of ulcer frequency in Western societies; geographical variations in ulcer rates; in sex ratios; in duodenal: gastric ulcer ratios; and in placebo healing rates; and seasonal variation in ulcer frequencies. This report examines each of these epidemiological observations to see if each of the environmental factors can explain the observations. The secular trends and the variation in ulcer rates can be related to all the environmental factors. The sex ratios can be explained on the basis of cigarette smoking and environmental stress, whereas the duodenal: gastric ulcer ratios may be ascribed to NSAID use. Placebo healing and seasonal occurrence of ulcer is probably more related to environmental stress. Helicobacter pylori infection alone cannot explain the sex ratios, the duodenal: gastric ulcer ratios, the placebo healing and the seasonal occurrence of ulcer. Cigarette smoking or NSAID use alone does not tally with the seasonal variation of ulcer frequencies. Environmental stress alone does not fit into the recent fall of ulcer rates in Western countries. This report supports the concept of heterogeneity in peptic ulceration.
Collapse
Affiliation(s)
- S K Lam
- Department of Medicine, University of Hong Kong, Queen Mary Hospital
| |
Collapse
|
39
|
Abstract
At the turn of the century, duodenal ulcer rose from rarity to affect 10% of males in their life time, subsequently declining in some countries such as UK, levelling off in others such as Germany, and continuing to increase in still others such as Hong Kong. The annual incidence per 1000 population varies from about 1 in Japan to 1.5 in Norway, 1.8 in USA and 2.7 in Scotland, and the frequency also varies within many individual countries, such as Australia, China and India, and among races such as a higher prevalence among whites than blacks in USA and among Chinese than Javanese in Indonesia. Ulcer frequency is higher in winter months, and this appears universal, being true in cold as well as in warm countries. Most places report a rise of ulcer rates among the elderly in recent decades. The male to female ratio also varies geographically, for example from 1:1 in USA to 18:1 in India, and with time such as moving from 2:1 to 1:1 in the last two decades in USA, and the duodenal ulcer to gastric ulcer ratio varies widely from place to place, for example from 0.8 in Japan to 19:1 in Africa and 32:1 in India. Placebo healing rates also differ geographically, ranging from 5% in Philippines to 78% in Mexico. These epidemiological data can only be explained by the presence of multiple aetiological factors, including analgesics, society stress, cigarette smoking, Helicobacter pylori, dietary factors, and genetic factors. Three lines of evidence support a genetic role: family studies, twin studies and blood group studies. Family aggregation occurs more commonly in patients with early-onset (< 30 yr) of symptoms. Blood group O prevalence is more associated with late-onset of symptoms. Other genetic markers include nonsecretor status, HLA antigens, phenylthiocarbamide taste sensitivity, and alpha-1-antitrypsin. Genetic syndromes such as MEN I also support a genetic role and give insight into pathogenetic mechanisms. The best physiological marker is still hyperpepsinogenemia I, which is transmitted by autosomal dominance, despite recent report of lower serum pepsinogen 1 after healing of Helicobacter pylori associated gastritis.
Collapse
Affiliation(s)
- S K Lam
- Department of Medicine, University of Hong Kong, Queen Mary Hospital
| |
Collapse
|
40
|
Holcombe C, Tsimiri S, Eldridge J, Jones DM. Prevalence of antibody to Helicobacter pylori in children in northern Nigeria. Trans R Soc Trop Med Hyg 1993; 87:19-21. [PMID: 8465385 DOI: 10.1016/0035-9203(93)90403-d] [Citation(s) in RCA: 34] [Impact Index Per Article: 1.1] [Reference Citation Analysis] [Abstract] [MESH Headings] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 01/30/2023] Open
Abstract
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.
Collapse
Affiliation(s)
- C Holcombe
- Academic Department of Surgery, University of Maiduguri, Northern Nigeria
| | | | | | | |
Collapse
|
41
|
Affiliation(s)
- D A Watters
- Department of Surgery, University Teaching Hospital, Lusaka, Zambia
| |
Collapse
|
42
|
Abstract
The author visited China in 1981 and 1984 and obtained data comparing the incidence of duodenal ulcer in the rice eating districts of the south with the incidence in the wheat, maize and millet eating areas of the north. The evidence suggested a higher prevalence of duodenal ulcer in the rice eating areas than in the wheat eating areas, and a low prevalence in association with millet eating. However, the differences were less marked than between similar rice and wheat eating areas of India. It is suggested that the lower prevalence of duodenal ulcer in the wheat eating areas of north India compared with the rice eating areas of south India may be due in part to the mucosal protective effect of wheat bran in the unrefined wheat that is used in making chappatis. In China white refined flour is used in the making of steamed bread with the loss of any protective effect of wheat bran.
Collapse
Affiliation(s)
- F I Tovey
- Department of Surgery, University College London, UK
| |
Collapse
|
43
|
Affiliation(s)
- C Holcombe
- Department of Surgery, Charing Cross Hospital, London
| |
Collapse
|
44
|
Glavin GB, Murison R, Overmier JB, Pare WP, Bakke HK, Henke PG, Hernandez DE. The neurobiology of stress ulcers. BRAIN RESEARCH. BRAIN RESEARCH REVIEWS 1991; 16:301-43. [PMID: 1790434 DOI: 10.1016/0165-0173(91)90012-w] [Citation(s) in RCA: 93] [Impact Index Per Article: 2.7] [Reference Citation Analysis] [Abstract] [MESH Headings] [Track Full Text] [Subscribe] [Scholar Register] [Indexed: 12/28/2022]
Abstract
We have reviewed the neurobiology of stress ulcers from animal models to potential pharmacotherapeutic mechanisms. The evidence strongly supports the hypothesis that certain stress-related gastric lesions are 'brain-driven' events which may be more effectively managed through central manipulations than by altering local, gastric factors. Recent advances in the use of anxiolytic and antidepressant drugs in the management of stress-related gastric mucosal injury further supports the contention that a brain-gut axis, which may have nervous, peptidergic and classic monoaminergic components, modulates the intricate and complicated pattern of communication between the brain and the stomach. Delineation of the precise pathways which make up this communication as well as their manipulation by various pharmacological agents will be the focus of future research endeavour.
Collapse
Affiliation(s)
- G B Glavin
- Department of Pharmacology and Therapeutics, University of Manitoba, Winnipeg, Canada
| | | | | | | | | | | | | |
Collapse
|
45
|
Affiliation(s)
- C Holcombe
- Department of Surgery, Charing Cross Hospital, London, UK
| |
Collapse
|
46
|
Tytgat GNJ, Langenberg ML, Rauws EAJ, Noach LA, Dankert J. Helicobacter pylori infection and duodenal ulcer. BMJ : BRITISH MEDICAL JOURNAL 1991. [DOI: 10.1136/bmj.302.6791.1535-b] [Citation(s) in RCA: 1] [Impact Index Per Article: 0.0] [Reference Citation Analysis] [Track Full Text] [Subscribe] [Scholar Register] [Indexed: 11/04/2022]
|
47
|
|
48
|
|
49
|
Dixon MF, Wyatt JI. Helicobacter pylori infection and duodenal ulcer. BRITISH MEDICAL JOURNAL 1991. [DOI: 10.1136/bmj.302.6791.1535-a] [Citation(s) in RCA: 2] [Impact Index Per Article: 0.1] [Reference Citation Analysis] [Track Full Text] [Subscribe] [Scholar Register] [Indexed: 11/04/2022]
|
50
|
Holcombe C. Duodenal ulcer: the villain unmasked? West J Med 1991. [DOI: 10.1136/bmj.302.6788.1333-b] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 11/04/2022]
|