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Helge L. Waldum - One of the best experts on this subject based on the ideXlab platform.

  • The Phylogeny and Biological Function of Gastric Juice-Microbiological Consequences of Removing Gastric Acid.
    International Journal of Molecular Sciences, 2019
    Co-Authors: Tom C. Martinsen, Reidar Fossmark, Helge L. Waldum
    Abstract:

    Gastric juice is a unique combination of hydrochloric acid (HCl), lipase, and pepsin. Acidic Gastric juice is found in all vertebrates, and its main function is to inactivate microorganisms. The phylogenetic preservation of this energy-consuming and, at times, hazardous function (acid-related diseases) reflects its biological importance. Proton pump inhibitors (PPIs) are one of the most widely used drugs in the world. Due to the reduced prevalence of Helicobacter pylori infection as well as the increased use of inhibitors of Gastric acid secretion, the latter has become the most important cause of Gastric Hypoacidity. In the present manuscript, we review the microbiological consequences of removing Gastric acidity. The resulting susceptibility to infections has not been studied extensively, and focus has mainly been restricted to bacterial and parasitic agents only. The strongest evidence concerning the relationship between hypochlorhydria and predisposition to infections relates to bacterial infections affecting the gastrointestinal tract. However, several other clinical settings with increased susceptibility to infections due to inhibited Gastric acidity are discussed. We also discuss the impact of hypochlorhydria on the gut microbiome.

  • The Enterochromaffin-like [ECL] Cell—Central in Gastric Physiology and Pathology
    International Journal of Molecular Sciences, 2019
    Co-Authors: Helge L. Waldum, Øystein Sørdal, Patricia Mjønes
    Abstract:

    Background: Studies on the regulation of Gastric and pancreatic secretion began more than 100 years ago. Secretin was the first hormone postulated to exist, initiating the field of endocrinology. Gastrin produced in the antral mucosa was the second postulated hormone, and together with histamine and acetylcholine, represent the three major Gastric acid secretagogues known since 1920. For a long time, the mast cell was the only recognized histamine-producing cell in the oxyntic mucosa and, in the mid-1980s, the ECL cell was recognized as the cell producing histamine, taking part in the regulation of Gastric acid secretion. Methods: This review is based upon literature research and personal knowledge. Results: The ECL cell carries the gastrin receptor, and gastrin regulates its function (histamine release) as well as proliferation. Long-term hypergastrinemia results in Gastric neoplasia of variable malignancies, implying that Gastric Hypoacidity resulting in increased gastrin release will induce Gastric neoplasia, including Gastric cancer. Conclusions: The trophic effect of gastrin on the ECL cell has implications to the treatment with inhibitors of acid secretion.

  • Helicobacter pylori and Gastric acid: an intimate and reciprocal relationship
    Therapeutic Advances in Gastroenterology, 2016
    Co-Authors: Helge L. Waldum, Per Martin Kleveland, Øystein Sørdal
    Abstract:

    Helicobacter pylori (Hp) is the main cause of gastritis, peptic ulcer disease and Gastric cancer. There are still unanswered questions related to the interaction between Hp and man, like what determines the susceptibility for the initial infection and the mechanisms for the carcinogenic effect. The initial infection seems to require a temporal Gastric Hypoacidity. For Hp to survive in the Gastric mucous layer, some acidity is necessary. Hp itself is probably not directly carcinogenic. Only when inducing oxyntic mucosal inflammation and atrophy with Hypoacidity, Hp predisposes for Gastric cancer. Gastrin most likely plays a central role in the Hp pathogenesis of duodenal ulcer and Gastric cancer.

  • and Gastric acid: an intimate and reciprocal relationship
    SAGE Publishing, 2016
    Co-Authors: Helge L. Waldum, Per Martin Kleveland, Øystein Sørdal
    Abstract:

    Helicobacter pylori (Hp) is the main cause of gastritis, peptic ulcer disease and Gastric cancer. There are still unanswered questions related to the interaction between Hp and man, like what determines the susceptibility for the initial infection and the mechanisms for the carcinogenic effect. The initial infection seems to require a temporal Gastric Hypoacidity. For Hp to survive in the Gastric mucous layer, some acidity is necessary. Hp itself is probably not directly carcinogenic. Only when inducing oxyntic mucosal inflammation and atrophy with Hypoacidity, Hp predisposes for Gastric cancer. Gastrin most likely plays a central role in the Hp pathogenesis of duodenal ulcer and Gastric cancer

  • Gastrin May Mediate the Carcinogenic Effect of Helicobacter pylori Infection of the Stomach
    Digestive Diseases and Sciences, 2015
    Co-Authors: Helge L. Waldum, Øystein Sørdal, Øyvind Hauso, Reidar Fossmark
    Abstract:

    Gastric cancer occurs almost exclusively in patients with gastritis. Since Helicobacter pylori (Hp) was proved to cause gastritis, Hp was also expected to play a role in Gastric carcinogenesis. Despite extensive studies, the mechanisms by which Hp cause Gastric cancer are still poorly understood. However, there is evidence that the anatomical site of Hp infection is of major importance. Infection confined to the antral mucosa protects against Gastric cancer but predisposes to duodenal ulcer, whereas Hp infection of the oxyntic mucosa increases the risk of Gastric cancer. Hp infection does not predispose to cancers in the Gastric cardia. In patients with atrophic gastritis of the oxyntic mucosa, the intraGastric pH is elevated and the concentration of microorganisms in the stomach is increased. This does not lead to increased risk of Gastric cancer at all anatomical sites. The site specificity of Hp infection in relation to cancer risk indicates that neither Hp nor the changes in Gastric microflora due to Gastric Hypoacidity are carcinogenic per se. However, reduced Gastric acidity also leads to hypergastrinemia, which stimulates the function and proliferation of enterochromaffin-like (ECL) cells located in the oxyntic mucosa. The ECL cell may be more important in human Gastric carcinogenesis than previously realized, as every condition causing long-term hypergastrinemia in animals results in the development of neoplasia in the oxyntic mucosa. Patients with hypergastrinemia will far more often develop carcinomas in the Gastric corpus. In conclusion, hypergastrinemia may explain the carcinogenic effect of Hp.

Reidar Fossmark - One of the best experts on this subject based on the ideXlab platform.

  • The Phylogeny and Biological Function of Gastric Juice-Microbiological Consequences of Removing Gastric Acid.
    International Journal of Molecular Sciences, 2019
    Co-Authors: Tom C. Martinsen, Reidar Fossmark, Helge L. Waldum
    Abstract:

    Gastric juice is a unique combination of hydrochloric acid (HCl), lipase, and pepsin. Acidic Gastric juice is found in all vertebrates, and its main function is to inactivate microorganisms. The phylogenetic preservation of this energy-consuming and, at times, hazardous function (acid-related diseases) reflects its biological importance. Proton pump inhibitors (PPIs) are one of the most widely used drugs in the world. Due to the reduced prevalence of Helicobacter pylori infection as well as the increased use of inhibitors of Gastric acid secretion, the latter has become the most important cause of Gastric Hypoacidity. In the present manuscript, we review the microbiological consequences of removing Gastric acidity. The resulting susceptibility to infections has not been studied extensively, and focus has mainly been restricted to bacterial and parasitic agents only. The strongest evidence concerning the relationship between hypochlorhydria and predisposition to infections relates to bacterial infections affecting the gastrointestinal tract. However, several other clinical settings with increased susceptibility to infections due to inhibited Gastric acidity are discussed. We also discuss the impact of hypochlorhydria on the gut microbiome.

  • Gastrin May Mediate the Carcinogenic Effect of Helicobacter pylori Infection of the Stomach
    Digestive Diseases and Sciences, 2015
    Co-Authors: Helge L. Waldum, Øystein Sørdal, Øyvind Hauso, Reidar Fossmark
    Abstract:

    Gastric cancer occurs almost exclusively in patients with gastritis. Since Helicobacter pylori (Hp) was proved to cause gastritis, Hp was also expected to play a role in Gastric carcinogenesis. Despite extensive studies, the mechanisms by which Hp cause Gastric cancer are still poorly understood. However, there is evidence that the anatomical site of Hp infection is of major importance. Infection confined to the antral mucosa protects against Gastric cancer but predisposes to duodenal ulcer, whereas Hp infection of the oxyntic mucosa increases the risk of Gastric cancer. Hp infection does not predispose to cancers in the Gastric cardia. In patients with atrophic gastritis of the oxyntic mucosa, the intraGastric pH is elevated and the concentration of microorganisms in the stomach is increased. This does not lead to increased risk of Gastric cancer at all anatomical sites. The site specificity of Hp infection in relation to cancer risk indicates that neither Hp nor the changes in Gastric microflora due to Gastric Hypoacidity are carcinogenic per se. However, reduced Gastric acidity also leads to hypergastrinemia, which stimulates the function and proliferation of enterochromaffin-like (ECL) cells located in the oxyntic mucosa. The ECL cell may be more important in human Gastric carcinogenesis than previously realized, as every condition causing long-term hypergastrinemia in animals results in the development of neoplasia in the oxyntic mucosa. Patients with hypergastrinemia will far more often develop carcinomas in the Gastric corpus. In conclusion, hypergastrinemia may explain the carcinogenic effect of Hp.

  • Spontaneous ECL cell carcinomas in cotton rats: natural course and prevention by a gastrin receptor antagonist
    2015
    Co-Authors: Tom C. Martinsen, Reidar Fossmark, Gunnar Qvigstad, Shiro Kawase, Rolf Haêkanson, Sverre H. Torp, Arne K. S, Helge L. Waldum
    Abstract:

    In our inbred strain of cotton rats (Sigmodon hispidus) 50 % of the females develop spontaneous ECL cell-derived tumors in the acid-producing part of the stomach due to hypergastrinemia secondary to Gastric Hypoacidity. Although the mechanism behind the Hypoacidity is unknown, the female cotton rat is an excellent model for studying ECL cell-related tumorigenesis. In this study we wanted to explore the malignancy potential of these tumors and the ability of a gastrin receptor antagonist (YF476) to prevent their development. First, nine hypergastrinemic female cotton rats (10 months of age) were diagnosed by laparotomy as having Gastric tumors. They were killed 6 months later. Second, 18 female cotton rats (2 months of age) were dosed monthly for 6 months with YF476 (500 mmol/kg body wt) by s.c. injection, while 21 age

  • The distressing overuse of Gastric acid inhibitors.
    Digestive Diseases and Sciences, 2013
    Co-Authors: Reidar Fossmark, Helge L. Waldum
    Abstract:

    Gastric acid secretion by parietal cells is an energy consuming process that concentrates H? one million-fold. The energy required is produced by abundant mitochondria. High Gastric acidity in combination with the proteolytic enzyme, pepsin, and the lipolytic enzyme, lipase, plays a key role in killing ingested microorganisms including bacteria [1, 2], viruses [3], and prions [4]. This corrosive juice can, however, overwhelm mucosal defense mechanisms leading to erosion and ulceration. Stress ulcers and less severe damage to the Gastric mucosa may develop in critically ill patients. The damage, which occurs predominantly in the oxyntic mucosa, is thought to be caused by tissue hypoxia [5, 6]. Hypovolemic or hypotensive patients are at obvious risk of developing such ulcers, but severe illness also increases the risk of stress ulcers [7, 8], particularly in patients requiring mechanical ventilation. Experimental studies have suggested that antisecretory medications, e.g. proton pump inhibitors (PPIs) and histamine H2-receptor antagonists (H2RAs), reduce development of ulcers in the oxyntic mucosa by decreasing energy expenditure as well as raising intraGastric pH [9, 10]. In this issue of Digestive Diseases and Sciences, Koczka et al. [11] report the overuse of stress ulcer prophylaxis in a large medical center. This adds to a large body of literature reporting the inappropriate overprescription of PPIs. Although the use of Gastric acid inhibitors may reduce the risk of stress ulcers, it is important to target the therapy to patients at significant risk since PPIs have recently been associated with numerous adverse events, including infections. Gastric Hypoacidity leads to bacterial overgrowth in the stomach and small intestine, in particular, an increase in gram negative and anaerobic bacteria [12, 13]. PPIs also increase the risk for Clostridium difficile infection (CDI) [14] and may predispose cirrhotic patients for spontaneous bacterial peritonitis [15, 16]. PPIs may also be associated with increased risk for respiratory infections, although the data are less clear [17, 18]. Nevertheless, in patients disposed to develop stress ulcers (that is patients with hypovolemia and/or hypoxia), it seems justified to prescribe prophylaxis with PPIs since the benefits of preventing a significant bleed in these very sick patients outweigh potential risks [19]. Critically ill patients probably profit from PPI stress ulcer prophylaxis, whereas in less ill patients with a minute risk of development of stress ulcers, the side effects may represent a greater risk for the patients than a possible small reduction in the risk of stress ulcer bleeding. In the present issue Koczka et al. [11] compared the attitude to stress ulcer prophylaxis between attending physicians and residents in a medical center in New York, reporting that half of the attending physicians thought that stress ulcer prophylaxis was indicated outside critical care settings. Perhaps even more problematic than short-term overuse of PPIs during the hospital stay is the fact that most of these patients are discharged on PPIs and thus probably remain on these drugs for prolonged periods without a proper indication [20, 21]. After patients are on PPIs for more than 3 months, stopping may be difficult due to rebound acid hypersecretion-induced dyspepsia [22, 23]. In conclusion, stress ulcer prophylaxis with PPIs is indicated in critically ill patients with hypovolemia and/or R. Fossmark H. Waldum (&) Department of Gastroenterology and Hepatology, St. Olavs Hospital, Prinsesse Kristinas Gate 1, 7006 Trondheim, Norway e-mail: helge.waldum@ntnu.no

  • Treatment of Gastric Carcinoids Type 1 With the Gastrin Receptor Antagonist Netazepide (YF476) Results in Regression of Tumours and Normalisation of Serum Chromogranin A
    Alimentary Pharmacology & Therapeutics, 2012
    Co-Authors: Reidar Fossmark, Gunnar Qvigstad, Constantin S. Jianu, Øystein Sørdal, Ivar Skjåk Nordrum, Malcolm Boyce, Helge L. Waldum
    Abstract:

    Summary Background Patients with chronic atrophic gastritis have long-term Gastric Hypoacidity, and secondary hypergastrinaemia. Some also develop Gastric ECL cells carcinoids (type 1 GC). Most type 1 GC remain indolent, but some metastasise. Patients undergo surveillance, and some are treated with somatostatin analogues, endoscopic resection or surgery. Netazepide (YF476) is a highly selective, potent and orally active gastrin receptor antagonist, which has anti-tumour activity in various rodent models of Gastric neoplasia driven by hypergastrinaemia. Netazepide has been studied in healthy volunteers. Aim To assess the effect of netazepide on type 1 GC. Methods Eight patients with multiple type 1 GC received oral netazepide once daily for 12 weeks, with follow-up at 12 weeks in an open-label, pilot trial. Upper endoscopy was performed at 0, 6, 12 and 24 weeks, and carcinoids were counted and measured. Fasting serum gastrin and chromogranin A (CgA) and safety and tolerability were assessed at 0, 3, 6, 9, 12 and 24 weeks. Results Netazepide was well tolerated. All patients had a reduction in the number and size of their largest carcinoid. CgA was reduced to normal levels at 3 weeks and remained so until 12 weeks, but had returned to pre-treatment levels at 24 weeks. Gastrin remained unchanged throughout treatment. Conclusions The gastrin receptor antagonist netazepide is a promising new medical treatment for type 1 Gastric carcinoids, which appear to be gastrin-dependent. Controlled studies and long-term treatment are justified to find out whether netazepide treatment can eradicate type 1 Gastric carcinoids.

Gene D. Morse - One of the best experts on this subject based on the ideXlab platform.

  • Delavirdine malabsorption in HIV-infected subjects with spontaneous Gastric Hypoacidity.
    The Journal of Clinical Pharmacology, 2003
    Co-Authors: Mark J. Shelton, Ross G. Hewitt, John M. Adams, Steve R. Cox, James H. Chambers, Gene D. Morse
    Abstract:

    To determine the impact of Gastric Hypoacidity and acidic beverages on delavirdine mesylate pharmacokinetics in HIV-infected subjects, matched subjects with (n = 11) and without (n = 10) Gastric Hypoacidity received delavirdine 400 mg tid with either water or an acidic beverage (usually orange juice). The pharmacokinetics of delavirdine and its N-desalkyl metabolite were determined over 8 hours after 14 days of each treatment. Gastric pH was measured at baseline and during each pharmacokinetic evaluation. Delavirdine exposure (Cmax, AUC0-->8 h, and Cmin) was approximately 50% lower and the extent of delavirdine metabolism was higher in subjects with Gastric Hypoacidity. Orange juice produced a lower mean Gastric pH compared to water and increased delavirdine absorption by 50% to 70% in subjects with Gastric Hypoacidity. However, orange juice had a marginal impact on delavirdine exposure in subjects without Gastric Hypoacidity. HIV-infected subjects with Gastric Hypoacidity significantly malabsorb delavirdine. Delavirdine administration with acidic beverages improves, but dose not normalize, absorption in these subjects.

  • previous infection with helicobacter pylori is the primary determinant of spontaneous Gastric Hypoacidity in human immunodeficiency virus infected outpatients
    Clinical Infectious Diseases, 1998
    Co-Authors: Mark J. Shelton, Ross G. Hewitt, John M. Adams, Gene D. Morse
    Abstract:

    To investigate the incidence and demographics of Gastric Hypoacidity among persons infected with human immunodeficiency virus (HIV), 146 asymptomatic subjects were evaluated with use of a radiotelemetry device (Heidelberg capsule). Gastric Hypoacidity (minimum Gastric pH of > or = 3) occurred in 24 subjects (17%). Demographic characteristics, CD4 cell counts, and Helicobacter pylori serological status were evaluated for an association with Gastric pH. Subjects with Hypoacidity were more likely to have positive H. pylori serology than were subjects without Hypoacidity (15 of 24 vs. 23 of 74, respectively; P = .004). Multivariate analysis indicated that a positive H. pylori serology was the most significant predictor of Hypoacidity, accounting for an increase in Gastric pH of 39%. A history of injection drug use, heterosexual transmission of HIV, and male gender were also associated with an elevated Gastric pH. CD4 cell counts did not contribute to predictions of Gastric pH. A history of H. pylori infection is relatively common in HIV-positive black and Hispanic populations and is a predictor of Gastric pH.

  • Previous Infection with Helicobacter pylori Is the Primary Determinant of Spontaneous Gastric Hypoacidity in Human Immunodeficiency Virus—Infected Outpatients
    Clinical Infectious Diseases, 1998
    Co-Authors: Mark J. Shelton, Ross G. Hewitt, John M. Adams, Gene D. Morse
    Abstract:

    To investigate the incidence and demographics of Gastric Hypoacidity among persons infected with human immunodeficiency virus (HIV), 146 asymptomatic subjects were evaluated with use of a radiotelemetry device (Heidelberg capsule). Gastric Hypoacidity (minimum Gastric pH of > or = 3) occurred in 24 subjects (17%). Demographic characteristics, CD4 cell counts, and Helicobacter pylori serological status were evaluated for an association with Gastric pH. Subjects with Hypoacidity were more likely to have positive H. pylori serology than were subjects without Hypoacidity (15 of 24 vs. 23 of 74, respectively; P = .004). Multivariate analysis indicated that a positive H. pylori serology was the most significant predictor of Hypoacidity, accounting for an increase in Gastric pH of 39%. A history of injection drug use, heterosexual transmission of HIV, and male gender were also associated with an elevated Gastric pH. CD4 cell counts did not contribute to predictions of Gastric pH. A history of H. pylori infection is relatively common in HIV-positive black and Hispanic populations and is a predictor of Gastric pH.

  • Effects of Spontaneous Gastric Hypoacidity on the Pharmacokinetics of Zidovudine and Didanosine
    Pharmacotherapy, 1997
    Co-Authors: Mark J. Shelton, Ross G. Hewitt, John M. Adams, Cindy Steinwandel, Mary Deremer, Steve Cousins, Gene D. Morse
    Abstract:

    Study Objective. To determine the effect of spontaneous Gastric Hypoacidity on the pharmacokinetics of zidovudine and didanosine in subjects infected with the human immunodeficiency virus (HIV). Design. Controlled, open-label, single-dose, pharmacokinetic study. Subjects. Thirty-two asymptomatic HIV-infected subjects. Interventions. Gastric pH studies were conducted in all 32 subjects, and 20 of these subjects (8 women, 12 men) were enrolled into the pharmacokinetic study. They were stratified into two groups according to fasting Gastric pH: those without and with Gastric Hypoacidity (minimum Gastric pH < 3 and ≥ 3, respectively). Gastric pH was measured using the Heidelberg pH monitoring system in all subjects before and during pharmacokinetic analysis of zidovudine 100 mg or didanosine 200 mg (given as two 100-mg tablets dissolved in 6 oz water). Plasma samples were collected over 8 hours after dosing. Measurements and Main Results. Six (20%) of 30 subjects had a minimum Gastric pH of 3 or above on at least two occasions, and the remaining 2 had variable Gastric pH. Although Gastric pH was unchanged during the administration of zidovudine, it increased to greater than 9 in 11 of 12 subjects with didanosine, regardless of baseline value. For both drugs, there were no statistically significant differences in peak plasma concentration (Cmax), time to reach peak plasma concentration (Tmax), elimination rate constant (ke), and area under the plasma concentration-time curve from time zero to infinity (AUC0–∞) between subjects with and without Gastric Hypoacidity despite sufficient statistical power to detect a 56% difference in clearance for either drug (α 0.05, β 0.1). Conclusion. Gastric Hypoacidity occurs in approximately 20% of HIV-infected patients and does not appear to influence zidovudine or didanosine pharmacokinetics.

Nancy F. Crum-cianflone - One of the best experts on this subject based on the ideXlab platform.

  • Salmonellosis and the gastrointestinal tract: More than just peanut butter
    Current Gastroenterology Reports, 2008
    Co-Authors: Nancy F. Crum-cianflone
    Abstract:

    Nontyphoidal salmonellosis is the leading cause of foodborne illness in the United States, causing about 1.4 million infections annually. Most cases of salmonellosis are due to ingestion of contaminated food items such as eggs, dairy products, and meats, but almost any foodstuff can be implicated, including peanut butter, as seen during a recent outbreak of more than 600 Salmonella infections. Although outbreaks often gain national media attention, the majority of nontyphoidal Salmonella infections in the United States occur sporadically. Risk factors for salmonellosis include Gastric Hypoacidity, recent use of antibiotics, extremes of age, and immunosuppressive conditions. Clinical manifestations of the infection most commonly involve self-limited gastroenteritis, but bacteremia and endovascular and localized infections may occur. Most cases of gastrointestinal involvement are self-limited, and antibiotic therapy is reserved for persons at risk for complicated disease. Preventive strategies by both industry and consumers are advocated to further reduce the occurrence of nontyphoidal salmonellosis.

G. Delle Fave - One of the best experts on this subject based on the ideXlab platform.

  • Systematic review: impaired drug absorption related to the co-administration of antisecretory therapy.
    Alimentary Pharmacology & Therapeutics, 2009
    Co-Authors: Edith Lahner, Bruno Annibale, G. Delle Fave
    Abstract:

    Summary Background  Due to suppression of Gastric acidity during antisecretory therapy, an impaired absorption of co-administered drugs may occur. Aim  To review evidence of impaired drug absorption related to the use of co-administered PPIs or H2RAs. Methods  Systematic search of MEDLINE/EMBASE/SCOPUS databases (1980–September 2008) for English articles with keywords: drug malabsorption and absorption, stomach, anti-secretory/acid inhibitory drugs, histamine H2 antagonists, PPIs, Gastric acid, pH, hypochlorhydria, Gastric Hypoacidity. From 2126 retrieved articles, 16 randomized crossover studies were identified investigating impaired absorption of nine different drugs in association with co-administration of PPIs or H2RAs. Information on investigated drug, study type, features of investigated subjects, study design, type of intervention, and study results were extracted. Results  The identified studies investigated the absorption kinetics of nine drugs. Acid suppression reduced absorption of ketoconazole, itraconazole, atazanavir, cefpodoxime, enoxacin and dipyridamole (median Cmax reduction by 66.5%). An increased absorption of nifedipine and digoxin (median AUC increase by 10%) and a 2-fold-increase in alendronate bioavailability were observed. Conclusions  Gastric pH appears relevant for absorption of some cardiovascular or infectious disease agents. Antisecretory treatment may significantly modify the absorption of co-administered drugs.

  • Systematic review: Heliocobacter pylori infection and impaired drug absorption
    Alimentary Pharmacology & Therapeutics, 2008
    Co-Authors: Edith Lahner, Bruno Annibale, G. Delle Fave
    Abstract:

    Summary Background  Impaired acid secretion may affect drug absorption and may be consequent to corporal Heliocobacter pylori-gastritis, which may affect the absorption of orally administered drugs. Aim  To focus on the evidence of impaired drug absorption associated with H. pylori infection. Methods  Data sources were the systematic search of MEDLINE/EMBASE/SCOPUS databases (1980–April 2008) for English articles using the keywords: drug malabsorption/absorption, stomach, Helicobacter pylori, gastritis, Gastric acid, Gastric pH, hypochlorhydria, Gastric Hypoacidity. Study selection was made from 2099 retrieved articles, five studies were identified. Data were extracted from selected papers, investigated drugs, study type, main features of subjects, study design, intervention type and results were extracted. Results  In all, five studies investigated impaired absorption of l-dopa, thyroxine and delavirdine in H. pylori infection. Eradication treatment led to 21–54% increase in l-dopa in Parkinon’s disease. Thyroxine requirement was higher in hypochlorhydric goitre with H. pylori-gastritis and thyrotropin levels decreased by 94% after treatment. In H. pylori- and HIV-positive hypochlorhydric subjects, delavirdine absorption increased by 57% with orange juice administration and by 150% after eradication. Conclusions  A plausible mechanism of impaired drug absorption is decreased acid secretion in H. pylori-gastritis patients. Helicobacter pylori infection and hypochlorhydria should be considered in prescribing drugs the absorption of which is potentially affected by intraGastric pH.