Association of Helicobacter pylori and Crohn’s Disease Incidence: An Inversion Reaction?

Bartels, Lars Erik; Dahlerup, Jens Frederik

doi:10.1007/s10620-017-4561-7

Cited by 4 publications

(8 citation statements)

References 10 publications

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“…H.p. induces activation of most components of innate (epithelial, neutrophil, macrophage and dendritic cells) and adaptive immunity (B and T cells) [ 30 , 33 , 34 , 35 ]. H.p., especially with specific virulent strains, in addition to a local reaction results in systemic low-grade inflammation [ 36 , 37 , 38 ].…”

Section: Brief Overview Of Helicobacter Pylori mentioning

confidence: 99%

Helicobacter pylori Related Diseases and Osteoporotic Fractures (Narrative Review)

Fisher

Smith

2020

JCM

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Osteoporosis (OP) and osteoporotic fractures (OFs) are common multifactorial and heterogenic disorders of increasing incidence. Helicobacter pylori (H.p.) colonizes the stomach approximately in half of the world’s population, causes gastroduodenal diseases and is prevalent in numerous extra-digestive diseases known to be associated with OP/OF. The studies regarding relationship between H.p. infection (HPI) and OP/OFs are inconsistent. The current review summarizes the relevant literature on the potential role of HPI in OP, falls and OFs and highlights the reasons for controversies in the publications. In the first section, after a brief overview of HPI biological features, we analyze the studies evaluating the association of HPI and bone status. The second part includes data on the prevalence of OP/OFs in HPI-induced gastroduodenal diseases (peptic ulcer, chronic/atrophic gastritis and cancer) and the effects of acid-suppressive drugs. In the next section, we discuss the possible contribution of HPI-associated extra-digestive diseases and medications to OP/OF, focusing on conditions affecting both bone homeostasis and predisposing to falls. In the last section, we describe clinical implications of accumulated data on HPI as a co-factor of OP/OF and present a feasible five-step algorithm for OP/OF risk assessment and management in regard to HPI, emphasizing the importance of an integrative (but differentiated) holistic approach. Increased awareness about the consequences of HPI linked to OP/OF can aid early detection and management. Further research on the HPI–OP/OF relationship is needed to close current knowledge gaps and improve clinical management of both OP/OF and HPI-related disorders.

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Section: Brief Overview Of Helicobacter Pylori mentioning

confidence: 99%

Helicobacter pylori Related Diseases and Osteoporotic Fractures (Narrative Review)

Fisher

Smith

2020

JCM

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“…Interestingly, and perhaps partly accounting for the lower rate of H. pylori among cases with GG and CD in our cohort, H. pylori infection is reportedly lower among patients with inflammatory bowel disease, especially CD 55 . Hypotheses that have been proposed to account for this inverse correlation include the use of antibiotics or other medications among CD patients that may eradicate H. pylori organisms; altered gut microbiota or inflammatory cells/mediators in the setting of H. pylori infection that may make CD less likely; H. pylori being a marker for other factors such as lifestyle or (childhood) environmental exposures that may, in turn, be protective against CD; selection bias, whereby CD patients, due to more frequent doctor contact, result in being tested and treated for H. pylori more often; or any combination of the above 56–58 …”

Section: Discussionmentioning

confidence: 67%

“…55 Hypotheses that have been proposed to account for this inverse correlation include the use of antibiotics or other medications among CD patients that may eradicate H. pylori organisms; altered gut microbiota or inflammatory cells/mediators in the setting of H. pylori infection that may make CD less likely; H. pylori being a marker for other factors such as lifestyle or (childhood) environmental exposures that may, in turn, be protective against CD; selection bias, whereby CD patients, due to more frequent doctor contact, result in being tested and treated for H. pylori more often; or any combination of the above. [56][57][58] Other authors have concluded that H. pylori can cause GG, including a study from Korea, where H. pylori prevalence is higher and CD prevalence lower than the United States. 7,40 It is unclear whether these authors excluded granulomatous inflammation due to crypt damage, given that most granulomas in their study were located in superficial mucosa, in close contact with damaged pits; however, they mentioned that extravasated mucin was not seen.…”

Section: Discussionmentioning

confidence: 99%

Clinicopathological characteristics and aetiological factors of granulomatous gastritis

2021

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Clinicopathological characteristics and aetiological factors of granulomatous gastritisAims: To examine the clinicopathological characteristics of granulomatous gastritis (GG) among different aetiologies, particularly Crohn disease (CD), and determine the contribution of Helicobacter pylori and the clinical significance of isolated GG. Methods and results: We identified 269 GG cases overall (0.19% prevalence): 220 had an underlying granulomatous disease (CD, sarcoidosis, tuberculosis) and only eight of these (3.6%) had H. pylori, fewer than the 10.3% rate among non-GG biopsies (P < 0.001). Conversely, among 49 GG cases without known cause (foreign body, undetermined, idiopathic), 13 (26.5%) had H. pylori more than background (P = 0.001). Most patients (n = 185/68.8%) had CD and these were more probably male (P < 0.001), younger (P < 0.001), white (P < 0.001) and had single (P = 0.010), smaller (P = 0.005) and antral (P = 0.027) granulomas amid inflammation (P = 0.005) compared to non-CD GG cases; younger age was independently associated with CD [P = 0.003; odds ratio (OR) = 1.13, 95% confidence interval (CI) = 1.04-1.22]. Among CD patients, younger age (P = 0.003; OR = 1.04, 95% CI = 1.01-1.07) and upper gastrointestinal (GI) symptoms (P = 0.017; OR = 2.53, 95% CI = 1.18-5.43) were associated with new (versus established) diagnosis, whereas multiple gastric granulomas (P = 0.003; OR = 4.67, 95% CI = 1.67-13.04) and lack of upper GI symptoms (P < 0.001; OR = 6.75, 95% CI = 2.94-15.49) were associated with lower GI granulomas. Of 86 isolated GG cases (i.e. no prior diagnosis or lower GI granulomas), 51 (59.3%) were eventually diagnosed with CD, and this was independently associated with younger age (P = 0.014; OR = 1.11, 95% CI = 1.02-1.21) and upper GI symptoms (P = 0.033; OR = 19.27, 95% CI = 1.27-293.31). The positive predictive value of finding isolated GG towards a CD diagnosis in patients aged <30 years was 91%, increasing in males (93%), with single (94%), antral (97%) granulomas or upper GI symptoms (94%). Conclusions: GG does not correlate with H. pylori in patients with granulomatous disease, but may be associated with the organism when such diagnosis is lacking. In CD patients with GG, younger age and upper GI symptoms are associated with a new CD diagnosis, whereas multiple gastric granulomas and lack of upper GI symptoms correlate with lower GI granulomas. GG, including in isolated cases with no prior clinical history or granuloma, probably signifies CD, particularly in younger, male patients or those with single, antral granulomas or upper GI symptoms.

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“…A number of hypotheses have been proposed to explain this discovery. For instance, if patients with Crohn's disease received antibiotics prior to an H. pylori eradicating H. pylori, the rate of H. pylori infections in Crohn's disease patients would be smaller [33,[35][36][37]. This would lead to a reduction in the prevalence of H. pylori infections in patients with CD.…”

Section: Epidemiological Correlation Between CD and H Pylorimentioning

confidence: 99%

“…Alternatively, it may be a case of selection biases where patients seeing doctor regularly get tested for H. pylori more often than those patients seeing doctors for a cause [38]. There are various potential sources of bias and confounding variables, including the fact that individuals with Crohn's disease may have received other medical treatments that have an effect on H. pylori, or the fact that publishing biases may have distorted the findings [35,39].…”

Section: Epidemiological Correlation Between CD and H Pylorimentioning

confidence: 99%

Helicobacter Pylori Infection Correlates with Lower Prevalence and Subsequent Incidence of Crohn’s Disease

Hu¹,

Lei²,

Tai³

et al. 2024

Helicobacter Pylori Infection - An Up to Date on the Pathogenic Mechanisms, Diagnosis and Clinical Management

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According to some researchs, Crohn’s disease (CD) and Ulcerative colitis (UC), two chronic inflammatory bowel illnesses, may be protected against Helicobacter pylori infection. Many case–control studies have revealed that individuals with CD and UC had lower H. pylori prevalence than healthy controls. However, whether or not H. pylori plays a protective role in the development of Crohn’s disease is debatable. CD was more common in H. pylori-negative individuals than in H. pylori-positive patients. After eradication of H. pylori, the CD was more common in the H. pylori-negative group than in the H. pylori-positive group over the previous research follow-up period. Although it has been strongly indicated in previous studies that H. pylori infection plays a significant role and triggers autoimmune reactions and may be implicated in the pathogenesis of autoimmune diseases, the role of H. pylori in inflammatory bowel disease, including Crohn’s disease, is unclear.

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Association of Helicobacter pylori and Crohn’s Disease Incidence: An Inversion Reaction?

Cited by 4 publications

References 10 publications

Helicobacter pylori Related Diseases and Osteoporotic Fractures (Narrative Review)

Helicobacter pylori Related Diseases and Osteoporotic Fractures (Narrative Review)

Clinicopathological characteristics and aetiological factors of granulomatous gastritis

Helicobacter Pylori Infection Correlates with Lower Prevalence and Subsequent Incidence of Crohn’s Disease

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