Effect of Helicobacter pylori and its virulence factors on portal hypertensive gastropathy and interleukin (IL)-8, IL-10, and tumor necrosis factor-alpha levels

Abbas, Zaigham; Yakoob, Javed; Usman, Muhammad Waqas; Shakir, Tanzila; Salehiniya, Hamid; Jafri, Wasim

doi:10.4103/1319-3767.129477

Cited by 25 publications

(29 citation statements)

References 20 publications

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“…Misoprostol applied to gastric mucosa caused ulcers associated with PHG [173] . Contrariwise, Sathar et al [174] reported an association between H. pylori infection and PHG in cirrhotic patients, but this study apparently had limitations, including low specificity and low sensitivity of H. pylori serology in cirrhotic patients, potential selection bias, and underreporting of H. pylori seroprevalence [174][175][176][177][178] .…”

Section: Angiogenesismentioning

confidence: 99%

Portal hypertensive gastropathy: A systematic review of the pathophysiology, clinical presentation, natural history and therapy

Gjeorgjievski¹

2016

WJH

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AIM:To describe the pathophysiology, clinical presentation, natural history, and therapy of portal hypertensive gastropathy (PHG) based on a systematic literature review. METHODS:Computerized search of the literature was performed via PubMed using the following medical subject headings or keywords: "portal" and "gastropathy"; or "portal" and "hypertensive"; or "congestive" and "gastropathy"; or "congestive" and "gastroenteropathy". The following criteria were applied for study inclusion: Publication in peer-reviewed journals, and publication since 1980. Articles were independently evaluated by each author and selected for inclusion by consensus after discussion based on the following criteria: Well-designed, prospective trials; recent studies; large study populations; and study emphasis on PHG. RESULTS:PHG is diagnosed by characteristic endoscopic findings of small polygonal areas of variable erythema surrounded by a pale, reticular border in a mosaic pattern in the gastric fundus/body in a patient with cirrhotic or non-cirrhotic portal hypertension. Histologic findings include capillary and venule dilatation, congestion, and tortuosity, without vascular fibrin thrombi or inflammatory cells in gastric submucosa. PHG is differentiated from gastric antral vascular ectasia by a different endoscopic appearance. The etiology of PHG is inadequately understood. Portal hypertension is necessary but insufficient to develop PHG because many patients have portal hypertension without PHG. Portal hypertensive gastropathy: A systematic review of the pathophysiology, clinical presentation, natural history and therapy PHG increases in frequency with more severe portal hypertension, advanced liver disease, longer liver disease duration, presence of esophageal varices, and endoscopic variceal obliteration. PHG pathogenesis is related to a hyperdynamic circulation, induced by portal hypertension, characterized by increased intrahepatic resistance to flow, increased splanchnic flow, increased total gastric flow, and most likely decreased gastric mucosal flow. Gastric mucosa in PHG shows increased susceptibility to gastrotoxic chemicals and poor wound healing. Nitrous oxide, free radicals, tumor necrosis factor-alpha, and glucagon may contribute to PHG development. Acute and chronic gastrointestinal bleeding are the only clinical complications. Bleeding is typically mild-to-moderate. Endoscopic therapy is rarely useful because the bleeding is typically diffuse. Acute bleeding is primarily treated with octreotide, often with concomitant proton pump inhibitor therapy, or secondarily treated with vasopressin or terlipressin. Nonselective β-adrenergic receptor antagonists, particularly propranolol, are used to prevent bleeding after an acute episode or for chronic bleeding. Iron deficiency anemia from chronic bleeding may require iron replacement therapy. Transjugular-intrahepaticportosystemic-shunt and liver transplantation are highly successful ultimate therapies because they reduce the underlying portal hypertension. SYSTEMA...

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Section: Angiogenesismentioning

confidence: 99%

Portal hypertensive gastropathy: A systematic review of the pathophysiology, clinical presentation, natural history and therapy

Gjeorgjievski¹

2016

WJH

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“…It is known that H. pylori infection leads to inflammation of the stomach, associated with the production of inflammatory cytokines, such as TNF-α, as demonstrated by studies observing increased levels of TNF-α in infected patients (38,39). However, a study by Abbas et al (40) conducted on patients with liver cirrhosis observed no statistically significant difference in the levels of TNF-α expression when comparing positive and negative H. pylori groups, or groups with moderate and severe gastropathy (41). TNF-α is a key cytokine in tumor promotion; therefore, it is important to clarify how the pro-inflammatory cytokines induced by H. pylori are involved in the development of gastric cancer (42).…”

Section: Discussionmentioning

confidence: 78%

Effect of Helicobacter pylori on NFKB1, p38α and TNF-α mRNA expression levels in human gastric mucosa

Oliveira

Biolchi

Medeiros

et al. 2016

Experimental and Therapeutic Medicine

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Abstract.Helicobacter pylori infects ~50% of the world population, causing chronic gastritis and other forms of cellular damage. The present study assessed the influence of H. pylori on the mRNA expression levels of nuclear factor-κB1 (NFKB1), p38α and tumor necrosis factor-α (TNF-α) in human gastric mucosa in a southern Brazilian population. Human gastric tissue was collected by upper endoscopy and H. pylori diagnosis was performed using a rapid urease test and histological analysis. Total RNA was extracted and purified for subsequent cDNA synthesis and analysis by quantitative polymerase chain reaction (qPCR). The gastric tissue samples were divided into four groups as follows: Normal, inactive chronic gastritis, active chronic gastritis and intestinal metaplasia. The SDHA gene was classified as the most stable when compared with ACTB, GAPDH, B2M and HPRT1 genes, and was therefore selected as the reference gene for qPCR data normalization. TNF-α mRNA expression was significantly higher in samples that were positive for H. pylori and with active chronic gastritis. However, no difference was detected in the mRNA expression levels of NFKB1 and p38α between the groups. The present study concluded that the presence of H. pylori is associated with TNF-α upregulation in human gastric mucosa, but had no effect on NFKB1 and p38α mRNA expression levels.

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“…Portal hypertensive gastropathy include changes in mucosa of the stomach of patients with liver cirrhosis It is associated with tortuosity and dilation of the submucosal vessels, increased area of the gastric mucosa occupied by vessels and thinning of the vascular wall, and [11] there is activation of growth factors and cytokines, such as tumor necrosis factor-alpha (TNF-α) and interleukin (IL)-6 [12]. TNF-α activates endothelial nitric oxide synthase and endothelin-1 in the gastric mucosa of patients with portal hypertension [13].…”

Section: Discussionmentioning

confidence: 99%

Can Hellicobacter Pylori Infection Increase the Risk of Variceal Bleeding in Patients with Liver Cirrhosis?

ELGhany¹

2018

JLRDT

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Background and Study Aims: Gastro-oesphageal varices carry high risk of bleeding which may be fatal in some circumstances. Many patients with varices have Helicobacter pylori (H.pylori) infection in their gastric mucosa. The relationship between H.pylori infection and the incidence of upper GIT bleeding was not well studied. Our study was aimed to study the role of H.pylori infection in gastro-oesphageal variceal bleeding. Patients and Methods:The subjects were 392 cirrhotic patients who were admitted to the Zagazig University Hospital to treat their gastro-oesphageal varices, consisted of 190 with upper GIT bleeding (bleeder group) and 202 with non bleeding episodes but came for prophylactic purposes either primary or secondary prevention (non bleeder group). For the diagnosis of H. pylori infection, rapid urease test was done for endoscopic gastric biopsies.Results: Gastro-oesphageal variceal bleeding was seen in 31.6 % (n = 60) of the H.pylori infected patients and in 68.4% (n = 130) of the no infected patients (total number was 190 patients) (P < 0.001). The H.pylori infection was associated with low incidence of bleeding in patients with gastro-eosphageal varices. Conclusion:These results suggest that H.pylori infection may have a protective effect against gastro-esophageal variceal bleeding.

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Effect of Helicobacter pylori and its virulence factors on portal hypertensive gastropathy and interleukin (IL)-8, IL-10, and tumor necrosis factor-alpha levels

Cited by 25 publications

References 20 publications

Portal hypertensive gastropathy: A systematic review of the pathophysiology, clinical presentation, natural history and therapy

Portal hypertensive gastropathy: A systematic review of the pathophysiology, clinical presentation, natural history and therapy

Effect of Helicobacter pylori on NFKB1, p38α and TNF-α mRNA expression levels in human gastric mucosa

Can Hellicobacter Pylori Infection Increase the Risk of Variceal Bleeding in Patients with Liver Cirrhosis?

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