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Safatle‐Ribeiro, Adriana Vaz; Ribeiro, Ulysses; Clarke, Martha; Sakai, Paulo; Ishioka, Shinichi; Garrido, Arthur B.; Gama-Rodrigues, Joaquim; Safatle, Nadim; Reynolds, James C.

doi:10.1023/a:1026681829083

Cited by 22 publications

(3 citation statements)

References 30 publications

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“…A firm link has been established between H. pylori and gastric malignancies such as adenocarcinoma of the distal stomach and low-grade gastric mucosa-associated lymphoid tissue lymphoma [5, 6]. …”

Section: Introductionmentioning

confidence: 99%

Diagnostic Accuracy of 13C-Urea Breath Test in the Diagnosis of Helicobacter pylori Infection in Patients with Partial Gastric Resection due to Peptic Ulcer Disease

Schilling

Jakobs

Peitz³

et al. 2001

Digestion

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Aims: We investigated the diagnostic properties of the ¹³C-urea breath test (¹³C-UBT) prospectively. These are well validated in nonresected patients before and after treatment of Helicobacter pylori infection but not in patients with partial gastric resection due to peptic ulcer disease. Methods: Hospitalized patients with previous gastric resection and indications for upper gastrointestinal endoscopy were recruited for the study. Biopsy specimens were obtained from the fundus mucosa and the gastric remnant adjacent to the gastroenteric anastomosis for histological examination and rapid urease test (HUT test). Histological slides were evaluated after hematoxylin and eosin and Warthin-Starry dye staining. 200 ml orange juice was given orally after two baseline breath samples had been taken, and 30 min after ingestion of 75 mg ¹³C urea two more breath samples were obtained and analyzed by ratio mass spectrometry. The Warthin-Starry dye-stained sample was taken as reference. Results: 68 patients (47 male, 21 female, mean age 62 years; 52 Billroth II resection, 17 Billroth I resection) were included in the study. The overall prevalence of histologically proven H. pylori infection was 36.7%. The sensitivity of the ¹³C-UBT was 52%, the specificity 93%. The positive predictive value was 81.25%, the negative predictive value 76.9% and the accuracy was 77.9%. The sensitivity of the HUT test reached 60%, and the specificity 97%. Conclusion: The diagnostic accuracy of ¹³C-UBT compared with the Warthin-Starry dye staining is low. The breath test, performed in the above-described manner, cannot be recommended as a noninvasive diagnostic tool for diagnosis of H. pylori infection in patients after partial gastrectomy as a result of peptic ulcer disease.

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Section: Introductionmentioning

confidence: 99%

Diagnostic Accuracy of 13C-Urea Breath Test in the Diagnosis of Helicobacter pylori Infection in Patients with Partial Gastric Resection due to Peptic Ulcer Disease

Schilling

Jakobs

Peitz³

et al. 2001

Digestion

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“…Similar to the case for the mouse TAA model of ICC, cell-fate conversion can be observed in many types of injured/diseased tissues and organs in mammals. For example, acinar cells can change their fate to that of hepatocyte-like cells in the damaged pancreas of adult rats maintained on a copper-deficient diet 9 , and human gastric epithelial cells can be converted into cells that form intestinal villi during intestinal metaplasia induced by mucosal injury associated with Helicobacter pylori infection 10 11 . In mouse models of diabetes, β cells constituting islets of the pancreas dedifferentiate into progenitor-like cells, resulting in loss of insulin secretion from β cells 12 .…”

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confidence: 99%

Kupffer cells induce Notch-mediated hepatocyte conversion in a common mouse model of intrahepatic cholangiocarcinoma

Terada

Horisawa

Miura

et al. 2016

Sci Rep

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Intrahepatic cholangiocarcinoma (ICC) is a malignant epithelial neoplasm composed of cells resembling cholangiocytes that line the intrahepatic bile ducts in portal areas of the hepatic lobule. Although ICC has been defined as a tumor arising from cholangiocyte transformation, recent evidence from genetic lineage-tracing experiments has indicated that hepatocytes can be a cellular origin of ICC by directly changing their fate to that of biliary lineage cells. Notch signaling has been identified as an essential factor for hepatocyte conversion into biliary lineage cells at the onset of ICC. However, the mechanisms underlying Notch signal activation in hepatocytes remain unclear. Here, using a mouse model of ICC, we found that hepatic macrophages called Kupffer cells transiently congregate around the central veins in the liver and express the Notch ligand Jagged-1 coincident with Notch activation in pericentral hepatocytes. Depletion of Kupffer cells prevents the Notch-mediated cell-fate conversion of hepatocytes to biliary lineage cells, inducing hepatocyte apoptosis and increasing mortality in mice. These findings will be useful for uncovering the pathogenic mechanism of ICC and developing prevenient and therapeutic strategies for this refractory disease.

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“…The presence of type II or III IM is found to be related to a 20-fold greater risk of GC [62]. Some studies also proved the link between H. pylori-induced gastritis and IM [63,64]. Three mechanisms could generate this risk: (i) the metaplastic tissue is an early step in a multi-step induction process of gastric carcinogenesis; (ii) IM exhibits epigenetic changes, raises the pH of gastric juice by replacing oxyntic mucosa, and favors the growth of H. pylori capable of producing endogenous mutagens; (iii) IM is only a marker for chronic gastritis due to H. pylori infection or pernicious anemia [55,60].…”

Section: The Link Between H Pylori-triggered Ag Im and Gcmentioning

confidence: 98%

Helicobacter pylori-Induced Inflammation: Possible Factors Modulating the Risk of Gastric Cancer

2021

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Chronic inflammation and long-term tissue injury are related to many malignancies, including gastric cancer (GC). Helicobacter pylori (H. pylori), classified as a class I carcinogen, induces chronic superficial gastritis followed by gastric carcinogenesis. Despite a high prevalence of H. pylori infection, only about 1–3% of people infected with this bacterium develop GC worldwide. Furthermore, the development of chronic gastritis in some, but not all, H. pylori-infected subjects remains unexplained. These conflicting findings indicate that clinical outcomes of aggressive inflammation (atrophic gastritis) to gastric carcinogenesis are influenced by several other factors (in addition to H. pylori infection), such as gut microbiota, co-existence of intestinal helminths, dietary habits, and host genetic factors. This review has five goals: (1) to assess our current understanding of the process of H. pylori-triggered inflammation and gastric precursor lesions; (2) to present a hypothesis on risk modulation by the gut microbiota and infestation with intestinal helminths; (3) to identify the dietary behavior of the people at risk of GC; (4) to check the inflammation-related genetic polymorphisms and role of exosomes together with other factors as initiators of precancerous lesions and gastric carcinoma; and (5) finally, to conclude and suggest a new direction for future research.

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Cited by 22 publications

References 30 publications

Diagnostic Accuracy of <sup>13</sup>C-Urea Breath Test in the Diagnosis of <i>Helicobacter pylori</i> Infection in Patients with Partial Gastric Resection due to Peptic Ulcer Disease

Diagnostic Accuracy of <sup>13</sup>C-Urea Breath Test in the Diagnosis of <i>Helicobacter pylori</i> Infection in Patients with Partial Gastric Resection due to Peptic Ulcer Disease

Kupffer cells induce Notch-mediated hepatocyte conversion in a common mouse model of intrahepatic cholangiocarcinoma

Helicobacter pylori-Induced Inflammation: Possible Factors Modulating the Risk of Gastric Cancer

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