المؤلفون: Rocco, Alba, Compare, Debora, Sgamato, Costantino, Coccoli, Pietro, Chiodini, Paolo, Nardone, Gerardo

المصدر: Alimentary Pharmacology & Therapeutics; Mar2021, Vol. 53 Issue 5, p608-615, 8p, 2 Charts, 3 Graphs

مصطلحات موضوعية: OMEPRAZOLE, PROTON pump inhibitors, CYTOCHROME P-450, BREATH tests, CIRRHOSIS of the liver, CYTOCHROME c

مستخلص: Summary: Background: Chronic use of proton pump inhibitors (PPIs) in patients with impaired liver function may worsen cytochrome P450 (CYP450) activity, predisposing them to clinically relevant drug–drug interactions. The 13C‐aminopyrine breath test (13C‐ABT) is a non‐invasive tool to study CYP450‐dependent liver function. Aims: To assess 13C‐ABT modifications with different PPIs in patients with cirrhosis Methods: Sixty consecutive patients with HCV‐related cirrhosis and indication to start PPI therapy were randomised to receive omeprazole 20 mg/day, esomeprazole 20 mg/day, lansoprazole 15 mg/day, pantoprazole 40 mg/day or rabeprazole 20 mg/day. 13C‐ABT was performed at baseline and on the 15th day of PPI therapy. Results: At baseline, mean values of max 13C% dose/h and 13C% cum dose at 120 minutes did not differ significantly among groups. On the 15th day of therapy, max 13C% dose/h and 13C% cum dose at 120 minutes did not significantly differ with respect to baseline for pantoprazole (P = 0.184 and P = 0.309, respectively) or rabeprazole (P = 0.536 and P = 0.286, respectively), but were significantly decreased on omeprazole (P = 0.013 and P = 0.015, respectively), esomeprazole (P = 0.009 and P = 0.001, respectively), and lansoprazole (P = 0.033 and P = 0.035, respectively). Conclusions: In patients with cirrhosis, omeprazole, esomeprazole and lansoprazole inhibit microsomal activity while pantoprazole and rabeprazole do not have a significant impact. Should our data be confirmed in larger cohort studies, pantoprazole and rabeprazole could be safely recommended for patients with cirrhosis. [ABSTRACT FROM AUTHOR]

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المؤلفون: Castiglione, Fabiana, Imperatore, Nicola, Testa, Anna, De Palma, Giovanni Domenico, Nardone, Olga Maria, Pellegrini, Lucienne, Caporaso, Nicola, Rispo, Antonio

المصدر: Alimentary Pharmacology & Therapeutics; Apr2019, Vol. 49 Issue 8, p1026-1039, 14p, 1 Diagram, 3 Charts, 4 Graphs

مصطلحات موضوعية: CROHN'S disease, INFLAMMATORY bowel diseases, GROWTH factors, TUMOR necrosis factors, CLINICAL trials, GLYCOPROTEINS

مستخلص: Summary: Background: While mucosal healing has been proved to predict relevant clinical outcomes in Crohn's disease (CD), little is known about the long‐term significance of transmural healing. Aims: To prospectively assess the 1‐year clinical outcomes in CD patients achieving transmural healing following treatment with biologics, and to compare them with those in patients reaching only mucosal healing or no healing. Methods: Observational longitudinal study, evaluating 1‐year outcomes in terms of steroid‐free clinical remission, rate of hospitalisation and need for surgery in a group of CD patients treated with anti‐tumour necrosis factor (TNF) alpha for 2 years. Bowel sonography was used in all patients to determine transmural healing. Results: Of 218 patients who completed a 2‐year treatment course with anti‐TNF alpha, 68 (31.2%) presented transmural (plus mucosal) healing (bowel wall thickness ≤3 mm at bowel sonography), 60 (27.5%) mucosal healing only, and 90 (41.3%) did not achieve any intestinal healing. Transmural healing was associated with a higher rate of steroid‐free clinical remission (95.6%), lower rates of hospitalisation (8.8%) and need for surgery (0%) at 1 year compared to mucosal (75%, 28.3% and 10%, respectively) and no healing (41%, 66.6% and 35.5%, respectively) (P < 0.001). Furthermore, transmural healing was associated with longer intervals until clinical relapse (HR, hazard ratio 0.87, P = 0.01), hospitalisation (HR 0.88, P = 0.002) and surgery (HR 0.94, P = 0.008) than mucosal healing. Also among patients discontinuing treatment with biologics, transmural healing predicted better clinical outcomes at 1 year than mucosal healing (P = 0.01). Conclusions: Transmural healing is an ambitious and powerful treatment goal associated, to a greater extent than mucosal healing, with improvement of all clinical outcomes. Additionally, transmural healing is associated with better long‐term clinical outcomes than mucosal healing also after discontinuation of biologics. [ABSTRACT FROM AUTHOR]

: Copyright of Alimentary Pharmacology & Therapeutics is the property of Wiley-Blackwell and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

المؤلفون: Alice Di Rocco, Peter Malfertheiner, Gerardo Nardone

المصدر: Alimentary Pharmacology & Therapeutics. 20:261-270

مصطلحات موضوعية: medicine.medical_specialty, Hepatology, biology, business.industry, Stomach, Gastroenterology, Intestinal metaplasia, Cancer, Inflammation, Helicobacter pylori, medicine.disease, biology.organism_classification, medicine.anatomical_structure, Dysplasia, Internal medicine, DNA methylation, medicine, Cancer research, Pharmacology (medical), Gastritis, medicine.symptom, business

الوصف: Gastric cancer can be divided into intestinal type and diffuse type that differ substantially in epidemiology and pathogenesis. The most important aetiological factor associated both with intestinal and diffuse gastric cancer, is Helicobacter pylori. Exposure of gastric epithelial cells to H. pylori results in an inflammatory reaction with the production of reactive oxygen species and nitric oxide that, in turn, deaminates DNA causing mutations. The complex interplay between H. pylori strain, inflammation and host characteristics may directly promote diffuse type gastric cancer or induce a cascade of morphological events, i.e. atrophy, intestinal metaplasia and dysplasia, finally leading to intestinal type gastric cancer. Two mechanisms, genetic and epigenetic have been held to play a role in the molecular alterations underlying gastric carcinogenesis. The former, comprising changes in the DNA sequence, is irreversible; the latter, involving DNA methylation, is potentially reversible by eliminating the triggering agents. If H. pylori is eradicated before development of stable mutations, the risk of gastric cancer will likely be prevented. Thus, eradication of H. pylori might immediately reduce the risk of diffuse type gastric cancer, whereas prevention of intestinal type gastric cancer may be less effective if patients are treated later in the evolution of the carcinogenic process.

الوصول الحر: https://explore.openaire.eu/search/publication?articleId=doi_________::120275edfaed50600846ffd08ff12adcTest
https://doi.org/10.1111/j.1365-2036.2004.02075.xTest

المؤلفون: Gerardo Nardone

المصدر: Alimentary Pharmacology & Therapeutics. 17:75-81

مصطلحات موضوعية: Genetics, Hepatology, biology, Cell, Gastroenterology, Cancer, Helicobacter pylori, medicine.disease, biology.organism_classification, Phenotype, Transformation (genetics), medicine.anatomical_structure, medicine, Environmental Risk Factor, Pharmacology (medical), Microsatellite Mutator Phenotype, Gene

الوصف: Gastric cancer is constituted by two histomorphological entities 'intestinal' and 'diffuse', however lesions with similar morphologies may differ in biological aggressiveness and response to therapy. Two distinct molecular pathways have been identified in gastric carcinogenesis: the microsatellite mutator phenotype and a phenotype associated with chromosomal and intrachromosomal instability. Mounting evidence suggests that microsatellite mutator phenotype alterations and expression of the products of cancer-related genes are early markers of cell transformation, and may serve to identify the gastric carcinoma histotypes. The lack of a clear genetic basis, lends weight to the notion that gastric cancer is not a monomorphic entity but may be affected by environmental factors. Helicobacter pylori is the most important environmental risk factor associated with sporadic gastric cancer. Exposure of gastric epithelial cells to bacterium results in the generation of reactive oxygen species and inducible nitric oxide synthase that in turn may cause genetic alterations leading to cancer in a subset of subjects. Thus, gastric cancer may be considered the result of an interplay between host genetic profile and environmental toxic agents. The new technologies of molecular analysis will help to establish an individual's risk of developing gastric cancer and will lead to novel biological therapeutic strategies.

الوصول الحر: https://explore.openaire.eu/search/publication?articleId=doi_________::6336552fb0116464b7237e5e3c1f3d86Test
https://doi.org/10.1046/j.1365-2036.17.s2.10.xTest

المؤلفون: Gerardo Nardone, Alba Rocco, T. Balzano, Gabriele Budillon

المصدر: Alimentary Pharmacology & Therapeutics. 13:1429-1436

مصطلحات موضوعية: medicine.medical_specialty, Gastrointestinal bleeding, Gastrointestinal tract, Cirrhosis, Hepatology, Vascular disease, business.industry, Stomach, Gastroenterology, Octreotide, medicine.disease, Surgery, medicine.anatomical_structure, Concomitant, Internal medicine, medicine, Pharmacology (medical), Angiodysplasia, business, medicine.drug

الوصف: Background : The treatment of angiodysplasia and watermelon stomach, vascular abnormalities implicated in gastrointestinal bleeding of obscure origin, is a major clinical problem. Aim : To determine the efficacy of octreotide in patients with long-standing gastrointestinal bleeding due to acquired angiodysplasia and watermelon stomach, resistant to previous treatments and not suitable for surgery because of old age and/or concomitant disorders. Patients and methods : We treated 17 patients (seven had isolated angiodysplasia, seven had multiple upper and lower gastrointestinal angiodysplasia, and three had watermelon stomach) with octreotide (0.1 mg subcutaneous t.d.s. for 6 months). Six of the patients had liver cirrhosis, one had Glanzmann-type platelet derangement, two had cardiovascular diseases and one had chronic uraemia. Results : Octreotide treatment stopped bleeding in 10 patients. A transient improvement was observed in four, who needed subsequent cyclical retreatment to correct low haemoglobin levels. No effect was observed in three, probably due to the severity of the concomitant disorders. Conclusions : Octreotide is a safe drug that may be useful to control the recurrent gastrointestinal bleeding due to acquired angiodysplasia and watermelon stomach, especially in patients who are not candidates for surgery due to old age and/or concomitant disorders.

الوصول الحر: https://explore.openaire.eu/search/publication?articleId=doi_________::55abd93a36262fdd8009b3479de43887Test
https://doi.org/10.1046/j.1365-2036.1999.00647.xTest

المؤلفون: Rocco, Alba, Compare, Debora, Sgamato, Costantino, Coccoli, Pietro, Nardone, Gerardo

المصدر: Alimentary Pharmacology & Therapeutics; Mar2021, Vol. 53 Issue 5, p665-666, 2p

مصطلحات موضوعية: PROTON pump inhibitors, CIRRHOSIS of the liver, PUZZLES

مستخلص: LINKED CONTENT This article is linked to Rocco et al and Celsa & Cammà papers. To view these articles, visit https://doi.org/10.1111/apt.16239Test and https://doi.org/10.1111/apt.16250Test [ABSTRACT FROM AUTHOR]

: Copyright of Alimentary Pharmacology & Therapeutics is the property of Wiley-Blackwell and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

المؤلفون: MARTIN, G., WEX, T., TREIBER, G., MALFERTHEINER, P., NARDONE, G.

المصدر: Alimentary Pharmacology & Therapeutics; Sep2008, Vol. 28 Issue 6, p782-788, 7p, 1 Color Photograph, 2 Black and White Photographs, 1 Chart, 2 Graphs

مصطلحات موضوعية: ASPIRIN, GASTRIC mucosa, POLYMERASE chain reaction, CYTOPLASM, CELL lines, PROTEINS

مستخلص: Background Gastrokine 1 (GKN1), one of the most abundant transcripts in normal stomach, is down-regulated by Helicobacter pylori infection. Aspirin (ASA), which is often used for secondary prevention of cardiovascular events, can damage gastric-duodenal mucosa within 1 or 2 h of ingestion. Aim To study the gastric mucosal expression of GKN1 during acute low-dose ASA consumption. Methods Ten H. pylori-negative human volunteers took 100 mg ASA per day for 1 week, and underwent multiple upper GI endoscopies. GKN1 expression was analysed in antral and corpus mucosa by quantitative reverse-transcriptase polymerase chain reaction, western blot and immunohistochemistry (IHC). Gastric mucosal damage was detected endoscopically and histologically. Results Gastrokine 1 was similarly expressed in both antral and corpus mucosa. The use of low-dose ASA led to a significant decrease (3.07 a.u. vs. 0.23 a.u., P < 0.001) in antrum at day 7, while GKN1 transcript levels in corpus mucosa were slightly elevated (twofold, P < 0.005). Western blot and IHC confirmed these changes at the protein level. Furthermore, IHC revealed a vesicular staining pattern in the cytoplasm for GKN1 that was confirmed by transfected human gastric adenocarcinoma cell line expressing GKN1. Conclusion Our data demonstrated that low-dose ASA downregulates GKN1 expression specifically in antral mucosa. [ABSTRACT FROM AUTHOR]

: Copyright of Alimentary Pharmacology & Therapeutics is the property of Wiley-Blackwell and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

المؤلفون: NARDONE, G.¹ (AUTHOR), ROCCO, A.¹ (AUTHOR), STAIBANO, S.² (AUTHOR), MEZZA, E.² (AUTHOR), AUTIERO, G.¹ (AUTHOR), COMPARE, D.¹ (AUTHOR), ROSA, G.² (AUTHOR), BUDILLON, G.¹ (AUTHOR)

المصدر: Alimentary Pharmacology & Therapeutics. Dec2005, Vol. 22 Issue 11/12, p1139-1146. 8p. 6 Charts, 1 Graph.

مصطلحات موضوعية: *GASTRIC mucosa, *MUSCULAR atrophy, *PEPSINOGEN, *GENETICS, *THERAPEUTICS

مستخلص: Background : Histology is the gold standard for diagnosis of atrophy but is hampered by observer variation. A reliable method to overcome this issue is morphometric analysis of gastric mucosa. Serum pepsinogens and gastrin have been proposed in the diagnostic work-up of gastric atrophy although diagnostic accuracy of these tests is considered unsatisfactory. Aim : To evaluate the diagnostic accuracy of gastric serum profile in relation both to morphological and morphometric diagnosis of gastric atrophy. Methods : Ninety-four dyspeptic out-patients underwent upper endoscopy and evaluation of serum levels of PGI, PGII and 17-gastrin. Diagnostic accuracy of gastric serum profile was tested by receiver operating characteristic curves and by evaluation of sensitivity and specificity in relation to both histology and morphometric analyses. Results : As far as concern to histological evaluation, only PGI/PGII ratio showed an acceptable diagnostic accuracy in discrimination of gastric atrophy, while, when morphometric analysis was considered as reference, both serum PGI level and PGI/PGII ratio showed an excellent performance. However, both PGI and PGI/PGII ratio showed low sensitivity and high specificity. Conclusions : Serological gastric profile corresponds better with the morphometric diagnosis of atrophy, even if, because of the low sensitivity, today this could only be used as screening test of chronic atrophic gastritis. [ABSTRACT FROM AUTHOR]

المؤلفون: Nardone, G.¹ (AUTHOR), Rocco, A.¹ (AUTHOR), Malfertheiner, P.² (AUTHOR)

المصدر: Alimentary Pharmacology & Therapeutics. Aug2004, Vol. 20 Issue 3, p261-270. 10p. 2 Charts.

مصطلحات موضوعية: *HELICOBACTER pylori, *GASTRIC diseases, *EPIDEMIOLOGY, *CARCINOGENESIS, *THERAPEUTICS

مستخلص: Gastric cancer can be divided into intestinal type and diffuse type that differ substantially in epidemiology and pathogenesis. The most important aetiological factor associated both with intestinal and diffuse gastric cancer, is Helicobacter pylori. Exposure of gastric epithelial cells to H. pylori results in an inflammatory reaction with the production of reactive oxygen species and nitric oxide that, in turn, deaminates DNA causing mutations. The complex interplay between H. pylori strain, inflammation and host characteristics may directly promote diffuse type gastric cancer or induce a cascade of morphological events, i.e. atrophy, intestinal metaplasia and dysplasia, finally leading to intestinal type gastric cancer. Two mechanisms, genetic and epigenetic have been held to play a role in the molecular alterations underlying gastric carcinogenesis. The former, comprising changes in the DNA sequence, is irreversible; the latter, involving DNA methylation, is potentially reversible by eliminating the triggering agents. If H. pylori is eradicated before development of stable mutations, the risk of gastric cancer will likely be prevented. Thus, eradication of H. pylori might immediately reduce the risk of diffuse type gastric cancer, whereas prevention of intestinal type gastric cancer may be less effective if patients are treated later in the evolution of the carcinogenic process. [ABSTRACT FROM AUTHOR]

المؤلفون: Nardone, G.¹

المصدر: Alimentary Pharmacology & Therapeutics. Jun2003 Supplement 2, Vol. 17, p75-81. 7p.

مصطلحات موضوعية: *STOMACH cancer, *MORPHOLOGY, *THERAPEUTICS, *PHENOTYPES

مستخلص: Summary Gastric cancer is constituted by two histomorphological entities ‘intestinal’ and ‘diffuse’, however lesions with similar morphologies may differ in biological aggressiveness and response to therapy. Two distinct molecular pathways have been identified in gastric carcinogenesis: the microsatellite mutator phenotype and a phenotype associated with chromosomal and intrachromosomal instability. Mounting evidence suggests that microsatellite mutator phenotype alterations and expression of the products of cancer-related genes are early markers of cell transformation, and may serve to identify the gastric carcinoma histotypes. The lack of a clear genetic basis, lends weight to the notion that gastric cancer is not a monomorphic entity but may be affected by environmental factors. Helicobacter pylori is the most important environmental risk factor associated with sporadic gastric cancer. Exposure of gastric epithelial cells to bacterium results in the generation of reactive oxygen species and inducible nitric oxide synthase that in turn may cause genetic alterations leading to cancer in a subset of subjects. Thus, gastric cancer may be considered the result of an interplay between host genetic profile and environmental toxic agents. The new technologies of molecular analysis will help to establish an individual's risk of developing gastric cancer and will lead to novel biological therapeutic strategies. [ABSTRACT FROM AUTHOR]