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Background Dermatitis herpetiformis (DH) is a rare gluten-sensitive blistering itchy skin disease, strictly related to coeliac disease (CD). Direct immunofluorescence, demonstrating IgA granular deposits localized either in the dermal papillae or along the dermo-epidermal junction, is currently the gold standard for diagnosis of DH. It has been shown that DH immunocomplexes contain epidermal transglutaminase (eTG) and that sera from patients with DH contain antibodies specifically directed against eTG. Objectives We studied the usefulness of serum eTG antibodies in discriminating between DH, CD and other gastrointestinal and dermatologic diseases. Methods eTG antibodies were tested in 308 adult patients' sera: 44 patients with untreated dermatitis herpetiformis (UDH), 99 patients with untreated coeliac disease (UCD), 70 dermatological controls and 95 gastrointestinal controls. Results In UDH eTG antibody levels were significantly higher than in DH patients on gluten-free diet, UCD, gastrointestinal controls and dermatological controls. In UCD eTG antibodies strongly correlated with tissue transglutaminase (tTG) antibodies, whereas in UDH no significant correlation was observed. Conclusion Serum IgA eTG antibody determination can efficiently distinguish UDH from other dermatological itchy diseases and is highly sensitive to gluten-free diet. [ABSTRACT FROM AUTHOR]

This study provides data on the genetic structuring of the pipefish Syngnathus abaster in the western Mediterranean and Adriatic Seas. A total of 109 specimens were collected in brackish-water biotopes. The control region and three other regions of the mitochondrial genome were analysed. The most relevant result was the high genetic structuring found by Bayesian inference ( BI), maximum likelihood ( ML) and network analyses, which were consistent in showing three well-separated clusters of S. abaster populations. Furthermore, BI and ML did not support the monophyly of the taxon S. abaster. These results suggest the occurrence of a species complex in the study area, whose differentiation may have occurred since the Pleistocene. The results also show a very high genetic variability at the inter-population level, with no shared haplotypes among sites. Evolutionary forces due to the fragmented nature of the brackish-water habitats may account for the high genetic divergence found among the groups and populations. Finally, although dispersal by rafting over long distances may occasionally occur, this study suggests linear stepping-stone model of colonization to be most likely. The complexity of the results obtained suggests that further studies are needed to elucidate the phylogeny of S. abaster. [ABSTRACT FROM AUTHOR]

Background: Data on mortality in coeliac disease are contrasting., Aims: To systematically review the literature on all-cause and cause-specific mortality in coeliac disease compared to the general population, and evaluate differences across clinical phenotypes, geographical regions, and over time., Methods: We searched PubMed and Embase from 1 January 1970 to 31 December 2022 for eligible studies reporting on all-cause and cause-specific mortality in coeliac disease compared to the general population or controls. The protocol was registered on Open Science Framework (https://doi.org/10.17605/OSF.IO/852DN)., Results: We included 25 studies. All-cause mortality (HR 1.16, 95% CI 1.05-1.27, I 2  = 89%), mortality due to malignancies (HR 1.21, 95% CI 1.08-1.36, I 2  = 65%) and respiratory disease (HR 1.39, 95% CI 1.04-1.86, I 2  = 76%) were increased. Mortality due to non-Hodgkin lymphoma (HR 10.14, 95% CI 2.19-46.88, I 2  = 96%) was markedly increased. Mortality significantly decreased in recent decades: 1989-2004 (HR 1.61, 95% CI 1.27-2.03, I 2  = 91%), 2005-2014 (HR 1.16, 95% CI 0.99-1.36, I 2  = 89%), 2015-2022 (HR 1.19, 95% CI 1.05-1.35, I 2  = 93%). All-cause mortality was not increased in dermatitis herpetiformis (HR 0.85, 95% CI 0.73-0.99, I 2  = 40%) and undiagnosed coeliac disease (HR 1.09, 95% CI 0.95-1.25, I 2  = 0%). Mortality was increased in the UK (HR 1.23, 95% CI 1.03-1.47, I 2  = 91%) but not Scandinavia (HR 1.01, 95% CI 0.91-1.13, I 2  = 81%). Limitations include high heterogeneity and lack of data for many countries., Conclusion: Mortality in coeliac disease is increased, predominantly due to malignancies-particularly non-Hodgkin lymphoma-although differing significantly across disease phenotypes. Mortality of patients with coeliac disease has significantly decreased in recent decades. These results may influence diagnosis and management., (© 2024 The Authors. Alimentary Pharmacology & Therapeutics published by John Wiley & Sons Ltd.)

Background: Although enteropathy due to angiotensin II receptor blockers (ARBs) has been known for over 10 years, clinicians' awareness of this condition is still low., Aims: To systematically review the literature about clinical phenotypes, distribution of mucosal changes throughout the gastrointestinal tract and prognosis of enteropathy due to ARBs., Methods: According to PRISMA guidelines, we searched PubMed and Embase for relevant articles up to November 6, 2023. We included full-text papers, letters, case reports and case series describing enteropathy due to ARBs. Patients were classified into subgroups based on endoscopic and histological findings of different regions of the gastrointestinal tract. The protocol was registered with Open Science Framework (https://doi.org/10.17605/OSF.IO/TK67C)., Results: We included 94 articles reporting 183 cases (101 female, mean age at diagnosis 69 ± 10 years). The clinical picture at diagnosis was characterised by severe diarrhoea (97%) and weight loss (84%, median -13 kg), leading to hospital admission in 167 (95%) patients. Olmesartan (90%) was most frequently implicated. Villous atrophy (VA) was reported in 164/183 (89%) patients. One hundred and nine had only VA, 12 had pan-gastrointestinal involvement, 23 had VA and gastric involvement and 19 had VA and colon involvement (predominantly microscopic colitis). Outcomes were reported for 178/183 (97%) patients, who all recovered clinically on ARBs withdrawal. Histological recovery occurred in all 96 patients with VA at baseline who underwent follow-up duodenal biopsy., Conclusions: Enteropathy due to ARBs is characterised by severe malabsorption often requiring hospital admission and can involve the entire gastrointestinal tract. Clinician awareness can lead to prompt diagnosis and excellent prognosis., (© 2024 The Authors. Alimentary Pharmacology & Therapeutics published by John Wiley & Sons Ltd.)

Background: Information on the management of Helicobacter (H.) pylori infection by gastroenterologists and gastroenterology fellows are scarce. We aimed to assess practice of gastroenterologists and gastroenterology fellows and their adherence to guidelines for diagnosis and treatment of H. pylori infection in Italy., Materials and Methods: All gastroenterologists and gastroenterology fellows attending the National Congress of Digestive Diseases - FISMAD were invited to fill-in an on-line questionnaire. The questionnaire included questions on the diagnosis and treatment of H. pylori infection., Results: A total of 279 gastroenterologists and 61 gastroenterology fellows participated to the study. The 13 C-urea breath test was the most preferred method among gastroenterologists and fellows for the diagnosis of H. pylori infection (40.4% and 57.6%, respectively) and the confirmation of eradication (61.3% and 70%, respectively). Sequential therapy was the most preferred first-line treatment of H. pylori for both gastroenterologists and gastroenterology fellows (31.8% and 44%, respectively), followed by bismuth quadruple therapy (31% and 27.6%, respectively) and clarithromycin triple therapy (26.8% and 22.4%, respectively). Only 30% of gastroenterologists and 38.5% of fellows used the clarithromycin triple therapy for the recommended duration of 14 days. Bismuth quadruple therapy was the most preferred second-line therapy for both gastroenterologists and fellows. The majority of gastroenterologists and fellows would prefer an empirical therapy at third line (72.6% and 62.5%, respectively) and a susceptibility-guided therapy at fourth line (46.7% and 71.4%, respectively)., Conclusions: Practices of gastroenterologists and gastroenterology fellows are in line with guidelines' recommendations, apart for the first-line treatment of H. pylori infection. Targeted educational interventions to improve adherence to guidelines are needed., (© 2021 The Authors. Helicobacter published by John Wiley & Sons Ltd.)

Background: Seronegative coeliac disease is poorly defined., Aims: To study clinical phenotypes and long-term outcomes of seronegative coeliac disease in a multicentre cohort over 20 years., Methods: Seronegative coeliac disease was diagnosed in HLA-DQ2/DQ8-positive patients with villous atrophy (VA), negative IgA endomysial (EmA), tissue transglutaminase (tTG) and deamidated-gliadin antibodies (DGP), clinical and histological response to a gluten-free diet (GFD), and no alternative causes for VA. In patients with IgA deficiency, coeliac disease was diagnosed through VA, positive IgG EmA/tTG/DGP and clinical/histological response to a GFD (coeliac disease+IgAd). Patients with seropositive coeliac disease served as controls., Results: Of 227 patients previously diagnosed with seronegative coeliac disease, true seronegative coeliac disease was confirmed in 84, coeliac disease+IgAd in 48, and excluded in 55. Lack of follow-up duodenal biopsy precluded diagnosing seronegative coeliac disease in 40 patients. 2084 patients with seropositive coeliac disease served as controls. True seronegative coeliac disease had more severe symptoms at diagnosis and a higher risk of complications (HR 10.87, 95% CI 6.11-19.33, P < 0.001) and mortality (HR 2.18, 95% CI 1.12-4.26, P < 0.01) than seropositive coeliac disease. There were no differences between true seronegative coeliac disease and coeliac disease+IgAd. On multivariate analysis, age at diagnosis, lack of clinical response to a GFD, true seronegative coeliac disease, coeliac disease+IgAd, and classical presentation predicted complications. Age at diagnosis, complications and absence of clinical response to a GFD predicted mortality., Conclusions: Seronegative coeliac disease has a more aggressive disease phenotype than seropositive coeliac disease. These data argue against over-reliance on serology for the diagnosis of coeliac disease and support a strict clinical and histologic follow-up in seronegative coeliac disease., (© 2021 John Wiley & Sons Ltd.)

Background: A-gliadin residues 31-49 (peptide A) binds to HLA-DQ2 and is toxic to coeliac small bowel. Analogues of this peptide, which bind to DQ2 molecules but are non-toxic, may be a potential route to inducing tolerance to gliadin in patients with coeliac disease., Methods: Toxicity was investigated with small bowel organ culture in six patients with untreated coeliac disease, four with treated coeliac disease and six controls. Analogue peptides comprised alanine substituted variants of peptide A at L31 (peptide D), P36 (E), P38 (F), P39 (G) and P42 (H)., Results: Peptides D and E were toxic in biopsies from some patients. Peptides F, G and H were not toxic., Conclusions: Peptide F, which binds to DQ2 more strongly than peptide A, is not toxic in patients with coeliac disease in-vitro; this could be an initial step towards investigation of the induction of tolerance to gliadin in patients affected by coeliac disease.

Severe hyposplenism has been recently documented in alcoholic liver disease, and it has been suggested that alcohol itself is important in the derangement of splenic function, despite a lack of evidence of a direct toxic effect of alcohol on the spleen. The aim of the present study was to assess splenic function in alcoholic patients without severe liver disease and to correlate these data with the degree and duration of alcohol intake. Fifty-two alcoholics, 31 subjects with current alcohol abuse (group A)-13 abstinent from alcohol for 1 to 6 months (group B) and B abstinent from alcohol for 6 months to several years (group C)- and 26 healthy social drinkers were studied. Splenic function was assessed by counting the percentage of pitted red cells. An in vitro experiment was performed to verify whether the presence of pitted red cells could be due to an effect of alcohol on red cell morphology. The percentage of pitted red cells in subjects from group A was significantly higher than in subjects from group B (p < 0.01), from group C (p < 0.005), and from controls (p < 0.001). There was no significant difference between group B, group C, and controls. Ten subjects from group A and 1 from group B and no subject from group C had evidence of splenic hypofunction. There was no significant correlation between the percentage of pitted red cells and daily alcohol intake or years of alcohol addiction. In conclusion, our study shows that, in patients with alcoholism but without any severe liver damage, a significant but slight increase in pitted red cells is present. Further studies are needed to clarify whether this is due to a mild form of splenic hypofunction or merely indicates erythrocyte membrane alterations.