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Purpose Despite the absorption of oral thyroxine (T4) occurs in the small bowel, several patients with gastric disorders show an increased need for T4. In vitro evidence suggested that medium pH variations interfere with T4 dissolution. This study was aimed at finding the proof of concept of a direct relationship between the minimal effective dose of T4 and the actual gastric juice pH. Patients and methods Among 311 consecutively thyroxine-treated patients, 61 bearing Hashimoto’s thyroiditis (52 F/9 M; median age = 51 years) who complained persistent dyspepsia and/or upper abdominal symptoms following a noninvasive workup for gastrointestinal disorders, underwent EGDS with multiple biopsies and gastric juice pH measurement. All patients accepted to take thyroxine in fasting conditions, abstaining from eating or drinking for one hour. Results Thyroxine requirement increased along with the rising gastric pH (ρ = 0.4229; p = 0.0007). A multivariate analysis revealed that gastric pH was, beside body mass index, the far more important independent variable in determining the effective dose of T4 (p = 0.001). The ROC curve revealed that the pH threshold for an increased thyroxine requirement was at 2.28, being the AUC by 78%. Subdividing patients by the histologic findings, it appeared a significant increase (p = 0.0025) along with the progressive damage of gastric mucosa. Conclusion The in vivo measurement of gastric pH highlighted its key role in determining the minimal effective dose of oral T4 and may explain the interference of food, of some drugs and gut disorders on levothyroxine treatment

Proton pump inhibitors (PPIs) are common medications within the practice of gastroenterology. These drugs, which act through the irreversible inhibition of the hydrogen/potassium pump (H+/K+-ATPase pump) in the gastric parietal cells, are used in the treatment of several acid-related disorders. PPIs are generally well tolerated but, through the long-term reduction of gastric acid secretion, can increase the risk of an imbalance in gut microbiota composition (i.e., dysbiosis). The gut microbiota is a complex ecosystem in which microbes coexist and interact with the human host. Indeed, the resident gut bacteria are needed for multiple vital functions, such as nutrient and drug metabolism, the production of energy, defense against pathogens, the modulation of the immune system and support of the integrity of the gut mucosal barrier. The bacteria are collected in communities that vary in density and composition within each segment of the gastrointestinal (GI) tract. Therefore, every change in the gut ecosystem has been connected to an increased susceptibility or exacerbation of various GI disorders. The aim of this review is to summarize the recently available data on PPI-related microbiota alterations in each segment of the GI tract and to analyze the possible involvement of PPIs in the pathogenesis of several specific GI diseases.

Helicobacter pylori (Hp) is responsible for one of the most common infections in the world. The prevalence exceeds 50% of the population in developing countries, and approximately one-third of the adults are colonized in North Europe and North America. It is considered a major pathogenic agent of chronic gastritis, peptic ulcer, atrophic gastritis, gastric cancer, and mucosa-associated lymphoid tissue lymphoma (MALT). Hp colonization modifies the composition of gastric microbiota that could drive the development of gastric disorders. Currently, an emerging problem in Hp treatment is represented by the increasing rate of antimicrobial therapy resistance. In this context, the search for adjuvant agents can be very useful to overcome this issue and probiotics administration can represent a valid option. The aim of this review is to describe the gastric microbiota changes during Hp colonization, the mechanisms of action, and a possible role of probiotics in the treatment of this infection.

In this review, we discuss the problem of antibiotic resistance, heteroresistance, the utility of cultures and antibiotic susceptibility tests in Helicobacter pylori (Hp) eradication, as well as the updated treatment strategies for this infection. The prevalence of antibiotic resistance is increasing all over the world, especially for metronidazole and clarithromycin, because of their heavy use in some geographical areas. Heteroresistance (simultaneous presence of both susceptible and resistant strains in different sites of a single stomach) is another important issue, as an isolate could be mistakenly considered susceptible if a single biopsy is used for antimicrobial tests. We also examined literature data regarding eradication success rates of culture-guided and empiric therapies. The empiric therapy and the one based on susceptibility testing, in Hp eradication, may depend on several factors such as concomitant diseases, the number of previous antibiotic treatments, differences in bacterial virulence in individuals with positive or negative cultures, together with local antibiotic resistance patterns in real-world settings. Updated treatment strategies in Hp infection presented in the guidelines of the Toronto Consensus Group (2016) are reported. These suggest to prolong eradication therapy up to 14 days, replacing the old triple therapy with a quadruple therapy based on proton pump inhibitor (PPI), bismuth, metronidazole, and tetracycline for most of the patients, or as an alternative quadruple therapy without bismuth, based on the use of PPI, amoxicillin, metronidazole, and clarithromycin. The new drug vonoprazan, a first-in-class potassium-competitive acid blocker recently approved in Japan, is also considered to be a promising solution for Hp eradication, even for clarithromycin-resistant strains. Furthermore, there is growing interest in finding new therapeutic strategies, such as the development of vaccines or the use of natural resources, including probiotics, plants, or nutraceuticals.

Outcome of Helicobacter pylori infection is different according to gastritis extension (i.e. antrum-restricted gastritis or pangastritis). The aim of this study is to evaluate whether different gastritis patterns are associated with specific gastrointestinal symptoms or clinical signs that could be suggestive of the topography of gastritis. 236 consecutive symptomatic outpatients were recruited in two tertiary centers. They filled in a validated and self-administered Rome III modular symptomatic questionnaire, and underwent gastroscopy with histological sampling. 154 patients with Helicobacter pylori infection were included. Clinical presentation did not differ between antrum-restricted gastritis and pangastritis, gastro-esophageal reflux disease being present in 48.2 and 54.1 % of patients and dyspepsia in 51.8 and 45.9 %, respectively. However, pangastritis statistically differed from antrum-restricted gastritis in that the presence of clinical signs (p

Background: Nonceliac gluten sensitivity (NCGS) is an emergent condition, the framework of which is yet unclear, whereas the diagnosis is suggested only by gluten-dependent symptoms after excluding wheat allergy and celiac disease (CD). Our goal was to highlight intestinal, systemic, and oral alterations to clarify the NCGS pathogenesis and identify new diagnostic tools. Study: A total of 60 NCGS patients, 20 untreated CD, 20 treated CD, and 20 healthy volunteers were recruited. The differential diagnosis among gluten-related disorders was performed by serological, allergy, and histologic tools. NCGS patients were also subjected to antigliadin antibody (AGA) detection and HLA typing. All participants underwent an oral mucosa patch test for gluten (GOMPT), whereas an oral provocation test (OPT) for gluten was performed in 26 NCGS patients. Results: About 6/60 (10%) NCGS patients showed IgG AGA-positive results, whereas 45/60 (75%) patients carried HLA-DQ2 and/or HLA-DQ8 genes. GOMPT showed positive results in 45/60 (75%) NCGS patients, 3/20 (15%) untreated CD patients, 5/20 (25%) treated CD patients, and in no healthy volunteers. No significant difference was found between the severity of symptoms reported by NCGS patients subjected to OPT with gluten-containing croissants and those who underwent OPT with gluten-free croissants. Conclusions: GOMPT seems to be a specific tool for NCGS diagnosis, although further investigations are needed to overcome limits due to the small population studied and to contextualize GOMPT false-positive results.

The long-term results of microsurgical shunts for idiopathic varicocele are reported in the present paper. Sixty-two patients with a total of 65 varicoceles (three were bilateral) were followed up for 1 to 8 years. Pre- and postoperative ultrasonographic evaluation of varicocele size was considered of great importance in order to reduce the bias of subjective clinical diagnosis and to achieve a reliable and objective follow-up. Microsurgical shunts were tailored to the type of reflux: renospermatic (76.9%), iliospermatic (10.8%) or mixed type (12.3%); 94% of patients experienced a complete morphologic disappearance of varicosities, while in 6% of the cases a consistent reduction of size was objectified although varicosities were still detectable at ultrasonographic examination. In patients with severe infertility a significant increase of seminal parameters was observed postoperatively and this improvement showed a higher statistical significance in patients aged

The authors report a case of massive intraoperative bleeding complicating a post-pancreatic abscess. Hemorrhage was due to erosion of the splenic artery, which eventually ruptured within the abscess c

Introduction Massive bleeding may complicate the course of either acute or chronic pancreatitis. Although the latter is more frequently involved when bleeding occurs in the acute form, a poorer prognosis is to be expected. Abscess, severe inflammation, regional necrosis, and pseudocysts may cause major vessel erosion, with or without pseudoaneurysm formation, whose eventual rupture may result in massive bleeding into the gastrointestinal tract, retroperitoneum, and peritoneal cavity. Aims To define the most important pathophysiologic mechanisms and factors that might contribute to a better understanding, better prevention, and more efficient treatment of severe hemorrhage complicating acute necrotizing pancreatitis. Awareness of high-risk conditions occurring during the natural evolution of the disease (from extensive local severe enzymatic damage to late septic sequelae), avoidance of a too early and too aggressive approach to sterile pancreatic necrosis, and providing prompt and effective treatment of local septic complications, when they occur, are crucial steps for bleeding prevention. Methodology Forty-four cases of severe bleeding following acute pancreatitis that were reported during the last decade since 1992 (including the six cases reported here) are reviewed, analyzed, and summarized. Results The overall mortality rate was 34.1%. Splenic artery, portal vein, spleen, and unspecified peripancreatic vessels were the most commonly involved sources of bleeding, with associated mortality rates of 33.3%, 50.0%, 30%, and 28.5%, respectively. Massive hemorrhage was more frequently associated with severe necrosis, with a mortality rate of 37.9%. Conclusion The increased use of diagnostic and interventional radiology, in association with prompt surgical treatment, appears to be the way to improve survival rates in cases of arterial bleeding. Venous bleeding due to lesion of major peripancreatic veins or diffuse bleeding represents a therapeutic challenge, and treatment of these conditions should be tailored to the individual case, as no general rule can be suggested. In extreme cases, open packing or salvage emergency pancreatectomy may represent the only chances for survival.

Bleeding in pancreatitis may be due either to gastroduodenal causes (e.g., acute gastric erosions, mucosal congestions, peptic ulceration, Mallory-Weiss syndrome, and alcoholic gastritis), which are usually managed with conservative treatment [1], or to direct involvement of vascular structures by pancreatitic local sequelae. The latter, although uncommon, is usually characterized by massive hemorrhage, which is considered the most severe and rapidly lethal complication of pancreatitis [2, 3]. It may be associated with either acute or chronic pancreatitis and is caused by major vessels’ erosion, followed in most cases by vessel disruption or pseudoaneurysm formation. Pseudocysts, severe inflammation, regional necrosis, and infection are the most important pathogenetic factors [4, 5]. Although the incidence of major bleeding in pancreatitis is relatively low (1.7%–2.5%), it is associated with a prohibitively high mortality rate reaching 40%–80% [6, 7, 8].

Microsurgical drainage of spermatic veins tailored to the hemodynamic type of varicocelle was performed in 20 patients. In 14 cases the procedure was indicated as prophylaxis and in 6 cases as treatment of infertility. Complete regression of varicosities was observed in 75 percent as early as six days postoperatively, in 85 percent at two weeks, and in 90 percent at twelve months. In the remaining 10 percent, a consistent reduction of varicocele was found. No patient experienced progression of the disease. Eighty-three percent of the patients with altered seminal parameters showed an improvement of them at a mean follow-up of 9.1 months.

A fatal case of acute fulminant bleeding in pancreatitis associated with portal hypertension and caused by rupture of the splenic vein is reported, and the pathological and clinical features of this u