Alcohol consumption pattern and risk of Barrett's oesophagus and erosive oesophagitis: an Italian case-control study.

Knowledge about the association between alcohol and Barrett's oesophagus and reflux oesophagitis is conflicting. In this case-control study we evaluated the role of specific alcoholic beverages (red and white wine, beer and liquors) in 339 Barrett's oesophagus and 462 oesophagitis patients compared with 619 endoscopic controls with other disorders, recruited in twelve Italian endoscopic units. Data on alcohol and other individual characteristics were obtained from structured questionnaires. No clear, monotonic significant dose-response relationship was pointed out for red wine. However, a generalised U-shaped trend of Barrett's oesophagus/oesophagitis risk due to red wine consumption particularly among current drinkers was found. Similar results were also found for white wine. Liquor/spirit consumption seemed to bring about a 1·14-2·30 risk excess, although statistically non-significant, for current Barrett's oesophagus/oesophagitis drinkers. Statistically significant decreasing dose-response relationships were found in Barrett's oesophagus for frequency and duration of beer consumption. Similar, but less clear downward tendencies were also found for oesophagitis patients. In conclusion, although often not statistically significant, our data suggested a reduced risk of Barrett's oesophagus and oesophagitis with a low/moderate intake of wine and beer consumption. A non-significant increased risk of Barrett's oesophagus/oesophagitis was observed with a higher intake of any type of heavy alcohol consumption, but no conclusion can be drawn owing to the high number of non-spirit drinkers and to the small number of drinkers at higher alcohol intake levels.

Smoking as an independent determinant of Barrett's esophagus and, to a lesser degree, of reflux esophagitis.

PURPOSE: To evaluate the role of smoking in Barrett's esophagus (BE) and erosive esophagitis (E) compared to endoscopic controls with no BE or E. Smoking is considered a cause of both BE and E, but results on this topic are quite controversial. METHODS: Patients with BE (339), E (462) and controls (619: 280 with GERD (gastroesophageal reflux disease)-negative and 339 with GERD-positive anamnesis) were recruited in 12 Italian endoscopy units. Data were obtained from structured questionnaires. RESULTS: Among former smokers, a remarkable upward linear trend was found in BE for all smoking-related predictors. In particular, having smoked for more than 32 years increased the risk more than two times (OR 2.44, 95 % CL 1.33-4.45). When the analysis was performed in the subgroup of subjects with GERD-negative anamnesis, the risk of late quitters (<9 years) passed from OR 2.11 (95 % CL 1.19-3.72) to OR 4.42 (95 % CL 1.52-12.8). A noticeably positive dose-response relationship with duration was seen also among current smokers. As regards E, no straightforward evidence of association was detected, but for an increased risk of late quitters (OR 1.84, 95 % CL 1.14-2.98) in former smokers and for early age at starting (OR 3.63, 95 % CL 1.19-11.1) in GERD-negative current smokers. CONCLUSIONS: Smoking seems to be an independent determinant of BE and, to a lesser degree, of E. The elevation in risk is independent from GERD and is already present in light cigarette smokers. Smoking cessation may reduce, but not remove this risk.

History of cancer in first degree relatives of Barrett's esophagus patients: a case-control study.

BACKGROUND AND OBJECTIVE: Familial clusters of Barrett's esophagus (BE) and esophageal adenocarcinoma (EAC) have been reported. This study evaluates the history of cancer in BE patients families. METHODS: In two years, patients with BE (272), esophagitis (456) and controls (517) were recruited in 12 Italian Endoscopy Units. Cancer family history in first-degree (FD) relatives was determined by a questionnaire. RESULTS: Approximately 53% of BE, 51% of esophagitis, and 48% of controls had at least one relative affected by any type of malignancy. Probands with at least one esophageal or gastric (E/G) cancer-affected relative showed a BE risk which was at least eighty-five percent higher than that of probands without affected relatives. The relative risk of BE was 4.18, 95% CL=0.76-23.04 if a FD relative had early (mean age ≤ 50 years) onset E/G cancer compared to late onset E/G cancer. CONCLUSION: In this sample there was no evidence that a family history of cancer was associated with the diagnosis of BE. An intriguing result was the association between the occurrence of E/G cancers at earlier ages (< 50 years) among BE relatives with respect the control group. This could suggest a genetic contribution in onset of these tumors, but the sample was too small to demonstrate a significant association. Further exploration of family history of E/G cancer and a diagnosis of BE in larger samples is warranted.

Increased incidence of small intestinal bacterial overgrowth during proton pump inhibitor therapy.

BACKGROUND & AIMS: Proton pump inhibitors (PPIs) can cause diarrhea, enteric infections, and alter the gastrointestinal bacterial population by suppressing the gastric acid barrier. Among patients that received long term PPI treatment, we evaluated the incidence of small intestinal bacterial overgrowth (SIBO; assessed by glucose hydrogen breath test [GHBT]), the risk factors for development of PPI-related SIBO and its clinical manifestations, and the eradication rate of SIBO after treatment with rifaximin. METHODS: GHBTs were given to 450 consecutive patients (200 with gastroesophageal reflux disease who received PPIs for a median of 36 months; 200 with irritable bowel syndrome [IBS], in absence of PPI treatment for at least 3 years; and 50 healthy control subjects that had not received PPI for at least 10 years). Each subject was given a symptoms questionnaire. RESULTS: SIBO was detected in 50% of patients using PPIs, 24.5% of patients with IBS, and 6% of healthy control subjects; there was a statistically significant difference between patients using PPIs and those with IBS or healthy control subjects (P < .001). The prevalence of SIBO increased after 1 year of treatment with PPI. The eradication rate of SIBO was 87% in the PPI group and 91% in the IBS group. CONCLUSIONS: SIBO, assessed by GHBT, occurs significantly more frequently among long term PPI users than patients with IBS or control subjects. High dose therapy with rifaximin eradicated 87%-91% of cases of SIBO in patients who continued PPI therapy.

[Esophageal transit and esophageal motility disorders in patients with nontoxic goiter and recurrent dysphagia]. / Transito esofageo e disordini della motilità esofagea in pazienti con gozzo non tossico e con disfagia ricorrente.

Esophageal motor function was studied in 14 patients affected with diffuse and (multi)nodular nontoxic goiter, with dysphagia and neck discomfort, and in 10 age-matched controls without thyroid and/or gastroesophageal diseases. Esophageal manometry was employed to evaluate upper esophageal sphincter pressure (UESP) and lower esophageal sphincter pressure (LESP), amplitude, duration and propagation velocity of peristaltic contractions and the presence of simultaneous deglutitive pressure waves. Esophageal transit was evaluated by radioisotopical method, at different times, in proximal, middle and distal esophagus. LESP was significantly lower (p < 0.001) in goitrous patients compared with controls. No difference was, on the contrary, found in the UESP, esophageal peristaltic wave amplitude and duration. Significantly (p < 0.05) increased propagation velocity of the peristaltic contractions and the presence of simultaneous deglutitive pressure waves in distal esophagus were observed in goitrous patients. Esophageal transit delay was found early in proximal and middle, and, at all times, in distal part of the esophagus of nontoxic goitrous patients. It is concluded that esophageal transit delay, early in the upper and prolonged in the lower part of the esophagus, represents the main findings of the esophageal dysfunction in the patients with nontoxic goiter and dysphagia.