Cyclic Vomiting Syndrome and Cannabis Hyperemesis Syndrome: The State of the Science.

This article provides a narrative review of the state of the science for both cyclic vomiting syndrome and cannabis hyperemesis syndrome along with a discussion of the relationship between these 2 conditions. The scope of this review includes the historical context of these conditions as well as the prevalence, diagnostic criteria, pathogenesis, and treatment strategies for both conditions. A synopsis of the endocannabinoid system provides a basis for the hypothesis that a lack of cannabidiol in modern high-potency Δ 9 -tetrahydrocannabinol cannabis may be contributory to cannabis hyperemesis syndrome and possibly other cannabis use disorders. In concluding assessment, though the publications addressing both adult cyclic vomiting syndrome and cannabis hyperemesis syndrome are steadily increasing overall, the state of the science supporting the treatments, prognosis, etiology, and confounding factors (including cannabis use) is of moderate quality. Much of the literature portrays these conditions separately and as such sometimes fails to account for the confounding of adult cyclic vomiting syndrome with cannabis hyperemesis syndrome. The diagnostic and therapeutic approaches are, at present, based generally on case series publications and expert opinion, with a very limited number of randomized controlled trials and a complete absence of Level 1 evidence within the cyclic vomiting literature overall as well as for cannabis hyperemesis syndrome specifically.

Risk factors for Barrett's esophagus among patients with gastroesophageal reflux disease: a community clinic-based case-control study.

OBJECTIVES: Our aim was to measure the relative risks of Barrett's esophagus (BE) associated with demographic factors, measures of adiposity, and smoking among patients with gastroesophageal reflux disease (GERD). METHODS: Patients newly diagnosed with specialized intestinal metaplasia (SIM) (n=197) were compared with patients with GERD (n=418) in a community clinic-based case-control study. Case subgroups included those with any visible columnar epithelium (VBE) (n=97), and those with a long segment (>or=2 cm) of columnar epithelium (LSBE) (n=54). RESULTS: Risks increased with older age (adjusted odds ratio (aOR) per decade for SIM=1.3, 95% confidence interval (CI)=1.1-1.5; VBE aOR=1.4, CI=1.1-1.6; LSBE aOR=1.5, CI=1.2-1.9), male gender (SIM aOR=1.5, CI=1.1-2.2; VBE aOR=2.7, CI=1.6-4.5; LSBE aOR=3.9, CI=1.9-8.1), and possibly Asian race. Increased risk of BE was observed with high waist-to-hip ratio (WHR, male high: >or=0.9, female high: >or=0.8) (SIM aOR=1.3, CI=0.9-2.1; VBE aOR=1.9, CI=1.0-3.5; LSBE aOR=4.1, CI=1.5-11.4). These associations were independent of body mass index (BMI) for the VBE and LSBE case groups but not for SIM, which was the only case group in which BMI was a significant risk factor. Ever having smoked cigarettes increased risk similarly for all case groups (SIM aOR=1.8, CI=1.2-2.6; VBE aOR=1.6, CI=1.0-2.6; LSBE aOR=2.6, CI=1.3-4.9), although a dose-response relationship was not detected for duration or intensity of smoking. CONCLUSIONS: Older age, male gender, and history of smoking increased risk of SIM and BE among GERD patients independent of other risk factors for BE. Central adiposity was most strongly related to risk of VBE and LSBE. These results may be useful in the development of risk profiles for screening GERD patients.

Comprehensive self-management for irritable bowel syndrome: randomized trial of in-person vs. combined in-person and telephone sessions.

OBJECTIVES: Psychological and behavioral therapies are being increasingly used for symptom management in patients with irritable bowel syndrome (IBS). The aims of this study were to compare two delivery modes for a comprehensive self-management (CSM) intervention, primarily by telephone vs. entirely in person, and to compare each with usual care (UC). METHODS: Adults with IBS were recruited through community advertisement. Subjects (N=188) were randomly assigned to three groups: one in which all nine weekly CSM sessions were delivered in person, one in which six of the nine sessions were conducted over telephone, and one in which subjects received UC. Primary outcome measures were a gastrointestinal (GI) symptom score based on six symptoms from a daily diary and disease-specific quality of life (QOL). These and other outcomes were assessed at baseline and at 3, 6, and 12 months after randomization. Mixed model analyses tested for differences between the three groups in each outcome variable at the three follow-up occasions, controlling for the baseline level of each outcome. RESULTS: Both GI symptom score and QOL showed significantly greater improvement in the two CSM groups than in the UC group (P<0.001), with the magnitude of this difference being quite similar for the three follow-up time points. The two CSM groups experienced a very similar degree of improvement, and there were no statistically significant differences between the two. CONCLUSIONS: A CSM program is efficacious whether delivered primarily by telephone or totally in person, and there is no evidence that replacing six of the in-person sessions by telephone sessions reduces the efficacy of the intervention.

Central adiposity and risk of Barrett's esophagus.

BACKGROUND AND AIMS: Aside from chronic reflux, the etiology of Barrett's esophagus (BE) remains largely unknown. This case-control study investigated body mass index (BMI), central adiposity, and cigarette smoking and risk of BE. METHODS: Washington residents newly diagnosed with specialized intestinal metaplasia on at least 1 of 4 esophageal biopsy specimens taken at community gastroenterology clinics (cases [n = 193]) were compared with matched population controls (n = 211). Case subgroups included those with any visible columnar epithelium (visible BE) and those with at least 2 cm of columnar epithelium (long-segment BE [LSBE]). Interviewers conducted personal interviews and took anthropometric measurements. RESULTS: All measures of central adiposity were strongly related to BE risk, particularly for LSBE. For the high category of waist-to-hip ratio (WHR), the adjusted odds ratios were 2.4 (95% confidence interval [CI]: 1.4-3.9) for all cases, 2.8 (95% CI: 1.5-5.1) for visible BE, and 4.3 (95% CI: 1.9-9.9) for LSBE. In contrast, the associations with BMI were weaker. When BMI and WHR were modeled simultaneously, the associations with BMI were greatly attenuated, whereas those with WHR remained strong. Further adjustment for frequency of heartburn did not change these results. Cigarette smoking moderately increased risk but with no evidence of a dose-dependent response or increasing strength by case group. CONCLUSIONS: These observations indicate the importance of identifying the mechanisms underlying obesity's role in BE and esophageal adenocarcinoma, and suggest that weight loss might be a fruitful approach to the prevention of these diseases.

Gastric fluid bile concentrations and risk of Barrett's esophagus.

Patients with Barrett's esophagus are at high risk of progression to adenocarcinoma. A growing, but conflicting body of evidence implicates bile reflux as a contributor to Barrett's esophagus. To investigate whether duodenogastric reflux was associated with an increased risk of Barrett's esophagus, a case-control study of incident Barrett's esophagus was performed. Cases (n=72) were identified by new histologically-confirmed diagnosis of specialized intestinal metaplasia (indicative of Barrett's esophagus) following upper endoscopy for refractory gastroesophageal reflux between October 1997 and September 2000. Cases were compared to gastroesophageal reflux patients without specialized intestinal metaplasia (controls; n=72). There was no difference in total bile acid concentrations between cases and controls. Risk of Barrett's esophagus did not significantly vary with increasing concentrations of total or free bile acids, respectively (OR 0.35 (95% CI 0.12, 1.02) and 0.60 (95% CI 0.22, 1.66)). Low gastric fluid pH (toxic range 3-5), was associated with a non-significant increase in the risk of Barrett's esophagus. In conclusion, no significant association between Barrett's esophagus and total or free bile acids in gastric refluxate was found. Patients with low gastric fluid pH (3-5) may represent a subset of patients at high risk of developing Barrett's esophagus.