Increased intragastric pressure gradients are involved in the occurrence of acid reflux in gastroesophageal reflux disease.

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Functional dyspepsia and irritable bowel syndrome in patients with achalasia and its association with non-cardiac chest pain and a decreased health-related quality of life.

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Persisting symptoms and decreased health-related quality-of-life in a cross-sectional study of treated achalasia patients

Copyright © 2007 The Authors The definitive version is available at www.blackwell-synergy.comSummaryBackgroundLittle is known about symptom characteristics of treated achalasia patients and their effect on health‐related quality‐of‐life (HRQoL).AimsTo examine clinical remission, achalasia‐associated symptoms and HRQoL in treated achalasia patients.MethodsThe Eckardt clinical symptom score, RAND‐36 and a disease‐specific HRQoL questionnaire were sent to 171 treated achalasia patients.Results76.6% of the patients returned their questionnaire. 44.9% of them were not in symptomatic remission. Prevalence of frequent dysphagia (at least daily) and chest pain (at least weekly) was 46% and 38%, respectively. Achalasia patients had lower general HRQoL scores than control subjects (all RAND‐36 subscales, except health change; P ≤ 0.002). Patients with frequent symptoms of chest pain and dysphagia showed lower HRQoL than patients with less frequent symptoms on three RAND‐36 subscales (pain, social functioning and general health perceptions; P < 0.003). Patients in clinical remission showed higher HRQoL than patients who were not, however HRQoL in the ‘remission group’ remained significantly impaired as compared to controls (all RAND‐36 subscales except emotional role limitations and mental health; P < 0.001).ConclusionsMany achalasia patients remain severely symptomatic after treatment and have decreased HRQoL. Frequent symptoms are associated with lower HRQoL. Patients in clinical remission show substantially improved, but not restored HRQoL.R. Frankhuisen, M. A. Van Herwaarden, R. Heijkoop, A. J. P. M. Smout, A. Baron, J. R. Vermeijden, H. G. Gooszen and M. Samso

Timing and impact of infections in acute pancreatitis

Contains fulltext : 81117.pdf (publisher's version ) (Closed access)BACKGROUND: Although infected necrosis is an established cause of death in acute pancreatitis, the impact of bacteraemia and pneumonia is less certain. METHODS: This was a cohort study of 731 patients with a primary episode of acute pancreatitis in 2004-2007, including 296 patients involved in a randomized controlled trial to investigate the value of probiotic treatment in severe pancreatitis. Time of onset of bacteraemia, pneumonia, infected pancreatic necrosis, persistent organ failure and death were recorded. RESULTS: The initial infection in 173 patients was diagnosed a median of 8 (interquartile range 3-20) days after admission (infected necrosis, median day 26; bacteraemia/pneumonia, median day 7). Eighty per cent of 61 patients who died had an infection. In 154 patients with pancreatic parenchymal necrosis, bacteraemia was associated with increased risk of infected necrosis (65 versus 37.9 per cent; P = 0.002). In 98 patients with infected necrosis, bacteraemia was associated with higher mortality (40 versus 16 per cent; P = 0.014). In multivariable analysis, persistent organ failure (odds ratio (OR) 18.0), bacteraemia (OR 3.4) and age (OR 1.1) were associated with death. CONCLUSION: Infections occur early in acute pancreatitis, and have a significant impact on mortality, especially bacteraemia. Prophylactic strategies should focus on early intervention

Association Analysis of Genetic Variants in the Myosin IXB Gene in Acute Pancreatitis

Introduction: Impairment of the mucosal barrier plays an important role in the pathophysiology of acute pancreatitis. The myosin IXB (MYO9B) gene and the two tight-junction adaptor genes, PARD3 and MAGI2, have been linked to gastrointestinal permeability. Common variants of these genes are associated with celiac disease and inflammatory bowel disease, two other conditions in which intestinal permeability plays a role. We investigated genetic variation in MYO9B, PARD3 and MAGI2 for association with acute pancreatitis. Methods: Five single nucleotide polymorphisms (SNPs) in MYO9B, two SNPs in PARD3, and three SNPs in MAGI2 were studied in a Dutch cohort of 387 patients with acute pancreatitis and over 800 controls, and in a German cohort of 235 patients and 250 controls. Results: Association to MYO9B and PARD3 was observed in the Dutch cohort, but only one SNP in MYO9B and one in MAGI2 showed association in the German cohort (p <0.05). Joint analysis of the combined cohorts showed that, after correcting for multiple testing, only two SNPs in MYO9B remained associated (rs7259292, p = 0.0031, odds ratio (OR) 1.94, 95% confidence interval (95% CI) 1.35-2.78; rs1545620, p = 0.0006, OR 1.33, 95% CI 1.16-1.53). SNP rs1545620 is a non-synonymous SNP previously suspected to impact on ulcerative colitis. None of the SNPs showed association to disease severity or etiology. Conclusion: Variants in MYO9B may be involved in acute pancreatitis, but we found no evidence for involvement of PARD3 or MAGI2