Association of CCK1 Receptor Gene Polymorphisms and Irritable Bowel Syndrome in Korean

INTRODUCTION: Cholecystokinin (CCK) belongs to a group of endogenous molecules known as brain-gut neuropeptides and functions as a neuropeptide as well as a gut hormone. It remains unclear whether genetic variation of the CCK receptor plays a role in irritable bowel syndrome (IBS). The aim of this study was to determine and compare the allele and genotype frequencies of the CCK1 receptor polymorphisms between healthy controls and patients with IBS. METHODS: Genotyping of 80 patients with IBS (who met the Rome III criteria) and 76 healthy controls was performed. We performed PCR amplification for the CCK1 receptor intron 1 779 T > C and Exon 1 G > A. We confirmed polymorphisms by direct sequencing method. RESULTS: There was a significantly different trend for genotypic distributions of the CCK1 receptor polymorphism between patients with IBS and healthy controls (p for trend = 0.048). The CCK1 receptor intron 1 779 T >C polymorphic type was more common in patients with 'IBS-constipation predominant (IBS-C) and IBS-mixed (IBS-M) forms' (19/31, 61.3%) than healthy controls 32/76, 42.1% adjusted odd ratio 2.43, 95% Confidence interval 1.01-5.86). The genotypic distributions of the CCK1 receptor exon 1 polymorphism were not significantly different between the two groups (p for trend = 0.223). CONCLUSIONS: CCK1 receptor polymorphisms were associated with IBS. In particular, the CCK1 receptor intron 1 779 T > C polymorphic type was associated with 'IBS-C and IBS-M'. Further studies are needed in larger number of patients with an even distribution of IBS subtypes.

A Case of Duodenal Fistula Caused by Intra-abdominal Tuberculous Lymphadenopathy during Anti-tuberculous Medication / 대한소화기내시경학회지

Recently, the proportion of extrapulmonary tuberculosis in patients has increased in Korea. Though intestinal tuberculosis in not infrequent, a duodenal fistula caused by tuberculosis is a rare condition. A 29-year-old man was admitted to the Department of Internal Medicine because of fever and weight loss. The patient was a doctor participating in a resident fellowship. The patient was diagnosed with intra-abdominal tuberculous lymphadenopathy and was given anti-tuberculous medication. One month after the administration of medication, the patient showed symptoms and signs of duodenal obstruction because of marked duodenal wall edema and a deep ulcer on the second portion of the duodenum. A computerized tomogram and duodenography revealed the formation of a fistula at the second portion of the duodenum and the presence of abscess-forming tuberculous lymphadenopathy. The use of continuous anti- tuberculous medication resulted in the improvement of the clinical symptoms, with complete healing of the duodenal fistula and tuberculous lymphadenitis. This case suggests that transient clinical worsening in intra-abdominal tuberculous lymphadenitis may occur during an early period of anti- tuberculous medication.