Association between hypokalemia and small bowel capsule endoscopy completion rates in patients in South China: A prospective single-center study.

BACKGROUND/AIMS: Approximately 20-30% of small bowel capsule endoscopies (SBCEs) do not reach the cecum at the completion of the examination. We aimed to determine whether hypokalemia influences the completion rate and small bowel transit time (SBTT) of SBCE. PATIENTS AND METHODS: From January to December 2017, 112 patients (18-75 years old) who underwent SBCE were assessed consecutively for enrolment in our study. On the day of the procedure, a blood test was performed prior to capsule ingestion. The completion rate, gastric transit time (GTT), SBTT, and diagnostic yield were recorded for each SBCE. RESULTS: The SBCE completion rate was lower in the hypokalemia group than that in the normal potassium group (55.6% (15/27) vs. 76.5% (65/85), P = 0.036). The median GTT was 55.5 ± 47.1 min in the hypokalemia group and 46.7 ± 44.5 min in the normal potassium group (P > 0.05). The median SBTT was 412.8 ± 123.3 min in the hypokalemia group and 367.3 ± 172.5 min in the normal potassium group (P > 0.05). The diagnostic yields of the hypokalemia and normal potassium groups were 74.1% and 78.8%, respectively (P = 1.00). CONCLUSION: Hypokalemia may decrease the SBCE completion rate. Physicians should consider the possibility of hypokalemia after bowel preparation because this condition is not rare. Potassium deficiencies should be rectified prior to performing SBCE procedures to increase the SBCE completion rate.

BTLA associates with increased Foxp3 expression in CD4(+) T cells in dextran sulfate sodium-induced colitis.

Ulcerative colitis (UC) is an inflammatory bowel disease, and its pathogenesis involves a variety of genetic, environmental, and immunological factors such as T helper cells and their secreted cytokines. B and T lymphocyte attenuator (BTLA) is an immunoregulatory receptor that has a strong suppressive effect on T-cell function. However the role of BTLA in UC remains poorly understood. Here we demonstrated that the frequency of BTLA-expressing CD3(+) T cells, especially CD4(+) T cells, increased in blood and mucosa in mice with DSS-induced colitis. The frequency of Foxp3-expressing cells in BTLA+ CD4(+) T cell from lamina propria mononuclear cells (LPMCs) was much higher in DSS-treated mice than that in controls. Similarly, the proportion of IL-17+ cells in BTLA+ CD4(+) T cells from LPMCs in DSS-treated mice is much higher than that in controls, while no perceptible difference for the proportion of IFN-γ+ cells in BTLA+ CD4(+) T cells was noted between DSS-treated mice and controls. Treatment of mesalazine, an anti-ulcerative colitis drug, down-regulated Foxp3 and IL-17 expression in BTLA positive T cells along with attenuated severity for colitis. Our findings indicate that BTLA may be involved in the control of inflammatory responses through increasing Foxp3 expression, rather than attenuating IL-17 production, in DSS-induced colitis.