Respiration and circulation affected by gas leakage into the abdominal cavity during endoscopic esophageal submucosal dissection after gastrostomy: a case report.

BACKGROUND: Pneumoperitoneum is a common complication of percutaneous endoscopic gastrostomy (PEG). We report a case of circulatory and respiratory depression due to pneumoperitoneum caused by PEG dislodgement during endoscopic submucosal dissection (ESD) surgery. CASE PRESENTATION: A 46-year-old man with PEG for dysphagia underwent ESD for esophageal cancer under general anesthesia. The patient developed a gradual increase in peak inspiratory pressure, followed by a decrease in peripheral oxygen saturation (SpO2) and blood pressure, as well as an increase in heart rate (HR) during endoscopic submucosal ESD for esophageal cancer. We suspected mediastinal emphysema due to esophageal perforation, but the surgery was successfully completed. Postoperative computed tomography (CT) revealed that the abdominal and gastric walls, which had been fixed by PEG, were detached, resulting in a large amount of intra-abdominal gas and mediastinal emphysema. CONCLUSIONS: ESD in patients with PEG should be performed carefully because of the possibility of intraoperative PEG dislodgement and pneumoperitoneum caused by insufflation gas leakage.

Mild Maternal Hypothyroxinemia During Pregnancy Induces Persistent DNA Hypermethylation in the Hippocampal Brain-Derived Neurotrophic Factor Gene in Mouse Offspring.

BACKGROUND: Thyroid hormones are essential for normal development of the central nervous system (CNS). Experimental rodents have shown that even a subtle thyroid hormone insufficiency in circulating maternal thyroid hormones during pregnancy may adversely affect neurodevelopment in offspring, resulting in irreversible cognitive deficits. This may be due to the persistent reduced expression of the hippocampal brain-derived neurotrophic factor gene Bdnf, which plays a crucial role in CNS development. However, the underlying molecular mechanisms remain unclear. METHODS: Thiamazole (MMI; 0.025% [w/v]) was administered to dams from two weeks prior to conception until delivery, which succeeded in inducing mild maternal hypothyroxinemia during pregnancy. Serum thyroid hormone and thyrotropin levels of the offspring derived from dams with mild maternal hypothyroxinemia (M offspring) and the control offspring (C offspring) were measured. At 70 days after birth, several behavior tests were performed on the offspring. Gene expression and DNA methylation status were also evaluated in the promoter region of Bdnf exon IV, which is largely responsible for neural activity-dependent Bdnf gene expression, in the hippocampus of the offspring at day 28 and day 70. RESULTS: No significant differences in serum thyroid hormone or thyrotropin levels were found between M and C offspring at day 28 and day 70. M offspring showed an impaired learning capacity in the behavior tests. Hippocampal steady-state Bdnf exon IV expression was significantly weaker in M offspring than it was in C offspring at day 28. At day 70, hippocampal Bdnf exon IV expression at the basal level was comparable between M and C offspring. However, it was significantly weaker in M offspring than in C offspring after the behavior tests. Persistent DNA hypermethylation was also found in the promoter region of Bdnf exon IV in the hippocampus of M offspring compared to that of C offspring, which may cause the attenuation of Bdnf exon IV expression in M offspring. CONCLUSIONS: Mild maternal hypothyroxinemia induces persistent DNA hypermethylation in Bdnf exon IV in offspring as epigenetic memory, which may result in long-term cognitive disorders.