Vitamin D is known to be critical to brain function and has neuroprotective effects (Anjum et al., 2018). Low levels of blood vitamin D accelerate cognitive impairment, and it especially results in executive dysfunction and episodic memory impairment (Miller et al., 2015). This is known to happen through regulating the release of neurotrophic factors, increasing antioxidant capacity, and decreasing the production of inflammation markers (Eyles et al., 2005;Grant, 2009;Moore et al., 2005). The high density of vitamin D receptors (VDR) in the hippocampus, hypothalamus, thalamus, cortex, and substantia nigra suggests the potential of vitamin D to influence neurological conditions (Fleet, 2004). Vitamin D contributes to neuronal development by regulating the synthesis of nerve growth factor (NGF) and various neurotransmitters such as acetylcholine (Ach), dopamine (DA), and gamma-aminobutyric acid (GABA)
Distal gastrectomy with Billroth I or II reconstruction may cause duodenogastroesophageal reflux (DGER), thereby resulting in digestive or respiratory symptoms. The mainstay of treatment is medication with proton pump inhibitors. However, these drugs may have limited effects in DGER. Laparoscopic fundoplication has been proven to be highly effective in treating gastroesophageal reflux disease (GERD), but it cannot be performed optimally for GERD that develops after gastrectomy. We report the case of a 72-year-old man with a history of distal gastrectomy and Billroth I anastomosis due to early gastric cancer. GERD due to bile reflux occurred after surgery and was refractory to medical therapy. The patient underwent Roux-en-Y conversion from Billroth I gastroduodenostomy and hiatal hernia repair with only cruroplasty. Fundoplication was not performed. His symptoms improved significantly after the surgery. Therefore, laparoscopic hiatal hernia repair and Roux-en-Y conversion can be an effective surgical procedure to treat medically refractory DGER after Billroth I gastrectomy.
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