Acute gastric volvulus is a life threatening condition requiring early diagnosis and aggressive management. Diagnosis of gastric volvulus remains a challenge for clinicians due to variable, non-specific clinical presentation, which requires a high level of suspicion. It should be considered in patients presenting with chest pain and/or epigastric pain, especially in the elderly population. Endoscopic de-rotation could be initially attempted as a therapeutic modality especially in patients who cannot undergo surgery. However, surgery remains the main stay of treatment. Delay in diagnosis can lead to complications like mucosal ischemia, necrosis or perforation, shock, which substantially increase the morbidity and mortality.

Intermittent gastric volvulus plagued a 61-year-old white woman with chest pain for months before it was observed on esophagogastroduodenoscopy (EGD). She presented to the Emergency Department with complaints of progressively worsening localized, burning, left-sided and substernal chest pain that was identical to her previous myocardial infarction. Her chest pain was associated with nausea, vomiting, and shortness of breath. She experienced no relief with the administration of sublingual nitroglycerin and aspirin. Due to her prior history of coronary artery disease with left anterior descending artery stent placement, acute coronary syndrome was highest on her differential diagnosis list during her visits to the hospital. In fact, the concern was so great that she underwent a nuclear medicine stress test, followed by a left heart catheterization 2 weeks prior to this hospitalization in another state during an acute episode of chest pain. During that hospitalization, the stress test showed no evidence of inducible myocardial ischemia and the left heart catheterization showed only mild to moderate stenosis of the left anterior descending artery with a patent stent. Further confounding her diagnosis was the lack of hematemesis prior to her admission, prior history of gastrointestinal bleed, or use of high-risk medications such as nonsteroidal anti-inflammatory drugs.Her past medical history was significant for coronary artery disease with left anterior descending artery stent placement, chronic kidney disease stage 3, hiatal hernia with gastroesophageal reflux disease, and depression. Her Funding: None.

Abstract. Hepatocellular dysfunction occurs early in sepsis and this appears to be caused by Kupffer cell-derived TNF-· production from the liver as a result of the increased release of the sympathetic neurotransmitter, norepinephrine, from the gut. Ghrelin, a novel stomach-derived peptide, is downregulated in sepsis and administration of ghrelin into rodents decrease pro-inflammatory cytokines, attenuates hepatic and other organ injuries and improves survival. Ghrelin's beneficial effect in sepsis is mediated by the inhibition of the sympathetic nervous system (SNS), as evidenced by the reduced gutderived norepineprine (NE) release in sepsis after ghrelin treatment. Recent data suggest that MKP-1, the MAPK phosphatase-1, is involved in the innate immune responses. To determine that the beneficial effect of ghrelin in sepsis is mediated by MKP-1, rats were subjected to sepsis by cecal ligation and puncture (CLP) alone, or treated with ghrelin, beginning at 5-h post-CLP and liver tissues were harvested and examined for MKP-1 mRNA and protein expression. CLP alone produced a significant decrease in MKP-1 gene expression in liver tissues at 20 h after CLP (P<0.05). MKP-1 mRNA was decreased by 30-40% at 2 and 5 h after CLP, but not statistically significant. MKP-1 protein expression was significantly decreased as early as 2 h after CLP and remained low at 5-20 h after CLP. While septic rats treated with vehicle produced significant decreases from sham rats, ghrelin treatment improved both mRNA and protein from vehicle group (0.58±0.069 vs. 0.91±0.16, P<0.05; 0.14±0.027 vs. 0.22±0.017, P=0.013), respectively. Since ghrelin's inhibitory effect is mediated by the SNS, we hypothesized that NE treatment in Kupffer cells may downregulate MKP-1. Kupffer cells were treated with NE and examined for MKP-1.Treatment with NE for 60 min showed an average of 46.9% decrease in MKP-1 mRNA expression compared to untreated cells (P<0.001). Likewise, NE treatment in RAW264.7 cells produced significantly lower MKP-1 mRNA than that of control cells. To further confirm the effect of NE on MKP-1, normal rats were infused with NE for 2 h through the portal vein and MKP-1 mRNA from the liver was examined. Infusion with NE produced a significant 73.7% decrease in MKP-1 mRNA. Therefore, ghrelin's inhibitory effect on gut-derived NE release in sepsis leading to the downregulation of proinflammatory cytokines is mediated by MKP-1.