IntroductionAcute pancreatitis is an inflammatory process of the pancreas, which can range from mild, self-limited disease to severe disease potentially resulting in death. Although overall mortality has decreased, the incidence of acute pancreatitis is increasing. Severe episodes of acute pancreatitis are more likely to result in prolonged hospitalisation and increased mortality. Reliable means of early detection and indicators of severity in acute pancreatitis remain a challenge, hence the continued efforts of the medical community toward developing improved prognostic tools. There are various scoring systems available that are aimed at classifying severity of acute pancreatitis; however, many of these scores are cumbersome and remain underutilised. As a result, the investigation of biological markers with potential to predict prognosis of acute pancreatitis has been a topic of interest.AimTo investigate the utility of peripheral venous bicarbonate levels as a biomarker in predicting severity of acute pancreatitis, defined as increased length of stay, organ failure, need for intervention, and/or mortality.Material and methodsPatients between the ages of 18 and 80 who were admitted from September 2015 to August 2017 with acute pancreatitis were selected via chart review. The associations between peripheral venous bicarbonate level obtained on admission and length of stay, encounter type, organ failure and need for intervention were analyzed.ResultsThere was a significant association between bicarbonate levels and both discharge type and organ failure. Expired patients and patients with more incidences of organ failure during their hospitalization were found to have lower peripheral venous bicarbonate levels on admission. There was no significant association found between bicarbonate level and length of stay or need for intervention.ConclusionsOur retrospective study found that lower peripheral venous bicarbonate levels were significantly associated with increased incidence of organ failure and mortality in acute pancreatitis. Peripheral venous sampling can be promptly and easily obtained in most clinical settings, making this biological marker worthy of further investigation.

INTRODUCTION: Over the past decade immune-checkpoint inhibitors have been playing an increasing role in cancer treatment. One of the targets of these therapies is the Programmed Death (PD-1) protein; a protein that prevents T cells from recognizing and attacking inflamed tissues and cancer cells. Our reports describes a case in which a patient treated with nivolumab, a PD-1 inhibitor, presented with endoscopic findings characteristic of ulcerative colitis (UC). CASE DESCRIPTION/METHODS: Our case involves a 69-year-old male with past medical history of metastatic melanoma who presented with complaints of diarrhea rectal bleeding. Patient was on nivolumab 3 mg/kg every 2 weeks which was started 5 months ago. He reported lower abdominal cramping, bright rectal bleeding and diarrhea ongoing for 4 days. Physical examination was significant for moderate tenderness to palpation in lower abdomen. Initial abnormal laboratory results including hemoglobin of 11.2 g/dL otherwise unremarkable comprehensive metabolic panel. On computed tomography (CT) of abdomen and pelvis he was noted to have marked colitis involving the ascending, transverse and descending colon. All the following stool testing was negative for clostridium difficile, stool cultures camplyobacter, salmonella, shigella, ova and parasite. Patient was noted to have pancolitis on colonoscopy and pathology showed acute and chronic inflammation with superficial ulceration. Nivolumab was stopped and he was started on IV methylprednisolone 80 mg TID. Patient had little improvement over the next three days and hemoglobin decreased to 8.0 g/dL. Therefore he was given a dose of infliximab 5 mg/kg. His symptoms improved and he was in complete clinical remission soon after discharge. Patient was continued on oral prednisone 100 mg daily and instructed to taper slowly over the coming months. DISCUSSION: The PD-1 pathway will continue to be manipulated in future cancer treatments. Inhibition of PD-1 pathway in mice has resulted in various autoimmune diseases. In a safety profile study with 576 patients on nivolumab dosing of 3 mg/kg the most common adverse effect was noted to be a fatigue in 25% of patients. The incidence of grade 3 or 4 colitis was noted to be present in 0.7% of patients or 4 in total. Although the incidence of severe colitis may be low, infectious etiology must be ruled out prior to initiating immunosuppressive therapy. Patients with corticosteroid resistant colitis should have prompt initiation of infliximab therapy.

A 65-year-old woman presented with right lower quadrant (RLQ) abdominal pain of three days duration. During her hospitalization, she underwent computed tomography (CT) of the abdomen, duplex ultrasound of the abdomen, esophagogastroduodenoscopy (EGD), and colonoscopy as part of a diagnostic workup. The workup identified high-grade obstructions of the celiac artery (CA), superior mesenteric artery (SMA), atypical appearing gastric ulcers, and a diffusely ulcerated cecum, which created a mass-like appearance. The patient developed cecal perforation despite mesenteric vessel stenting and ultimately required right hemicolectomy for definitive management. This case report represents a rare presentation of simultaneous gastric ischemia and cecal ischemia with necrosis in a patient with underlying peripheral vascular disease.

INTRODUCTION: Double pylorus is a rare endoscopic finding that has been reported in 0.001% to 0.4% of upper gastrointestinal endoscopies, consisting of a gastroduodenal fistula extending from the prepyloric gastric antrum to the duodenal bulb through an accessory channel. In the majority of cases, it is a complication when peptic ulcers erode and create a fistula between the duodenal bulb and the distal stomach. It usually presents on the lessor curvature of the gastric antrum and on a superior wall of the duodenal bulb. It is commonly an endoscopic finding, since clinical presentation is similar to other peptic diseases. CASE DESCRIPTION/METHODS: The patient was a 62-year-old female presented to the emergency room for evaluation of intractable nausea and vomiting. The patient reported sudden onset of symptoms day prior, with multiple episodes of brown-colored liquid emesis. Patient denied any associated abdominal pain, no postprandial association with food. CT showed significant mucosal thickening of the gastric antrum to proximal duodenum, resulting in severe dilation of the stomach with air fluid level. Nasogastric tube was then placed for decompression and serial KUB showed adequate position and non-obstructive bowel gas pattern. An esophagogastroduodenoscopy revealed moderate gastritis and antral duodenal fistula, an accessory channel was noted on the lesser curvature side and once engaged was able to be passed with the endoscope. Pathology returned reactive mucosal changes suggestive of focal erosions, Helicobacter Pylori returned negative. DISCUSSION: The majority of reported cases of double pylorus are acquired and are attributed to complications of ulcers at the antrum-pyloric area or at the duodenal bulb. Acquired double pylorus typically present symptomatic with chronic upper abdominal pain, vomiting, dyspepsia, or upper gastrointestinal bleeding. Patients often have a long history of treatment with NSAIDs or corticosteroids, which should prompt an investigation for Helicobacter pylori and eventual treatment if found positive. Medications for the reduction of peptic acid should be taken and ulcerogenic medications should be avoided. The majority of patients respond well to medical treatment, according to a retrospective follow-up study in patients treated with H2 receptor antagonist or proton pump inhibitor after the diagnosis of acquired double pylorus, the fistula remained open in the majority of patients (64%), fused with normal pylorus in 27% of patients and closed only in 9% of cases.

INTRODUCTION: Anabolic-androgenic steroid abuse has been steadily increasing in the general population. According to a 2014 study, approximately 1 in 50 students in the 12th grade reported using anabolic steroids. Trenbelone acetate is a synthetic anabolic androgen which is an agonist of the androgen receptor and most often used in cattle. CASE DESCRIPTION/METHODS: A 23 year old male with no significant past medical history presented with complaints of jaundice and generalized weakness which began 10 days prior to presentation. Patient endorsed weekly IM trenbelone 1000 mg weekly over the last 8 weeks. Physical examination was remarkable for icterus and appropriate mentation. Initial investigations reflected a total bilirubin of 13.44 mg/dL, AST 159 IU/L, ALT 425 IU/L, PT 11.0, INR 1.0, and Alk Phos of 142. Serologies were negative for viral hepatitis, anti-mitochondrial antibody, anti-smooth muscle antibody and ANA of 1:40. A liver ultrasound reported normal liver size without biliary obstruction. Patient's liver chemistries improved over the next three days and he was discharged with total bilirubin of 12.54 mg/dL, AST 135 IU/L, ALT 320 IU/L, PT 11.0, INR 1.0 and Alk Phos of 121. Patient advised to abstain from any future use of trenbelone. On repeat labs in 10 days, his total bilirubin of 29.50 mg/dL, AST 78, ALT 123, PT 20.1, INR 1.85 and Alk Phos 242. Physical examination noted worsening jaundice overall along with icterus but mentation remained appropriate. Patient denied any new medications and no further use of trenbelone since discharge. Patient's liver chemistries remained stable and he underwent MRI abdomen which was unremarkable. Patient was discharged home on ursodiol 300 mg BID. Patient's liver chemistry improved in one week and returned to baseline in one month. DISCUSSION: Anabolic steroids have been linked to four different forms of liver injury including an acute cholestatic syndrome such as in our patient, elevation in serum enzymes, chronic vascular injury and hepatic tumors including adenomas and hepatocellular carcinoma. Mechanism of cholestatic syndrome is not well defined in this type of injury. Urosdiol has been used in the past for treatment however efficacy has not been shown in a study. Healthcare provides managing patients with elevated liver chemistries should able to recognize anabolic induced liver injury given increasing use and ease of availability of such performance enhancing drugs.