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Background: Esophageal high-resolution manometry (HRM) is performed for evaluation of dysphagia or the pre-operative evaluation before esophageal surgery. The esophageal manometry parameters, interpreted as per the Chicago classification (CC), are meant to be acquired in an awake state. At times, the patient intolerance or inability to traverse the manometry catheter across the esophagogastric junction (EGJ) renders incomplete esophageal motility evaluation; hence, sedation or endoscopy assistance is required. There have been concerns raised regarding the use of sedation and resultant alteration of the manometry parameters. The aims were to study the effects of intravenous sedation on esophageal motility parameters and analyze its impact on outcomes of patients with dysphagia who are intolerant to awake manometry procedure., Methods: The study population comprised patients who had sedation or the endoscopy assistance for the HRM. The indication for HRM, necessity for the sedation, manometry findings, barium esophagogram results, procedural timings and patient outcomes were reviewed. The diagnostic impact of the 10% correction in integrated relaxation pressure (IRP) was also studied., Results: There were 14 patients from 179 awake manometry procedures that required the sedation or the endoscopy assistance. The mean age was 60.7 years and there was equal gender distribution. Dysphagia (n = 9) remained the predominant indication for the HRM, followed by the pre-operative evaluation for the esophageal surgery (n = 5). In eight patients, awake manometry failed due to the coiling of the catheter above the EGJ and six patients were intolerant to awake catheter insertion technique. Six patients were diagnosed with achalasia and two with EGJ obstruction. The correction of the possible 10% inflation of the IRP did not alter the final diagnosis in majority except one patient with the EGJ obstruction. The findings of the barium esophagogram corroborated the manometry diagnosis., Conclusion: Esophageal HRM should be done in awake state as much as possible. Sedation may be a feasible option as against aborting the further workup in patients who fail with current techniques involving awake catheter insertion. However, one needs to be mindful of sedation effects on manometry parameters and interpret results carefully., Competing Interests: All authors declare no conflict of interest.

Hepatocellular carcinoma (HCC) affects more than half a million people worldwide each year. Paraneoplastic syndromes associated with HCC include erythrocytosis, hypercalcemia, hypercholesterolemia, hypoglycemia and thrombocytosis. Thrombocytosis is a rare paraneoplastic syndrome in HCC mediated by thrombopoietin (TPO) production. We report a case of thrombocytosis as a paraneoplastic syndrome in a patient with HCC and hepatitis C cirrhosis. A 56-year-old patient was evaluated with abdominal distension and pain of 1-month duration. He had a history of hepatitis C infection with liver cirrhosis, CTP (Child-Turcotte-Pugh) class C, MELD (model for end-stage liver disease) score 22, methadone dependence, alcohol abuse and depression. His physical examination was remarkable for distended abdomen with shifting dullness, palpable hepatomegaly and scleral icterus. Routine laboratory tests showed a platelet count of 754 k/µL, white blood cell count 12.4 k/µL, serum sodium level 128 mEq/L, alanine aminotransferase 93 U/L, aspartate aminotransferase 871 U/L, total serum bilirubin 4.3 mg/dL, direct serum bilirubin 2.8mg/dL and albumin 2.6 g/dL. Computed tomography of the abdomen and pelvis revealed hepatomegaly with numerous hypodensities suspicious for HCC. Abdominal paracentesis was done, serum ascites albumin gradient (SAAG) was 2.4 g/dL consistent with portal hypertension, and spontaneous bacterial peritonitis was ruled out. Magnetic resonance imaging of the liver was consistent with infiltrating HCC, portal vein thrombosis and retroperitoneal lymphadenopathy. His alpha fetoprotein (AFP) level was 79,102 ng/mL and TPO level was 126 pg/mL. JAK2 mutation was negative and no other cause of reactive thrombocytosis could be identified. One year prior to this admission, the patient was noted to have a normal platelet count and AFP level. He was not considered a candidate for liver transplantation due to ongoing substance abuse, and expired 1 month later. Thrombocytosis is a rare paraneoplastic condition seen in HCC. It is presumed to be secondary to increased production of TPO by the tumor. We observed an elevated level of TPO in our patient. Thrombocytosis in HCC is associated with a high tumor burden, portal vein thrombosis (PVT), serum AFP levels and a poor prognosis. Thrombocytosis in a cirrhotic patient should alert the presence of HCC and is associated with poor outcomes.

Malignant mesothelioma is a rare neoplasm of the serosal linings. Mesothelioma has been linked to asbestos exposure, with prior asbestos exposure linked to 33-50% of malignant peritoneal mesotheliomas. We describe a case of malignant peritoneal mesothelioma (MPM) without any prior exposure to asbestos in a 40-year-old Hispanic female who presented to the emergency department with worsening abdominal pain and distension. She had a history of beta thalassemia trait and iron deficiency anemia. Examination revealed a distended abdomen with protruding umbilicus and positive shifting dullness. Laboratory tests showed anemia. Computed tomography (CT) of the abdomen revealed massive complex ascites suspicious of a malignant process. Ascitic fluid analysis showed serum ascites albumin gradient (SAAG) of 1.1 g/dL with a total protein of 5.2 g/dL. She underwent laparoscopic peritoneal biopsy which yielded epithelioid type malignant mesothelioma. She was started on chemotherapy with cisplatin and pemetrexed. The last follow-up was 27 months after the diagnosis. MPM is a rare and life-threatening malignancy. Frequently, the symptoms are non-specific. This poses a diagnostic challenge for physicians and probably the reason why the diagnosis is often delayed, especially in the absence of risk factors.

We present a case of an 18-year-old male who presented with complains of abdominal pain, nausea and vomiting for 2 years. An esophagogastroduodenoscopy (EGD) revealed a 3 mm nodule on the lesser curvature of the stomach and prominent gastric folds. Biopsy of the nodule revealed a well-differentiated neuroendocrine tumor (NET) in lamina prop with focal extension into muscularis mucosa consistent with a gastric carcinoid. Tumor cells stained with neuron-specific enolase (NSE), chromogranin and synaptophysin only. The prominent gastric fold biopsy revealed gastric fundic mucosa with mucosal edema and focal mild chronic inflammation. Serum gastrin level was found to be 2,083 pg/mL. Abdomen CT and endoscopic ultrasound (EUS) revealed a mass near the pancreatic neck. These findings were consistent with a functional gastrin producing well-differentiated grade 1 neuroendocrine neoplasm (gastrinoma). The patient underwent exploratory laparotomy with resection of the mass and resulting in normalization of gastrin levels., Competing Interests: None of the authors have any financial conflict of interest.

There is an epidemic of obesity worldwide. The prevalence of obesity has doubled over the last three decades. Obesity, especially abdominal obesity is associated with insulin resistance that can lead to pancreatic steatosis and non-alcoholic fatty pancreatic disease (NAFPD). NAFPD describes a phenotype entity ranging from deposition of fat in the pancreas to pancreatic inflammation, and resultant fibrosis, which is similar to that of non-alcoholic fatty liver disease (NAFLD). NAFPD may represent a meaningful manifestation of metabolic syndrome. Pancreatic steatosis can be diagnosed on ultrasound, computed tomography (CT) scan or magnetic resonance imaging (MRI). In addition to a correlation between pancreatic steatosis and metabolic syndrome, pancreatic steatosis may lead to a worse outcome in pancreatitis and may be an etiological factor in pancreatic cancer, but we need further research to examine the associations, pathophysiology, and the impact of pancreatic steatosis and NAFPD on the human health.