BYPASS-OMA: Hypoglycemic Hyperinsulinemic Nesidioblastosis after Gastric Bypass Surgery-A Case Report and Review of the Literature.

This rare case vignette describes hypoglycemic, hyperinsulinemic nesidioblastosis in a female patient with prior Roux-en-Y gastric bypass. The patient presented with severe symptomatic hypoglycemia resistant to IV dextrose and diazoxide, requiring surgical resection. Traditional imaging found nonspecific findings, and biochemical analysis was inconsistent with insulinoma. A gallium-68 dotatate PET scan was utilized to successfully localize the tumor in the distal pancreas. She underwent laparoscopic resection of the distal pancreatic lesion with resolution of her symptoms and return to euglycemia. The histological evaluation confirmed the diagnosis of nesidioblastosis. Nesidioblastosis is a rare complication of bariatric surgery that may be more clinically relevant with rising prevalence of obesity. Diagnosis with conventional imaging modalities may be challenging; however, the dotatate PET scan may have high utility in detecting lesions. It is essential for clinicians to consider nesidioblastosis in the differential diagnosis of hyperinsulinemic hypoglycemic conditions and recognize there may be a link with increasing rates of bariatric surgery.

Acute Pancreatitis with an Ongoing Pancreatic Duct Leak Complicated by Refractory Pleural Effusion: A Case Report.

BACKGROUND Acute pancreatitis causes a significant systemic inflammatory response that affects multiple organs. Pulmonary complications include pleural effusions, hypoxia, atelectasis, and acute respiratory distress syndrome. Pleural effusion is an indicator of poor prognosis in pancreatitis. This case report supports the few existing reports about best practice for the diagnosis and treatment of a pancreatic duct leak causing refractory right pleural effusion. CASE REPORT In this case report, a woman with long-term rheumatoid arthritis and recent severe gallstone pancreatitis required hospital readmission for progressive shortness of breath from recurrent massive right pleural effusion from the pancreatitis with an ongoing pancreatic leak and a pseudocyst. She had diagnostic thoracentesis and magnetic resonance cholangiopancreatography (MRCP) that was followed by endoscopic retrograde cholangiopancreatography (ERCP) and stent placement as a therapeutic procedure, with complete resolution of her symptoms. CONCLUSIONS This case report demonstrates an atypical presentation of complications from severe pancreatitis. MRCP is the criterion standard and best initial test for diagnosing a fistula. When possible, ERCP is preferred for the initial evaluation and treatment of pancreatic leaks and fistulas. In the present case report, treatment with endoscopic cystogastrostomies was effective for the internal drainage of the pseudocyst, pancreatic duct leak, and eventual resolution of the pleural effusion.

Adverse events associated with ribavirin in sofosbuvir-based therapies for patients with chronic hepatitis C: A community practice experience.

OBJECTIVE: Due to high sustained virological response (SVR) rates, sofosbuvir-based regimens are currently a mainstay for hepatitis C virus (HCV) therapies. The addition of pegylated interferon (PEG-IFN) and ribavirin impacts patients' quality of life during treatment. This study aimed to compare severe adverse events (SAEs) amongst therapeutic combinations for HCV in a community clinic setting. METHODS: From December 2013 to July 2014, 128 chronic HCV-infected patients were treated with sofosbuvir, ribavirin and weekly PEG-IFN for 12 weeks (cohort 1), 12 or 24 weeks of sofosbuvir and ribavirin (cohorts 2 and 3) or sofosbuvir plus simeprevir for 12 weeks (cohort 4). Adverse events were recorded from baseline to 12 or 24 weeks of treatment. RESULTS: SAEs appeared in 15.6-53.8% of ribavirin-inclusive treated patients compared to 4.8% of the ribavirin-free regimen. PEG-IFN, sofosbuvir plus ribavirin had the highest frequencies of fatigue, headache and rash compared to either 12 or 24 weeks of ribavirin and sofosbuvir. However, sofosbuvir and ribavirin regimens led to significant increases in dyspnea, need for ribavirin dose reductions and withdrawal from treatment due to SAEs. Anemia was also more frequent in ribavirin-inclusive combinations (P < 0.001). Conversely, sofosbuvir plus simeprevir reached similar SVR rates at week 12 post-treatment compared to all ribavirin-containing regimens, but with significantly fewer adverse events (P = 0.006). At week 12 post-treatment, cirrhotic patients experienced a higher virological relapse rate than non-cirrhotic patients (P = 0.019). CONCLUSIONS: Ribavirin-inclusive HCV therapies increased the frequencies of SAEs, had higher dropout rates and increased patient morbidity.

Predicting clinical outcomes in patients with HBsAg-positive chronic hepatitis.

BACKGROUND AND AIMS: The progression of HBsAg-positive chronic hepatitis is insidious and unpredictable. Identification of factors leading to either a benign or more serious clinical outcome may assist in decision making for antiviral therapy. METHODS: From 1989 to 1998, 130 untreated patients with chronic hepatitis were enrolled in a prospective study and followed every 3-6 months with liver and virologic tests, platelet counts and alpha-fetoprotein (AFP) measurements. RESULTS: During a mean follow-up of 107 ± 86 months, 16 (12.3 %) chronic hepatitis patients progressed to cirrhosis (annual rate 1.4 %), and 23 (17.7 %) reverted to being inactive carriers (annual rate 2.1 %). Compared to baseline values, chronic hepatitis patients who progressed to cirrhosis exhibited declines in mean platelet counts (225.7-195.2 mm(3), p = 0.008-0.04) during the first 4 years of follow-up, while those who reverted to being inactive carriers had substantial reductions in mean levels of AST (83.5-27.2 u/l, p < 0.001-0.002) and ALT (100.2-29.2 u/l, p < 0.001-0.007). In addition, during spontaneous alanine aminotransferase (ALT) flares, patients progressing to cirrhosis had concomitant elevations of AFP levels, while patients who became inactive carriers maintained normal AFP values during ALT flares (13.45 vs. 4.65 ng/ml, p = 0.001). These AFP differences during episodes of ALT flares were similarly observed when analyzed in two separate cohorts of cirrhosis and inactive carrier patients. CONCLUSION: Patients with chronic hepatitis who progressed to cirrhosis exhibited declines in platelet counts and had AFP elevations during ALT flares. To prevent progression, serial measurements of these parameters during the chronic hepatitis stage will assist in identifying patients requiring antiviral therapy.

Familial clustering of hepatocellular carcinoma in HBsAg-positive patients in the United States.

PURPOSE: The impact of familial clustering of hepatocellular carcinoma (HCC) in hepatitis B virus (HBV)-infected persons in a low HBV endemic area was investigated. METHODS: Four hundred thirteen HBsAg-positive patients, 173 with HCC and 240 without HCC, were subgrouped into those with or without a family history of HCC and analyzed for risk factors associated with HCC development. In families with HCC clustering, the ages of HCC onset in parents and siblings were compared. RESULTS: Forty-four of 173 (25.4 %) HCC patients, all of Asian descent, had 82 other blood relatives with HCC. Of these, 69 (84.1 %) were first-degree relatives. Compared to HCC patients without HCC family history, male HCC patients with family history developed HCC at a younger age than either their mothers or fathers with HCC (45.2 ± 10.3 years vs. 63.0 ± 6.8 years, p < 0.001 and 41.2 ± 14.8 years vs. 60.5 ± 5.5 years, p = 0.001, respectively); however, this was not observed in female HCC patients. In mothers of index HCC cases, 22/26 (84.6 %) tested were HBsAg positive and 14 (63.6 %) had HCC; in fathers, 11/21 (52.4 %) tested were HBsAg positive and 10 (90.9 %) had HCC. By multivariate analysis, independent risk factors for HCC development included family history (OR = 2.58, p = 0.05), male gender (OR = 3.23, p = 0.03), cirrhosis (OR = 2.4, p = 0.04), Child-Pugh classification (OR = 7.62, p = 0.004), AFP per log10 increase (OR = 1.68, p = 0.01), precore mutation (OR = 3.77, p = 0.003), and basal core promoter mutation (OR = 8.33, p < 0.001). CONCLUSIONS: HBsAg-positive male HCC patients presented at a younger age than their parents with HCC. In adult patients with an HCC family history, HCC surveillance should begin at the time of the initial clinic encounter.