A 64-year-old woman with traumatic brain injury and chronic percutaneous endoscopic gastrostomy (PEG) tube presented to the emergency room with nonradiating acute epigastric abdominal pain for 3 days. The external PEG bumper measured 8 cm. Lipase was 550 U/L (ref: 0-160 U/L), and abdominal computed tomography revealed migrated inflated PEG balloon into the duodenal bulb resulting in extrinsic mass effect on the pancreatic segment of the common bile duct with notable dilation of the common bile duct (Figures 1 and 2). The PEG tube was repositioned, and the bumper was adjusted to 4 cm. Abdominal X-ray showed the PEG balloon within the midgastric body (Figure 3). Her pancreatitis improved, and she was ultimately discharged. PEG tubes are commonly used for enteral nutrition in patients incapable of maintaining adequate oral intake and are generally safe and effective. 1,2 Complications of PEG include hemorrhage, infection, intestinal perforation, and peritonitis, whereas pancreatitis is rare and has only been reported sparingly. 3 The external bumper may dislodge, leading to tube migration, and therefore warrants frequent checks to ensure the bumper is firmly in place. 3,4 Resolution of symptoms in other cases occurred with tube repositioning, as seen in our patient. [3][4][5]

Although the relationship between androgens and hepatocellular tumor development has been noted since 1975, cases involving hepatocellular carcinoma (HCC) or cholangiocarcinoma development in patients on chronic androgen therapy or anabolic androgenic steroid (AAS) use are few, and far between. We present three cases of patients who developed hepatic and bile duct malignancies in the setting of AAS use and testosterone supplementation, arising from a single tertiary referral center. Additionally, we review the literature for the mechanisms behind the possible androgen-mediated malignant transformation of these liver and bile duct tumors.

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584 Background: Cholangiocarcinoma (CCA) is a rare cancer of the bile ducts but has been increasing in incidence. The mainstay of treatment of CCA is resection or chemoradiation for more advanced disease, with immunotherapy being an evolving field in treatment. A better understanding of CCA pathogenesis will pave new avenues for treatment. Methods: We employed our STARGEO platform to conduct a meta-analysis of public data from NCBI's Gene Expression Omnibus. We performed meta-analysis with 259 CCA tumor samples against 16 normal intrahepatic duct samples as a control. We then analyzed the signature in Ingenuity Pathway Analysis. Results: Our analysis revealed FXR/RXR and LXR/RXR activation as top canonical pathways. Top upstream regulators identified included HNF1A (with predicted inhibition) and ERBB2 (with predicted activation). The most upregulated genes included several extracellular matrix proteins implicated in cancer including COL1A1, LAMC2 (correlated with poor prognosis in CCA), KRT17 (a keratin implicated in various malignancies but not well described in CCA), and LAMB3 (exerts tumorigenesis through PI3k/Akt signaling). Additionally, we found stark upregulation of the immunophillin FKPBP1A, which is involved in mTOR activation. We also noted upregulation of ubiquitin-associated gene UBASH3B, which inhibits endocytosis in EGFR and has been described in breast cancer but not CCA. From our investigation of immune checkpoint inhibitors, we found upregulation of classically described inhibitors such as CTLA4, TIGIT, and BTLA. In addition, we found upregulation of SIGLEC7, which has been recently shown to suppress immune function by binding to terminal sialic acid on glycans on the surface of immune cells. Conclusions: Our analysis highlights the possible role of ERBB2 and several extracellular genes in the pathogenesis of CCA. We also identify the role of genes not previously described in CCA such as FKBP1A and UBASH3B. Lastly, our results promote the promise of immunotherapy in CCA treatment.

Introduction: Hepatitis C virus (HCV) is a lymphotropic virus that promotes HCV-mediated B-cell proliferation and transformation to Non-Hodgkin Lymphoma (NHL). Here we present a case of reactivation of HCV presenting as an aggressive intra-abdominal B cell lymphoma. Case Description/Methods: A 68-years-old-male with history of eradicated HCV with recombinant interferon-alfa and resolved HBV infection presented with painless jaundice and pruritus. CT abdomen revealed a 9.6 x 11.5 x 9.5 cm heterogeneous mass causing CBD and intrahepatic biliary duct dilation. Labs revealed reactivation of HCV infection with worsening of liver function tests with total bilirubin of .40mg/dl. FNA biopsy confirmed mature B-cell lymphoma. Given persistent worsening jaundice despite biliary stent, trial of high dose steroid was initiated to improve lymphoma burden in order to get a window to initiate chemotherapy. After tumor board discussion, he received radiation therapy for tumor shrinkage for this aggressive lymphoma. Prior to initiation of planned R-CHOP chemotherapy, he developed severe sepsis with hepatic abscess. Patient and family opted for hospice care and comfort care was initiated. Discussion: Chronic HCV is a fast-growing epidemic in the U.S.A which carries an enormous threat to general population and healthcare. HCV becomes chronic in .70% of infected patients with risk for cirrhosis, hepatocellular carcinoma and lymphoma. HCV can cause NHL via lymphocyte proliferation from viral antigenic stimulation, HCV replication inside B-cell and mutation via B-cell damage. Among patient who achieve sustained viral response (SVR), reactivation occurs in 1%, 11% and 15% among low-risk monoinfected HCV, high-risk monoinfected HCV and HIV/HCV coinfected group respectively. Treatment of HCV with resolution of NHL has been reported and there is some literature with sequential chemotherapy followed by antiviral therapy (AVT) showing promising results in HCV-NHL cases. Concurrent use of AVT and chemotherapy is primarily discouraged due to hematological toxicity. More evidence and studies need to be explored for such aggressive HCV-NHL management. Patient with SVR should have at least an annual testing and periodic follow-up to access for HCV reactivation or reinfection. Hepatitis C education regarding risk factors reduction and transmission prevention should be encouraged at every healthcare level and in general community and only then we can achieve WHO aim of eradication by 2030.