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Budd-Chiari syndrome (BCS) is a rare vascular disorder characterized by an obstruction of the hepatic venous outflow. Nodular regenerative hyperplasia (NRH) may develop as a result of an underlying autoimmune disease such as hepatic sarcoidosis. Only a few case reports have described cases with either NRH or hepatic sarcoidosis associated with BCS. We present a 42-year-old man presenting with BCS and signs of portal hypertension who was found to have an underlying pathological diagnosis of both hepatic sarcoidosis and NRH and who was successfully treated with a transjugular intrahepatic portosystemic shunt.

INTRODUCTION: Antidepressants are one of the most prescribed medications in the United States with duloxetine being reported as one of the top fifty drug prescriptions. Self-limited liver test abnormalities have been reported with duloxetine use but only a few case reports describe clinically apparent hepatitis following duloxetine use. CASE DESCRIPTION/METHODS: A 35-year-old African American woman with a past medical history of depression presented with few days of worsening upper abdominal pain, nausea and multiple episodes of non-bloody emesis. Initial laboratory tests revealed liver test abnormalities with ALT of 1176 U/L, AST of 596 U/L, bilirubin of 1.6 mg/dL (but with normal ALP) and INR of 1.65. Full workup including viral hepatitis, EBV, CMV, drug toxicology screen (including acetaminophen), lipase, and ceruloplasmin among others turned out to be negative. Autoimmune hepatitis markers were negative other than mild elevation of anti-smooth muscle antibody at 33 units (normal < 19). Abdominal ultrasound with Doppler showed no abnormalities without any evidence of biliary obstruction. The patient denied any alcohol or illicit drug use. Patient endorsed having a recent contact with a sick squirrel so leptospira IgM was ordered which was non-reactive. The patient denied taking any medications other than duloxetine which she was started on within the last two months but she stopped taking it when she started to vomit a few days before presentation. In the second day of hospitalization, patient's LFTs peaked with ALT above 7000 U/L and AST of 5409 U/L but it then started to decrease in the following days with normalization of her bilirubin and INR as well as improvement of her symptoms with supportive care. No corticosteroids or antibiotics were given. Patient's clinical presentation with the timeline of her duloxetine use and laboratory finding indicate that duloxetine was the likely cause of her acute hepatitis. DISCUSSION: Few cases described clinically evident hepatotoxicity following duloxetine treatment. Most duloxetine-induced hepatotoxicity was seen in females with symptoms starting in the first few months following initiation of duloxetine. Typically there was an elevation of ALT > AST and with some cases having bilirubin elevation as well as elevation of one of the autoimmune hepatitis markers in some cases. Clinicians should be vigilant toward possible hepatotoxicity following initiation of antidepressant even in patients with no pre-existing chronic liver disease or alcohol abuse history.

INTRODUCTION: Esophageal stents are used to treat a wide variety of problems, most commonly malignant dysphagia as a form of palliation. Delayed complications include tumor ingrowth/overgrowth, stent migration, hemorrhage, and delayed perforation. We present a rare case of osteomyelitis secondary to a stent that was placed for the closure of a tracheoesophageal fistula. CASE DESCRIPTION/METHODS: A 55-year-old female presented with stage IV non-small-cell lung cancer with distant metastases. She was started on chemotherapy (gemcitabine and carboplatin) as well as immunotherapy (pembrolizumab). A bronchoscopy had revealed extensive cancer in the bronchial tree and detected a tracheoesophageal fistula, which required placement of an esophageal stent for closure. The stent had been repositioned twice for better location and patient comfort. Four months after the last stent, she presented with fevers, which was initially attributed to her malignancy. However, her symptoms eventually progressed to dysphagia, cough, chest and back pain. Serologic evaluation was notable for an elevated ESR at 112 and an elevated CRP of 105. Subsequent CT of the chest revealed erosive endplate changes at the T1-T2 vertebral level with soft tissue density adjacent to the proximal aspect of the stent. These findings were concerning for osteomyelitis in the setting of an esophageal stent erosion. The decision was made to reposition the stent endoscopically. EGD revealed that the proximal end of the stent was embedded into the esophageal wall without clear erosions or evidence of perforation. Attempt to reposition the esophageal stent was performed, but follow up CT revealed minimal change from endoscopic repositioning. No further endoscopic intervention was performed and she was treated for osteomyelitis with intravenous antibiotics. DISCUSSION: Few cases have reported osteomyelitis related to esophageal stent migration. Whether the stent-related osteomyelitis is potentiated by the effects of chemotherapy on the esophageal wall or related to pressure erosion caused by the stent is not entirely clear. With newer therapies for malignancies and increased life expectancies, new complications may emerge. The decision to perform endoscopic manipulation would largely depend on patients’ clinical status and a discussion of risks versus benefits in a case-based scenario. This case illustrates the importance of having a high index of clinical suspicion for osteomyelitis in a patient with previous esophageal intervention.

INTRODUCTION: Current guidelines recommend esophagectomy for Esophageal Adenocarcinoma stage T1b. There are limited data regarding multimodality therapy for Esophageal Adenocarcinoma T1b using endoscopic therapy instead of a surgical option. We present a case of EAC stage T1b patient who was successfully treated by multimodality treatments. CASE DESCRIPTION/METHODS: An 84 years old female with a history of Barrett’s esophagus underwent an endoscopy and was found to have esophageal adenocarcinoma with deep submucosal invasion (T1b) with no surrounding lymphadenopathy on EUS. She was recommended to have an esophagectomy but refused and requested a less invasive approach. She was offered endoscopic mucosal resection (EMR) and cryoablative treatments. Over the course of one year, the patient underwent several sessions of endoscopic EMR followed by cryoablative therapy. The fourth EMR specimen revealed positive deep margins involving the submucosa with lymphovascular invasion (LVI). Further sessions of cryoablation and EMR were done and she was also referred to oncology for adjuvant therapy. Oncology recommended both chemotherapy (with paclitaxel and carboplatin) as well as radiotherapy. However, the patient couldn’t tolerate more than two sessions of chemotherapy so it was discontinued while radiotherapy was continued. Few months after the patient finished radiotherapy she underwent a follow-up EGD with multiple biopsies which showed no evidence of dysplasia or malignancy. DISCUSSION: Endoscopic eradication therapy is the treatment of choice for early esophageal cancer. Surgical management for T1b is recommended given higher rates of LVI. Our case represents a successful case of eradicated adenocarcinoma using a multidisciplinary approach involving gastroenterology, thoracic surgery, medical oncology, and radiation oncology. More data will be helpful in assessing the effectiveness of a multimodality approach in treating T1b esophageal adenocarcinoma with LVI without invasive surgery.