Background Eosinophilic esophagitis, once considered a rare disorder, has been increasingly recognized as a leading cause of dysphagia and food impaction in children and adults over the last few decades. It predominantly occurs in young men with a history of atopy. Dysphagia and food impaction are the most common presentations. However, rarely, spontaneous perforation (Boerhaave’s syndrome) may occur in association with eosinophilic esophagitis. Case presentation A 40-year-old white woman with known history of eosinophilic esophagitis, who was non-compliant with treatment, presented with chest pain and developed acute spontaneous transmural esophageal perforation while eating a snack. Surgical repair was required. Conclusion In a relatively young patient who presents with spontaneous esophageal perforation, eosinophilic esophagitis should always be ruled out as subsequent treatment may prevent recurrent perforation.

Neuroendocrine tumors (NETs) of gastrointestinal tract are rare entities. Their presence as synchronous lesions with adenocarcinoma has rarely been described in the literature. Cases of synchronous lesions of adenocarcinoma with neuroendocrine component have been described in the colon in the past. However, synchronous presence in the ampulla of Vater is quite uncommon. In the duodenum, NETs constitute 5.7 to 7.9% of the neuroendocrine neoplasms of the gastroenteropancreatic tract. We present a case of 65-year-old male who presented with abdominal symptoms and weight loss, was found to have adenocarcinoma of the ampulla of Vater on biopsy via endoscopic retrograde cholangiopancreatography (ERCP), for which he underwent Whipple’s surgery and was found to have neuroendocrine component along with adenocarcinoma postoperatively on histology.

INTRODUCTION: Amyloidosis is characterized by extracellular deposition of amyloid protein. It affects most commonly heart, kidney and GI tract. It can occur sporadically or in association with other conditions like multiple myeloma, chronic inflammatory diseases, infections etc. It has variable manifestations in GI tract from involving the stomach to the large bowel including liver. CASE DESCRIPTION/METHODS: This is 55 year old Caucasian male with past medical history of recent diagnosis of multiple myeloma, chronic kidney disease, hypertension, atrial flutter who presented to the hospital with chief complaints of multiple episodes of nausea and vomiting, diffuse abdominal pain, subjective fevers and chills from past 2 days. On presentation, vitals were stable. CBC- wnl, CMP – wnl, CT abdomen/pelvis without contrast revealed partial small bowel obstruction. Patient had similar symptoms in prior admissions. During the initial hospitalization 1 month ago, he underwent exploratory laparotomy with no findings to suggest mechanical small bowel obstruction. Subsequently, he had an EGD with push enteroscopy which identified enteritis and a Mallory-Weiss tear. Small bowel biopsies were performed with pathology noting: focal acute cryptitis and a background of moderate chronic nonspecific inflammation. Repeat EGD with push enteroscopy revealed non erosive esophagitis, mild gastritis and severe duodenitis, biopsies were obtained. Congo red staining of the biopsy revealed amyloidosis of the small bowel but the gastric biopsy was negative. The patient was then referred to higher center for consideration of bone marrow transplant. The fat pad biopsy was never obtained for systemic amyloidosis. DISCUSSION: The AL amyloidosis which is most commonly associated with monoclonal free light chains deposition, which was also previously called primary amyloidosis is most common. The AA amyloidosis (also called as secondary amyloidosis) is secondary to chronic inflammation in the body due to infection, rheumatoid arthritis etc. Diagnosis of amyloid, irrespective of the type, depends upon clinical, laboratory and histological findings. Serum and urine immunoelectrophoresis are the initial laboratory tests, but confirmation requires histological evaluation. Overall median survival in untreated patients or nonresponders with systemic amyloidosis is <2 years. Treatment should be directed at the underlying cause. GI complications are managed with symptomatic control.

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