Eosinophilic gastroenteritis (EGE) is a digestive disorder in children and adults that is characterized by eosinophilic infiltration in the stomach and intestine. The underlying molecular mechanisms predisposing to this disease are unknown, but it seems that hypersensitivity response plays a major role in its pathogenesis, as many patients have a history of seasonal allergies, food sensitivities, asthma, and eczema. Symptoms and clinical presentations vary, depending on the site and layer of the gastrointestinal wall infiltrated by eosinophils. Laboratory results, radiological findings, and endoscopy can provide important diagnostic evidence for EGE; however, the cornerstone of the diagnosis remains the histological examination of gastric and duodenal specimens for evidence of eosinophilic infiltration (>20 eosinophils per high-power field), and finally clinicians make the diagnosis in correlation with and by exclusion of other disorders associated with eosinophilic infiltration. Although spontaneous remission is reported in around 30%–40% of EGE cases, most patients require ongoing treatment. The management options for this disorder include both dietary and pharmacological approaches, with corticosteroids being the mainstay of therapy and highly effective. The subsequent course is quite variable. Some patients have no recurrences, while a few experience recurrent symptoms during or immediately after corticosteroid interruption. An alternative therapeutic armamentarium includes mast-cell stabilizers, leukotriene antagonists, antihistamines, immunomodulators, and biological agents. In this review, we provide a summary of the different diagnostic tools utilized in practice, as well as the different therapeutic approaches available for EGE management.

Percutaneous endoscopic gastrostomy (PEG) is a well-recognized procedure for providing enteral feeding and long-term enteral nutritional support. Although it is mostly well tolerated, complications, sometimes mechanical in nature, do occur. Rare, and often initially unrecognized, late complications of PEG tube placement are gastric outlet obstruction and duodenal obstruction. Simple adjustment of the gastrostomy tube will lead to the improvement of the patient’s clinical condition and prevent further complications. Physicians should be aware of and suspect gastric outlet and duodenal obstruction as rare late complications of PEG tube placement. Simple adjustment of the gastrostomy tube can resolve the problem without unnecessary medical tests and overly aggressive care. Here, we present two interesting cases of elderly women who developed mechanical obstruction after inadvertent migration of the gastrostomy tube.

Hypercalcemia due to primary or secondary hyperparathyroidism is a rare and obscure cause of acute pancreatitis. Although a rare occurrence to begin with, hyperparathyroidism commonly manifests with symptoms of hypercalcemia. Thus, it would reason that a patient might develop pancreatitis by way of hypercalcemia due to primary or secondary hyperparathyroidism. We present a case of an 88-year-old female with acute pancreatitis and only after an extensive work-up, was it determined that her severe acute pancreatitis resulted from primary hyperparathyroidism caused by a left parathyroid adenoma.

An esophageal mucosal bridge is a rare finding that is seldom encountered on upper endoscopy. They most commonly present secondary to an underlying inflammatory disorder and cause chest pain and dysphagia, among other symptoms. More rarely, they present asymptomatically with no identifiable inflammatory conditions. Our case consists of a 31-year-old woman who presented with an asymptomatic, noninflammatory mucosal bridge of the esophagus. To our knowledge, this makes the third such case. The rarity of this condition coupled with the lack of epidemiologic data available make this case worthy for literature review.

Chilaiditi syndrome is a very rare disorder characterized by abdominal pain due to the entrapment of the colon between the liver and the diaphragm. However, it is rare to have bowel perforation as a complication of this syndrome with only 2 cases reported to date. In this article, we present the case of a 56-year-old woman with medical history of scleroderma who presents with abdominal pain and was found to have colonic perforation from Chilaiditi syndrome. She was also incidentally found to have cecal adenocarcinoma. Sometimes abdominal pain in patients with Chilaiditi syndrome may be more than benign and calls for increased attention from clinicians regarding this.