The objective of this article is to highlight the clinical features, screening, diagnosis, treatment, and prevention of gastric cancer (GC). Early GC is often asymptomatic leading to frequent delays in diagnosis. Weight loss and persistent abdominal pain are the most common symptoms at initial diagnosis. The diagnosis of GC typically involves a combination of endoscopy, biopsy, and imaging studies. Endoscopic resection techniques are emerging as successful treatment options for early GC. Treatment options for advanced GC include surgery and chemotherapy. The first line chemotherapy for advanced GC consists of doublet therapy with a combination of platinum and fluoropyrimidines. Trastuzumab, a monoclonal antibody, is used in the treatment of human epidermal growth factor 2 positive GCs. Anti-angiogenic agents and immunotherapy are also useful in the treatment of GC. Currently there are no GC screening guidelines in the United States, but they exist in other regions where there is increased prevalence of GC. Prevention strategies for GC include Helicobacter pylori eradication and adoption of a healthy diet consisting of fruits and vegetables.

Langerhans cell histiocytosis (LCH) is an idiopathic and rare disease that ranges in clinical severity based on location and organ involvement. LCH most commonly affects the skin and bones. The involvement of the gastrointestinal tract (GI) in adults is exceedingly rare and only 10 cases have been reported in the literature. We present the case of a 60-year-old male who was referred for a routine screening colonoscopy. Numerous 3-5 mm nodular lesions were present throughout the colon. A histopathological examination revealed diffuse aggregates of histiocytes within the lamina propria of the mucosa and immunohistochemical staining further confirmed the presence of Langerhans cells with a positive CD1-a stain. Although extremely rare, LCH involving the GI tract should be considered as a differential diagnosis when polyps or nodular lesions are witnessed on screening colonoscopies. In addition, the lesions must be biopsied to confirm the diagnosis of LCH and additional follow-up is essential to rule out systemic disease.

Esophagitis dissecans superficialis (EDS) is a rare and underdiagnosed esophageal lesion characterized by sloughing of the esophageal mucosa that has been associated with medications, various autoimmune disorders, and exposure to some chemical irritants. Anatomically, EDS is most commonly seen in the middle and distal thirds of the esophagus. When present, EDS is best treated by discontinuing the offending agent and initiating pharmacologic therapy with proton pump inhibitors. Steroids may also be effective if the etiology is autoimmune in nature. Our case highlights a 65-year-old female diagnosed with EDS after incidental ingestion of hair dye containing resorcinol and para-phenylenediamine (PPD).

Background. Hepatocellular carcinoma (HCC) is a leading cause of cancer morbidity and mortality. Findings of microvascular invasion (MVI) in patients with HCC have emerged as an important prognostic factor for poor survival after tumor resection. Aim. This study evaluated the relation between MVI and HCC within various anatomical Couinaud’s segments of the liver. Method. A multicenter retrospective review of HCC records was conducted from 2012 to 2017. HCC cases were identified using ICD-9 and 10 codes 155, C22.0, and C22.8. HCC patients who underwent liver transplants were included in this study. Liver segment of the location of HCC was obtained from radiographic records, and MVI information was obtained from pathology reports. Segmental distributions of HCC in MVI versus non-MVI groups were compared using Wilcoxon rank sum tests. value was set at <0.05. Results. We analyzed 120 HCC patients who underwent liver transplantation. The mean age of our cohort was 57 years, and the most common etiology of liver disease was hepatitis C at 58.3%. The median HCC size was 3.1 cm, and MVI was present in 23.3% of the explanted specimens. MVI was 2 to 3 times significantly higher in patients with HCC affecting segments 2 and 3 and segments 4b and 5 ( ). Moreover, median survival was significantly lower in patients with MVI versus those without MVI (50 vs. 137 months, ). Conclusion. MVI was significantly higher in HCC tumors located in liver segments 2 and 3 and 4b and 5, and survival was lower in patients with MVI compared with those without.

Idiosyncratic drug-induced liver injury (iDILI) is the second-most-common cause of acute liver injury. When it is caused by ibuprofen, it is quite rare, especially when not accompanied by systemic signs or symptoms. A young female patient presented with an ibuprofen overdose suicide attempt and then developed an acute liver injury within a few days. Given its rarity, ibuprofen-induced iDILI was initially a secondary differential, but when her course did not improve as expected, she was quickly evaluated for liver transplant. She fully recovered without needing the transplant, but this case highlights the importance of not only early suspicion/detection but also early referral to a transplant hepatology service.

Gastrointestinal stromal tumors (GISTs) are rare neoplasms of the digestive tract. The clinical behavior of GISTs varies greatly, has extended follow-up, and almost all of the tumors have malignant potential. The introduction of imatinib has led to extraordinary improvements in the treatment of individuals with GISTs (as well as those with Philadelphia chromosome-positive chronic myeloid leukemia (CML) and Philadelphia chromosome-positive acute lymphoblastic leukemia (ALL)). However, there have been notable postmarketing reports of adverse drug reactions of hepatotoxicity with the use of imatinib. By our search, among individuals taking imatinib for the treatment of GIST, only six cases of drug-induced liver injury (DILI) have been reported. Here, we present an interesting case of an elderly woman who developed DILI after taking imatinib for the treatment of GIST. As the liver function tests (LFTs) initially did not improve, it was decided to proceed with an interventional radiology (IR)-guided liver biopsy, which showed a histologic pattern of acute hepatitis, consistent with DILI. Ultimately, discontinuation of the antineoplastic agent led to recovery in the patient’s clinical condition along with normalization of her LFTs over the next several weeks. Thus, it is essential that physicians remain alert for and suspect DILI for any patient being treated with imatinib who presents with a sudden elevation of LFTs. The key to making the diagnosis is stopping the offending agent and closely monitoring the liver enzymes for improvement. When discontinuation of imatinib alone does not lead to improvement in LFTs and the patient’s clinical status, a detailed history should be taken and initial diagnostic testing performed to exclude other etiologies. And, if they are negative, a liver biopsy should be considered.