INTRODUCTION: Gastric cancer incidence and mortality has continued to steadily decline but remains the second leading cause of cancer death worldwide. Predominantly, gastric cancers are known to arise from a single lesion whereas gastric cancer arising from multiple lesions is uncommon. We present a case of a 67 year-old female who was initially found with gastritis in the antrum that evolved into a multifocal gastric cancer within 1 year. CASE DESCRIPTION/METHODS: The patient was a 67 year-old female who was first seen in Hepatology clinic for chronic hepatitis C with early fibrosis. After successful treatment, she underwent upper endoscopy for non-specific gastric symptoms. EGD showed gastritis in the antrum and biopsy revealed intestinal metaplasia and H-Pylori was negative so repeat endoscopy was recommended in a year. Upon returning for repeat endoscopy, evaluation revealed a small antral erosion and a raised area of erythematous mucosa in the fundus. Unexpectedly, biopsies revealed extensive intestinal metaplasia and high-grade dysplasia in both lesions. The patient was immediately referred to an academic center for upper endoscopic ultrasound and mucosal resection. Both studies were unremarkable, so the patient returned to our facility and underwent upper chromo-endoscopy. By this time, the antral erosion had markedly increased in size and became an ulcer with circumferential induration and staining centrally with methylene blue. There was also methylene blue uptake in two other erosions within the fundus. Repeat biopsy of the ulcers now showed nascent well-differentiated adenocarcinoma associated with high-grade dysplasia. Whole body computerized tomography showed no evidence of metastasis so patient underwent total gastrectomy. Surgical pathology revealed multiple foci of intestinal type gastric adenocarcinoma in the background of high-grade dysplasia and intestinal metaplasia. All lymph nodes and margins were negative. DISCUSSION: There have been less than 50 cases of multifocal gastric cancer reported in the literature with even fewer cured by total gastrectomy. Upper gastrointestinal endoscopy remains the gold standard for diagnosing gastric lesions. Generally, surveillance isn’t recommended for findings of intestinal metaplasia. However, our case serves to highlight the importance of diligent endoscopic surveillance and tissue sampling, even if findings convey low suspicion. Our patient was successfully cured of multifocal gastric cancer, a disease that usually carries a very poor prognosis.

Introduction: Colorectal Cancer (CRC) is the 3rd most diagnosed cancer worldwide with a high incidence in the USA. Most common sites of involvement with metastatic colorectal cancer (mCRC) are liver and lungs. Brain metastasis (BM) and osseous metastasis (OM) are rarely seen, let alone as the initial presentation of CRC. BM confers poor prognosis among patients with CRC. Diagnosing BM remains critical, as early surgical intervention improves outcome. This is an unusual case of mCRC presenting with neurological deficits as a feature of atypical metastatic sites -brain and bone, with concurrent lung metastasis. Case Description/Methods: A 62-year-old healthy female presented with 3 days of right upper extremity weakness. She denied any other neurological or GI complaints. Her mentation was intact but motor deficit of 2/5 in the right upper extremity was present. Labs were consistent with microcytic anemia (Hg 7.6 g/dL, MCV 71.5 fL), and elevated CEA level (36 ng/mL); transaminases were normal. CT head showed left frontal and right temporoparietal masses with vasogenic edema and mass effect upon left lateral ventricle. MRI brain was deferred due to claustrophobia. CTA chest revealed multiple nodules in bilateral lung fields and NM bone scan showed increased tracer uptake in bilateral ribs concerning for metastatic disease in lungs and bones, respectively. Concurrently, irregular wall thickening of the rectosigmoid colon suspicious for neoplasm was noted on CT abdomen. Dexamethasone was initiated and patient underwent right craniotomy with tumor resection. Pathology was positive for APC, tp53 and kras mutations, consistent with metastatic adenocarcinoma of colorectal origin. Patient was ultimately discharged home with hospice care and colonoscopy was deemed futile. Discussion: Most common sites of mCRC are liver (50%) and lungs (36%), whereas metastasis to brain and bone is very rare and is often a late presentation. Increased risk of BM and OM is associated with known lung metastasis and KRAS mutation in a patient with primary CRC. The average time between detection of OM and diagnosing CRC is reported to be 21 months. We did not find any case describing simultaneous metastasis to lung, brain and bones from primary CRC at the time of diagnosis especially in the absence of hepatic lesions. Lastly, neurological deficit, as seen in our patient, is an uncommon presentation for CRC. Increased awareness of BM and OM in mCRC is crucial for early diagnosis and intervention.

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Introduction: Hepatitis E virus (HEV) can cause acute or chronic viral hepatitis and is a common cause of acute viral hepatitis worldwide and is an important public health concern. A high level of HEV, hepatitis A virus (HAV), cytomegalovirus (CMV), and Epstein-Barr virus (EBV) cross reactivity can occur, which indicates that serology can sometimes be unreliable in the diagnosis of acute viral hepatitis. Case Description/Methods: A 28-year-old Pakistani male presented with right upper quadrant abdominal pain, general malaise, and deranged liver function tests. Work-up for his abnormal liver tests was unremarkable except for detection of Hepatitis E antibody, Hepatitis E IgM antibody, and Epstein-Barr Virus IgM antibody with polymerase chain reaction (PCR) analysis revealing no detection of Epstein-Barr Virus DNA. The patient was diagnosed with acute hepatitis E with a false-positive EBV infection due to serological cross-reactivity. Supportive care was continued, liver function tests trended down, and the patient clinically improved and was discharged with outpatient follow-up. Discussion: The incubation time for HEV infection can last up to six weeks and HEV RNA, anti-HEV IgM, and anti-HEV IgG antibodies can be detected at the time of diagnosis. Anti-HEV IgM antibodies have a short window of positivity at three to four months, whereas HEV RNA can be detected in the blood within three weeks with viral shedding lasting up to six weeks in the stool. The enzyme immunoassay is the most widely used serological method for the identification of anti-HEV IgG and IgM antibodies, but the identification of anti-HEV IgM and rising titers of anti-HEV IgG antibodies are inadequate for diagnosis due to the lack of specificity for these antibodies. Confounding the diagnosis of HEV is the incidence of HEV, HAV, CMV, and EBV cross reactivity, which is posited to be due to polyclonal B-cell stimulation. The diagnosis of HEV infection in the clinical setting relies on the performance of assays of anti-HEV IgM, and subsequently the awareness of factors influencing diagnostic accuracy is crucial regarding potential treatment options. This case suggests that both anti-HEV IgM and EBV IgM should be interpreted with caution in acute HEV infection and that confirmatory testing with PCR analysis should be conducted to evaluate for false-positive serological cross-reactivity. We conclude that the diagnosis of viral hepatitis should be based on characteristic symptoms, elevated liver enzymes, serology, and confirmatory PCR testing.