Case Description/Methods: 66-year-old Hispanic male, with no significant medical, family, or social history presented to the hospital with syncope. Further history revealed three weeks of melena, fatigue, exertional dyspnea, and 50 lb weight loss. Upon evaluation, the patient was found to have HGB of 3.2. CT abdomen with contrast showed a mass in the antrum of the stomach, most prominent posteriorly and around the greater curvature. EGD revealed normal esophagus and a 15 cm, oozing, fungating, and partially circumferential gastric mass. It was located in the antrum, involving the entire posterior wall with extension into the greater curvature. The gastric mass was 5 cm below the GE junction, without evidence of esophageal involvement. Biopsy of the mass revealed poorly differentiated squamous cell carcinoma and Helicobacter pylori infection. Colonoscopy then revealed a 4 cm lesion near the splenic flexure which was confirmed to also be poorly differentiated squamous cell carcinoma. The patient was placed on triple therapy for his H. pylori infection. PET scan showed known gastric and colonic mass with multiple enlarged and hypermetabolic perigastric and retroperitoneal lymph nodes consistent with metastasis. He was seen by oncology and started on systemic chemotherapy (Figure 1). Discussion: PGSCC is a rare form of gastric malignancy accounting for roughly 0.2% of primary gastric cancer reported. Compared to the more common gastric adenocarcinoma, SCC tends to be more aggressive with poorer outcomes. Unfortunately, the pathogenesis remains obscure, making early detection difficult. Our case was associated with H. pylori infection which is one of the most significant risk factors for the development of gastric cancer due to the chronic inflammation caused by infection. Additionally, metastasis to the colon is exceptionally rare with most cases metastasizing to liver, peritoneum, lung and bone. Further investigation and studies are needed to understand this rare disease.[3659] Figure 1. Primary gastric tumor (left panel), submucosal colonic mass (right panel).
Case Description/Methods: The patient had a two-year history of non-bloody diarrhea which worsened (7 bowel movements/day) in the two months prior to presentation. She described associated nausea, reflux, and abdominal pain. Notably, her mother had similar symptoms, requiring small bowel resection (records not available). Previous workup included a colonoscopy and an esophagoduodenoscopy (EGD) showing duodenal ulcerations with negative biopsies for celiac disease. She was started on a proton-pump inhibitor (PPI), colestipol, and loperamide without improvement. Medication review, stool infectious studies, and cross-sectional imaging had been unrevealing. On presentation, she had stable vitals and physical exam significant for diffuse abdominal tenderness. Labs were notable for a hemoglobin of 10.2 gm/ dL (grams per deciliter) and an acute kidney injury (AKI). Abdominal Computed Tomography (CT) suggested multiple, small duodenal ulcers with a polypoid lesion in the gastric antrum (Figure). EGD revealed esophagitis, multiple small duodenal ulcerations (D1, D2), and gastric mucosal atrophy. Repeat colonoscopy was unremarkable. The fasting gastrin level was 211 pg/mL (picogram per milliliter). The secretin stimulation test showed serum gastrin blood levels of 121, 258, and 483 pg/mL at 2, 5, and 10 minutes respectively consistent with Zollinger-Ellison Syndrome. The Dotatate PET/CT scan showed metastatic somatostatin receptor expressing portocaval adenopathy without a tracer-avid primary neuroendocrine tumor. She was started on lanreotide and is now referred to oncology. Discussion: This case represents an instructive example of Zollinger Ellison Syndrome (ZES), often discussed, but rarely diagnosed. In this case, the patient presented with progressive diarrhea, a subtle family history, and with several prior evaluations. ZES is a rare gastrin-secreting neuroendocrine tumor (NET) associated with multiple endocrine neoplasia (MEN-1), which leads to refractory acid reflux and chronic diarrhea, as seen in our patient. Non-specific gastrointestinal symptoms and empiric PPI use can delay the diagnosis. The gastric pH, gastric level, secretin stimulation, and Dotatate PET/CT are used to evaluate and localize the tumor.[3363] Figure 1. A, B: Computed Tomography (CT) abdomen showed multiple, small duodenal ulcers and 4 millimeter (mm) enhancing polyp at the gastric antrum (red arrows).
Anion gap is a value calculated by determining the difference between major plasma cations (sodium, sometimes additionally potassium) and anions (namely bicarbonate and chloride), with “normal” levels falling somewhere between 8 and 16 mEq/L. Elevations in anion gap are classically described in a variety of different clinical disease states, including but not limited to uremia, ketoacidoses, lactic acidosis, and a number of drug toxicities. Comparatively little is understood about the etiology of low and negative (<0) anion gap measurements; however, certain patient populations and pathologic states have been associated with negative anion gap measurements, such as multiple myeloma and hypertriglyceridemia (Kraut, 2007). We reviewed laboratory chemistries for 340,354 pediatric and adult patients over a ten-year period (2009-2018). Laboratory testing included values from basic and comprehensive metabolic panels and blood gas analyses. Chart review was performed on adult patients with anion gaps measuring less than 0 mEq/L to assess for medical trends or other explanations such as analytical interference or data errors. Additionally, blood gas analyses from patients being cared for in the neonatal intensive care unit (NICU) over the same ten-year period were also reviewed. Of the adult patients, 0.046% (157 samples) had an anion gap measuring below 0 mEq/L. Samples obtained as part of a blood gas analysis made up 52% of all negative gaps. While no definitive trends were noted, 23 samples were noted to be from patients with history of malignancy (solid tumor and hematopoietic), including multiple myeloma (4 patients).[mkrasows1] In addition to malignancy, 17 patients with hypertriglyceridemia were also found to have negative anion gaps. Negative anion gaps were rare in outpatient populations. Negative anion gaps as a result of a laboratory error were also rare, constituting only 1.3% of cases (2 patients). Negative anion gaps were comparatively more common in the NICU population, with 983 patients having a negative anion gap[mkrasows2] (0.289 %). NICU patients constituted 91% of all blood gas analyses with a negative anion gap, demonstrating that negative anion gaps are much more prevalent in this patient population than they are in other pediatric and adult populations. Negative anion gaps are relatively rare occurrences in the adult outpatient population; however, they can be seen in association with certain underlying disease states such as malignancy. By comparison, negative anion gaps are much more common in critically-ill populations, most notably NICU patients.
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