ABSTRACT
A 53-year-old woman was referred to our hospital for management of gastric varices that ran transversely across the greater curvature of the gastric body, detected during routine upper gastrointestinal endoscopy. CT identified a low-density calcified mass near the tail of the pancreas and the splenic hilum. Based on the results of radiographic and pathological investigations, the tumor was diagnosed as solid pseudopapillary neoplasm (SPN), and the gastric varices were considered to have developed secondary to occlusion of the splenic vein by the tumor mass. This is a rare case of SPN associated with splenic vein occlusion and left-sided extrahepatic portal hypertension.
Subject(s)
Carcinoma, Papillary/diagnosis , Esophageal and Gastric Varices/diagnosis , Hypertension, Portal/diagnosis , Pancreatic Neoplasms/diagnosis , Splenic Vein/pathology , Carcinoma, Papillary/complications , Diagnosis, Differential , Esophageal and Gastric Varices/complications , Female , Humans , Hypertension, Portal/etiology , Middle Aged , Pancreatic Neoplasms/complicationsABSTRACT
BACKGROUND: Gastric atrophy caused by Helicobacter pylori (H. pylori) infection is a risk factor for gastric cancer. We aimed to evaluate the relationship between gastric cancer risk and tumor markers in the general population. MATERIALS AND METHODS: A total of 688 volunteers were examined to test their serum pepsinogen (PG) levels and anti-H. pylori antibodies, in addition to a total of 22 serum tumor markers. The participants were classified into four groups according to their anti-H. pylori antibody and serum PG serological status. Accordingly, groups A and D were negative, whereas groups B and C were positive for anti-H. pylori antibodies; and groups A and B were normal, whereas groups C and D were abnormal for serum PG levels. All the blood examination results were statistically evaluated using Student's t-test among these groups. RESULTS: There were 424, 202, 50, and 12 individuals in groups A, B, C, and D, respectively. Because of the small number of participants in groups C and D, we combined these two groups. Compared to the normal group (A), a statistically significant higher in adenosine deaminase level was found in group C+D (p=0.01). CONCLUSION: This result supports a previous study indicating that adenosine deaminase is involved in the regulatory system of chronic atrophic gastritis and gastric cancer risk.
