Influence of Helicobacter pylori status and eradication on the serum levels of trefoil factors and pepsinogen test: serum trefoil factor 3 is a stable biomarker.

BACKGROUND AND AIM: Emerging data indicate that serum trefoil factors (TFFs), especially TFF3, could be potential biomarkers for gastric cancer risk. We aimed to evaluate the influence of Helicobacter pylori (H. pylori) status and eradication on serum TFFs and the pepsinogen test. METHODS: Healthy individuals who underwent a thorough medical checkup were enrolled in study 1, and gastric ulcer patients who undertook H. pylori eradication therapy were enrolled in studies 2 and 3. Serum levels of the TFFs (TFF1, TFF2 and TFF3), H. pylori antibody and pepsinogen test were examined in all studies. In study 3, TFF expressions in biopsy samples of the gastric mucosa were additionally examined before and 2 months after eradication. RESULTS: In 1,260 healthy individuals enrolled in study 1, serum TFF1 and TFF2 levels were markedly different between H. pylori antibody-positive and -negative participants (P < 0.0001). Differences in serum TFF3 levels between H. pylori antibody-positive (5.85 ± 3.93 ng/ml) and -negative subjects (5.27 ± 2.38 ng/ml) were statistically significant (P = 0.002) but small in absolute value. In 178 gastric ulcer patients enrolled in study 2, serum TFF1, TFF2 and positive rates of the pepsinogen test significantly decreased 2 months after H. pylori eradication therapy (P < 0.001). In contrast, serum TFF3 levels and positive rates of high TFF3 levels (≥7 ng/ml) did not significantly change with H. pylori-eradication until 5 years after eradication. In 18 gastric ulcer patients (study 3), TFF1 and TFF2 were mainly expressed in the foveolar epithelium, and TFF2 was additionally expressed in the pyloric glands. These expressions significantly decreased with H. pylori eradication. TFF3s were scarcely expressed in the gastric mucosa except in goblet cells of intestinal metaplasia, which did not change with H. pylori eradication. CONCLUSION: In serum TFFs and pepsinogen tests, only serum TFF3s were not significantly affected by H. pylori eradication, suggesting that serum TFF3 could be a stable biomarker of gastric cancer risk even after H.pylori eradication in contrast with the pepsinogen test.

A case of chemical peritonitis and pleuritis caused by spontaneous rupture of a benign cystic ovarian teratoma that improved without surgical intervention.

Rupture of a benign cystic ovarian teratoma may result in severe chemical granulomatous peritonitis, a condition mimicking peritonitis carcinomatosa, with patients complaining of common abdominal symptoms. As the precipitating cause of rupture is often indeterminate and the rupture itself is hard to recognize, it is difficult to differentiate from peritonitis of other etiologies, such as gastrointestinal malignancy. We report the case of a 72-year-old female who presented with recurrent pyrexia and abdominal distension. Laboratory data showed signs of inflammation and a high level of carbohydrate antigen 125. Imaging examinations showed left-side-dominant pleural effusion, ascites with peritoneal adhesions, and a left cystic ovarian teratoma. Repeat paracentesis of both the pleural effusion and ascites demonstrated exudative characteristics, but there was no indication of malignancy or signs of infection, including those of tuberculosis. Although exploratory laparotomy was then recommended for conclusive diagnosis and ruling out such gynecological malignancy, the patient declined. Fortunately, laboratory data, radiological images, and other clinical findings gradually improved over the following 12 months. Moreover, a retrospective review of the computed tomography images revealed lipid particles in the ascites, indicative of teratoma rupture. The final diagnosis was chemical peritonitis and pleuritis caused by spontaneous rupture of the benign cystic teratoma. The present case was extremely rare with regard to its diagnosis and clinical progression. Our experience suggests that chemical peritonitis should be included in the differential diagnosis of peritonitis.