Primary hepatic gastrinoma being diagnosed preoperatively: a case report and literature review

Background A majority of gastrinomas causing Zollinger–Ellison syndrome are located in the duodenum or pancreas. Primary hepatic gastrinomas are rare and difficult to diagnose. We report a rare case of primary hepatic gastrinoma, which could be diagnosed preoperatively. Case presentation A 29-year-old man with a 55-mm tumor in segments 5 and 6 (S 5/6) of the liver was admitted to our hospital. After thorough investigations, he was treated for a suspected inflammatory pseudotumor and advised to undergo routine follow-up. Two years later, he revisited our hospital with a complaint of abdominal pain, vomiting, and diarrhea. Upper gastrointestinal endoscopy revealed multiple duodenal ulcers. His serum gastrin level was 2350 pg/mL (normal: 37–172 pg/mL), suggesting Zollinger–Ellison syndrome. Abdominal computed tomography showed a 78-mm hypervascular tumor with cystic degeneration in the S 5/6 region of the liver, with a potential to increase over time. The tumor showed hypointensity on T2-weighted and hyperintensity on diffusion-weighted abdominal contrast-enhanced magnetic resonance imaging. Somatostatin receptor scintigraphy (SRS) only detected a hepatic tumor. No tumors in the gastrinoma triangle were detected by endoscopic ultrasonography. Hence, selective arterial calcium injection (SACI) test was performed to determine the location of the gastrinoma. The serum gastrin concentration increased from 4620 pg/mL to 23,600 pg/mL at 20 s after calcium gluconate injection into the proper hepatic artery. Conversely, no effect on serum gastrin level was observed after the injection into any other arteries. Extended right hepatic lobectomy and cholecystectomy were performed after percutaneous transhepatic portal vein embolization. A histopathological examination of the liver tumor revealed a gastrinoma. The patient’s serum gastrin concentration on postoperative day 1 decreased to 65 pg/mL. Conclusion We report a surgical case of primary hepatic gastrinoma correctly diagnosed preoperatively. The patient underwent extended right hepatic lobectomy, resulting in a histological definitive diagnosis of primary hepatic gastrinoma.

Impact of Helicobacter pylori Infection on Gastric Variceal Bleeding among Patients with Liver Cirrhosis

Background and Aims. Currently, it is well known that Helicobacter pylori- (H. pylori-) related peptic ulcer is one of the main causes of nonvariceal bleeding in cirrhotic patients. However, there is a lack of data to identify the exact effect ofH. pyloriinfection on variceal bleeding. This study was conducted to identify the impact ofH. pyloriinfection on gastric variceal bleeding in cirrhotic patients.Patients and Methods. 76 cirrhotic patients with gastric varices were included in this prospective study and divided into 2 groups: nonbleeding gastric varices (32 patients) and bleeding gastric varices (44 patients). The fasting serum gastrin level was measured. Mucosal biopsies from the gastric body and antrum were examined to determine the patterns of gastritis and the presence ofH. pylori.Results. The frequency ofH. pyloriinfection in the studied patients was 59.2%. There were significant differences between both groups regarding liver decompensation (P=0.001), red color sign over gastric varices (P=0.0011), prevalence ofH. pyloriinfection (P=0.0049), histological patterns of gastritis (P=0.0069), and serum gastrin level (P=0.0200). By multivariate analysis, Child C cirrhosis, red color sign over gastric varices, andH. pylori-induced follicular gastritis were independent risk factors for bleeding from gastric varices.Conclusion.H. pylori-induced follicular gastritis is considered as an additional risk factor for bleeding from gastric varices.

Poster Presentation on Adrenal, Pituitary, and Other Endocrine Glands, Parathyroid Gland, Thyroid Gland

ABSTRACT BACKGROUND AND AIMS Gastrointestinal and pancreatic neuroendocrine tumors (NET) are classified as low grade (G1), intermediate grade (G2), and high grade (G3) by mitotic rate and/or Ki-67 index. The basic treatment for neuroendocrine carcinoma (NEC, G3) with remote metastasis is platinum-based systemic chemotherapy. In contrast, for patients with NET G1 or G2 with remote metastasis, multidisciplinary treatment is necessary in order to prolong patients' survival and relieve symptoms. We report here a patient with pancreatic G1 gastrinoma and its multiple liver metastases. METHODS The patient was a 42 years old male who had been suffering from diarrhea for 2 years, and his serum level of gastrin was as high as 4200 pg/mL before treatment. Needle biopsy of the liver proved the tumor was positive for chromogranin A, gastrin, and somatostatin receptor type 2A. RESULTS First, we chose an induction drug therapy with sunitinib and octreotide. The size of the liver tumors decreased dramatically and the serum gastrin level became lower than 500 pg/mL. About 1 year after diagnosis, we performed distal pancreatectomy and right hepatic lobectomy. After surgery, the serum gastrin level was normalized, and the activity of daily living (ADL) of the patient was much improved by the consecutive therapies. During the 2-year postoperative follow-up time, the course was favorable and no recurrent lesion was found. CONCLUSION Even when there are remote metastases, multidisciplinary treatment including surgical resection should be considered for G1/ G2 NET. Further, it should be necessary to study in a larger number of patients if perioperative drug therapy for G1/G2 NET with remote metastases is effective.

Treatment of Gastrin-Secreting Tumor With Sustained-Release Octreotide Acetate in a Dog

An 8 yr old, intact male Shiba Inu was presented with loose stool, polydipsia, hematuria, vomiting, and anorexia. On abdominal ultrasonography, numerous nodules were detected in the hepatic parenchyma distributed diffusely throughout all lobes. Excisional biopsy of one of the nodules was performed via exploratory laparotomy. A histopathological diagnosis of the lesion was carcinoid, and the tumor cells stained positive to chromogranin A and gastrin. The serum gastrin level of the dog was 45,613 pg/mL (reference range: 160–284). In addition to medical treatment with omeprazolec and famotidinee, suppression of gastrin secretion was attempted with octreotide acetate. A test dose of octreotide acetate significantly decreased the serum gastrin level to approximately one third of the baseline in 2 hr and the effect lasted approximately for 6 hr. On day 21, treatment with sustained-release formulation of octreotide acetatea (5 mg intramuscular, q 4 wk) was initiated. The serum gastrin concentration gradually decreased over 32 days and then progressively increased in parallel with the progression of the hepatic nodules. The dog gradually developed recurrence of initial clinical signs, and was lost to follow-up on day 510.