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A case of nonfunctioning islet cell tumor with hyperammonemia and hyperamylasemia
Author(s) -
Matsuo Shigetoshi,
Shinozaki Takuo,
Yamaguchi Satoshi,
Tsuda Nobuo,
Matsuoka Uichiro,
Kanematsu Takashi
Publication year - 1994
Publication title -
journal of hepato‐biliary‐pancreatic surgery
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.63
H-Index - 60
eISSN - 1868-6982
pISSN - 0944-1166
DOI - 10.1007/bf01211927
Subject(s) - hyperamylasemia , hyperammonemia , islet , medicine , endocrinology , cancer research , chemistry , biochemistry , insulin , enzyme , amylase
A case of nonfunctioning islet cell tumor with hyperammonemia and hyperamylasemia is reported. A 67‐year‐old female was admitted in an unconsciousness state, with a large abdominal mass about 10×10 cm in size. Hyperammonemia and hyperamylasemia were evident. Blood sugar levels, electroencephalogram (EEG), and brain scan were normal. After admission, lactulose and gabexate mesilate were administered for the hyperammonemia and hyperamylasemia. Serum ammonia levels returned to the normal range within 2 weeks, but serum amylase levels failed to decrease. Results of the oral glucose tolerance test were normal. A contrast computed tomographic (CT) scan revealed a tumor with a homogeneous enhancement pattern. Angiography demonstrated a hypervascular pancreatic tumor. Distal pancreatectomy with splenectomy was performed on the basis of a preoperative diagnosis of pancreatic tumor with extrapancreatic growth. Histological examination showed nonfunctioning islet cell tumor, with evidence of vascular invasion of tumor cells. Production of pancreatic hormones was not noted. The patient promptly returned to normal consciousness, and no elevation of ammonia or amylase was observed other than an incidental elevation of the latter due to pseudocyst formation. The hyperamylasemia was obviously related to tumor growth, and the pancreatic tumor itself may have contributed to the hyperammonemia.