In patients with postprandial and/or fasting neuroglycopenia NIPHS may be suspected when insulin levels are low but inadequately suppressed and localization studies failed to show a distinct pancreatic tumor.

The rarity of malignant insulinoma limits reports on therapeutic strategies and outcome. The treatment and follow-up of 10 patients, all presenting an insulinoma with metastatic disease of the liver and newly diagnosed between 1992 and 2002, is reported. Pancreatic surgery with successful removal of the primary tumor preferentially located in the tail was performed in 7 women and 3 men, median age 55 years (range 36-82 years). If appropriate, 5 patients underwent additional hepatic surgery and lymph node resections. Liver metastases as the major cause of postoperatively persistent hypoglycemia were subsequently treated by repeated transarterial hepatic chemoembolization and chemoperfusion protocols using high-dose transhepatic streptozocin perfusions (3-4 g per session). The current median survival time for all 10 patients is 2.6 years (range: 1.6-9.7 years). Six patients are currently alive with a median survival of 3.7 years (1.7-9.7 years), five of them with stable disease and free of hypoglycemia. Four patients died after a median survival of 1.8 years (range: 1.6-7.5 years) from complications of unmanageable hypoglycemia. It is concluded that the necessity to treat debiliating and life-threatening hypoglycemia in metastatic malignant insulinoma warrants the option of radical endocrine surgery in combination with extended and repeated postoperative chemoembolization of liver metastases.

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Thirty-one cases of thyroid malignancies which were originally classified as anaplastic carcinoma were reexamined immunohistochemically using PAP methods (peroxidase:antiperoxidase) for IgM, IgG, IgA, cytokeratin, calcitonin, lysozyme and alpha-1-antitrypsin. The reclassification results were compared with patient data such as clinical symptoms, treatment modalities, and clinical outcome. Postoperative radiotherapy was carried out in more than 80% of cases, chemotherapy in none. Seven of 31 tumors showed a positive staining for IgM (n = 4), IgG (n = 2), and IgA (n = 1) antibodies. All of these cases were negative for epithelial markers. Surprisingly, not only all small cell tumors (n = 3) but also 4 tissues with predominantly giant cell areas were among those reclassified as primary malignant lymphoma.

The role of the complement system in the initial membrane lesion of acute pancreatitis was investigated. In the experimental sodium-taurocholate pancreatitis of the rat a sudden and steady decline of serum complement was observed. The deposition of C3 component of complement in acute pancreatitis could be demonstrated by immunofluorescence. To rule out mere deposition or activation of complement in the interstitial exsudative fluid, single acinar cells of rat and rabbit pancreatic tissue were prepared and transfered to culture medium. In contrast to heat inactivated serum and C6 deficient serum these cells were lysed by trypsin activated fresh serum. Consequently, an acute pancreatitis could be induced by activating exclusively the complement system by injection of cobra venom factor into the pancreatic duct of rats. The activated complement system is thought to be responsible for initial membrane lesion in exsudative inflammation, as could be shown in acute pancreatitis.