Background-The pathology of nonalcoholic chronic pancreatitis has not yet been suYciently studied. Aims-To identify the major changes of pancreatic tissue in patients surgically treated for non-alcoholic chronic pancreatitis. Patients-Pancreatectomy specimens from 12 patients with non-alcoholic chronic pancreatitis, including four patients with autoimmune or related diseases (Sjögren's syndrome, primary sclerosing cholangitis, ulcerative colitis, and Crohn's disease), were reviewed. Methods-Morphological changes were studied histologically and immunohistochemically (to type inflammatory cells) and compared with the pancreatic alterations found in 12 patients with alcoholic chronic pancreatitis. Results-In patients with non-alcoholic chronic pancreatitis, with or without associated autoimmune or related diseases, pancreatic inflammation particularly involved the ducts, commonly resulting in duct obstruction and occasionally duct destruction. None of these features was seen in alcoholic chronic pancreatitis which, however, showed pseudocysts and calcifications. Conclusion-The pancreatic changes in patients with non-alcoholic chronic pancreatitis clearly diVer from those with alcoholic chronic pancreatitis. The term chronic duct destructive pancreatitis is suggested for this type of pancreatic disease.

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Our analysis shows that colorectal mini-de novo carcinoma is not a purely Japanese phenomenon, and that these carcinomas are being diagnosed with increasing frequency as the awareness of their existence and macroscopic growth characteristics increases.

Whipple's disease is not quite as rare as commonly assumed. There is no obvious geographic predominance. During the past three decades, the demography of WD patients has changed.

The effect of the occlusion of the pancreatic duct system with a new alcoholic solution of amino acids has been studied in animal experiments. The solution becomes solid in the duct system, is microbiologically indifferent and becomes disintegrated within 11 days. This time, however, is sufficient to keep a high-grade atrophy of the exocrine parenchyma. With this method one doesn't risk the provocation of an acute pancreatitis. The development of fistulas following exploratory excision is prevented by the filling of the duct system. The solution could be qualified for a therapeutical acceleration of the "burning-out" of the chronic pancreatitis.