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Clinical research into patients with idiopathic chronic pancreatitis points to a possible immunopathogenetic process in a number of cases. In order to examine the behaviour between the exocrine pancreas under the influence of anti-rat-pancreas immune serum produced in rabbits, a 1.00 ml immune serum is administered once a week over a maximum 26 week period into Wistar-rats by intraperitoneal injection. By electrone-microscopy a much reduced production of enzymes apparently takes place, though to differing extent. There is also destruction of the basal membrane of acinocytes: the production of interstitial oedema, the new formation of collagen fibres and the proliferation of connective tissue cells. Under a conventional light microscope the first changes become noticeable after 8-12 weeks of study. These take the form of localised cell decay, deterioration and lysis of acinocytes; and an increasing non-specific inflammation. There is also the new formation of connective tissue. After 20-26 weeks the exocrine pancreas is characterised by reduction of parenchyma, acino-ductal metaplasia, chronic inflammatory infiltrates of differing density, fibrous and irregular calibres of the smaller and larger ducts. The findings are almost identical to the structural changes of chronic idiopathic pancreatitis in human beings. The results support the view of an immuno-pathologic aetiology for human chronic idiopathic pancreatitis.
Clinical research into patients with idiopathic chronic pancreatitis points to a possible immunopathogenetic process in a number of cases. In order to examine the behaviour between the exocrine pancreas under the influence of anti-rat-pancreas immune serum produced in rabbits, a 1.00 ml immune serum is administered once a week over a maximum 26 week period into Wistar-rats by intraperitoneal injection. By electrone-microscopy a much reduced production of enzymes apparently takes place, though to differing extent. There is also destruction of the basal membrane of acinocytes: the production of interstitial oedema, the new formation of collagen fibres and the proliferation of connective tissue cells. Under a conventional light microscope the first changes become noticeable after 8-12 weeks of study. These take the form of localised cell decay, deterioration and lysis of acinocytes; and an increasing non-specific inflammation. There is also the new formation of connective tissue. After 20-26 weeks the exocrine pancreas is characterised by reduction of parenchyma, acino-ductal metaplasia, chronic inflammatory infiltrates of differing density, fibrous and irregular calibres of the smaller and larger ducts. The findings are almost identical to the structural changes of chronic idiopathic pancreatitis in human beings. The results support the view of an immuno-pathologic aetiology for human chronic idiopathic pancreatitis.
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