Petr Dítě, Ivo Novotný, Bohuslav Kianička, Pavel Klvaňa, Hana Nechutová, Martina Bojková, Arnošt Martínek, Arpád Bodai, Miroslav Souček,
Our present knowledge on aetiological factors is documented by a disease classification called TIGARO. Besides “classical” toxonutritive factors, important factors are genetic and autoimmune influence and condition indicating pancreatic duct obstruction. It is known that no more than 10 % of alcoholics will suffer from chronic pancreatitis, out of which is logical a necessity of coexistence of other risk factors for induction of fibrotic gland changes, e.g. combination of alcohol abuse and smoking. An independent factor inducing chronic pancreatitis is the presence of PRSS gene, pro cationic trypsinogen, known as a causal gene of hereditary pancreatitis. Other genes related to origination of chronic pancreatitis, i.e. CFTR mutation and SPINK1 gene do not evoke the disease, but e.g. with alcohol these factors are crucial. In the recent years also a relation between these genes to a tropic form of chronic pancreatitis was proved. Aetiopathogenesis of autoimmune pancreatitis is not exactly known, a characteristic finding is a positivity of immunoglobulin G4 in blood serum and also in pancreatic tissues. But an autoimmune form of pancreatitis is not a homogeneous condition; everything above mentioned is valid for 1st type of the disease, which is the most common. In the second type of the disease IgG4 is not increased, but histologically the findings are virtually equal, with the exception of presence or non-presence of granular endothelial lesions (EGL). The therapy of the autoimmune form was based on administration of steroids and at failure of immunosupressives. Aetiopathogenesis of chronic pancreatitis is apparently multifactorial with differences concerning a clinical course and therapy. Despite of all new knowledge about aetiopathogenesis of the disease it is possible to state that we are only able to treat chronic pancreatitis but not to cure it.