Does the neurotrophic factor artemin influence the extent of neural damage and growth in chronic pancreatitis?
Overexpression of artemin in chronic pancreatitis might function as a compensatory upregulation in order to repair neural damage incurred by ongoing pancreatic inflammation. Upregulation of TGFbeta1 seems not only to increase pancreatic fibrosis but also to contribute to neural alteration by stimulating artemin expression in hPSCs. However, overexpression of endogenous artemin does not seem to be sufficient to prevent pain in chronic pancreatitis.
Hematological changes in AN, as assessed by peripheral blood parameters and MRI patterns of bone marrow, are correlated with total body FM depletion, suggesting that the reduction of adipose tissue adversely affects hematopoiesis.