Transforming growth factor beta, fibrogenesis and hyperglycemia in patients with chronic pancreatitis

• Published in: Journal of medicine Vol. 29; no. 5-6; p. 277
• Main Authors: Fogar, P, Pasquali, C, Basso, D, Floreani, A, Piva, M G, De Paoli, M, Melis, A, Sperti, C, Pedrazzoli, S, Plebani, M
• Format: Journal Article
• Language: English
• Published: United States 1998
• Subjects: Adult; Aged; Bilirubin - blood; Biomarkers; Blood Glucose - metabolism; Chronic Disease; Female; Fibrosis; Follow-Up Studies; Humans; Hyperglycemia - metabolism; Laminin - blood; Liver Cirrhosis - metabolism; Liver Cirrhosis - virology; Male; Middle Aged; Pancreatitis - complications; Pancreatitis - metabolism; Pancreatitis - pathology; Procollagen - metabolism; Transforming Growth Factor beta - blood
• ISSN: 0025-7850

It has been suggested that transforming growth factor beta (TGFb) mediates liver fibrosis, which can be monitored by the serum determination of the N-terminal peptide of type III procollagen (PIIIP) and laminin. Fibrosis is also an important phenomenon in patients with chronic pancreatitis (CP). In 23 patients with CP, 38 with liver cirrhosis (LC) and 20 healthy controls we compared the serum patterns of PIIIP, laminin and TGFb and assessed whether in CP these markers are correlated with exocrine and endocrine function. In patients with LC, PIIIP and laminin levels were significantly higher, whereas TGFb levels were significantly lower than those of controls. In CP patients, no significant variations were found for PIIIP and laminin, although levels were high in 7/23 and in 5/23 patients, respectively. TGFb levels in CP patients were higher than those in LC patients, levels being raised in 6/23 patients. In LC patients an inverse correlation was found between PIIIP and TGFb, whereas in CP patients, a direct correlation was found between TGFb and PIIIP. Moreover, in CP patients, there was also a positive correlation between TGFb and fasting serum glucose levels, while laminin was correlated with PABA test results.
serum biochemical markers of liver fibrosis can be considered of limited value in assessing pancreatic fibrosis; in liver cirrhosis there may be a negative feed-back regulation between TGFb production and the fibrogenetic process; and in chronic pancreatitis TGFb appears to favor fibrosis on the one hand and the development of hyperglycemia on the other.