Treatment for chronic pancreatitis (CP) should be started early to prevent further pancreatic fibrosis and managed with a multidisciplinary approach to prevent complications and to maintain a good quality of life. The management strategies of CP can be divided into medical, endoscopic, and surgical treatment. The role of pancreatic enzymes and antioxidants for pain relief is not clearly defined, but their role in maintaining nutritional support by correcting exocrine insufficiency is well established. Endoscopic treatment is applied for resolution of pancreatic or bile duct strictures, clearance of pancreatic duct stones, and pseudocyst drainage. Endosonography-guided celiac plexus or celiac ganglia block for pain relief are known to be safe procedures but evidence for their effectiveness is still lacking. Surgery is commonly recommended when endoscopic therapy fails or there is suspicion of malignancy. New evidence-based guidelines for the management of CP are needed.
Antioxidants/therapeutic use ; Cholangiopancreatography, Endoscopic Retrograde ; Endosonography ; Enzyme Replacement Therapy ; Fibrosis ; Gallstones/therapy ; Humans ; Lithotripsy ; Pancreas/pathology ; Pancreatitis, Chronic/*drug therapy/pathology

Autoimmune pancreatitis has recently been described as a clinical entity that causes chronic pancreatitis. This unique form of chronic pancreatitis is characterized by minimal attacks of abdominal pain, irregular narrowing of the pancreatic duct, and a diffuse enlargement of the pancreas. Autoimmune pancreatitis is associated with hypergammaglobulinemia. In addition, there is histological evidence of lymphoplasmacytic inflammation, the occasional coexistence of other autoimmune diseases, and has a favorable response to glucocorticoid treatment. Recently autoimmune pancreatitis has been increasingly reported particularly in Japan. We report two patients with autoimmune pancreatitis who were treated successfully with corticosteroid therapy.
Anti-Inflammatory Agents/*therapeutic use ; Autoimmune Diseases/*drug therapy/pathology/radiography ; Cholangiopancreatography, Endoscopic Retrograde ; Chronic Disease ; Human ; Male ; Middle Aged ; Pancreatitis/*drug therapy/pathology/radiography ; Prednisolone/*therapeutic use ; Tomography, X-Ray Computed

OBJECTIVETo investigate the effect of modified Xiaochaihu Decoction (, MXD) on transforming growth factor-β1/Sma- and Mad-related proteins (TGF-β1/Smads) signaling pathway in rats with chronic pancreatitis (CP) induced by dibutyltin dichloride.

METHODSThirty healthy male Wistar rats were randomly divided into the normal control group, CP group and CP+MXD-treated group. CP was induced by injection of dibutyltin dichloride (DBTC, 7 mg/kg of body weight) into the right caudal vein, and the control rats were treated with vehicle. MXD was given daily by gavage at a dose of 10 g/kg of body weight, starting from the day after CP induction. After 28-day treatment, the n-benzoyl-tyrosyl para-aminobenzoic acid (NBT-PABA) test was carried out to evaluate exocrine pancreatic function. Then, rats were sacrificed, and pancreatic tissues were harvested for histological evaluation. In addition, the mRNA expression of TGF-β1, TGF-β1 type II receptor (TGFβRII), Smad3 and Smad7 was determined in pancreatic tissues by using real-time polymerase chain reaction.

RESULTSTreatment of CP with MXD improved the PABA recovery, decreased the histological lesion, and reduced the mRNA expression of TGF-β1, TGFβRII and Smad3 (P<0.05). However, MXD had no effect on Smad7 mRNA level.

CONCLUSIONSMXD could protect the pancreas against chronic injury and improve pancreatic exocrine function in DBTC induced rat CP model. Its mechanism may involve inhibition of the TGF-β1/Smads signaling pathway.

Amylases ; blood ; Animals ; Base Sequence ; Blood Glucose ; metabolism ; Body Weight ; drug effects ; Chronic Disease ; DNA Primers ; Disease Progression ; Drugs, Chinese Herbal ; therapeutic use ; Lipase ; blood ; Male ; Pancreatitis ; drug therapy ; metabolism ; pathology ; RNA, Messenger ; genetics ; Rats ; Rats, Wistar ; Real-Time Polymerase Chain Reaction ; Signal Transduction ; drug effects ; Smad Proteins ; genetics ; metabolism ; Transforming Growth Factor beta1 ; metabolism