ABSTRACT
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.
Subject(s)
Humans , Antioxidants/therapeutic use , Cholangiopancreatography, Endoscopic Retrograde , Endosonography , Enzyme Replacement Therapy , Fibrosis , Gallstones/therapy , Lithotripsy , Pancreas/pathology , Pancreatitis, Chronic/drug therapyABSTRACT
A significant increase in serum lipase, amylase, capase-1 and myeloperoxidase activities, oxidative stress index (OSI), IL-1β and IL-18 was observed in rats receiving ethanol (EtOH) and high fat diet (HFD). Thymoquinone (TQ) supplementation along with EtOH and HFD significantly decreased the levels of serum lipase, amylase, capase-1, myeloperoxidase, OSI and maintained the antioxidant status when compared to untreated EtOH and HFD fed rats. Among the 4 doses, 100 mg of TQ/kg body weight was found to provide optimum protective effect on pancreas against EtOH and HFD induced abnormal changes. Histological observations added more evidence for the anti-inflammatory effect of TQ.
Subject(s)
Animals , Antioxidants/metabolism , Benzoquinones/pharmacology , Body Weight , Diet, High-Fat/adverse effects , Dose-Response Relationship, Drug , Ethanol/adverse effects , Glutathione/metabolism , Inflammation , Interleukin-18/metabolism , Interleukin-1beta/metabolism , Lipase/blood , Lipid Peroxides/chemistry , Male , Oxidative Stress , Pancreatitis, Chronic/chemically induced , Pancreatitis, Chronic/drug therapy , Peroxidase/metabolism , Rats , Rats, WistarABSTRACT
Chronic pancreatitis occurs by the prolonged inflammation of pancreatic tissue that induces the irreversible destruction of the organ, leading to a global pancreatic insufficiency. The most common manifestations are abdominal pain, diarrhea, malabsorption, and possibly diabetes mellitus. Chronic pancreatitis treatment includes dietary restrictions, enzymatic supplementation, vitamins, and endoscopic or surgical methods depending on the degree of ductal involvement. In addition to the known therapies, new therapies are under development and research.
La pancreatitis crónica se desarrolla por la inflamación prolongada del tejido pancreático que induce la destrucción irreversible del órgano, llevando a una insuficiencia pancreática global. Las manifestaciones más frecuentes son dolor abdominal, diarrea, malabsorción y eventualmente diabetes mellitus. El tratamiento en pancreatitis crónica incluye restricciones dietarias, suplementación enzimática, vitamínica, y métodos endoscópicos o quirúrgicos, dependiendo del grado de compromiso ductal. Además de lo descrito, están en desarrollo y experimentación nuevas terapias.
Subject(s)
Humans , Pancreatitis, Chronic/surgery , Pancreatitis, Chronic/diet therapy , Pancreatitis, Chronic/drug therapy , Antioxidants/therapeutic use , Abdominal Pain/etiology , Abdominal Pain/therapy , Endoscopy, Digestive System , Steatorrhea/etiology , Steatorrhea/therapy , Pancreatitis, Chronic/complications , Malabsorption Syndromes/etiology , Malabsorption Syndromes/therapy , Enzyme Therapy , Genetic TherapyABSTRACT
Fibrocalculous pancreatitis diabetes (FCPD), a late stage of tropical chronic pancreatitis (TCP), is classified as a secondary cause of diabetes mellitus resulting from pancreatic exocrine dysfunction. The distinctive features of FCPD and TCP are young age at onset, presence of large intraductal pancreatic calculi, and reported mainly in tropical developing countries. Their etiology is still obscure, but the autodigestion due to aberrant intraductal activation of zymogens by trypsin is thought to be a primary common event. Recently, mutations in SPINKI gene encoding a pancreatic secretory trypsin inhibitor have been reported in association with an increased risk of pancreatitis. We describe a heterozygous mutation, IVS3+2 T>C, of SPINK1 gene in a young Thai female patient with typical presentation of FCPD. To our knowledge, this is the first report of the SPINK1 gene mutation in a FCPD patient in Southeast Asia.
Subject(s)
Adolescent , Carrier Proteins/genetics , Female , Humans , Insulin/therapeutic use , Mutation , Pancreatitis, Chronic/drug therapyABSTRACT
No abstract availble.
Subject(s)
Humans , Autoimmune Diseases/drug therapy , Glucocorticoids/therapeutic use , Pancreatitis, Chronic/drug therapyABSTRACT
BACKGROUND/AIMS: Autoimmune chronic pancreatitis (AIP) is a clinically attractive entity because of its dramatic response to steroid therapy. But the long-term results after steroid therapy have not been reported yet in Korea. The purpose of this study was to assess the long-term results and prognosis after steroid therapy in patients with AIP. METHODS: We retrospectively analyzed the clinical, radiologic, and laboratory features and evaluated clinical outcomes in 19 patients with AIP who have been treated with oral corticosteroid. All patients were initially treated with prednisolone (30-40 mg/d) for 1 or 2 months. After the confirmation of clinical improvement in radiologic imaging and laboratory findings, the daily dose of prednisolone was then gradually tapered by 5-10 mg per month to the maintenance dose (2.5-7.5 mg/d). RESULTS: All the patients showed normalization or marked improvement in symptoms, laboratory and imaging findings after steroid therapy. There were 4 cases (21%) of recurrence during the mean follow-up period of 27 months. All the patients with recurrence responded to oral steroid again. Among the 10 patients with diabetes mellitus, seven patients were able to stop or reduce the medication for diabetes after completion of steroid therapy. The biliary stents were additionally inserted in 10 patients who showed distal common bile duct stricture and obstructive jaundice. The accompanying autoimmune diseases were also improved with oral corticosteroid. CONCLUSIONS: Steroid therapy is very effective for AIP and is also effective in the cases of recurrence. A definitive protocol of steroid therapy for AIP should be established in the future.