![]() Chronic Pancreatitis. Definition. Chronic pancreatitis (CP) is a progressive inflammatory disease of the pancreas, characterized by irreversible morphologic changes and gradual fibrotic replacement of the gland. Loss of exocrine and endocrine function results from parenchymal fibrosis. The primary symptoms of CP are abdominal pain and maldigestion. Because of diagnostic and therapeutic challenges, an interdisciplinary management strategy is required. Back to Top. Epidemiology. The incidence of CP ranges from 1. Chronic pancreatitis in the United States results in more than 1. Back to Top. Pathophysiology. Grossly, the pancreas may be enlarged or atrophic, with or without cysts or calcifications. The ducts may be dilated, irregular, or strictured. Essential pathologic features include irregular and patchy loss of acinar tissue, chronic inflammation, ductal changes, and fibrosis. These gross changes are end- manifestations of complex pathogenic mechanisms that are associated with gene mutations, metabolic and environmental factors. Several past theories have been developed to explain the pathogenesis of chronic pancreatitis. The premise of the oxidative stress hypothesis is that reactive by- products of hepatic mixed function oxidase activity damage the pancreas through chronic reflux of bile into the pancreatic duct. The toxic- metabolic theory is that alcohol is directly toxic to the acinar cell through a change in intracellular metabolism. The stone and duct obstruction theory suggests that alcohol increases the lithogenicity of pancreatic juice and causes stone formation. Chronic contact of the stones with duct epithelial cells produces ulceration, scarring, and obstruction of the acinar glands. ![]() The necrosis- fibrosis theory emphasizes that acute and chronic pancreatitis represents a spectrum of disease. Inflammation from acute pancreatitis leads to scarring and extrinsic compression of the pancreatic ductules. Recently, research in the immunology of pancreatitis has demonstrated the primary role of pancreatic stellate cells. The sentinal acute pancreatitis event (SAPE) hypothesis encompasses past theories and the new knowledge about pancreatic stellate cells. This model includes 3 sequential phases on a continuum – pre acute pancreatitis, the sentinel attack of acute pancreatitis and progression phase. It presupposes that CP occurs in patients who are genetically or environmentally at risk of pancreatitis (pre- acute pancreatitis stage). The sentinel event of pancreatitis (second stage) in a predisposed patient leads to triggering of chronic inflammation in pancreas and importantly, activation and recruitment of stellate cells. Perpetuation of these immune responses from variety of insults (e. In contrast to other causes, alcohol- related CP is associated with more- severe pain, extensive calcification and ductal changes, and more rapid progression to endocrine and exocrine insufficiency. Most patients experience recurrent episodes of acute pancreatitis for several years before CP develops. Interestingly, only 3% of alcoholics develop CP, implying the presence of cofactors that amplify the effect of alcohol. A high- fat diet and smoking might also contribute to pancreatic disease in alcoholics. Smoking adversely affects pancreatic bicarbonate and water secretion, induces oxidative stress, and increases the rate of pancreatic calcification. Indeed, there have been several studies that demonstrated smoking as an independent risk factor for both development and progression of chronic pancreatitis. Tropical pancreatitis is endemic to certain developing regions, such as India, Africa, and South America. Antibiotics for Crohn's disease. Metronidazole (Flagyl) is an antibiotic that is used for treating several infections caused by parasites (for example, giardia. ![]() Episodic abdominal pain begins in childhood and is followed by rapid progression to endocrine and exocrine insufficiency. Nutritional factors such as micronutrient deficiencies (zinc, copper, and selenium) may be involved in the pathogenesis of tropical pancreatitis. Causes of obstructive CP include pancreatic adenocarcinoma, neuroendocrine tumors, and intrapapillary mucinous tumors. Autoimmune pancreatitis is a recently described disorder which resides on the continuum of Ig. G4 related sclerosing disease. Pancreatic involvement often presents with obstructive jaundice or acute recurrent pancreatitis due to pancreatic swelling and ductal strictures compressing the bile duct or pancreatic duct. Laboratory features include an elevated immunoglobulin Ig. G4 level. Imaging features include focal or diffuse pancreatic enlargement and a narrowed pancreatic duct. The clinical and radiographic features of the disease improve rapidly with corticosteroid therapy. Important discoveries have been made in the genetic basis of pancreatic disease. ![]() ![]() Hereditary pancreatitis is a rare autosomal dominant disease that causes recurrent painful episodes of acute pancreatitis in childhood, leading to CP and pancreatic cancer in adulthood. Hereditary pancreatitis occurs through a mutation of the cationic trypsinogen gene (PRSS1), leading to loss of autoregulation of activated trypsin. Additionally, studies have demonstrated a high prevalence of CFTR gene mutations in patients presenting with idiopathic acute and chronic pancreatitis. Although 8. 5% of cystic fibrosis patients have the severe form of cystic fibrosis, with respiratory disease and pancreatic insufficiency, the remaining 1. Celiac Disease Research Fundraiser Support Celiac research through our own community sponsored internship! Our goal is to raise $3,000. ![]() Most patients who present with pancreatitis as the sole phenotypic feature of cystic fibrosis have one or two mild CFTR mutations. Other susceptibility genes that have been established include the pancreatic secretory trypsin inhibitor gene (SPINK1), the chymotrypsinogen C gene (CTRC), and the calcium sensing receptor gene (CASR). Severe hypercalcemia is known to trigger episodes of acute pancreatitis through trypsin- mediated mechanisms and can progress to CP. Chronic renal failure is associated with an increased prevalence of CP, perhaps related to a direct toxicity of uremia on the pancreas. Hypertriglyceridemia and gallstones rarely cause CP. Ten percent to 3. CP possess no identified risk factors. Idiopathic CP has a bimodal age presentation. Early- onset idiopathic CP manifests with severe abdominal pain in childhood, with relatively few structural and functional changes. Late- onset idiopathic CP manifests in late adulthood, often with minimal pain and pronounced exocrine insufficiency. A commonly used etiologic classification of CP is Toxic Idiopathic Genetic Autoimmune Recurrent Obstructive (TIGAR- O) system that reflects different underlying mechanisms of pancreatic injury. TIGAR- O Etiologic Classification of Chronic Pancreatitis.
Etiologic Risk Factors. Toxic Metabolic. Alcoholic. Tobacco smoking. Hypercalcemia. ![]() Hyperlipidemia. Chronic renal failure. Idiopathic. Tropical. Cause unknown; likely genetic. Genetic. Autosomal dominant. Cationic trypsinogen. Autosomal- recessive/modifier genes. CFTR mutations. SPINK1 mutations. Alpha- 1- antitrypsin deficiency. Autoimmune. Isolated autoimmune chronic pancreatitis. Associated with the following: Primary sclerosing cholangitis. Sj. Pancreatic pain is dull or boring in quality and worsens after eating. The pain is located in the epigastric area and often radiates to the back. There may be associated nausea and vomiting with exacerbations of pain. Two patterns of abdominal pain have been described in CP. Type A pain is characterized by short relapsing episodes lasting days to weeks, separated by pain- free intervals. ![]() Type B pain implies prolonged, severe, unrelenting pain. Recent study suggests that type B pain is associated with worse quality of life, greater healthcare need and disability. Pain exacerbations are not always associated with elevations of serum amylase and lipase levels. Previously, results of some studies suggested diminishment of pancreatic pain with progression of CP. However, subsequent large prospective studies refuted this notion and findings suggest progression of disease may in fact lead to a state where pain management is less effective. There are several proposed pathogenic mechanisms of pancreatic pain in CP, including intraductal hypertension, neural inflammation, upregulation of pain mediators, and proliferation of unmyelinated nerve fiber, neurohormonal changes, and abnormal feedback mechanisms. Concomitant gastroparesis, and complications of CP (see section on complications (Table 2)) can contribute to abdominal pain and appropriately investigated if suspected. Some patients develop nonvisceral (central) pain, often after years of narcotic dependency. ![]() Gradual pancreatic fibrosis produces a steady deterioration in enzyme output, leading to steatorrhea and weight loss. Clinically apparent steatorrhea does not occur until 9. The sudden development of steatorrhea suggests main pancreatic duct obstruction by inflammatory strictures, stones, or cancer. Endocrine insufficiency does not occur until late in the disease course. Pancreatic diabetes requires insulin and is typically brittle because of concomitant glucagon deficiency. Weight loss in CP is multifactorial, related to maldigestion, fear of eating, anorexia, nausea, and vomiting. Severe or rapid weight loss is a red flag for pancreatic cancer. Back to Top. Complications. Complications of chronic pancreatitis are listed in Table 2. Table 2. Complications of Chronic Pancreatitis. Signs and Symptoms. Treatment. Pseudocysts. Increased pain. Vomiting. Mild elevations in amylase and lipase levels. Drainage for large or symptomatic pseudocysts. Endoscopic drainage (transmural or transpapillary)Surgical drainage (cyst gastrostomy or cyst jejunostomy). Biliary Obstruction. Jaundice. Drainage of obstructing pseudocyst. Endoscopic decompression. Surgical decompression. Gastric Outlet Obstruction. Abdominal pain. Early satiety. Nausea and vomiting. Drainage of pseudocyst. Surgical gastrojejunostomy. Pancreatic Adenocarcinoma. Increased pain. Weight loss. Consider surgical resection. Palliation. Pancreatic Ascites. Increased abdominal girth. High- amylase ascites. Endoscopic stent placement. Total parenteral nutrition. Pleural effusion. Approach Considerations, Symptomatic Therapy/Supportive Care, Overview of Stepwise Therapy. World Gastroenterology Organisation (WGO). World Gastroenterology Organisation Global Guideline. Inflammatory bowel disease: a global perspective. Munich, Germany: World Gastroenterology Organisation (WGO); 2. 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