eMedicine Specialties > Gastroenterology > Pancreas

Pancreatitis, Chronic

Author: Kamil Obideen, MD, Assistant Professor of Medicine, Division of Digestive Diseases, Emory University School of Medicine; Consulting Staff, Division of Gastrointestinal Endoscopy, Atlanta Veterans Affairs Medical Center
Coauthor(s): Paul Yakshe, MD, Assistant Professor of Medicine, University of Minnesota, Medical Director of Pancreas and Biliary Clinic, Department of Medicine, Division of Gastroenterology, Hepatology, and Nutrition, Fairview University Medical Center; Mohammad Wehbi, MD, Assistant Professor of Medicine, Associate Program Director, Department of Gastroenterology, Atlanta Veterans Affairs Medical Center, Emory University School of Medicine
Contributor Information and Disclosures

Updated: Jun 16, 2008

Introduction

Background

Chronic pancreatitis is commonly defined as a continuing chronic inflammatory process of the pancreas, characterized by irreversible morphological changes. This chronic inflammation can lead to chronic abdominal pain and/or impairment of endocrine and exocrine function of the pancreas. Chronic pancreatitis usually is envisioned as an atrophic fibrotic gland with dilated ducts and calcifications. However, findings on conventional diagnostic studies may be normal in the early stages of chronic pancreatitis, as the inflammatory changes can be seen only by histologic examination.

By definition, chronic pancreatitis is a completely different process from acute pancreatitis. In acute pancreatitis, the patient presents with acute and severe abdominal pain, nausea, and vomiting. The pancreas is acutely inflamed (neutrophils and edema), and the serum levels of pancreatic enzymes (amylase and lipase) are elevated. Full recovery is observed in most patients with acute pancreatitis, whereas in chronic pancreatitis, the primary process is a chronic irreversible inflammation (monocyte and lymphocyte) that leads to fibrosis with calcification. The patient with chronic pancreatitis clinically presents with chronic abdominal pain and normal or mildly elevated pancreatic enzyme levels; when the pancreas lose its endocrine and exocrine function, the patient presents with diabetes mellitus and steatorrhea.

Pathophysiology

The proposed pathologic mechanisms of chronic pancreatitis are as follows:

  • Intraductal plugging and obstruction (eg, ETOH abuse, stones, tumors)
  • Direct toxins and toxic metabolites: These act on the pancreatic acinar cell to stimulate the release of cytokines, which stimulate the stellate cell to produce collagen and to establish fibrosis. Cytokines also act to stimulate inflammation by neutrophils, macrophages, and lymphocytes (eg, ETOH, tropical sprue).
  • Oxidative stress (eg, idiopathic pancreatitis)
  • Necrosis-fibrosis (recurrent acute pancreatitis that heals with fibrosis)
  • Ischemia (from obstruction and fibrosis), which is important in exacerbating or perpetuating disease rather than in initiating disease
  • Autoimmune disorders: Chronic pancreatitis has been found in association with other autoimmune diseases, such as Sjögren syndrome, primary biliary cirrhosis, and renal tubular acidosis. 

Autoimmune pancreatitis is a recently described new entity. Clinical characteristics include symptomatic or asymptomatic diffuse enlargement of the pancreas, diffuse and irregular narrowing of the main pancreatic duct, increased circulating levels of gamma globulin, the presence of autoantibodies, and a possible association with other autoimmune diseases. Fibrosis with lymphocytic infiltration is seen on pathology. The disorder is associated with elevated immunoglobulin G4 (IgG4) concentrations. While alcohol greatly influences the understanding of its pathophysiology because it is the most common etiology (60-70%), approximately 20-30% of cases are idiopathic and 10% of cases are due to rare diseases.

Although a linear relationship exists between the amount of alcohol ingested and the risk of developing chronic pancreatitis, the fact that fewer than 10% of people with alcoholism actually develop the disease is not understood.

In the affected gland, alcohol appears to increase protein secretion from acinar cells while decreasing fluid and bicarbonate production from ductal epithelial cells. The resulting viscous fluid results in proteinaceous debris becoming inspissated within the lumen, causing ductular obstruction, upstream acinar atrophy, and fibrosis. GP2, which is secreted from the acinar cell and homologous to a protein involved in renal tubular casts, is an integral component of these ductal plugs. Lithostathine (formerly pancreatic stone protein), which also is produced by acinar cells, accounts for about 5% of secretory protein and inhibits the growth of calcium carbonate crystals. Abnormal lithostathine S1, whether inherited or acquired through trypsin digestion, appears to play a role in stone formation; it is insoluble at the neutral pH of pancreatic juice and is the major constituent of pancreatic stones.

A competing theory suggests that the persistent demands of metabolizing alcohol (and probably other xenobiotics, such as drugs, tobacco smoke, environmental toxins, and pollution) causes oxidative stress within the pancreas and may lead to cellular injury and organ damage, especially in the setting of malnutrition. Both oxidative and nonoxidative pathways metabolize ethanol. Alcohol dehydrogenase oxidatively metabolizes ethanol first to acetaldehyde and then to acetate. When the alcohol concentration increases, cytochrome P-450 2E1 is induced to meet the metabolic demands. Although these reactions occur principally in the liver, further increases in ethanol concentration induce pancreatic cytochrome P-450 2E1, and the level of acetate within the pancreas begins to approach that observed in the liver. Reactive oxygen species produced by this reaction may overwhelm cellular defenses and damage important cellular processes.

In an effort to explain why so few people with alcoholism actually develop chronic pancreatitis, researchers have studied genetic polymorphisms of ethanol-oxidizing enzymes; to date, none have correlated with a susceptibility to alcohol-induced pancreatitis. Although nonoxidative metabolism of ethanol is a minor pathway, the fatty acid ethyl esters produced by this reaction may cause cellular injury and are synthesized in the pancreas to a greater extent than in other organ systems.

Whatever the etiology of chronic pancreatitis, pancreatic fibrogenesis appears to be a typical response to injury. This involves a complex interplay of growth factors, cytokines, and chemokines, leading to deposition of extracellular matrix and fibroblast proliferation. In pancreatic injury, local expression and release of transforming growth factor–beta (TGF-beta) stimulates the growth of cells of mesenchymal origin and enhances synthesis of extracellular matrix proteins, such as collagens, fibronectin, and proteoglycans.

Recent evidence indicates involvement of distinct chemokines in the initiation and perpetuation of chronic pancreatitis.

Frequency

United States

Based on estimates from hospital discharge data in the United States, approximately 87,000 cases of pancreatitis occur annually.

International

Comparing the hospital admissions data from several cities around the globe, the overall frequency is similar. Expressed as number of cases per 1000 hospital admissions, the value for Marseille is 3.1, for Cape Town is 4.4, for Sao Paulo is 4.9, and for Mexico City is 4.4. When the data from several centers are compared over time, the incidence of chronic pancreatitis from 1945-1985 appears to be increasing.

Mortality/Morbidity

No data exist on the extent of the disability resulting from benign pancreatic diseases.

Race

Hospitalization rates for blacks are 3 times higher than for whites in the United States.

Sex

  • In population studies, males are affected more commonly than females (6.7 vs 3.2 per 100,000 population).
  • Differences in the hospitalization rates of patients with chronic pancreatitis exist with respect to sex. Rates in males peak at age 45-54 years and then decline; female rates reach a plateau, which remains stable after age 35 years.
  • Sex differences with respect to etiology also exist. Alcohol-induced illness is more prevalent in males, idiopathic and hyperlipidemic-induced pancreatitis is more prevalent in females, and equal sex ratios are observed in chronic pancreatitis associated with hereditary pancreatitis.

Age

In aggregate, the mean age at diagnosis is 46 years, plus or minus 13 years. In idiopathic chronic pancreatitis, a bimodal age distribution has been reported, designated as early-onset form (median age 19.2 y) and late-onset form (median age 56.2 y).

Clinical

History

For most patients with chronic pancreatitis, abdominal pain is the presenting symptom. Either the patient's age or the etiology of the disease has some influence on the frequency of this presentation. Ninety-six percent of those with early-onset idiopathic pancreatitis present with abdominal pain, compared with 77% with alcohol-induced disease and 54% with late-onset idiopathic chronic pancreatitis.

Clinically, the patient experiences intermittent attacks of severe pain, often in the mid or left upper abdomen and occasionally radiating in a bandlike fashion or localized to the mid back. The pain may occur either after meals or independently of meals, but it is not fleeting or transient and tends to last at least several hours. Unfortunately, patients often are symptomatic for years before the diagnosis is established; the average time from the onset of symptoms until a diagnosis of chronic pancreatitis is 62 months, add or subtract 4 months. The delay in diagnosis is even longer in people without alcoholism, in whom the average time is 81 months from onset of symptoms to diagnosis.

  • The natural history of pain in chronic pancreatitis is highly variable. Most patients experience intermittent attacks of pain at unpredictable intervals, while a minority of patients experience chronic pain. In most patients, pain severity either decreases or resolves over 5-25 years. Nevertheless, ignoring pain relief with the expectation that the disease eventually will resolve itself is inappropriate. In alcohol-induced disease, eventual cessation of alcohol intake may reduce the severity of pain. Variability in the pain pattern contributes to the delay in diagnosis and makes determining the effect of any therapeutic intervention difficult.
  • Other symptoms associated with chronic pancreatitis include diarrhea and weight loss. This may be due either to fear of eating (eg, postprandial exacerbation of pain) or due to pancreatic exocrine insufficiency and steatorrhea.
  • A small percentage of patients (20%) have painless chronic pancreatitis and present with signs or symptoms of pancreatic exocrine or endocrine insufficiency.

Physical

  • In most instances, the standard physical examination does not help to establish a diagnosis of chronic pancreatitis; however, a few points are noteworthy.
  • During an attack, patients may assume a characteristic position in an attempt to relieve their abdominal pain (eg, lying on the left side, flexing the spine and drawing the knees up toward the chest).
  • Funduscopic examination may reveal a milky white hue in the retinal blood vessels when hyperlipidemia is present.
  • Occasionally, a tender fullness or mass may be palpated in the epigastrium, suggesting the presence of a pseudocyst or an inflammatory mass in the abdomen. Patients with advanced disease (ie, patients with steatorrhea) exhibit decreased subcutaneous fat, temporal wasting, sunken supraclavicular fossa, and other physical signs of malnutrition.

Causes

  • The cause of chronic pancreatitis usually is metabolic in nature.
    • Excessive alcohol consumption is the most common cause, accounting for about 60% of all cases. Because fewer than 5-10% of people with alcoholism develop the disease, other factor(s) must place these individuals at risk. Recently, a mutation in the gene encoding the serine protease inhibitor, Kazal type 1, was identified in patients with chronic pancreatitis. The N34S mutation was detected in 5.8% of 274 patients with alcoholic chronic pancreatitis compared to 1.0% of people with alcoholism without pancreatitis. Although all patients were heterozygous for the mutation, it provides evidence for abnormalities in the pancreatic protease/protease inhibitor system playing a role in the pathogenesis of alcoholic chronic pancreatitis.
    • Several inherited disorders also are considered metabolic in origin. Hereditary pancreatitis is an autosomal dominant disorder with an 80% penetrance, accounting for about 1% of cases. Research of families with hereditary pancreatitis has led to the identification of several mutations in the cationic trypsinogen gene on chromosome 7. These mutations apparently render the activated enzyme resistant to second-line proteolytic control mechanisms. Mutations were found in the pancreatic secretory serine protease inhibitor Kazal type 1 (SPINK1) gene in 18 of 96 patients with idiopathic or hereditary chronic pancreatitis.
    • Cystic fibrosis, one of the most common genetic abnormalities, is an autosomal recessive disorder accounting for a small percent of patients with chronic pancreatitis. The cystic fibrosis transmembrane regulator (CFTR) gene transcribes a protein important in regulating chloride transport across cellular membranes. Several hundred mutations of the CFTR gene have been identified, and the clinical manifestation of any given mutation depends on how severely it affects the protein's ability to regulate chloride transport. This leads to clinical manifestations ranging from severe chronic pancreatitis associated with classic pulmonary disease to chronic pancreatitis associated with relatively normal respiratory function.
    • Hyperlipidemia (usually type I and type V) also may cause chronic pancreatitis; however, it usually presents with repeated attacks of acute pancreatitis.
    • Hypercalcemia due to hyperparathyroidism now is a rare cause of chronic pancreatitis, probably because automation of serum chemistries reveals hypercalcemia before it results in pancreatitis.
    • Nutritional, or tropical, chronic pancreatitis is rare in the United States, but it is an important cause of disease in other parts of the world.
    • Medications are an infrequent, or possibly underrecognized, cause of chronic pancreatitis.
  • Idiopathic chronic pancreatitis, which accounts for approximately 30% of cases, has been subdivided into early-onset and late-onset forms arbitrarily. While the cause is not yet known, some evidence points to atypical genetic mutations in CFTR, cationic trypsinogen, and possibly other proteins.
  • Obstruction of the flow of pancreatic juice can cause chronic pancreatitis. Obstructive forms account for less than 10% of cases and may be congenital or acquired.
    • Congenital abnormalities, such as pancreas divisum and annular pancreas divisum, are uncommon (even rare) causes of chronic pancreatitis and usually require an additional factor to induce chronic pancreatitis. For example, while pancreas divisum usually does not cause chronic pancreatitis, patients with divisum and minor papilla stenosis are at risk. In these patients, clear evidence of disease exists in the dorsal pancreas, whereas the ventral pancreas is normal histologically.
    • Acquired obstructive forms typically result from blunt abdominal trauma or accidents involving motor vehicles, bicycles, horses, and, on occasion, severe falls. In these cases, the pancreas is whiplashed against the spine, causing trauma to the ductal system, resulting in a stricture close to the surgical genu. In rare instances, chronic inflammatory conditions affecting the duodenum, or primarily the duodenal papilla, can induce fibrosis and papillary stenosis in a subset of patients, leading to chronic pancreatitis.
  • Autoimmune pancreatitis is uncommon and accounts probably for less than 1% of cases of chronic pancreatitis. Clinical characteristics include symptomatic or asymptomatic diffuse enlargement of the pancreas, diffuse and irregular narrowing of the main pancreatic duct, increased circulating levels of gamma globulin, the presence of autoantibodies, and a possible association with other autoimmune diseases. Fibrosis with lymphocytic infiltration is seen on pathology with an elevated level of IgG4. Secondary forms of autoimmune chronic pancreatitis are associated with primary biliary cirrhosis, primary sclerosing cholangitis, and Sjögren syndrome.

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Further Reading

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Keywords

continuing inflammatory disease of the pancreas, inflamed pancreas, pancreas inflammation, pancreatic inflammation, chronic pancreatitis, pancreatic disease, lithostathine, pancreatic stone protein, alcoholism, alcohol-induced pancreatitis, pancreatic fibrogenesis, abdominal pain, steatorrhea, pancreatic exocrine insufficiency, decreased subcutaneous fat, temporal wasting, sunken supraclavicular fossa, pancreatic fibrosis, alcoholic chronic pancreatitis, hereditary pancreatitis, serine protease inhibitor Kazal type 1 gene, SPINK1 gene, cystic fibrosis, cystic fibrosis transmembrane regulator gene, CFTR gene, hyperlipidemia, hypercalcemia, hyperparathyroidism, nutritional chronic pancreatitis, tropical chronic pancreatitis, idiopathic chronic pancreatitis, obstruction of the flow of pancreatic juice, annular pancreas divisum, minor papilla stenosis, blunt abdominal trauma, blunt abdominal accidents, papillary stenosis, autoimmune pancreatitis, hypergammaglobulinemia, eosinophilia, positive fluorescent antinuclear antibody, positive FANA, anticarbonic anhydrase II, antilactoferrin antibodies, primary biliary cirrhosis, primary sclerosing cholangitis, Sjögren syndrome

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Contributor Information and Disclosures

Author

Kamil Obideen, MD, Assistant Professor of Medicine, Division of Digestive Diseases, Emory University School of Medicine; Consulting Staff, Division of Gastrointestinal Endoscopy, Atlanta Veterans Affairs Medical Center
Kamil Obideen, MD is a member of the following medical societies: American College of Gastroenterology, American Gastroenterological Association, and American Society for Gastrointestinal Endoscopy
Disclosure: Nothing to disclose.

Coauthor(s)

Paul Yakshe, MD, Assistant Professor of Medicine, University of Minnesota, Medical Director of Pancreas and Biliary Clinic, Department of Medicine, Division of Gastroenterology, Hepatology, and Nutrition, Fairview University Medical Center
Paul Yakshe, MD is a member of the following medical societies: American College of Gastroenterology, American Pancreatic Association, and American Society for Gastrointestinal Endoscopy
Disclosure: Nothing to disclose.

Mohammad Wehbi, MD, Assistant Professor of Medicine, Associate Program Director, Department of Gastroenterology, Atlanta Veterans Affairs Medical Center, Emory University School of Medicine
Mohammad Wehbi, MD is a member of the following medical societies: American College of Physicians, American Gastroenterological Association, and American Medical Association
Disclosure: Nothing to disclose.

Medical Editor

Tushar Patel, MB, ChB, Professor of Medicine, Director of Hepatology, Ohio State University Medical Center
Tushar Patel, MB, ChB is a member of the following medical societies: American Association for the Study of Liver Diseases and American Gastroenterological Association
Disclosure: Nothing to disclose.

Pharmacy Editor

Francisco Talavera, PharmD, PhD, Senior Pharmacy Editor, eMedicine
Disclosure: Nothing to disclose.

Managing Editor

Noel Williams, MD, Professor Emeritus, Department of Medicine, Dalhousie University, Halifax, Nova Scotia, Canada; Professor, Department of Internal Medicine, Division of Gastroenterology, University of Alberta, Edmonton, Alberta, Canada
Noel Williams, MD is a member of the following medical societies: Royal College of Physicians and Surgeons of Canada
Disclosure: Nothing to disclose.

CME Editor

Alex J Mechaber, MD, FACP, Assistant Dean for Medical Curriculum, Associate Professor of Medicine, Division of General Internal Medicine, University of Miami Miller School of Medicine
Alex J Mechaber, MD, FACP is a member of the following medical societies: Alpha Omega Alpha, American College of Physicians-American Society of Internal Medicine, and Society of General Internal Medicine
Disclosure: Nothing to disclose.

Chief Editor

Julian Katz, MD, Clinical Professor of Medicine, Drexel University College of Medicine; Consulting Staff, Department of Medicine, Section of Gastroenterology and Hepatology, Hospital of the Medical College of Pennsylvania
Julian Katz, MD is a member of the following medical societies: American College of Gastroenterology, American College of Physicians, American Gastroenterological Association, American Geriatrics Society, American Medical Association, American Society for Gastrointestinal Endoscopy, American Society of Law Medicine and Ethics, American Trauma Society, Association of American Medical Colleges, and Physicians for Social Responsibility
Disclosure: Nothing to disclose.

 
 
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