Chronic Pancreatitis occurs most often in patients with alcoholism, sever malnutrition, or untreated hyperparathyroidism.
Chronic pancreatitis usually follows many years of alcohol abuse. Chronic pancreatitis occurs most often in patients with alcoholism, severe malnutrition, or untreated hyperparathyroidism. It may develop after only one acute attack, especially if there is damage to the ducts of the pancreas.
In the early stages, the healthcare provider cannot always tell whether the patient has acute or chronic disease. The symptoms may be the same. Damage to the pancreas from drinking alcohol may show no symptoms for many years, and then the patient suddenly can have an attack of pancreatitis. In more than 90 percent of adult patients, chronic pancreatitis appears to be caused by alcoholism. This is more common in men than women and often develops between 30 and 40 years of age. In other cases, pancreatitis may be inherited.
It may be hereditary or idiopathic. Recently, a gene for hereditary pancreatitis, transmitted as an autosomal dominant trait with variable penetrance, has been identified on chromosome 7.
In chronic pancreatitis, progressive fibrosis and destruction of functioning glandular tissue occur. Pancreaticolithiasis and obstruction of the duodenal end of the pancreatic duct are often present.
Chronic Pancreatitis disease is histologically characterized by infiltration with inflammatory cells and extended fibrosis. Epithelial cells of pancreatic ducts express HLA-DR antigens and secretory component of secretory IgA. As a consequence of this, we could find elevated levels of secretory component in pancreatic juice of chronic pancreatitis patients compared to normal controls.
Since chronic pancreatitis is a fibrotic disease leading to a more or less complete replacement of the exocrine pancreas by fibrotic tissue, it is one of the subjects of our research to investigate the role of extracellular matrix proteins in this disease. The serum level of procollagen-III-peptide (P-III-P), laminin, and hyaluronic acid by immunoassays may be elevated.
Symptoms of the disease are greatest in the upper abdomen, may be in the middle of the upper abdomen, may last from hours to days, eventually may be continuous, may be worse by eating or drinking, may be worse from alcohol, and may radiate to the back. Other symptoms may be nausea, vomiting, weight loss, and fatty stools. Likewise, additional symptoms that may also be associated with Chronic Pancreatitis may be overall swelling, colored clay stools, and abdominal indigestion.
Management of the symptoms of chronic pancreatitis is achieved by reducing pancreatic stimulation, alleviating fat indigestion, reducing pain, and treating diabetes with the following measures:
* Low-Fat Diet
* Fat-soluble vitamins and calcium in diet
* No alcohol use or caffeine
* Pain relief with analgesics
* Controlling blood sugar levels by giving insulin
* Pancreatic enzymes to correct underproduction
Surgery to alleviate an obstruction may be recommended if an anatomic lesion is found. In advanced cases, all or part of the pancreas may be removed. This is a serious disease that may lead to disability. The outcome is usually better if abstinence from alcohol is maintained.
Scientists do not know why the inherited form occurs. Patients with chronic pancreatitis tend to have three kinds of problems: pain, malabsorption of food leading to weight loss, or diabetes.
Some patients do not have any pain but most do. Pain may be constant in the back and abdomen, and for some patients, the pain attacks are disabling. In some cases, the abdominal pain goes away as the condition advances. Healthcare providers think this happens because pancreatic enzymes are no longer being made by the pancreas.
Patients with this disease often lose weight, even when their appetite and eating habits are normal. This occurs because the body does not secrete enough pancreatic enzymes to break down food, so nutrients are not absorbed normally. Poor digestion leads to loss of fat, protein, and sugar into the stool. Diabetes may also develop at this stage if the insulin-producing cells of the pancreas (islet cells) have been damaged.