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Query: UMLS:C0030305 (pancreatitis)
 16,014 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Chronic pancreatitis (CP) is characterized by progressive, chronic inflammation of the pancreas, resulting in loss of exocrine and endocrine function and chronic abdominal pain. In most cases, CP is induced by long-term alcoholism. The second most frequent diagnosis is idiopathic CP, in the absence of known causes of CP. However, the identification of genetic and immunological causes continuously reduces the number of cases classified as idiopathic pancreatitis. Common symptoms of CP comprise abdominal pain radiating to the back, diarrhea, steatorrhea and the development of diabetes. The diagnosis is mainly based on clinical features, typical morphological findings such as pancreatic calcifications, duct stenoses and dilatations, as well as pathologic pancreatic function tests. Treatment of CP includes watch and wait strategies in asymptomatic patients, symptomatic treatment of the clinical features such as pain, exocrine and endocrine insufficiency, as well as interventional or surgical therapy of complications such as pseudocysts, pancreatic duct stenosis, stones or biliary obstruction.
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PMID:[Diagnostics and therapy of chronic pancreatitis]. 1843 29

Retroperitoneal fibrosis is characterized by the presence of a retroperitoneal tissue, consisting of chronic inflammation and marked fibrosis, which entraps the retroperitoneal organs. In two-thirds of cases, the retroperitoneal fibrosis is idiopathic. The pathogenic mechanism is not clearly identified. We report a case of idiopathic retroperitoneal fibrosis associated with type 1 diabetes mellitus. A 61-year-old woman with C peptide negative insulindependent diabetes developed retroperitoneal fibrosis revealed by bilateral hydronephrosis. Anti-GAD 65 antibodies were positive. There were no signs of autoimmune pancreatitis: no steatorrhea, normal IgG4 isotype levels, and absence of pancreas morphological abnormalities.
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PMID:Type 1 diabetes and idiopathic retroperitoneal fibrosis: case report. 1899 43

This review discusses gastrointestinal manifestations of parathyroid diseases. Parathyroid hormone is the primary regulator of calcium physiology. Hypoparathyroidism can be idiopathic, hereditary, or secondary to surgery in the neck. Hyperparathyroidism is usually from adenomas or hyperplasia. Hypoparathyroidism is associated with steatorrhea that may improve with medium-chain triglycerides, correction of the hypoparathyroidism, or administration of vitamin D. Hyperparathyroidism results in constipation because of reduction in neuromuscular excitability by high calcium levels. According to old literature, the incidence of peptic ulcer disease (PUD) in patients with hyperparathyroidism is 9% compared with autopsy rates of 4% to 5%. Any association is difficult to prove today, as hyperparathyroidism is usually mild due to early detection of cases through routine automated measurements of calcium. In addition, PUD is less prevalent now than before the advent of proton pump inhibitors. The presence of ulcers or ulcer symptoms may correct in some patients after parathyroidectomy, suggesting an association. The incidence of pancreatitis in patients with primary hyperparathyroidism ranges from 1.5% to 12% and may be because of the hypercalcemia. Complicating the issue is secondary hyperparathyroidism in response to hypocalcemia from pancreatitis. Pancreatitis may improve in some individuals after parathyroidectomy. Pancreatitis may follow parathyroid surgery because of an acute rise in calcium levels with manipulation of the parathyroid glands or to a blunted response of calcitonin-producing cells from fatigue. Parathyroid diseases have a few distinct effects on the gut: steatorrhea in hypoparathyroidism, and constipation, PUD, and pancreatitis in hyperparathyroidism.
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PMID:The parathyroids and the gut. 2048 90

Pancreatitis may be acute or chronic. Although both can be caused by similar aetiologies, they tend to follow distinct natural histories. Around 80% of acute pancreatitis (AP) diagnoses occur secondary to gallstone disease and alcohol misuse. AP is commonly associated with sudden onset of upper abdominal pain radiating to the back that is usually severe enough to warrant the patient seeking urgent medical attention. Onset of pain may be related to a recent alcohol binge or rich, fatty meal. The patient may appear unwell, be tachycardic and have exquisite tenderness in the upper abdomen. Overall, 10-25% of AP episodes are classified as severe, leading to an associated mortality rate of 7.5%. Disease severity is best predicted from a number of clinical scoring systems which can be applied at diagnosis in association with repeated clinical assessment, measurement of acute inflammatory markers, and CT. All patients with suspected AP should be referred urgently. Chronic pancreatitis (CP) follows continued, repetitive or sustained injury to the pancreas and 70% of diagnoses occur secondary to alcohol abuse. The characteristic presenting feature of CP is insidious progression of chronic, severe, upper abdominal pain, radiating to the back, caused by a combination of progressive pancreatic destruction, inflammation and duct obstruction. Signs and symptoms include weight loss and steatorrhoea and later on diabetes. CP patients may also present with recurrent episodes mimicking AP, both symptomatically and metabolically. Diagnosis of CP should be based on symptom profile, imaging and assessment of exocrine and endocrine pancreatic function. CT should be the first-line imaging investigation.
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PMID:Managing acute and chronic pancreatitis. 2114 Dec 49

Pancreatic insufficiency is a major consequence of pancreatic diseases leading to a loss of pancreatic parenchyma, obstruction of the main pancreatic duct, decreased pancreatic stimulation, or acid-mediated inactivation of pancreatic enzymes. In addition, gastrointestinal and pancreatic surgical resections are frequent causes. Clinical manifestations include abdominal cramps, steatorrhea and malnutrition. Malnutrition, the main contributing factor of weight loss, has been related to a high morbidity and mortality secondary to an increased risk of malnutrition-related complications and cardiovascular events. Assessments of exocrine pancreatic function, such as fecal fat quantification and (13) C-triglyceride breath test, are the method of choice for diagnosis. In clinical practice, high-risk patient populations include those with severe necrotizing pancreatitis, gastrointestinal and pancreatic surgery, cancer of pancreas head, and those with pancreatic calcifications. Apart from relief of maldigestion-related symptoms, the main goal of pancreatic enzyme substitution therapy is to ensure a normal nutritional status. Therapy of pancreatic insufficiency is based on the oral administration of exogenous pancreatic enzymes. Restriction of fat intake, though traditionally important in conventional treatment, should be reconsidered. Enzyme substitution therapy should ideally mimic the physiological pattern of pancreatic exocrine secretion, and pancreatic enzymes in the form of enteric-coated minimicrospheres are considered as the most elaborated commercially available enzyme preparations. In general, pancreatic exocrine insufficiency in patients after surgery may be managed similarly to patients with chronic pancreatitis. This review focuses on current perspectives in diagnosis and treatment of pancreatic exocrine insufficiency and practical suggestions on its clinical management.
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PMID:Pancreatic exocrine insufficiency: diagnosis and treatment. 2132 92

Chronic pancreatitis is a progressive fibroinflammatory disease that exists in large-duct (often with intraductal calculi) or small-duct form. In many patients this disease results from a complex mix of environmental (eg, alcohol, cigarettes, and occupational chemicals) and genetic factors (eg, mutation in a trypsin-controlling gene or the cystic fibrosis transmembrane conductance regulator); a few patients have hereditary or autoimmune disease. Pain in the form of recurrent attacks of pancreatitis (representing paralysis of apical exocytosis in acinar cells) or constant and disabling pain is usually the main symptom. Management of the pain is mainly empirical, involving potent analgesics, duct drainage by endoscopic or surgical means, and partial or total pancreatectomy. However, steroids rapidly reduce symptoms in patients with autoimmune pancreatitis, and micronutrient therapy to correct electrophilic stress is emerging as a promising treatment in the other patients. Steatorrhoea, diabetes, local complications, and psychosocial issues associated with the disease are additional therapeutic challenges.
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PMID:Chronic pancreatitis. 2139 20

Pancreatic exocrine insufficiency with steatorrhea is a major consequence of pancreatic diseases (e.g. chronic pancreatitis, cystic fibrosis, severe acute necrotizing pancreatitis, pancreatic cancer), extrapancreatic diseases like celiac disease and Crohn's disease, and gastrointestinal and pancreatic surgical resections. Recognition of this entity is highly relevant to avoid malnutrition-related morbidity and mortality. Therapy of pancreatic exocrine insufficiency is based on the oral administration of pancreatic enzymes aiming at providing the duodenal lumen with sufficient amount of active lipase at the time of gastric emptying of nutrients. Administration of enzymes in form of enteric-coated minimicrospheres avoids acid-mediated lipase inactivation and ensures gastric emptying of enzymes in parallel with nutrients. Despite that, factors like an acidic intestinal pH and bacterial overgrowth may prevent normalization of fat digestion even in compliant patients. The present article critically reviews current therapeutic approaches to pancreatic exocrine insufficiency.
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PMID:Pancreatic enzyme replacement therapy for pancreatic exocrine insufficiency: when is it indicated, what is the goal and how to do it? 2145 May 58

We described a 45-year-old previously healthy man presenting with progressively worsening breathlessness for 10 days. Physical examination was suggestive of a left-sided pleural effusion. A chest X-ray was confirmatory. Analysis of aspirated fluid showed a lymphocytic exudate with grossly elevated amylase and lipase levels. CT revealed chronic calcific pancreatitis as the underlying cause of effusion. Retrospective questioning failed to identify classical symptoms of chronic pancreatitis including abdominal pain and steatorrhoea. The patient was managed with intercostal drainage and supportive care. Although unusual, chronic pancreatitis should be kept as a differential diagnosis in patients with unilateral exudative pleural effusion. Elevated fluid levels of amylase and lipase are useful clues to this uncommon diagnosis.
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PMID:Primary presentation of chronic calcific pancreatitis with massive unilateral pleural effusion. 2413 Feb 4

An observational cross-sectional study of 50 cases of chronic calcific pancreatitis patients was conducted in Bangabandhu Sheikh Mujib Medical University (BSMMU) and some other tertiary level hospitals of Dhaka city from August 2008 to July 2010. Patients required laparotomy for different modalities of surgical treatment to manage chronic calcific pancreatitis were included in the study. Biopsy was taken from panceatic duct containing stone during laparotomy to determine the histopathological changes. Among 50 cases female predominance was observed. Male, female ratio was 2:3. Majority (62%) patients were in 20 to 40 years age group. Female presented earlier than male (20-30 years and 30-40 years respectively). All patients complained recurrent attack of epigastric pain. Other presentations were diabetes (74%), malnutrition and weight loss (56%), steatorrhoea (24%) and jaundice (12%). Adenocarcinoma was found in 3(6%) patients (2 male and 1 female) and rests were chronic pancreatitis. Several studies showed the association between chronic calcific pancreatitis and pancreatic cancer. Further large scale study is required to find out the national incidence level.
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PMID:Chronic calcific pancreatitis and pancreatic cancer. 2517

Fibrocalculous pancreatic diabetes (FCPD) is an uncommon form of diabetes that occurs as a result of chronic calcific pancreatitis, in the absence of alcohol abuse. The disease is restricted to tropical regions of the world, and southern India has the highest known prevalence of FCPD. The typical patient with FCPD is a lean adolescent or young adult of either sex, presenting with history of recurrent bouts of abdominal pain and steatorrhea. Demonstration of large, discrete pancreatic calculi by plain radiographs or ultrasonography of the abdomen is diagnostic. While the exact etiology of FCPD is unknown, genetic, nutritional and inflammatory factors have been hypothesized to play a role. Diabetes in FCPD is often brittle and difficult to control; most patients require multiple doses of insulin for control of glycemia. However, in spite of high blood glucose levels, patients rarely develop ketosis. Malabsorption responds to pancreatic enzyme supplementation. Surgical removal of stones is indicated for symptomatic relief of intractable pain. While patients with FCPD develop microvascular complications as frequently as those with type 2 diabetes, macrovascular disease is uncommon. Development of pancreatic malignancy is the most dreaded complication and should be suspected in any patient who complains of weight loss, back pain or jaundice.
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PMID:Fibrocalculous pancreatic diabetes (FCPD). 2539 47


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