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

Chronic pancreatitis is defined by a persistent destruction of the pancreatic parenchyma replaced by fibrosis. The lesions generally start in the exocrine gland, islets being attacked later in the fibrosis. The two most frequent forms are: 1. Chronic calcifying pancreatitis which is a pancreatic lithiasis responsible for more than 95% of chronic pancreatitis. In its most frequent form, calculi are built up of more than 98% calcium salts together with fibres of a degraded residue of lithostathine, a secretory protein. This disease is related (i) in most countries to alcohol, protein, fat and tobacco and (ii) in certain tropical countries to malnutrition (low-fat, low-protein diet) for some generations. A causative role for cassava and kwashiorkor is improbable. The mechanism of calcium precipitation is partly explained by the calcium-saturation of pancreatic juice and the decreased biosynthesis of lithostathine S, the secretory protein preventing crystallization. As a rule, diabetes (and steatorrhoea) appear after a clinical evolution characterized by recurrent attacks of upper abdominal pain, generally lasting some days with transiently increased concentrations of pancreatic enzymes in serum. When diabetes appears, pain frequently disappears. Complications are mostly observed in the first 10 years of clinical evolution. 2. Obstructive pancreatitis is due to an obstacle (tumours, scars) in the pancreatic duct. It is rarely a cause of diabetes. Diabetes due to chronic pancreatitis is characterized by the low incidence of ketosis and the high incidence of insulin-induced hypoglycaemia. Patients are generally thin. Serum insulin levels, either basal or stimulated, are decreased. Glucagon is less affected. Angiopathies and retinopathies are less frequent than in non-insulin-dependent diabetes. Neural complications are fairly frequent. The diagnosis is generally easy because diabetes appears at a late stage of the disease. The treatment generally requires insulin.
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PMID:Chronic pancreatitis and diabetes. 144 67

Non-insulin-dependent (type II) diabetes mellitus is an inherited metabolic disorder characterized by hyperglycemia with resistance to ketosis. The onset is usually after age 40 years. Patients are variably symptomatic and frequently obese, hyperlipidemic and hypertensive. Clinical, pathological and biochemical evidence suggests that the disease is caused by a combined defect of insulin secretion and insulin resistance. Goals in the treatment of hyperglycemia, dyslipidemia and hypertension should be appropriate to the patient's age, the status of diabetic complications and the safety of the regimen. Nonpharmacologic management includes meal planning to achieve a suitable weight, such that carbohydrates supply 50% to 60% of the daily energy intake, with limitation of saturated fats, cholesterol and salt when indicated, and physical activity appropriate to the patient's age and cardiovascular status. Follow-up should include regular visits with the physician, access to diabetes education, self-monitoring of the blood or urine glucose level and laboratory-based measurement of the plasma levels of glucose and glycated hemoglobin. If unacceptably high plasma glucose levels (e.g., 8 mmol/L or more before meals) persist the use of orally given hypoglycemic agents (a sulfonylurea agent or metformin or both) is indicated. Temporary insulin therapy may be needed during intercurrent illness, surgery or pregnancy. Long-term insulin therapy is recommended in patients with continuing symptoms or hyperglycemia despite treatment with diet modification and orally given hypoglycemic agents. The risk of pancreatitis may be reduced by treating severe hypertriglyceridemia (fasting serum level greater than 10 mmol/L) and atherosclerotic disease through dietary and, if necessary, pharmacologic management of dyslipidemia. Antihypertensive agents are available that have fewer adverse metabolic effects than thiazides and beta-adrenergic receptor blockers. New drugs are being developed that will enhance effective insulin secretion and action and inhibit the progress of complications.
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PMID:Non-insulin-dependent (type II) diabetes mellitus. 174 94

The tropical calcifying pancreatitis and/or fibrous pancreatitis are responsible for a number of cases of juvenile insulin-dependent diabetes in the Third World countries. World wide distributed in the tropical areas of Asia, Africa and South America, they can also be observed in Europe, in migrants from these countries. Intensive epidemiological and biochemical studies are currently developed in order to shed light on the many obscure points. Classification of the typical calcifying pancreatitis and the related syndromes is a matter of debate. The pathological basis is calcification of the pancreas and echography of the gland may become a cheap convenient relatively specific tool for epidemiology. The clinical syndrome consists of chronic painful pancreatic episodes since childhood, associated with pancreatic exocrine insufficiency, followed by the onset, during adolescence, of diabetes mellitus, which is most of the times insulin dependent. Patients' history is free of chronic alcoholism, but includes constantly chronic caloric and proteic malnutrition. Although insulin dependent this diabetes in not prone to ketosis, due presumably to carnitine deficiency and relative glucagon deficiency (or suppressibility). Insulin resistance is traditionally noted, the pathophysiology of which is unknown. The mechanism of calcification appearance is also undetermined. Either a deficiency in pancreatic stone protein, or the toxic effect of cyanogen glucosides present in cassava and other tropical foodstuffs, or the malnutrition-related deficiency in sulphur-containing aminoacids may be causal factors. No valid experimental model of the disease is available.
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PMID:[Diabetogenic tropical pancreatitis]. 304 66

A diabetic patient is described who presented with the bizarre biochemical association of hyperglycaemia, ketosis and severe alkalosis. Investigation revealed hypercortisolaemia due to ectopic adrenocorticotrophic hormone secretion from an oat cell carcinoma of the bronchus and post-mortem studies demonstrated clinically unsuspected resolving pancreatitis. a possible mechanism for the metabolic upset is discussed.
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PMID:Diabetic ketoalkalosis due to ectopic ACTH production from an oat cell carcinoma. 627 31

Serum amylase shows the greatest increase among the various pancreatic enzymes that increase at the onset of acute pancreatitis. However, the diagnostic value of the total serum amylase activity has been questioned due to its lack of specificity. To differentiate hyperamylasemia due to pancreatic disease from that due to other causes, the activity of pancreatic amylase should be determined by using a monoclonal antibody that specifically binds to pancreatic or salivary amylase, or by electrophoresis. The most useful and accurate method for distinguishing pancreatic from salivary-type hyperamylasemia is isoamylase analysis by electrophoresis. In patients with acute pancreatitis, increase of Amylase-1 and -2 is accompanied by the appearance of Amylase-4, a minor component of the pancreatic-type isoamylases, and by disappearance of the salivary-type isoenzymes, thereby leaving a pattern of the pancreatic isoenzymes alone. This pancreatitis pattern persists for about 10 days after the onset of illness. Therefore, if such a pattern is found in a patient with clinical findings suggesting acute pancreatitis despite a normal serum amylase level, the patient can be diagnosed as having acute pancreatitis or a recent attack of the disease. However, the existence of an inherited trait of the pancreatitis pattern in some healthy individuals must be borne in mind. Patients with recurrent chronic pancreatitis also show pancreatic-type hyperamylasemia, whereas the pancreatic amylase activity decreases when pancreatic exocrine insufficiency progresses. Hyperamylasemia due to elevated salivary amylase activity is also common in patients with diabetic ketosis or malignancies such as lung cancer (adenocarcinoma). Hyperamylasemia is also found following various types of operation. In most cases, it is salivary-type hyperamylasemia.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Usefulness of amylase isoenzyme determination for the diagnosis of pancreatic diseases]. 754 79

The exocrine and endocrine pathophysiology of chronic calcific pancreatitis of the tropics (CCPT) remains elusive. The objective of this study was to evaluate the spectrum and correlates of the exocrine and endocrine pancreatic dysfunction in CCPT. Thirty-seven consecutive patients with a clinico-radiological diagnosis of CCPT were stratified into three subgroups: CCPT-normal glucose tolerance (NGT), CCPT-abnormal glucose tolerance (IGT) and CCPT-diabetes mellitus (DM). Ten ketosis resistant young diabetic (KRDY) patients, 10 classical insulin dependent diabetes mellitus (IDDM) patients and 18 healthy matched controls were included for comparison. Fecal chymotrypsin (FCT) levels and blood C-peptide levels (basal and post i.v. glucagon stimulation) were estimated for assessing the exocrine and endocrine pancreatic functions, respectively. Sonography was performed to evaluate the pancreatic size and ductal diameter. Pancreatic exocrine-endocrine correlation was examined by studying the C-peptide/fecal chymotrypsin ratio (CP/FCT) (CP/FCT of normal controls = 1). Mean FCT levels in all 3 subgroups of CCPT (NGT: 3.4 micrograms/g; IGT: 0.82 microgram/g; DM: 2.4 micrograms/g) were very low (87-96% reduction in exocrine pancreatic dysfunction; mean FCT in healthy controls was 22.8 micrograms/g) (P < 0.0001). In contrast, KRDY and IDDM patients displayed 50-54% reduction in pancreatic acinar function (P < 0.001). Basal and stimulated C-peptide levels progressively fell in the 3 CCPT subsets (NGT: 0.23 and 0.46 > IGT: 0.14 and 0.29 > DM 0.10 and 0.14) (P < 0.01). CCPT patients exhibited pancreatic atrophy and ductal dilation (> 3 mm).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Chronic calcific pancreatitis of the tropics (CCPT): spectrum and correlates of exocrine and endocrine pancreatic dysfunction. 760 50

The relationship between tropical calcific pancreatitis (TCP) and fibrocalculus pancreatic diabetes (FCPD) is still unclear. The clinical, biochemical and radiological data of age-matched TCP and FCPD subjects have been briefly discussed in the present review. Fibrocalculus pancreatic diabetes patients present with a significantly lower BMI compared with TCP patients. Analysis of the family history reveals that some kind of environmental factors seem to play a predominant role in the development of diabetes in FCPD patients, although these factors remain to be identified. Both TCP and FCPD patients predominantly come from a rural background. Fasting and 2 h blood glucose values as well as fructosamine levels in FCPD patients are approximately four-times higher than those of TCP patients. Measurements of early renal haemodynamic and microvascular changes (glomerular filtration rate, kidney size, microalbuminuria and microtransferrinuria) indicate an early renal involvement in FCPD patients. Tropical calcific pancreatitis subjects have approximately twice as high fasting C-peptide values compared with FCPD patients. Findings of single stranded DNA measurements suggest the involvement of oxidative damage in FCPD patients. Ketosis resistance is the most conspicuous clinical feature in the FCPD group and this relative absence of ketosis is probably due to a defect in the ketone body synthesis pathway and/or in the regulation of counterbalancing hormones. Endoscopic retrograde pancreatography findings of TCP and FCPD patients suggest that FCPD should not be considered only as a form of secondary diabetes consequent to generalized pancreatic damage in TCP.
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PMID:Tropical calcific pancreatitis and fibrocalculus pancreatic diabetes in Bangladesh. 919 12

Many animals with diabetes mellitus are severely ill on clinical presentation. The spectrum of disease is quite variable and includes diabetic ketoacidosis (DKA), ketosis without acidosis, hyperosmolar nonketotic syndrome (HNKS), and other nonketotic variants (negative urine ketones, serum osmolality < 340 mOsm/kg with or without acidosis). These more severe forms of diabetes are often precipitated by concurrent diseases such as pyelonephritis, pancreatitis, pyometra, hyperadrenocorticism, renal failure, and heart failure. To make matters worse, in-hospital treatment of diabetic dogs and cats is commonly associated with serious complications, including hypoglycemia, hypokalemia, and hypophosphatemia.
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PMID:Complications and concurrent disease associated with diabetes mellitus. 1088 75

Tropical chronic pancreatitis represents a juvenile nonalcoholic form of chronic pancreatitis prevalent in many tropical developing countries. Tropical chronic pancreatitis differs from temperate zone pancreatitis in its younger age of onset, more accelerated course, higher prevalence of pancreatic calculi and diabetes, and greater propensity to pancreatic malignancy. The diabetic stage of the disease is referred to as fibrocalculous pancreatic diabetes. The diabetes is severe and insulin requiring although ketosis resistant. Diabetic complications occur in fibrocalculous pancreatic diabetes just like in other primary forms of diabetes. The etiology of tropical chronic pancreatitis remains unclear, although malnutrition along with dietary cyanogen toxicity, antioxidant deficiency, and a genetic predisposition have been proposed. In the last few decades, the prognosis has markedly improved as a result of better management of diabetes. Yet a better understanding of the pathogenesis of tropical chronic pancreatitis could further improve treatment options and offer an opportunity for prevention of this disorder, which leads to severe morbidity in a large proportion of affected patients.
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PMID:Tropical chronic pancreatitis: an update. 1264 42

Tropical pancreatitis is a special type of chronic pancreatitis that is seen mainly in tropical countries. The prevalence of tropical pancreatitis is about 126/100,000 population in southern India. It occurs usually in young people, involves the main pancreatic duct and results in large ductal calculi. The etiology is not known, but genetic mutations such as the SPINK1 gene mutation and environmental factors are likely causes. Clinically, >90% of patients present with abdominal pain. About 25% of patients develop diabetes which generally requires insulin for its control but is ketosis-resistant. Painless diabetes is another clinical presentation in some patients. Most patients develop malnutrition during the course of the disease. Steatorrhea is less common. Patients with tropical pancreatitis may develop pancreatic cancer as a long-term complication. The diagnosis can be established by plain radiography of the abdomen, ultrasonography, computerized tomography scan of the abdomen or endoscopic retrograde cholangiopancreatography. Management is directed towards relief from pain and control of diabetes and steatorrhea. Pain relief can be obtained by analgesics and enzyme supplementation with preparations rich in proteases. Endotherapy coupled with stone fragmentation by extracorporeal shock wave lithotripsy is an effective therapy for those who fail to respond to medical therapy. Surgical decompression of the main pancreatic duct by lateral pancreato-jejunostomy is reserved for patients with severe pain non-responsive to other forms of therapy.
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PMID:Tropical pancreatitis. 1575 8


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