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 31,184 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

Seven young patients presenting with diabetic amyotrophy, unusual at their age, are described. Besides symptoms suggestive of proximal muscle weakness and occasionally of diabetes, all patients were underweight; abdominal pain occurred in all the patients. The diagnosis of amyotrophy was confirmed on electromyography and nerve conduction studies in all patients, and muscle biopsy in two patients. All patients recovered fully on control of diabetes with insulin. Only two episodes of stress induced ketosis were recorded in these 7 patients. These patients were not ketotic though they were severely uncontrolled on omission of insulin. They had normal lipid levels, and had no other complications of diabetes. Pancreatic calculi were found in only one patient. We describe here the clinical profiles of these patients and discuss the possible aetiologies of diabetes and the clinical implications.
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PMID:Amyotrophy in young diabetics: clinical profiles. 239 Dec 99

Fibrocalculous pancreatic diabetes of the tropics has not been previously identified in Papua New Guinea where the prevalence of Type 2 (non-insulin-dependent) diabetes is increasing. Four patients with this syndrome:--onset of diabetes before the age of 30 years, low body mass index, radiologic pancreatic calcification and marked hyperglycaemia with resistance to ketosis were recognized over three years at Port Moresby General Hospital. Two patients had a history of recurrent abdominal pain in childhood, and two patients had documented insulin requirement greater than 1.5 U/kg daily, and insulin resistance confirmed by intravenous insulin tolerance test. Plasma C-peptide was present in the three cases tested. In the two patients tested islet cell antibodies were not detected but in both there was a prominent diffuse acinar stain suggestive of antibodies to acinar tissue.
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PMID:Fibrocalculous pancreatic diabetes in Papua New Guinea. 329 81

Severe abdominal pain was the major indication for operation in 85 patients with chronic pancreatitis. Preoperative endoscopic retrograde cholangiopancreatography (50 patients) or intraoperative pancreatic ductograms (44 patients) demonstrated dilated or obstructed major pancreatic ducts in 50 patients (59%), nonvisualization of the distal duct in 10 patients (12%), and normal or small sized ducts in 34 patients (40%). Operative procedures, tailored according to duct morphology, included pancreatic duct drainage (46 patients), subtotal (40% to 80%) pancreatectomy (21 patients), near-total (85% to 95%) pancreatectomy alone (eight patients), and near-total or total pancreatectomy and intrahepatic islet autotransplantation (10 patients). Pancreatic duct drainage resulted in pain relief in 37/46 patients (80%) followed for 6 years. However, 20/46 patients (43%) had continued loss of pancreatic function after duct drainage as measured by the development of insulin-dependent diabetes (16 patients) or steatorrhea (seven patients). Seven years after subtotal pancreatectomy, pain relief was partial in 9/21 patients (43%) and complete in five patients (24%). A higher incidence of hypoglycemic or ketoacidotic complications was noted in patients treated by subtotal pancreatectomy (three patients, 14%) than by duct drainage (one patient, 2%). Near-total pancreatectomy was the most effective surgical procedure in relieving pain, but late sequelae in three patients (38%) included one hypoglycemic death and two ketoacidotic episodes. Five years after near-total pancreatectomy and islet autotransplantation, one patient remained permanently insulin independent; three patients were insulin independent for 4, 5, and 15 months, respectively, but subsequently developed nonketosis-prone diabetes (tested by insulin withdrawal) and require 15 to 30 U of insulin daily; three patients had immediate insulin requirements and currently need 20 to 30 U of insulin per day but are nonketosis prone; and two patients are ketosis prone and require 30 to 60 U of insulin daily. Our analysis suggests that 5-year survival of patients undergoing operation for chronic pancreatitis is similar after treatment by duct drainage, subtotal pancreatectomy, or near-total pancreatectomy, regardless of duct morphology. Five years after duct drainage or subtotal pancreatic resection, a high incidence of diabetes (59% and 48%) and/or continued pain (20%) and (35%) can be expected.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Chronic pancreatitis: long-term surgical results of pancreatic duct drainage, pancreatic resection, and near-total pancreatectomy and islet autotransplantation. 643 70

Because it may be difficult to evaluate gastrointestinal diseases in children with insulin-dependent diabetes mellitus (IDDM), this report highlights several clinical features unique to diabetes and emphasizes the relationship between gastrointestinal pathology and glycemic control. Two children with IDDM are described whose hyperglycemia, ketosis, and abdominal pain were the presenting features of H. pylori-positive duodenal ulcer disease and acute appendicitis, respectively. A third nondiabetic child developed persistent postprandial hyperglycemia as the initial manifestation of dumping syndrome. These patients illustrate the relationship between glycemic control and gastrointestinal pathology in children with diabetes and the effects of gastrointestinal dysfunction on glucose regulation in nondiabetic children. In children with IDDM, gastrointestinal pathology can be confused with ketoacidosis and complicate diabetes control and management. Early recognition and treatment of the underlying gastrointestinal disease often improves glycemic control. Furthermore, severe gastrointestinal dysfunction in nondiabetic children may deleteriously influence glycemic regulation and may be confused with childhood diabetes.
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PMID:Gastrointestinal symptoms and diabetes mellitus in children and adolescents. 907 23

Forty-three cases of diabetic ketosis were analysed to determine the mode of presentation, treatment modalities and outcome. Among these cases 62.8% were non-insulin dependent diabetes mellitus (NIDDM) patients and 37.2% belonged to the insulin dependent diabetes mellitus (IDDM) group. Six patients had blood glucose levels of more than 250 mg/dl but less than 300 mg/dl who were grouped separately for analysis under the term "euglycaemic diabetic ketoacidosis (EGDK)". Infection was the commonest precipitating factor in diabetic ketosis in all groups. Abdominal pain and vomiting occurred with NIDDM and EGDK cases. Drowsiness was common and coma was rare. Acute myocardial infarction (MI) and pulmonary oedema occurred with NIDDM cases. Shock, acidosis, acquired respiratory distress syndrome (ARDS) and mucor mycosis were seen with IDDM cases. Mortality was 7 out of 43(16.3%). Saline requirement was lower in NIDDM and EGDK cases. Intensive insulin therapy with hourly intravenous doses were needed for IDDM cases while majority of NIDDM cases could be managed with 6 hourly doses of insulin given subcutaneously or intramuscularly.
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PMID:Changing profile of diabetic ketosis. 956 97

The histopathology of Fibrocalculous Pancreatic Diabetes (FCPD) has been extensively studied, but there are no reports on alteration in patterns of hormone secreting cells using immunohistochemistry in islets of FCPD patients. In this study, we report on the histopathology and immunohistochemistry of islets of FCPD patients and its possible correlation with the clinical picture. Pancreatic biopsies were carried out in six patients with FCPD at the time of surgery for abdominal pain. Routine histopathology and immunohistochemistry studies were carried out with six primary antibodies namely insulin, glucagon, pancreatic polypeptide (PP), somatostatin, vasoactive intestinal peptide and gastrin. Histopathology of the pancreas showed a spectrum of changes ranging from moderate to severe atrophy, fibrosis of the parenchyma and degeneration of the ducts. Nesidioblastosis was present in three patients. Immunohistochemical studies showed a decrease in the number of islets but some patients showed evidence of hyperplasia. There was an overall decrease in the percent of insulin cells and the positivity in the islets correlated with plasma C-peptide levels and the duration of diabetes. There was no consistent relationship with glucagon with some patients showing increased and other decreased positivity. There was a marked decrease in PP and somatostatin positivity, the significance of which is not clear. The reduction, but partial preservation of insulin positivity is consistent with the ketosis resistance shown by patients with Fibrocalculous Pancreatic Diabetes.
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PMID:Histopathology and immunohistochemistry of pancreatic islets in fibrocalculous pancreatic diabetes. 1113 79

Tropical chronic pancreatitis (TCP) is a juvenile form of chronic calcific non-alcoholic pancreatitis, seen almost exclusively in the developing countries of the tropical world. The classical triad of TCP consists of abdominal pain, steatorrhoea, and diabetes. When diabetes is present, the condition is called fibrocalculous pancreatic diabetes (FCPD) which is thus a later stage of TCP. Some of the distinctive features of TCP are younger age at onset, presence of large intraductal calculi, more aggressive course of the disease, and a high susceptibility to pancreatic cancer. Pancreatic calculi are the hallmark for the diagnosis of TCP and in non-calcific cases ductal dilation on endoscopic retrograde cholangiopancreatography, computed tomography, or ultrasound helps to identify the disease. Diabetes is usually quite severe and of the insulin requiring type, but ketosis is rare. Microvascular complications of diabetes occur as frequently as in type 2 diabetes but macrovascular complications are uncommon. Pancreatic enzyme supplements are used for relief of abdominal pain and reducing the symptoms related to steatorrhoea. Early diagnosis and better control of the endocrine and exocrine dysfunction could help to ensure better survival and improve the prognosis and quality of life of TCP patients.
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PMID:Tropical chronic pancreatitis. 1465 69

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

Fibrocalculous pancreatopathy (FCPP) is a secondary form of diabetes mellitus (DM) with obscure etiology. Recently various gene mutations have been reported in patients with FCPP from the Indian subcontinent. Initially termed tropical pancreatic diabetes, FCPP is uncommon and is characterized by pancreatic calcifications. The diagnosis is made in the third decade of life in most patients with the onset of abdominal pain and DM. We report a female child with DM diagnosed at the age of 3 years who had been managed with insulin but was ketosis resistant. The diagnosis of FCPP was made 3 years later. There were no mutations at N34S and P55S in the SPINK1 gene.
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PMID:Juvenile fibrocalculous pancreatopathy--a patient report. 1699 76


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