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

In the majority of patients suffering from chronic pancreatitis an endocrine pancreatic insufficiency is correlated with exocrine dysfunction. The prevalence of impaired or diabetic glucose tolerance is 40-70%, half of these patients suffer from an insulin-dependent diabetes mellitus. In general the probability of endocrine insufficiency progressively increases within the ten years following diagnosis of chronic pancreatitis. Onset and severity of the endocrine dysfunction depend on parenchymal destruction of the pancreas but are also influenced by ongoing alcohol consumption. Pathological findings in the endocrine pancreas are a loss of B-cells with decrease in secretion of insulin but also a loss of B-cell responsiveness to glucose by impaired perisinusoidal diffusion. Disturbances of the enteroinsulinar axis with diminished levels of incretins due to an exocrine insufficiency are also discussed. In addition, an impaired A-cell function may be important, that is characterized by diminished levels of stimulated glucagon. Increased plasma levels of somatostatin were found, the source of which is unknown. The susceptibility to severe hypoglycemia in patients with diabetes mellitus secondary to chronic pancreatitis is higher than in Type I diabetics. This is mainly caused by the impaired glucagon secretion but also influenced by malnutrition and concomitant hepatic dysfunction due to the toxic affect of alcohol. Diagnostic procedures are the measurement of C-peptide-concentrations and profiles of blood glucose after fasting and stimulation with L-arginine or glucose. Especially in the beginning of the endocrine insufficiency the determination of basal levels of blood glucose or C-peptide are not useful. Unless treatment by diet is effective, the therapy of diabetes secondary to chronic pancreatitis should be done by insulin replacement. A certain degree of hyperglycemia may be tolerated due to the risk of hypoglycemia and the persistent alcohol consumption in these patients. Intensified insulin therapy should only be done in selected patients with good compliance. Long-term complications in patients with pancreatogenic diabetes are comparable to diabetes Type I and largely depend on the duration of the diabetes. Life expectancy is reduced, death in these patients is mainly due to persistent alcohol and nicotine abuse (cardiovascular disease, malignant tumors, etc.), in only a minority pancreatitis or diabetes (mainly hypoglycaemia) are relevant risk factors.
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PMID:[Secondary diabetes in chronic pancreatitis]. 1044 9

Alcohol consumption is the most important etiological factor of chronic pancreatitis (around 70%). Smoking, ethnic-racial predispositions, diets high and low in fat and high in protein may also contribute to the development of chronic pancreatitis. Non-alcoholic chronic pancreatitis of unknown cause makes up 10% to 30% of patients with chronic pancreatitis. Two subgroups have been reported: juvenile (about 25 years) and senile (up 65 years). Tropical pancreatitis has been observed in children and young men in many African and Asian countries. This disease develops because of fat and protein deficiency or nutritional deficiency in general, also due to cyanogenes present in cassava. Hereditary chronic pancreatitis is a rare disease connected with autosomal transmissions. Dr Whitcomb reported, that hereditary chronic pancreatitis developed because of trypsines mutation. Mutant "hypertrypsin" is not inactivated by enzymes; this way it leads to pancreas autodigestion. Obstructive chronic pancreatitis is caused by longterm pancreatic ducts obstruction. In many rare causes leading to chronic pancreatitis among other are: hypercalcaemia, hyperlipoproteinemia, some drugs and pancreatitis associated with autoimmune disorders. Newest information about etiology and pathogenesis of chronic pancreatitis is yielded by recent immunohistochemical research. This research shows increasing irregular improper antigens expression of class I and/or class II MHC in pancreas as well as the role of Transforming Growth Factor Alpha in chronic pancreatitis development. This illness is still a puzzling problem.
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PMID:[Contemporary opinions on the etiology of chronic pancreatitis]. 1050 45

Lipoprotein lipase (LPL) plays a crucial role in the regulation of lipoprotein metabolism by hydrolyzing the core triglycerides of circulating chylomicrons and very low-density lipoprotein. Deficiency in this enzyme usually results in disturbances in lipid levels. To understand the molecular defect that leads to a functional deficiency of LPL in patients with hypertriglyceridemia, we looked for mutations of the LPL gene by means of single-strand conformation polymorphism (SSCP) analysis and direct DNA sequencing in 24 patients. A single base C-->G substitution in codon 252 of the LPL gene, encoding a change of a leucine to a valine residue in the mature protein, was found in three women who had hypertriglyceridemia and recurrent pancreatitis. Two of these patients, who were homozygous for the L252V mutation, had variable and occasionally severe hypertriglyceridemia with undetectable or very low LPL activities, respectively. The third woman was heterozygous for this mutation. All three patients had poor post-heparin LPL activity. Site-directed mutagenesis experiments provided in vitro evidence that the mutation of codon 252 was responsible for the loss of LPL activity. In conclusion, we identified a novel LPL mutation that results in decreased LPL activity in Taiwanese patients with hypertriglyceridemia. The assessment of a causative link between the mutation and hyperlipidemia awaits further studies.
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PMID:Newly identified missense mutation reduces lipoprotein lipase activity in Taiwanese patients with hypertriglyceridemia. 1056 Feb 36

METHODS: Evaluated are surgical difficulties, management problems and weight loss in patients with distal gastric bypass as a revisionary procedure. Eighty patients were followed up to 3 years; four were lost to follow-up. Mean age was 43; mean prebariatric surgery weight 134 kg; height 1.65 meters; body mass index 40.1; ideal body weight 62.7 kg; excess weight 70.5 kg; per cent excess weight 214%. A 250 cm stomach-to-ileocecal valve segment of small bowel was used, and the biliopancreatic secretions were brought into the terminal ileum 100 6 in from the ileocecal valve. Mean pouch size was 63 cc; length of hospital stay 5 days; operative blood loss 616 cc; operative time 130 min. RESULTS: Intraoperative complications included three splenic injuries (without splenectomy). Early complications included one deep vein thrombosis, two marginal ulcers, one GI hemorrhage, one wound dehiscence, one pouch outlet obstruction and one pancreatitis. Late complications included: one death from protein malnutrition/ ARDS; 21 hypoproteinemia; six protein malnutrition, and of these, three had hyperalimentation; three cholecystitis; 27 anemia; 22 incisional hernia; two staple-line disruption (reoperated); 26 low serum iron; 11 prolonged (>6 months) diarrhea; three prolonged frequent vomiting; and two unrelated deaths (chronic myelogenous leukemia and amyotrophic lateral sclerosis). Mean excess weight loss was 83% at 12 months; 89% at 24 months; and 94% at 36 months. CONCLUSION: The distal gastric bypass is fraught with the operative and immediate post-operative complications experienced in any revisionary bariatric surgery. Distal gastric bypass is very effective in producing long-term weight loss. Nutritional problems are common but usually easily corrected. The most serious nutritional complication is protein malnutrition, which must be identified and corrected early. Success of this procedure is dependent upon patient compliance with proper nutrition and supplements, and regular office follow-up with monitoring of laboratory data. Patients who are noncompliant are at significant risk for complications.
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PMID:The Gastric Bypass for Failed Bariatric Surgical Procedures. 1072 55

The First Surgical Clinic of the First Medical Faculty Charles University and General Faculty Hospital Prague made operations of the pancreas ever since 1971. In the work sooner or later all approaches to surgical treatment of pancreatitis were reflected. The authors present a brief review of results and their own experience since 1994 when duodenum sparing operations were introduced. Indications for surgical treatment were based on the diagnosis by US, CT and ERCP, in exceptional cases MR, after evaluation by a pancreatologist, roentgenologist and surgeon. The group of patients with chronic pancreatitis was extended by 15 patients from a group operated because of preoperative suspicion of a malignant pancreatic tumour not confirmed during and after surgery. In those Whipple's operation was performed. The same operation was performed in three patients with chronic pancreatitis with serious changes in the area of the head of the pancreas. In 111 patients a drainage and duodenum sparing operation was performed. Of these in 46x according to Neger, 9x according to Frey, 10x modification of these operations, 37x Partington-Rochelle's procedure. The authors did not record postoperative complications after the classical Beger operation and the hospital stay was on average by five days shorter as compared with the classical method of Whipple. When evaluating postoperative complaints and problems (pain, malnutrition, physical constitution and social position) the authors recorded equally favourable results as after non-complicated duodenopancreatectomy. They varied, depending on the patient s co-operation round 87% while after longitudinal drainage of the duct a satisfactory result was recorded in 78% of the operated patients. The authors consider Beger's operation logical because of the removal of the main tissue mass of the head of the pancreas, responsible for pain, complications caused by fibrosis in the area round the bile duct and duodenum, responsible for the deterioration of the compartment syndrome in the left half of the gland. Its result is destruction of the remainder of exocrine and endocrine tissue. Of 170 operated patients one patient with decompensated diabetes died. Based on their own experience the authors do not consider repeated re-operations an absolute contraindication of Beger's operation when conditions permit. A problem is, in their opinion, fibrosis in the vicinity of the pancreas and portal overpressure.
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PMID:[6 years' personal experience with duodenum-sparing procedures in chronic pancreatitis]. 1096 70

Lipoprotein lipase (LPL) is the rate-limiting enzyme for the hydrolysis of triglycerides and the subsequent uptake of free fatty acids in extrahepatic tissues. Deficiency of LPL in humans (Type I hyperlipoproteinemia) is associated with massive chylomicronemia, low high density lipoprotein (HDL) cholesterol levels, and recurrent attacks of pancreatitis when not controlled by a strict diet. In contrast to humans, homozygous LPL knock-out mice (L0) do not survive suckling and die between 18 and 24 h after birth. In this study, an adenovirus-based protocol was utilized for the transient expression of LPL during the suckling period in an effort to rescue L0 mice. After a single intraperitoneal injection of 5x10(9) plaque-forming units of LPL-expressing virus immediately after birth, more than 90% of L0 mice survived the first days of life. 3% of L0 mice survived the entire suckling period and lived for up to 20 months, although LPL activity in mouse tissues and postheparin plasma was undetectable in all animals after 6 weeks of age. Adult LPL-deficient mice were smaller than their littermates until 2-3 months of age and exhibited very high triglyceride levels in the fed (4997 +/- 1102 versus 113.4 +/- 18.7 mg/dl) and fasted state (2007 +/- 375 versus 65.5 +/- 7.4 mg/dl). Plasma total cholesterol levels, free fatty acids, and ketone bodies were elevated in L0 mice, whereas plasma glucose was normal. Most strikingly, L0 mice lacked apoA-I-containing prebeta-HDL particles as well as mature HDL resulting in undetectable HDL cholesterol and HDL-apoA-I levels. HDL deficiency in plasma was evident despite normal apoA-I mRNA levels in the liver and normal apoA-I protein levels in plasma, which were predominantly found in the chylomicron fraction. The absence of prebeta-HDL and mature HDL particles supports the concept that the lipolysis of triglyceride-rich lipoproteins is an essential step for HDL maturation.
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PMID:Adenovirus-mediated rescue of lipoprotein lipase-deficient mice. Lipolysis of triglyceride-rich lipoproteins is essential for high density lipoprotein maturation in mice. 1143 68

Tropical chronic pancreatitis is a form of idiopathic chronic pancreatitis that has not previously been described in Spain. Typically it is related to dietary factors and malnutrition, although genetic factors may also play a significant role in the development of the disease. We report a case of chronic tropical pancreatitis in a 27-year-old woman from the Dominican Republic domiciled in Spain since 1992. The patient was admitted to our hospital for acute pancreatitis that fulfilled the diagnostic criteria (clinical and radiological) for chronic tropical pancreatitis. This case has led us to review this uncommon entity. Because of the increasing number of immigrants from tropical countries, chronic tropical pancreatitis will probably need to be taken into account in the differential diagnosis of chronic pancreatitis in our patients.
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PMID:[Tropical chronic pancreatitis in a young patient]. 1172 20

The case of a 24 year-old Comorian male patient consuming large amounts of cooked and uncooked cassava and suffering of malnutrition since his boyhood is reported. The patient presented a diabetes mellitus by chronic calcific pancreatitis with retinopathy and neuropathy. The protein deficiency associated with eating uncooked cassava may be recognised as a factor of calcific pancreatitis diabetes. Other factors might be associated such as the environment as well as immunological and genetic characteristics.
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PMID:[Is manioc a diabetogenic factor? Apropos of a case of diabetes mellitus with a large consumption of crude manioc]. 1184 23

Malnutrition may develop in acute pancreatitis (AP), accompanied by hypermetabolism and high nutritional requirements, and in chronic pancreatitis (CP). We measured the incidence of protein malnutrition in AP and CP by comparing different serum biomarkers of protein metabolism and inflammation. Thirty-five patients with acute (27 moderate, 8 severe), and 35 with chronic, pancreatitis were enrolled in the study. Serum transthyretin, albumin, transferrin and C-reactive protein (CRP) concentrations were measured in AP at admission, after 1 and 2 weeks of jejunal feeding, and in patients with CP at follow-up. In AP, at admission the transthyretin level was low in 74%, transferrin in 48%, and albumin in 29% of patients. In severe pancreatitis, transthyretin levels were significantly lower than in moderate forms (7.5 +/- 2.43 vs. 14.39 +/- 6.8 mg/dl, p < 0.005). Transthyretin levels increased significantly after 2 weeks of jejunal feeding (p < 0.05). In CP, transthyretin levels were decreased in 37%, transferrin in 27%, and albumin in 12% of patients. We found significantly lower transthyretin levels in alcohol-related CPthan in other forms (18.5 +/- 8.3 vs. 30.2 +/- 5.7, p < 0.01). Transthyretin correlated positively with albumin and transferrin and negatively with CRP Transthyretin seems to be a sensitive biomarker of protein status and metabolic stress. Monitoring nutritional status through measurement of serum proteins is important for optimal treatment of AP and CP.
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PMID:Protein status in pancreatitis--transthyretin is a sensitive biomarker of malnutrition in acute and chronic pancreatitis. 1255 37

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


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