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

Sixteen pancreatico-duodenal transplants were performed on 15 insulin-dependent diabetics, aged 25-46, during a 20-month period beginning May 1, 1988. Fourteen patients received a combined cadaveric pancreas/renal transplant with bladder drainage. One patient received a second pancreas transplant 24 hours after the first pancreas graft failed due to portal vein thrombosis. One patient received a pancreas graft 3 years after kidney transplantation. Complications included five cases of hematuria, two bladder leaks, two wound infections, one cytomegalovirus pneumonia, three cases of graft pancreatitis, one pseudocyst, one urine reflux pancreatitis requiring conversion to pancreatico-enterostomy, and two late deaths. Average time to discharge was 17 days following transplant, with 2.9 re-hospitalizations per patient and an average of 38 in-hospital days during the first 6-12 months. Seventeen rejection episodes occurred in 12 patients, diagnosed by declining urine amylase and pH and/or finding of rejection on kidney biopsy. Patient and kidney graft survival is 87 per cent. Pancreas graft survival is 81 per cent (1-20 months follow-up). All patients are insulin-independent and normoglycemic. Mean glycosylated hemoglobin concentration is 4.0 +/- 0.9 post-transplant vs. 7.5 +/- 0.6 pretransplant. Mean serum creatinine is 1.4 +/- 0.7 mg/dl. A new program of pancreas transplantation can be successful in carefully selected diabetic patients, with special attention to avoidance of preservation injury to the pancreas during multiorgan donor procurement. Combined pancreatic/renal transplantation is believed to be the therapeutic treatment of choice in Type I diabetic patients who have impaired renal function and have no significant cardiovascular disease.
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PMID:Pancreas transplantation. A new program. 199 66

In acute pancreatitis the mechanism involved in the auto-amplification of morbid phenomena can be suppressed in most of the cases by inhibiting the pancreatic secretion. This can also enhance the repair of pancreatic, duodenal and jejunal fistulae. On the basis of experimental studies carried out by Johnson, and on the clinical studies of Guttmann, as well as on original studies done by the authors, Ftorafur was included in the complex therapy of acute pancreatitis, and of pancreatic and duodenal fistulae. A group of 14 cases of acute pancreatitis, were treated. These included 5 necrotic-haemorrhagic pancreatitis, and 9 oedematous pancreatitis. The drug was given by continuous intravenous perfusion in doses of 1,200-1,600 mg per day, for a period of 6-12 days. In all the cases the clinical improvement of the patients as well as recovery of normal values of blood amylase were spectacular, and full recovery was achieved in all the cases. Ftorafur was also used in 3 cases of pancreatic fistulae, and in 2 cases of duodenal fistulae, and recovery was also achieved in a very short time. On the basis of this experience, although small, the authors recommend the introduction of Ftorafur in the complex therapy of acute pancreatitis, as well as in that of pancreatic and duodenal fistulae. Following administration of Ftorafur no adverse effects were noted, and in the doses mentioned above this drug did not delay the repair of surgical wounds.
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PMID:[5-fluorouracil treatment of acute pancreatitis and of pancreatic and duodenal fistulae]. 214 91

We investigated the effect of large volume replacement with balanced electrolyte solutions on extravascular lung water (EVLW) in 16 adult surgical patients with sepsis syndrome. Patients entered the study within the 24 h period following surgical interventions for acute necrotizing pancreatitis, intra-abdominal abscesses, and/or peritonitis. Sequential measurements (n = 108) were made at intervals of 6-12 h over a 48 h period. There were no significant differences between initial and final values of thermal-dye EVLW (5.0 +/- 1.1 vs. 5.7 +/- 1.1 ml/kg), plasma colloid osmotic pressure (COP, 13.3 +/- 2.5 vs. 13.2 +/- 2.9 mmHg), pulmonary artery wedge pressure (PAWP, 9.2 +/- 3.0 vs. 10.8 +/- 3.0 mmHg), and COP-PAWP gradient (4.0 +/- 3.5 vs. 2.4 +/- 3.9 mmHg). All results expressed as (mean +/- SD). The EVLW did not correlate with plasma COP, PAWP, or COP-PAWP gradient. We conclude that large volume replacement with balanced electrolyte solutions with the secondary decrease in plasma COP and COP-PAWP gradient do not necessarily contribute to a substantial increase in EVLW. This study fails to show any causal relationship between decrease in plasma COP or COP-PAWP gradient and oedema formation in the lung.
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PMID:Effect of large volume replacement with balanced electrolyte solutions on extravascular lung water in surgical patients with sepsis syndrome. 260 37

The aim of the study was to verify the hypothesis of complete recovery after acute gallstone pancreatitis (a.g.p) and to correlate findings of different diagnostic techniques. Thirty patients, aged 23-82 (mean 53.4 +/- 16.7), underwent a secretin-cerulein test (SCT), ultrasound (US) and computed tomography (CT) of the pancreas 6-12 months and 3-5 years after an attack of a.g.p. Exocrine pancreatic function impairment in SCT was found in 19 (63.3%) patients 6-12 months after a.g.p and in 9 (30%) patients 3-5 years after a.g.p. Imaging techniques revealed pancreatic structure abnormalities (pancreas enlargement, pseudocysts, Wirsung duct dilatation or calcifications) in 33.3% patients (US) and in 56.6% patients (CT) 6-12 months after a.g.p and in 13.3% (both US and CT) in patients 3-5 years after a.g.p. Nevertheless, the combination of recurrent attacks of abdominal pain, severe exocrine pancreatic function impairment requiring enzyme supplementation and pancreatic calcifications in imaging techniques 3-5 years after a.g.p. have been observed only in 4 (13.3%) patients. Those were the patients after multiple attacks of clinically severe, necrotic a.g.p., in which cholecystectomy has not been performed. We conclude that in most cases after acute gallstone pancreatitis pancreatic structure and function gradually return to normal. Nevertheless, patients after multiple episodes of clinically severe a.g.p., with gallbladder in situ should undergo a prospective pancreatic function and structure evaluation in order to early recognize and treat the revealed changes.
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PMID:The natural course of acute gallstone pancreatitis. 908 19

Trypsinogen activation peptide (TAP) is a useful marker of severe acute pancreatitis. However, it is sometimes difficult to detect an elevation of plasma TAP in patients with acute pancreatitis because TAP is rapidly cleared from plasma. Therefore, urine TAP has been evaluated to provide an accurate prediction of the outcome of pancreatitis. In the present study, we examined the time course of plasma and urine TAP simultaneously after induction of taurocholate-induced pancreatitis in rats. Plasma TAP levels peaked at 1 hour after the induction of pancreatitis and then gradually decreased, but was still higher than prepancreatitis levels at 48 hours. Significant increases in urine TAP levels were seen at 0-6, 6-12, and 30-36 hours after induction of pancreatitis. The peak level of urine TAP output and TAP/creatinine ratio was observed at 6-12 and 30-36 hours, respectively. Urine TAP concentration showed a significant correlation with both urine TAP/creatinine ratio and TAP output in urine (p < 0.01). In conclusion, plasma TAP increased immediately after the induction of pancreatitis, but excretion of TAP into urine was delayed several hours in taurocholate-induced pancreatitis in rats. The measurement of urine TAP concentration alone sufficiently can reflect the amount of TAP liberated in the pancreas at initial stage of acute pancreatitis.
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PMID:Urinary excretion of trypsinogen activation peptide (TAP) in taurocholate-induced pancreatitis in rats. 1113 66

Although the association between alcohol and pancreatitis has been recognized for centuries, the precise magnitude of the impact of alcohol remains poorly quantified. Epidemiologic research on this condition has been seriously handicapped by several factors. Classifications are based on morphology rather than on etiology; the diagnostic differences between acute and chronic pancreatitis are imprecise and confusing; and coding by the International Classification of Diseases (ICD) has been inadequate. The current ICD (ICD-10), used in the United States since 1999, identifies alcohol-induced chronic pancreatitis as a separate code for the first time, an enhancement that will greatly improve the quality of data collected in current and future studies. Unfortunately, no code yet exists for acute alcoholic pancreatitis. Of the approximately 2.4 million deaths in the United States in 1999, pancreatitis was listed as the underlying cause for 3289 deaths, making it the 235th leading cause of death. Acute pancreatitis accounted for 84% of these deaths, and chronic pancreatitis the remaining 16%. Alcohol is a primary cause of both acute and chronic pancreatitis in most developed countries. About one-third of acute pancreatitis in the United States is alcohol-induced. In the United States and other developed countries, 60%-90% of chronic pancreatitis is alcohol induced. Both forms are more common in men. The development of chronic pancreatitis is proportional to the dose and duration of alcohol consumption (minimum, 6-12 years of approximately 80 g of alcohol per day). Autopsy studies reveal subclinical chronic pancreatitis in another 10% of alcohol abusers. Yet, since <10% of chronic alcoholics develop chronic pancreatitis, clearly other predisposing factors besides alcohol are involved. Genetic variability and environmental exposures, such as diet, are prime candidates for further investigation. To date, there have been few large epidemiological studies of alcoholic pancreatitis in the United States or other developed countries. Additional studies are needed to improve the quality of existing baseline epidemiologic data and allow better assessment of risk. Improved diagnostic precision, more complete and specific coding, and greater understanding of covariables and mechanisms would also advance the field.
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PMID:The epidemiology of alcohol-induced pancreatitis. 1457 88

Autoimmune pancreatitis (AIP) has been characterized by unique clinical imaging, immunological findings, and the effectiveness of steroid therapy. A set of clinicopathological criteria for AIP was proposed by the Japan Pancreatic Society in 2002, and AIP has come to be widely recognized among general digestive clinicians. However, the indication of steroid therapy for AIP is still not well established, and furthermore the therapeutic doses and method of administration of steroid therapy is also unclear. Recently, an epidemiological survey of all the treatments used for AIP in Japan was conducted by the Research Committee of Intractable Pancreatic Diseases, and their report "Consensus for a Treatment of Autoimmune Pancreatitis" was produced. In a comparison of the results of steroid therapy and nonsteroid therapy for AIP in relation to the rate of complete remission, the recurrence rate, and the period needed to guarantee complete remission, it was thought that the administration of a steroid should be a standard therapy for AIP. However, if the diagnosis of AIP is still uncertain, steroid therapy should be given with caution. In addition, even when AIP still appears to be possible after a course of steroid therapy, a re-evaluation should be carried out taking pancreatic carcinoma into consideration. An initial steroid dose of 30-40 mg per day is recommended. With continuous and careful observations of the clinical manifestations, laboratory data, and imaging findings after administration of the initial dose of steroid for 2-4 weeks, the quantity of steroid can be reduced gradually to a maintenance dose in 2-3 months, and then reduced to 2.5-5 mg per day after remission. The recommended period of maintenance treatment is still unclear, but the administration of the steroid could be stopped after a period of about 6-12 months of treatment, although the patient should be monitored for clinical manifestations of improvement. In addition, the patient's progress should be followed taking recurrence into consideration. In order to evaluate the effectiveness of steroid therapy, follow-up observations should include biochemical examinations of blood findings such as serum gamma-globulin, IgG, and IgG 4, imaging findings, and clinical manifestations such as jaundice and abdominal discomfort.
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PMID:Treatment for autoimmune pancreatitis: consensus on the treatment for patients with autoimmune pancreatitis in Japan. 1752 Feb 24

Recently, autoimmune pancreatitis has been classified into two subtypes. Type 1 is related to immunoglobulin G4 and type 2 is related to granulocytic epithelial lesions, but pathogenetic mechanisms in both still remain unclear. Apart from type 2 autoimmune pancreatitis, the pathological features of type 1 autoimmune pancreatitis with increased serum immunoglobulin G4/immunoglobulin E levels, abundant infiltration of immunoglobulin G4+plasmacytes and lymphocytes, fibrosis, and steroid responsiveness are suggestive of abnormal immunity such as allergy or autoimmunity. Although pathophysiological conditions seem to be different in each, both respond well to steroid drugs. After remission, the patients with type 1 autoimmune pancreatitis show high relapse rates (30-50% within 6-12 months), whereas those with type 2 autoimmune pancreatitis seldom relapse. After remission, the steroid maintenance therapy and therapeutic strategy for relapsing patients with type 1 is different among local expertise. In this paper, recent advances in pathogenesis and clinical guidance for therapy are discussed.
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PMID:Autoimmune pancreatitis: pathogenesis, latest developments and clinical guidance. 2479 Jul 26