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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

The aim of the present study is to assess the frequency of pancreas divisum and the features of patients with pancreas divisum in order to assess the role of this anomaly in the occurrence of pancreatitis. A total of 1049 endoscopic retrograde pancreatographies were studied between 1978 and 1988. Patients with pancreas divisum were studied in terms of their clinical findings and their disease (pancreatitis or not). Pancreas divisum was diagnosed in 62 patients (5.9%). No statistical differences with regard to age and sex were found between patients with and without pancreas divisum. The frequency of pancreas divisum was similar in the different groups of disease, especially chronic pancreatitis, acute pancreatitis, recurrent pancreatitis and idiopathic pancreatitis. The study of pancreatograms showed that dorsal ductal abnormalities alone were found as frequently as ventral alterations alone. Our results show that pancreas divisum cannot be directly implicated in the occurrence of pancreatitis, and should not prompt a systematic sphincterotomy of the accessory papilla. This treatment should only be considered in the rare cases of acute recurrent idiopathic pancreatitis with dorsal ductal dilatation and stenosis of the accessory papilla.
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PMID:Pancreas divisum and pancreatitis: a coincidental association? 205 15

Few data exist regarding nutritional assessment during pancreatic abscess. We compared nonprotein caloric requirements calculated by Harris-Benedict equation and measured by indirect calorimetry in patients with pancreatic abscess. Seven patients with pancreatitis and pancreatic abscess had determinations of resting energy expenditure via Medicor metabolic cart with 20% added for activity. Caloric requirements were also estimated using the Harris-Benedict equation with stress factors. Determinations from indirect calorimetry ranged from 22.4-46.8 (mean 36.1) kcal/kg/d. Harris-Benedict calculations with stress factor 1.7 differed from indirect calorimetry by at least 15% in seven of ten determinations. Stress factor 1.9 results overestimated indirect calorimetry by over 25% in four of ten determinations. Energy requirements via indirect calorimetry of some patients with pancreatic abscess cover a wide range and do not correlate with Harris-Benedict calculations. Harris-Benedict equation with a stress factor of 1.9 may estimate adequate nonprotein calories for hyperalimentation, but there is risk of overfeeding.
Pancreas 1990
PMID:Nonprotein caloric requirements for patients with pancreatic abscess as measured by indirect calorimetry. 210 57

We reported two cases of acute recurrent pancreatitis lasting for 8 and 10 years, respectively, and characterized by acute abdominal pain associated with an increased serum level of pancreatic enzymes and in one case transient enlargement of the pancreas on sonography and CT scan. Exocrine and endocrine pancreatic function remained normal. Pain attacks were associated with headache or typical migraine, myalgia, pruritus, and diarrhea. In one case only, the IgE serum level was increased. In both cases, the symptoms were reproduced in the 2 h following the consumption of some particular food and cured for years by the suppression of this food and the use of cromoglycate, but recurred 1 month to 3 years after this treatment was stopped, to be again healed by the same treatment. We suggest that these cases are due to food allergy and that food allergy could be a rare cause of acute recurrent pancreatitis. Responsible foods were beef (twice), milk, potato, fish, and eggs, which is in agreement with the frequency of food allergens in southwestern Europe.
Pancreas 1990 Mar
PMID:Is food allergy a cause of acute pancreatitis? 210 39

Serum apolipoprotein A-I measurement was compared in alcoholic patients according to presence or absence of chronic pancreatitis and liver fibrosis. Among alcoholic patients without liver disease, apolipoprotein A-I was significantly lower in patients with chronic pancreatitis (157 +/- 70 mg/dl) than in patients without pancreatitis (209 +/- 74 mg/dl, p less than 0.001). In cirrhotic patients, apolipoprotein A-I was lower in patients with chronic pancreatitis (82 +/- 35 mg/dl) than in patients without pancreatitis (102 +/- 45 mg/dl), but this difference was not significant. The decrease of serum apolipoprotein A-I was independent of nutritional parameters whether or not there was cirrhosis. Immunohistochemical study of pancreatic samples with chronic pancreatitis showed that apolipoprotein A-I was located in the pancreatic fibrosis whereas lobules were unstained. This study suggests that apolipoprotein A-I is trapped by the pancreatic extracellular matrix and that this sequestration might explain, in part, the decrease of the serum apolipoprotein A-I.
Pancreas 1990 Sep
PMID:Serum apolipoprotein A-I in alcoholic patients with chronic calcifying pancreatitis. 212 44

A series of 10 cases of chronic calcifying pancreatitis from central Tunisia are reported. The mean age at presentation was 23 years and the male to female ratio was 1.5. The main clinical manifestations of the disease were abdominal pain (eight cases), weight loss (four cases), and diarrhea (three cases). Diabetes was recorded in four cases. The etiological investigations yielded negative results in all the patients. It is concluded that central Tunisia should be added to the regions where juvenile chronic calcifying pancreatitis of the "tropical type" may be observed.
Pancreas 1990 May
PMID:Juvenile idiopathic chronic calcifying pancreatitis: report of 10 cases from central Tunisia. 218 58

Monoclonal antibodies specific for luminal plasma membranes of acinar and duct cells of the exocrine pancreas were used to investigate changes in antigen expression during regeneration of the pancreas after acute pancreatitis and during fetal pancreatic development in mice. During regeneration after acute pancreatitis induced by supramaximal injections of cerulein or by a choline-deficient, ethionine-supplemented diet, morphologically identifiable acinar cells expressed the ductal antigen on their luminal surface, but at a lower level than this antigen is expressed on duct cells. As the pancreas regenerated, the ductal antigen was lost from acinar cells and was found only on duct cells. Characteristic tubular complexes formed in both pancreatitis models and were positive for the acinar antigen, demonstrating their acinar origin. In fetal pancreas, acinar cells between prenatal days 3 through 1, when zymogen granules were already abundant, expressed the duct-cell antigen on their luminal surface. By birth duct antigen was mostly present on ducts with only occasional label on acinar cells. The presence of a ductal antigen on acinar cells is associated with acinar-cell growth during regeneration and during fetal development and may reflect a less differentiated state.
Pancreas 1990 Jul
PMID:Growing pancreatic acinar cells (postpancreatitis and fetal) express a ductal antigen. 219 65

We created acute pancreatitis in cats by instilling ethanol (20 ml of a 40% solution) into the stomach and then perfusing activated pancreatic enzymes through the main pancreatic duct. Edematous pancreatitis developed within 24 h as the enzymes leaked out of the duct into the surrounding pancreatic parenchyma. We tested the effects of a number of agents on the amelioration of the severity of the pancreatic inflammation. Cimetidine (an H2 receptor blocker) and Benadryl (an H1 receptor blocker) given in combination decreased the incidence of pancreatic hemorrhage but not the overall degree of inflammation. Indomethacin (a cyclooxygenase inhibitor) had a similar effect. Terbutaline (a beta-agonist) given alone decreased the overall degree of inflammation, including the incidence of hemorrhage. All of the drugs given together were no more effective than terbutaline alone. The combination was effective even when given up to 12 h after the onset of pancreatitis.
Pancreas 1990 Sep
PMID:Treatment of acute alcoholic pancreatitis in cats. 223 68

Forty-nine patients with tropical calcific pancreatitis (TCP), 51 insulin-dependent diabetics (IDDMs), 87 non-insulin-dependent diabetics (NID-DMs), and 66 nondiabetic controls were studied to evaluate their exocrine pancreatic function by measurement of serum immunoreactive trypsin (IRT, normal for white caucasians from the U.K. of 140-414 micrograms/L), pancreatic isoamylase (PIA, normal of 35-125 U/L), and fecal chymotrypsin (FCT, normal of greater than 6.6 u/g). The majority of patients were studied within 1 year of diagnosis. TCP subjects included 7 nondiabetics, 6 with impaired glucose tolerance (IGT-TCP), and 36 diabetics [fibrocalculous pancreatic diabetes (FCPD)]. There was evidence of active pancreatitis (IRT greater than 800 micrograms/L) and partial preservation of function in nondiabetic TCP subjects [median IRT of 220 micrograms/L (range of 102-1,360 micrograms/L), FCT of 2.2 u/g (range 0.7-12.8 u/g)] and also in IGT-TCP subjects [IRT of 370 micrograms/L (range of 30-1,360 micrograms/L), FCT of 4.2 u/g (range of 1-38 u/g)]. FCPDs showed severely diminished exocrine function [IRT of 50 micrograms/L (range of 0-184 micrograms/L), FCT of 0.23 u/g (range of 0-10.4 u/g)]; none showed IRT greater than 800 micrograms/L. IDDMs and NIDDMs also showed diminished exocrine pancreatic function in approximately 30 and approximately 10%, respectively. Controls showed a wide range of IRT and FCT concentrations; IRT concentrations tended to be higher than those reported in white Caucasians from the U.K. Three controls, one IDDM, and two NIDDMs showed "pancreatic" IRT concentrations in the absence of symptoms. PIA concentrations were diminished in FCPD but were similar in IDDM and NIDDM subjects compared to controls.(ABSTRACT TRUNCATED AT 250 WORDS)
Pancreas 1990 Nov
PMID:Exocrine pancreatic function (serum immunoreactive trypsin, fecal chymotrypsin, and pancreatic isoamylase) in Indian diabetics. 228 Oct 79

A case of relapsing pancreatitis in a young man is presented. Stenosis of the main duct and cystic lesions of the tail of the pancreas were shown by ultrasonography, CT scan, and endoscopic retrograde cholangiopancreatography (ERCP). After a wrong diagnosis of cancer, the pathological examination demonstrated an eosinophilic infiltration of the pancreatic tail, spleen, lymph nodes, and spleen flexure of the colon. After treatment with oral cromoglycate, the previously increased rate of polynuclear eosinophils in blood returned to normal. Similar observations were found in the medical literature.
Pancreas 1990
PMID:Eosinophilic pancreatitis: report of a case. 229 10


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