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 277,896 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Thirty-seven patients treated for severe acute pancreatitis were investigated a mean of 6.2 years after the attack; 30 were found to be in good condition and 24 were working normally. Two-thirds of previously heavy drinkers had either reduced their intake considerably or become abstainers. The main complication observed on follow-up was diabetes mellitus, which affected 20 patients and required insulin treatment in nine. Of the remaining patients, four were taking oral antidiabetic agents and seven were on a strict diabetic diet. Before severe acute pancreatitis none had been diabetic. All patients who underwent resection of the pancreas developed diabetes. In 21 of 24 patients with over or imminent diabetes, pancreatitis had been primarily alcoholic in origin. Polyneuropathy, as diagnosed by clinical signs and/or neurophysiological tests, was observed in six patients, all of them heavy drinkers. It is concluded that patients with severe acute pancreatitis have a high chance of returning to normal activity and productive work. These results serve to encourage all those involved to persist with the exacting work involved in treating such patients.
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PMID:Good long-term results in patients surviving severe acute pancreatitis. 829 10

The author describes the development of medical research since the 16th century based on a literary review of the study of the anatomy, physiology and pathology of the pancreas. The anatomical basis was first created in the 17th century when the pancreatic duct was discovered (J.C. Wirsung 1642) and the duodenal papilla was described (J.K. Brunner 1683, C.B. Holdefreund 1713 and A. Vater 1750). The physiological function of the pancreas as a secretary gland was first experimentally investigated by R. Graaf (1671). A few decades later the enzymatic breakdown of nutrients by pancreatic juice was demonstrated in animal experiments (G. Valentin 1844, Cl. Bernard 1849). The earliest case reports of patients dying of suppurative inflammation or tumours of the pancreas were presented by S. Alberti (1578), J. Schenck (1600), and N. Tulp (1641). The presence of fatty necrosis in acute pancreatitis was first indicated by W. Balser (1882), and the autodigestive genesis was suspected by H. Chiari (1896). The discovery in the 19th century that diabetes mellitus occurs in dogs following total pancreatectomy (J. von Mering and O. Minkowski 1890) and the first operation on a pancreatic cyst by "marsupialisation" (C. Gussenbauer 1883) as well as the emergence of the connection between cholelithiasis and acute pancreatitis (E.L. Opie and W. St. Halsted 1901) laid the foundation for 20th century research.
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PMID:[Study of the pancreas and its inflammatory diseases from the 16th-19th century]. 830 65

We report a series of five patients with nonalcoholic chronic pancreatitis who underwent abdominal radiotherapy for Hodgkin's disease (n = 4) or seminoma (n = 1) at doses ranging from 3600 to 4050 rads, 6 to 20 years (median, 7 years) before the onset of pancreatitis. Patients were in complete remission for their malignant disease. Other causes of chronic pancreatitis were excluded. The manifestations of chronic pancreatitis (median follow-up after the diagnosis of pancreatitis, 5 years) were pancreatic pain (n = 5), acute pancreatitis (n = 3), pseudocysts (n = 3), common bile duct stenosis (n = 2), duodenal stenosis (n = 1), splenic vein obstruction (n = 1), diabetes mellitus (n = 4), steatorrhea (n = 4), and pancreatic calcifications (n = 1). Other abdominal radiation injuries were severe chronic ulcer of the genu superius (n = 1), stenosis at the junction of the right and left hepatic ducts (n = 1), and splenic and left renal atrophy (n = 1). In one patient, pathological examination of the pancreas showed signs of chronic pancreatitis, severe fibrous endarteritis, and lack of inflammation. Abdominal radiotherapy should be added to the list of causes of chronic pancreatitis. We suggest that the physiopathology of postradiotherapy chronic pancreatitis is a vascular process.
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PMID:Abdominal radiotherapy is a cause for chronic pancreatitis. 803 46

The medical records of 101 dogs with acute pancreatitis, diagnosed on the basis of medical histories of acute vomiting, with serum lipase or amylase activity greater than the reference range, or with gross signs of pancreatitis at surgery or histopathologic evidence at necropsy, were evaluated to identify potential risk factors for the development of acute pancreatitis. Age, sex, and breed of dogs with acute pancreatitis were compared with those from a reference population of 100 dogs admitted for other medical emergencies during the same period. Analysis of multiple regression models indicated that dogs > 7 years old were at increased risk for acute pancreatitis. Spayed dogs and castrated male dogs had an increased risk, compared with that of sexually intact males. Similarly, terrier and nonsporting breeds appeared to be at higher risk of developing acute pancreatitis than were other breed types. Most dogs in this study (63/101) had intercurrent diseases, including diabetes mellitus (n = 14), hyperadrenocorticism (n = 12), chronic renal failure (n = 8), neoplasia (n = 17), congestive heart failure (n = 6), and autoimmune disorders (n = 5). Fourteen dogs had undergone anesthesia or surgery in the week before admission; only 3 had undergone abdominal procedures. Recent medication use was listed in 52 of 101 cases. Antibiotics (n = 18) and corticosteroids (n = 18) were most frequently described. Anticancer chemotherapeutic agents (n = 5) and organophosphate insecticides (n = 5) also were listed.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Risk factors associated with acute pancreatitis in dogs: 101 cases (1985-1990). 840 36

Serum pancreatic stone protein (PSP) was determined in sera of pancreatic and nonpancreatic diseases using enzyme immunoassay specific to human PSP to study the diagnostic and pathophysiological significance of PSP. Serum PSP in acute pancreatitis (mean +/- SD = 1075.4 +/- 2849.1 ng/mL, n = 33) was significantly higher than that in controls (78.6 +/- 31.8 ng/mL, n = 37, p < 0.01), chronic pancreatitis (156.8 +/- 82.8 ng/mL, n = 32, p < 0.05), and pancreatic cancer (148.468.8 ng/mL, n = 26, p < 0.05). No significant difference was found between noncalcified and calcified chronic pancreatitis. Serum PSP levels were significantly higher in chronic renal failure under hemodialysis (1796.0 +/- 1492.9 ng/mL) than in other diseases such as peptic ulcer, liver cirrhosis, gallstone, and diabetes mellitus. Low but significant correlation was obtained between serum PSP and serum immunoreactive trypsin (r = 0.22, p < 0.05). Increased serum PSP levels in acute pancreatitis and chronic renal failure suggest that serum PSP levels reflect reflex from pancreatic secretion, release from damaged pancreatic acinar cells, or retention in circulation, and can be useful for diagnosis of acute pancreatitis, but not chronic calcified pancreatitis.
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PMID:Serum pancreatic stone protein in pancreatic diseases. 850 56

Serum lipid and lipoprotein concentrations in 10 obese and 16 control dogs were examined. The serum triglyceride (TG) concentration in obese dogs was significantly higher than in control dogs. The serum concentrations of TG and phospholipid (PL) in beta lipoprotein and PL in pre-beta lipoprotein were significantly higher in obese dogs, while the serum PL concentration in alpha 1 lipoprotein was significantly lower in obese animals. In the serum total cholesterol concentration in obese dogs, a higher tendency for beta and pre-beta lipoproteins and lower tendency for alpha 1 lipoprotein were observed. These abnormal lipoprotein profiles were similar to those in diabetes mellitus in men and acute pancreatitis in dogs.
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PMID:Serum lipid and lipoprotein concentrations in obese dogs. 851 83

Current data on patients treated with human growth hormone (GH) were analyzed for the following safety topics. New leukemia. Thirteen of 46 new cases of leukemia were in non-Japanese patients without risk factors for leukemia (compared with at least 13 new cases expected). A possible increased occurrence of leukemia with GH treatment appears to be limited to patients with risk factors. Nonleukemic extracranial neoplasms. The number of cases reported (10) does not differ significantly from the number expected. Acute pancreatitis. In five of the seven cases reported risk factors (renal failure, valproic acid use, insulin-dependent diabetes mellitus) were present. The available data do not indicate a clear cause-and-effect relation between GH therapy and pancreatitis. Prepubertal gynecomastia. Of 15 possible cases, two were pubertal, eight resolved or improved with continued GH therapy, and two resolved with the cessation of GH therapy. An effect of GH treatment on prepubertal gynecomastia remains unknown. Scoliosis. Scoliosis is reported in fewer than 1 percent of the patients in the National Cooperative Growth Study (general-population prevalence, 1.5% to 3%). Curvature progression can occur during growth acceleration, and a causal association with GH treatment is not substantiated. Pigmented nevi. Nevi growth may be increased with GH treatment. Biopsies have detected no neoplasia or premalignant nevi transformations.
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PMID:Safety of human growth hormone therapy: current topics. 1124 Oct 65

In humans chronic obstructive pancreatitis (COP) is thought to be a disease devoid of ductal stones. The aim of this study was to verify the presence and frequency of calcifications in patients with COP and compare them with those found in patients with chronic calcifying/calcific pancreatitis (CCP). We conducted a retrospective ERCP investigation in 115 patients with documented chronic pancreatitis. Only 75 could be safely classified as COP or CCP. Fifty-three patients (M:F ratio, 5.6:1; mean age, 36.1 +/- 12.2 years) had CCP, 46 of whom (86.8%) with calcifications. Twenty-two patients (M:F ratio, 3.4:1; mean age, 45.3 +/- 16.2 years; p < 0.05 vs. CCP) presented COP at endoscopic retrograde cholangiopancreatography, 8 (36.4%) with ductal calcifications (p < 0.0001 vs. CCP). COP was secondary to acute pancreatitis in nine cases, to odditis in 11 cases, and to malignant tumor and hypertrophy of Oddi's sphincter, respectively, in the other two cases. The two patient groups showed no significant differences in drinking and smoking habits, number of painful relapses, disease duration, and incidence of diabetes, gallstones, and need for surgery. In conclusion, formation of ductal stones is by no means rare in COP and should be classified as a form of lithiasic pancreatitis. Early restoration of pancreatic outflow by removing the obstruction, or by shunt-type operations and abstinence from drinking and smoking, should resolve this type of disease.
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PMID:Chronic obstructive pancreatitis in humans is a lithiasic disease. 878 36

Acute and chronic pancreatitis present challenging problems for the physician. In acute pancreatitis, initial efforts should be directed toward supporting the patient hemodynamically. Recognition and early treatment of complications such as shock, renal failure, respiratory failure, hypocalcemia, abscess, hemorrhage, or unremitting symptoms caused by an impacted stone in the common bile duct are necessary. The cause of the pancreatitis must be identified, possibly for acute therapy, but certainly to prevent recurrences and progression of disease. In chronic pancreatitis, insufficiencies of pancreatic function must be identified and consequent malabsorption and diabetes treated appropriately. The major challenge is the relief of chronic pain. It is hoped that this can be accomplished medically, but in carefully selected cases, specific types of surgery may be required.
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PMID:Pancreatitis. Evaluation and treatment. 888 42

Clinical as well as experimental studies in insulinopenic diabetes mellitus have demonstrated abnormal pancreatic exocrine responses to cholecystokinin (CCK). In the present study, we examined pancreatic exocrine and endocrine function in the recently developed genetically diabetic Otsuka Long-Evans Tokushima fatty (OLETF) rats and compared them with those in the control Long-Evans Tokushima Otsuka (LETO) rats of the same age. Stepwise increasing doses of CCK octapeptide (CCK-8; 0.027-7.0 nmol.kg-1.h-1) evoked a characteristic biphasic dose-response curve for pancreatic juice and protein output in the LETO rats, whereas the OLETF rats were totally insensitive to CCK-8 stimulation. However, the responsiveness and the sensitivity to both carbamylcholine and secretin were similar in the two groups. Intraduodenal infusion of casein (500 mg/h) failed to stimulate pancreatic exocrine secretion in the OLETF rats despite a greater CCK response than in the LETO rats (peak response: 8.43 +/- 0.97 vs 5.12 +/- 0.30 pmol/l in LETO, P < 0.01). Intravenous infusion of CCK-8 (4.4 nmol.kg-1.20 min-1) caused a significant increase in serum insulin concentrations and a concomitant decrease in glucose levels in the LETO rats but not in the OLETF rats. On the other hand, an intravenous bolus injection of 1.1 mmol/kg glucose caused a greater insulin release in the OLETF rats than in the LETO rats. In contrast, gastric acid secretion in the OLETF rats was significantly high in basal and in response to intravenous infusion of CCK-8 compared with that in the LETO rats. Four subcutaneous injections of 20 micrograms/kg caerulein at hourly intervals over 3 h induced acute pancreatitis in the LETO rats but did not elicit any significant increase in serum amylase or lipase activities and pancreatic wet weight or histological evidence of acute pancreatitis in the OLETF rats. These results indicate that the exocrine and endocrine pancreas of the recently developed genetically diabetic OLETF rats are totally and specifically insensitive to exogenous and endogenous CCK stimulation, whereas parietal cells in these rats are sensitive to CCK stimulation.
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PMID:Defect in pancreatic exocrine and endocrine response to CCK in genetically diabetic OLETF rats. 892 5


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