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Query: UMLS:C0000737 (abdominal pain)
 31,184 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Between 1954 and 1975, 80 pancreaticojejunostomies were performed on 77 patients for intractable pain of chronic pancreatitis. All patients had a history of chronic alcoholism. Drainage operations done primarily for pseudocysts were excluded. Operative procedures included seven caudal pancreaticojejunostomies, 42 longitudinal pancreaticojejunostomies with splenectomy and implantation of the pancreas into the jejunum, and 31 side-to-side pancreaticojejunostomies. Eighty-one percent of the patients noted substantial improvement or complete resolution of their abdominal pain on follow-up that ranged up to 21 years. The operative mortality was 5%. Thirty-two patients died during the period of the follow-up. Continued alcohol abuse, carcinoma, and cardiovascular disease were the leading causes of mortality. Data from this review confirm the effectiveness of pancreaticojejunostomy in relieving the pain of chronic relapsing pancreatitis.
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PMID:Pancreaticojejunostomy for chronic pancreatitis. Two- to 21-year follow-up. 7 68

The efficiency of ultrasound in the diagnosis of pancreatic disease was compared prospectively with that of selenomethionine isotope scanning in 46 patients presenting with abdominal pain or weight-loss or with jaundice. Of 14 patients who later proved to have pancreatic carcinoma, all had an abnormal isotope scan and 13 had an abnormal ultrasound scan. Of 10 patients with chronic pancreatitis, all had an abnormal isotope scan and 9 had an abnormal ultrasound scan. The small advantage of selenomethionine was, however, offset by a higher false-positive rate: of 22 patients who proved not to have pancreatic disease, 13 had abnormal isotope scans compared with only 3 with ultrasound. Review of earlier experience with the two techniques yielded similar results: in pancreatic carcinoma and chronic pancreatitis, isotope scanning gave slightly fewer false-negative results than ultrasound but many more false-positives. Because of its lower false-positive rate, because it avoids ionising radiation, and because it can usually distinguish carcinoma from pancreatitis, ultrasound is the procedure of choice for initial investigation of patients with suspected pancreatic disease.
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PMID:Screening for pancreatic disease: A comparison of grey-scale ultrasonography and isotope scanning. 8 71

Records of 346 patients were studied to determine the reliability and diagnostic value of pancreatic scanning. In 157 the pancreatic diagnosis was established subsequent to scanning. The scan was abnormal in 28 of 34 patients (82%) with pancreatic neoplasm, and in 21 of 26 patients (81%) with chronic pancreatitis. Of 71 with normal scans, 56 (79%) had a normal pancreas, and 15 had pancreatic disease (a false negative rate of 21%). Of the 86 with abnormal scans, the pancreas was diseased in 56 (65%), and of the others, 14 had extrapancreatic conditions known to be associated with a high incidence of scan abnormalities. In obstructive jaundice all 21 patients with pancreatic carcinoma had abnormal scans (and the scan accurately diagnosed all four cases of bile duct carcinoma). A normal scan reliably indicated that the cause of jaundice was outside the pancreas. In chronic abdominal pain an abnormal scan was unreliable, but a normal scan excluded pancreatic disease with reasonable accuracy.
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PMID:Radionuclide pancreatic scanning: a retrospective analysis. 27 99

A 43-year old man with CRST syndrome (calcinosis, Raynaud's phenomenon, sclerodactyly and telangiectasia) and progressive systemic sclerosis presented with a four-year history of relapsing abdominal pain, the result of chronic pancreatitis, not associated with alcoholism, biliary disease, or any of the known causes of pancreatitis. He had a good response to retrograde pancreatic duct drainage but exhibited management problems and complications that may be peculiar to the systemic sclerosis patient with pancreatitis. A cause and effect relationship between progressive systemic sclerosis and pancreatic disease is not proven but we believe there is evidence to suggest such a relationship.
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PMID:Idiopathic calcific pancreatitis, CRST syndrome and progressive systemic sclerosis. 43

The authors report a case of macroamylasemia in which the diagnosis was made with some difficulty. A hyperamylasemia was discovered after the patient, an alcoholic, had been hospitalized for atypical abdominal pain and weight loss, and this was thought to be due to an acute episode of chronic pancreatitis. The absence of an incrase in amylasuria suggested the presence of a macroamylasemia, and both diagnoses were confirmed by suitable exploratory investigations. Alcoholic cirrhosis was also present. The two main known types of macroamylase and their iatrogenic variant are described as well as the incidence of this biological anomaly in the general population. Confirming the presence of this anomaly in the plasma is a delicate and complex procedure. Simultaneous study of amylase-creatinine clearance ratio was thought to be a decisive test, but this does not appear to be true.
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PMID:[Clinical and biological aspects of macroamylasemia (author's transl)]. 48 89

An analysis of 89 cases with chronic pancreatitis revealed 56% of chronic alcoholic pancreatitis (AP). The sex ratio was 47 males to 3 females and the mean age at onset was 42.4 years in AP and 49.3 years in chronic non-alcoholic pancreatitis (NAP). The 'total amount' of alcohol consumption was correlated to the onset. In AP, the abdominal pain was apt to relapse and severe in nature, furthermore painless pancreatitis was seen in 6%. The association with diabetes or calcification (38%) were more frequently seen in AP. The calcifications in AP appeared to be smaller in size and distributed diffusely or localized in cephalic portion. A striking frequency of liver dysfunctions (39 cases) were demonstrated, however, cirrhosis was rare in AP. The P-S test dysunctions in NAP were frequently reversible in the follow up study, while even some of chronic asymptomatic alcoholics developed clinical signs of pancreatitis during the observed period and proceeded to definite AP, of whom pancreatic dysfunctions showed fluctuation and eventual progression. In other words, even pain free intervals the pancreatic inflammation in susceptible persons may proceed to ultimated destruction of the pancreas. The fatality from chronic pancreatitis was rare (12.3%), which was related diabetes mellitus.
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PMID:A clinical investigation of chronic pancreatitis--comparative study between alcoholic pancreatitis and non-alcoholic pancreatitis--. 66 97

Information from 72 patients from 7 families in England and Wales confirms that hereditary pancreatitis is inherited as an autosomal dominant conditions with limited penetrance. The degree of penetrance is approximately 80%. These patients have had recurrent attacks of abdominal pain starting from childhood or young adult life. The mean age of onset in the 7 families studied was 13.6 years. There were two peaks, with maximum numbers at 5 years and 17 years. The second peak was thought to represent genetically susceptible individuals having pain brought on by alcohol rather than representing evidence of genetic heterogeneity. Five of the 7 families had members with both childhood and adult ages of onset. Only 4 patients out of 72 had life-threatening disease and in the majority of cases the attacks of pain were of nuisance value only. Hereditary pancreatitis was implicated in only 1 patient's death and this was not definite. Patients appear to get better after a period of symptoms usually as they approach middle age, or after a severe attack. In older patients alcohol, emotional upsets, and fatty food appear to precipitate attacks. Pancreatic insufficiency (5.5%), diabetes mellitus (12.5%), pseudocysts (5.5%), and haemorrhagic pleural effusion are uncommon complications. Portal vein thrombosis occurred definitely in 2 patients and was suspected in 3 others. Carcinoma of the pancreas was not found in any of 72 patients studied in detail; however, 2 members from a family not visited personally had chronic pancreatitis and malabsorption going on to carcinoma. They may have suffered from a different disease. Genetic linkage information was too slight for many definite conclusions. However, there was no suggestion of linkage with any of the markers tested.
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PMID:Hereditary pancreatitis in England and Wales. 67 83

The metabolic consequences and the clinical results of total pancreatectomy for end-stage chronic pancreatitis are detailed. This experience, accumulated between the years 1952 and 1976, adds 26 cases to the world's literature, which now contains 53 cases reported singly or in small series. The patients were selected on the basis of far-advanced, incapacitating disease in three patients and the failure of 62 previous related operations in 23 patients. Total pancreatectomy was performed with a zero hospital mortality but with serious inhospital morbidity. After discharge, 24 patients required 55 hospital readmissions and 18 related surgical operations; 12 patients have died, five of unrelated causes. Of 14 living patients, five consider themselves to be in good to excellent condition, six in fair condition, and three in poor condition. Twelve thought they were improved over their preoperative state. Our estimate of the result in living patients was similar. In those 12 who died, only four had satisfactory results. The results are also evaluated relative to level of activity, presence of abdominal pain, use of narcotics, weight, alcohol consumption, and the efficiency of endocrine and exocrine replacement. In general, the procedure is effective for relief or amelioration of pain, but the patients' personalities preclude complete adaptation to the apancreatic state rehabilitation. A failure to thrive is the common denominator.
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PMID:Total pancreatectomy of end-stage chronic pancreatitis. 68 97

The prevalence of diabetes due to chronic pancreatitis would appear to be increasing. In western countries this is associated with the known increase in alcohol consumption and AIP. Malnutrition may be etiologic in tropical areas. The incidence of diabetes in chronic pancreatitis is dependent on a number of factors. It is more common in alcohol-induced pancreatitis, rarely occurs after the first attack but tends to increase with time and rises markedly in calcific pancreatitis. Abnormal glucose tolerance occurred in 91% of patients with calcific pancreatitis and 70% of patients with noncalific AIP in our follow up of five to 12 years. This stresses the importance of serial regular glucose tolerance tests in these patients (Table I). The insulin-reserve is severely depleted in most patients who do not yet demonstrate abnormal glucose tolerance, indicating that pancreatitis regularly affects the islets and that nearly all patients are potential diabetics. The beta cells appear to respond better to oral glucose, glucagon or secretin than to i.v. glucose suggesting a selective glucose receptor loss or block to hyperglycemia in chronic pancreatitis. The alpha cells seem to be more resistant to the effects of chronic pancreatitis but true hypoglucagonemia was found in 16% of patients. In addition, stimulated growth hormone secretion may be deficient in pancreatic diabetes. These last two factors, among others, may be responsible for the protracted and even fatal hypoglycemia to which some patients with AIP on insulin therapy are liable. The danger of drug-induced hypoglycemia, coupled with the infrequency of vasculopathy, retinopathy and nephropathy in pancreatic diabetes has induced us to keep these patients hyperglycemic and glycosuric rather than in a sugar-free state, as long as symptoms are contained. Recurrent abdominal pain, marked weight loss and associated steatorrhea often raise special problems in the management of the pancreatic diabetic.
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PMID:Clinical and hormonal aspects of pancreatic diabetes. 80 21

Three cases of benign pancreatic ascites have been added to 94 cases reviewed from the literature. Common characteristic of this syndrome were chronic alcoholism, intermittent abdominal pain, nausea, vomiting and considerable weight loss which occurred despite fluid accumulation. Markedly elevated protein and amylase levels in the ascitic fluid, hyperamylasemia and hypoalbuminemia were the major diagnostic clues as to the pancreatic origin of ascites. Predominant pathological findings were chronic pancreatitis with or without pseudocysts, pancreatic duct disruption, lesion which were considered to be the major pathogenic factor besides lymphatic obstruction by leaking pancreatic juice into the peritoneal cavity. Early laparotomy for diagnosis and treatment is essential. ERP might be of great value in diagnosis.
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PMID:Massive pancreatic ascites without carcinoma. Report of three cases. 84 74


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