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

The influences of combined adrenalectomy and castration and of a replacement therapy with estradiol and glucocorticoids were examined in the rat pancreas. At the light microscope level, the surgical treatment changed the overall shape of the acini and caused widening of intralobular and interlobular spaces as well as partial depletion of zymogen granules. A significant reduction of the acinar lumen size was observed in castrated-adrenalectomized (CasX-AdreX) animals. This could be reversed by a replacement therapy with glucocorticoids. Moreover, triamcinolone even caused a significant lumen enlargement as compared to sham-operated animals. Such an enlargement was not observed with dexamethasone. Both these glucocorticoids caused an increase in zymogen granule content of the acinar cell. At the ultrastructural level, hitherto undescribed type of precipitates was observed in the acinar lumen of CasX-AdreX rats. Precipitates that exhibited a laminated aspect were identified as luminal laminated bodies. The latter could have some interest from the etiological point of view of certain pancreatic diseases, such as cystic fibrosis and pancreatitis. Replacement therapy with estradiol did not affect the frequency of these precipitates, but glucocorticoid had a significantly inhibitory effect. From our observation, it is clear that some steroid exert a profound influence on the acinar cell and that a replacement therapy with glucocorticoids or estradiol do not totally restore the normal aspect of the pancreas acinar tissue. It suggests that some unknown factors from adrenals or testis are still required in addition to glucocorticoids and estrogens for the maintenance of the structural integrity of the gland.
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PMID:Influence of steroids on the exocrine pancreas: presence of laminated bodies in the acinar lumen following castration and adrenalectomy. 275 43

We comment the case of a 25-year-old woman, diagnosed since the age of 7 as cystic fibrosis, who presented acute pancreatitis, an exceptional complication of the underlying disease. In the ultrasonographic exploration and endoscopic retrograde cholangiopancreatography was appreciated dilation of the pancreatic ducts, with mobile echoes and filling defects, respectively, compatible with mucus plugs. The etiopathogenesis of this type of acute pancreatitis and the procedure for reaching an etiological diagnosis are discussed. Although the patient presented moderate grade pancreatic failure, there is presently no agreement as to whether pancreatitis secondary to cystic fibrosis can be considered as chronic pancreatitis.
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PMID:[Acute pancreatitis: an infrequent complication of cystic fibrosis (mucoviscidosis)]. 276 30

We describe the computed tomographic (CT) and sonographic appearances of large pancreatic cysts found in a review of pancreatic ultrasonography of two patients with cystic fibrosis (CF). Both patients had clinical evidence of pancreatic insufficiency, and one also had evidence of calcification in the body of the pancreas. These cysts, which have rarely been seen in older patients with CF, are not associated with a history of trauma or pancreatitis. Cyst formation requires not only obstruction of the small pancreatic ducts by secretions and cellular debris but also the presence of some residual functioning acinar tissue proximal to the obstruction.
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PMID:Pancreatic cysts and calcification in cystic fibrosis. 295 Jan 13

Twenty-three patients with recent onset Type 1 (insulin-dependent) diabetes in whom residual insulin secreting B cells were present and 12 patients with disease of more prolonged duration (maximum 9 years), 8 of whom had residual B cells, were studied. Aberrant expression of Class II major histocompatibility complex molecules was demonstrated immunohistochemically on insulin secreting B cells in 21 out of 23 patients with recent onset disease and 6 of the patients with more prolonged disease. No such expression was seen on glucagon secreting A cells or somatostatin secreting D cells. Islets where there was marked hyperexpression of Class I major histocompatibility complex molecules on islet endocrine cells were seen in all cases in which residual B cells were present. Ninety-two per cent of insulin containing islets but only 1% of insulin deficient islets exhibited this phenomenon (p less than 0.001, Chi-squared test). There was evidence to suggest that both these abnormalities of major histocompatibility complex expression preceded insulitis within a given islet. They also appeared to be unique to Type 1 diabetes, being absent in pancreases of patients with Type 2 (non-insulin-dependent) diabetes, chronic pancreatitis, cystic fibrosis, graft-versus-host disease and Coxsackie B viral pancreatitis. The development of autoimmunity to B cells in Type 1 diabetes may be a "multistep" process in which abnormalities of major histocompatibility complex expression on islet endocrine cells are crucial events.
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PMID:Aberrant expression of class II major histocompatibility complex molecules by B cells and hyperexpression of class I major histocompatibility complex molecules by insulin containing islets in type 1 (insulin-dependent) diabetes mellitus. 330 84

In a study of pancreases from 75 patients who died at presentation of Type I diabetes there was selective destruction of beta cells associated with islet inflammation (insulitis). According to a recent hypothesis, aberrant expression of Class II major histocompatibility complex (MHC) products on a target cell may allow presentation of organ specific surface antigen(s) to potentially autoreactive T helper lymphocytes and thus lead to autoimmunity. Aberrant expression of Class II MHC was demonstrated immunohistochemically on beta cells in 21 out of 23 patients with recent onset diabetes. No such expression was seen on the other pancreatic endocrine cells. Ninety-four per cent of insulin-containing islets in these patients had marked hyperexpressions of Class I MHC affecting all endocrine cells in these islets. Insulin deficient islets were not thus affected. Both these abnormalities of MHC expression appeared to precede insulitis within a given islet and appeared to be unique to Type I diabetes, being absent in pancreases of patients with Type II diabetes, chronic pancreatitis, cystic fibrosis, graft-versus-host disease and Coxsackie B viral pancreatitis. The development of autoimmunity to beta cells in Type I diabetes may be a 'multistep' process in which abnormalities of MHC expression are crucial events.
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PMID:C. L. Oakley lecture (1987). The pathogenesis of beta cell destruction in type I (insulin-dependent) diabetes mellitus. 330 29

An increased echogenicity of the pancreas ("white pancreas") was sonographically found in 25 children with various pancreatic and systemic diseases. Fifteen patients with cystic fibrosis had a small white pancreas. Five patients with haemosiderosis, two with pancreatitis and one with Shwachman-syndrome presented with a normal-sized or slightly enlarged pancreas. Fatty infiltration and calcifications of the pancreas can also increase its echogenicity.
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PMID:The increased echogenicity of the pancreas in infants and children: the white pancreas. 331 85

We measured the activity of a non-lysosomal alpha-glucosidase with pH optimum near 6.0 in serum from a wide variety of patients, using the fluorogenic substrate, 4-methylumbelliferyl-alpha-D-glucopyranoside. Acutely ill patients with cystic fibrosis (CF) demonstrated significant increases in alpha-glucosidase compared with CF outpatients. The former group of CF patients experienced far more severe chronic pulmonary disease than did the latter, whereas both groups had similar degrees of gastrointestinal impairment. Patients with pancreatitis associated with trauma or complicated by severe necrosis, hemorrhage, or abscess also displayed greater increases in alpha-glucosidase than did patients with uncomplicated (edematous) pancreatitis. For CF outpatients and patients with either edematous pancreatitis or pancreatic cancer, the alpha-glucosidase activity was similar to that for the general hospital-patient population. Corresponding changes were not observed for other measured serum glycosidases (alpha-fucosidase, alpha-mannosidase, beta-glucuronidase, beta-N-acetylglucosaminidase). Measurement of serum alpha-glucosidase may be of value in assessing the clinical course in CF and in differentiating necrotizing from edematous pancreatitis.
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PMID:Measurement of alpha-glucosidase activity in serum from patients with cystic fibrosis or pancreatitis. 351 92

Twenty-nine children with acute pancreatitis were managed during the period 1971 to 1983. Aetiology included trauma (5), mumps (5), drug therapy (4), biliary disease (1), and cystic fibrosis (1); 13 cases were classified as idiopathic. Diagnosis could be difficult, and unnecessary laparotomies were performed in 7 instances for suspected appendicitis. One patient, however, had a well-justified laparotomy revealing coexisting severe appendicitis and pancreatitis. Morbidity included relapses (7), pseudocysts (3), obstructive duodenal hematoma (1), and miscellaneous problems (4). Improvements in management included endoscopic retrograde cholangio-pancreatography (ERCP) to exclude anatomical anomalies in relapsing cases, ultrasonography for the diagnosis of pseudocysts and for follow-up measurements in two such cases successfully managed conservatively, and increasing use of total parenteral nutrition in cases with protracted disease or serious complications.
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PMID:Acute pancreatitis in children. 388 28

No single pathophysiologic factor has been identified as the cause of recurrent acute pancreatitis. A systematic search should be undertaken in every patient to identify one of a myriad of factors that have been shown to play a part in causing this distressing illness. The abuse of alcohol remains the likeliest cause, and further research may reveal an inborn error of metabolism that jeopardizes some people. Biliary tract disease, gallstones, choledochal cyst, papillary stenosis, and duodenal diverticula show a clear relationship. Metabolic disorders such as hypercalcemia, hyperlipidemia, and hyperparathyroidism remain suspect. Systemic illnesses such as systemic lupus erythematosus and cystic fibrosis must be considered. Development anomalies such as pancreas divisum may precipitate acute pancreatitis through aberrant anatomic structures. Cancer must always be disproved. Not yet firmly established but worthy of thorough investigation are uncommon causes, such as the ingestion of certain drugs or combinations of drugs and trauma, either recent or past. Pancreatitis remains frightening for those with the disease and puzzling and frustrating for the medical people who treat it. A careful history and investigation in accordance with a systematic diagnostic plan that includes many disparate factors will lead to identification of the cause in the majority of patients.
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PMID:Pathophysiologic factors in recurrent acute pancreatitis. 393 40

We treated a patient with an unusual case of cystic fibrosis in whom the diagnosis was not made until age 42 years, the predominant clinical manifestation was recurrent pancreatitis, and the chest roentgenogram and results of pulmonary function tests were normal between bouts of pneumonia. As cystic fibrosis may simulate more benign conditions often seen in adults, the diagnosis must be suspected and confirmed for optimal management. Internists must play an increasingly important role in the diagnosis and management of this disease.
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PMID:Cystic fibrosis. An adult perspective. 397 Jun 29


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