Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0030305 (pancreatitis)
 16,014 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Mumps epidemics are followed by sporadic cases of insulin dependent diabetes mellitus (IDDM). We have studied beta-cell function in 11 subjects who had had a mumps infection. They had no clinical pancreatitis but were selected as they had abnormal pancreas iso-amylase values and/or glucosuria during the mumps virus infection. At the follow-up some years later the subjects were healthy. A few HbA1-values were noted in the upper part of the normal range. Total serum insulin values were normal, but the C-peptide values were low at first follow-up 1-3 years after infection in all but two patients. These values increased in 4/7 patients during the follow-up period but were subnormal in five subjects still 3-6 years after the infection. All five patients had HLA-DR 3 and/or 4. In 7 out of 11 patients islet cell surface antibodies could be demonstrated. Our results indicate that subclinical mumps pancreatitis may initiate a reaction towards the beta-cells recognized as subnormal C-peptide levels several years later in certain patients. This might contribute to manifest IDDM many years after infection.
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PMID:Mumps with laboratory signs of subclinical pancreatitis may cause a disturbed beta-cell function. 307 6

The reason why similar amounts of alcohol consumption cause different types of organ damage in alcoholics is obscure. Recent studies indicate that hepatitis B virus infection may influence the development of liver cirrhosis in alcoholics. We investigated the prevalence of markers of viruses known to cause hepatitis (HAV, HBV, EBV, CMV) in two groups of patients, one with alcoholic pancreatitis without known liver cirrhosis and one with alcoholic liver cirrhosis without known pancreatitis. We found signs of past infection with HAV and HBV more often in alcoholics with liver cirrhosis than in patients with alcoholic pancreatitis or in age-matched controls.
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PMID:Prevalence of markers of hepatotrophic viruses in alcoholics with symptomatic liver cirrhosis or pancreatitis. 608 3

Fifteen chickens, five broilers and ten layers, from the Pennsylvania 1983 outbreak of highly pathogenic avian influenza virus infection, were examined. Gross lesions in the broilers were limited to serosal petechiae and dehydration. In the layers there was comb edema, vesiculation, and necrosis. Microscopic lesions were mild to severe diffuse nonsuppurative encephalitis, very mild to severe diffuse necrotizing pancreatitis, and very mild to severe subacute necrotizing myositis involving numerous skeletal muscles and most severe in the external ocular muscles and limbs. While many of these lesions have been seen in experimental infections of chickens with influenza viruses, the pattern of organs involved in this group of chickens is distinctive.
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PMID:Lesions in broiler and layer chickens in an outbreak of highly pathogenic avian influenza virus infection. 651 76

Inter-alpha-trypsin inhibitor (ITI) is a serine protease inhibitor found in human plasma. Its antiprotease activity is due to bikunin which is effective in various types of experimental shock and pancreatitis. Therefore ITI, which releases bikunin by proteolytic cleavage, could be of therapeutic interest. A method for the large-scale isolation of ITI from human plasma is described. ITI was purified from the prothrombin complex concentrate (PCC) by diethylaminoethyl-Sepharose fast-flow chromatography followed by a chromatographic step on immobilized heparin designed to remove C4, factor X and protein C. With this procedure, which was performed under mild conditions, a homogeneous preparation of native ITI was obtained, as demonstrated by electrophoretic and chromatographic analyses. ITI maintained its biological activity, as exhibited by its specific antitryptic activity of 420 +/- 65 IU/g. In order to decrease or eliminate the risk of transmission of viral disease due to lipid-enveloped viruses, the process incorporated a solvent-detergent treatment. Animal studies on the final product revealed no adverse side-effects in terms of toxicity, thrombogenicity or hypotension. This preparation appears suitable for therapeutic evaluation in animal experimental models.
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PMID:Preparation and properties of a therapeutic inter-alpha-trypsin inhibitor concentrate from human plasma. 753 97

It has been noticed that hyperamylasemia occurs after hepatic resection. Between July 1973 and April 1991, hyperamylasemia was observed in 57 (42%) of 136 patients with hepatocellular carcinoma and 13 (32%) of 41 patients with metastatic liver cancer. The incidence was not correlated with extent of resection, blood loss, hypoxemia, disseminated intravascular coagulation, liver cirrhosis, or hepatitis B virus infection. There were three patterns: salivary-type dominant hyperamylasemia (type I), pancreatic-type dominant hyperamylasemia (type II), and a mixture of types I and II (type III). The point at issue is whether types II and III indicate postoperative pancreatitis. Although the pathogenesis remains unclear, surgeons should be alert to this complication and take reasonable measures with regard to the types of hyperamylasemia.
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PMID:Hyperamylasemia after hepatic resection. 768 77

Renal transplantation of patients with previous or ongoing hepatitis B virus infection has been tempered with a concern that immunosuppression may lead to viral replication and progressive liver damage. However, renal transplantation as therapy for end-stage renal failure in these patients improves quality of life and reduces the risk of body fluid exposure to their carers. To assess the long-term outcome of renal transplantation in hepatitis-BsAg-positive patients a retrospective study was carried out on the patients transplanted in this unit since 1969. Seventy-six patients received 98 grafts up to December 1991; follow-up was available on 68. Thirty-one of the 68 patients died; the causes of death were infective 23, cardiovascular 6, liver failure 4, pancreatitis 2, aspiration 1, GI haemorrhage 1, and stopped therapy 1. Serological markers of hepatitis B virus infection did not correlate with outcome. The risk of developing liver failure after renal transplantation appears small in the hepatitis-BsAg-positive patients and no patient should be denied a renal transplant on the basis of serological tests.
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PMID:Outcome of renal transplantation in hepatitis BsAg-positive patients. 781 99

Didanosine, a purine analogue with antiretroviral activity, is used in the treatment of human immunodeficiency virus disease. Associated toxic effects of didanosine include pancreatitis, peripheral neuropathy, and retinopathy. The retinal lesions associated with didanosine therapy were studied in a 6-year-old girl with acquired immunodeficiency syndrome. Gross examination disclosed multiple well-circumscribed depigmented lesions in the midperipheral retina. Microscopic examination of these lesions showed multiple areas of retinal pigment epithelial (RPE) loss, some surrounded by areas of hypertrophy or hypopigmentation of the RPE. Partial loss of the choriocapillaris and neurosensory retina were also noted in areas of diseased RPE. Transmission electron microscopy showed numerous membranous lamellar inclusions and cytoplasmic bodies in the RPE cells. These data show that didanosine primarily affects the RPE and that the choriocapillaris and overlying neurosensory retina are also dystrophic in areas of RPE loss.
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PMID:A clinicopathologic report of the retinal lesions associated with didanosine. 799 16

Review of autopsies of 28 children with severe combined immunodeficiency (SCID) or combined immunodeficiency (CID) and three with DiGeorge syndrome showed a high incidence of acute graft-versus-host disease (GVHD) in the pancreas. Acute GVHD (seven cases: four SCID, two CID, and one DiGeorge syndrome) was characterized by lymphocytes around large to medium ducts, damage to ductal epithelium (focal necrosis, reactive nuclear changes, inspissated secretions in duct lumens), and periductal edema. Changes were judged indeterminate but suspicious for GVHD when ductal damage was slight (six cases: three SCID, two CID, and one DiGeorge syndrome). All patients with pancreatic GVHD had received allogeneic bone marrow, fetal liver or thymus transplant, or nonirradiated blood products and had evidence of GVHD in other organs. Immunoperoxidase stain for HLA-DR showed strong-to-moderate staining of duct epithelium in two of four GVHD cases for which blocks were available. This change was nonspecific; weaker staining for HLA-DR was seen in cases with nonspecific abnormalities and in viral pancreatitis. Four cases had histological evidence of viral infection: two had cytomegalovirus pancreatitis, one had patchy parenchymal necrosis caused by adenovirus, and one had giant cell pancreatitis caused by parainfluenza virus. Mild nonspecific changes, such as focal fat necrosis or acinar dilatation, were seen in seven cases. One case had unexplained marked pancreatic atrophy and fibrosis. Acute pancreatic GVHD is not uncommon in autopsies of children with congenital immune deficiencies with GVHD of other organs; however, this finding may not have strong clinical implications in this group of patients. Careful attention to pancreatic ducts is necessary for diagnosis. Unusual viral pancreatitis may also be seen in this group, as well as nonspecific abnormalities.
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PMID:Pathology of the pancreas in severe combined immunodeficiency and DiGeorge syndrome: acute graft-versus-host disease and unusual viral infections. 808 66

Although the efficacy of switching from zidovudine (AZT) to didanosine (ddI) has already been evaluated in controlled studies, prior investigations were not specifically designed to evaluate this issue in patients with acquired immune deficiency syndrome (AIDS). This open, randomized, multicenter study (ISS 901) was designed to evaluate the clinical benefit in patients with AIDS of switching to ddI after 6-18 months of AZT and no major intolerance. Patients were randomized to continue AZT, maintaining the current dosage at randomization (n = 79), or to receive ddI (n = 80) at the dosage of 375 mg and 250 mg b.i.d. for body weight > 60 and < or = 60 kg, respectively. Primary efficacy measures were survival and time to new AIDS-defining events, analyzed by the intent-to-treat approach. The two groups were comparable for baseline characteristics, follow-up (15 months), and time spent on allocated treatment. At the end of the study, 104 patients (48 AZT, 56 ddI) had died and 90 had at least one new AIDS-defining event (44 AZT, 46 ddI). Kaplan-Meier estimates of survival and of time to first new AIDS-defining event showed no differences between the treatment groups. No differences were detected in other efficacy measurements (p24 antigenemia, CD4+ count, Karnofsky score, and body weight), occurrence of severe toxicities, and treatment modifications. Pancreatitis occurred only in ddI-treated patients (6%). In our population of patients with advanced disease, switching from AZT to ddI did not produce apparent benefits, suggesting that application of this strategy earlier in the course of human immunodeficiency virus disease should be considered.
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PMID:A randomized trial (ISS 901) of switching to didanosine versus continued zidovudine after the diagnosis of AIDS. 875 22

Chronic hepatitis B is a widespread viral illness with the serious sequelae of cirrhosis and hepatocellular carcinoma. Current therapy with interferon is not universally efficacious, and this has led to the evaluation of other antiviral agents. A recent Phase II trial of the nucleoside analogue, fluoroiodoarabinofuranosyluracil (fialuridine, FIAU) was halted because of the sudden development of severe multisystem toxicity characterized by hepatic failure, lactic acidosis, and pancreatitis, which resulted in the deaths of five patients. We systematically evaluated pre- and post-therapy biopsy, explant, and autopsy specimens from the 15 patients involved in this trial to define the hepatic changes of fialuridine toxicity and to determine whether the degree of pre-existing hepatitis contributed to the severity of toxicity. Severe hepatotoxicity from fialuridine was characterized by hepatomegaly with diffuse, predominantly microvesicular steatosis, hepatocellular glycogen depletion, marked bile ductular proliferation, and cholestasis. Ultrastructural examination revealed intracytoplasmic lipid droplets and marked mitochondrial injury. Patients in whom severe toxicity did not develop mainly showed changes caused by the underlying chronic hepatitis B alone. There was a subtle increase in the amount of microvesicular steatosis in two of six patients with mild or no symptoms of toxicity. The microscopic and ultrastructural pattern of injury and systemic symptoms in patients with fialuridine toxicity are consistent with severe mitochondrial and metabolic derangements. Similar hepatic pathologic findings have been reported rarely for other antiviral nucleoside analogues, which suggests that the mechanisms of toxicity might be related.
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PMID:Histopathologic changes associated with fialuridine hepatotoxicity. 907 26


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