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)

Disruption or absence of hepatocyte keratins 8 and 18 is associated with chronic hepatitis, marked hepatocyte fragility, and a significant predisposition to stress-induced liver injury. In contrast, pancreatic keratin disruption in transgenic mice that express keratin 18 Arg89 --> Cys (K18C) is not associated with an obvious pancreatic pathology. We compared the effects of keratin filament disruption on pancreatic acini or acinar cell viability, and on cholecystokinin (CCK)-stimulated secretion, in transgenic mice that overexpress wild-type keratin 18 and harbor normal extended keratin filaments (TG2) and K18C mice. We also compared the response of these mice to pancreatitis induced by a choline-deficient ethionine-supplemented diet or by caerulein. Despite extensive cytoplasmic keratin filament disruption, the apicolateral keratin filament bundles appear intact in the acinar pancreas of K18C mice, as determined ultrastructurally and by light microscopy. No significant pancreatitis-associated histologic, serologic, or F-actin/keratin apicolateral redistribution differences were noted between TG2 and K18C mice. Acinar cell viability and yield after collagenase digestion were lower in K18C than in TG2 mice, but the yields of intact acini and their (125)I-CCK uptake and responses to CCK-stimulated secretion were similar. Our results indicate that keratin filament reorganization is a normal physiologic response to pancreatic cell injury, but an intact keratin cytoplasmic filament network is not as essential in protection from cell injury as in the liver. These findings raise the possibility that the abundant apicolateral acinar keratin filaments, which are not as evident in hepatocytes, may play the cytoprotective role that is seen in liver and other tissues. Alternatively, identical keratins may function differently in different tissues.
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PMID:Effects of keratin filament disruption on exocrine pancreas-stimulated secretion and susceptibility to injury. 1069 32

We report on our experience with laparoscopic cholecystectomy in 15 patients, 12 females and 3 males (mean age: 44 years), with chronic acalculous cholecystitis. These patients presented with recurrent episodes of biliary colic together with a dysmorphic or dysfunctioning gallbladder as confirmed by ultrasound and/or cholescintiscan with 99m-Tc HIDA performed in fasting conditions and after meals. First of all, we considered the possible presence of concomitant digestive disease (peptic ulcer disease, recurrent pancreatitis, irritable bowel syndrome, chronic hepatitis) potentially responsible for the pain. Ultrasound investigations revealed a pathological gallbladder in 10 patients. Cholecystectomy was curative in 8/10. Cholescintiscan revealed a pathological gallbladder in 8 patients and cholecystectomy was curative in only 5 of these. No postoperative deaths or significant complications occurred. The mean duration of the operation (35 vs 48 min) and hospital stay (2.1 vs 2.8 days) were reduced in comparison to 346 cholecystectomies performed for gallstones. After 6-36 months' follow-up, resolution of symptoms was successful in 10/15 cases (66.6%); in 3 cases, only dyspepsia was reduced, whilst in the other 2 cases, who also presented concomitant irritable bowel syndrome and gastroduodenitis, there was no improvement in pain. In all but the latter two cases (86.6%), histological examination revealed chronic gallbladder inflammation. In conclusion, laparoscopic cholecystectomy was curative (66.6%) or led to an improvement in symptoms (20%) in patients with chronic acalculous cholcystitis. Cholescintiscans were not always diagnostic for the disease, whereas ultrasound findings were more useful as an indication for surgery.
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PMID:[Diagnostic problems and results of laparoscopic cholecystectomy in chronic acalculous cholecystitis]. 1119 May 28

Extrahepatic manifestations of chronic hepatitis C virus (HCV) infection have been well described. However, hyperlipasemia and/or pancreatitis have not been reported. Following the observation that several HCV patients had elevated lipase levels, this retrospective study was conducted to assess the association between hyperlipasemia and/or pancreatitis with hepatitis C infection. Of 204 subjects who underwent evaluation for hepatitis C, 103 had lipase levels determined at baseline. The control group consisted of 41 nonHCV subjects with a variety of gastrointestinal diseases including 18 with nonalcoholic liver disease. Twenty-five percent of HCV patients had elevated lipase at baseline as compared to 10% of controls (P = 0.04; OR = 3.1; 95% CI: 1.02-9.60). Mean lipase levels were 253 +/- 72 units/liter (normal range 114-286 units/liter and 210 +/- 42 units/liter for the HCV and control groups, respectively (P = 0.002). No significant difference in amylase was found between the groups. There was a significant association between ALT (> 1.5 times the upper limit of normal) and lipase (P = 0.02; OR = 3.0; 95% CI: 1.1-7.5). Among 30 patients who received interferon-based therapy +/- ribavirin, 11 had elevated lipase at baseline. Six of these patients responded to therapy and demonstrated normalization of lipase levels. In contrast, all nonresponders with baseline hyperlipasemia continued to have high lipase levels (P = 0.17; OR = 4.0; 95% CI: 0.6-28.4). Furthermore, only 3 of 8 (37.5%) patients with normal lipase responded to treatment as compared to 6 of 10 (60%) of hyperlipasemic patients (P = 0.36; OR = 2.5; 95% CI: 0.4-16.9). In conclusion, hyperlipasemia and/or subclinical pancreatitis may represent extrahepatic manifestations of HCV infection and should not preclude treatment.
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PMID:Hyperlipasemia associated with hepatitis C virus. 1292 63

An evaluation of the US Food and Drug Administration's Adverse Event Reporting System identified that patients coinfected with human immunodeficiency virus and chronic hepatitis C virus who were treated with a regimen of ribavirin and didanosine, with or without stavudine, were at increased risk for events associated with mitochondrial toxicity, including fatal hepatic failure, peripheral neuropathy, pancreatitis, and symptomatic hyperlactatemia/lactic acidosis. In response, the US product labels for didanosine and ribavirin have been revised to caution clinicians against coadministration of these drugs.
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PMID:Nucleoside analogues and mitochondrial toxicity. 1509 36

Acute pancreatitis is a rare complication of interferon (IFN) and ribavirin (RBV) therapy. The aim of this study was to determine the incidence, clinical presentation, and outcome of acute pancreatitis in patients with chronic hepatitis C virus (HCV) infection treated with IFN and RBV combination therapy. We conducted a retrospective review of 1706 HCV-infected patients treated with IFN alpha-2b and RBV. The diagnosis of drug-induced acute pancreatitis was made based on the presence of epigastric pain, elevated amylase and lipase levels, and the absence of other identifiable causes of pancreatitis. Acute pancreatitis was diagnosed in 7 of 1706 HCV-infected patients (0.4%; 95% CI, 0.2 to 0.8%) who were treated with IFN alpha-2b and RBV. The mean age of the patients (four males and three females) was 51.4 +/- 4.7 years and the median duration of therapy prior to development of pancreatitis was 12.0 weeks (range, 4.0-21.0 weeks). All patients presented with epigastric pain associated with nausea, vomiting, and/or fever. The median amylase and lipase values at the time of diagnosis of pancreatitis were 330.0 U/L (range, 182.0-1813.0 U/L) and 500.0 U/L (range, 171.0-2778.0 U/L), respectively. IFN and RBV were discontinued in all patients at the time of diagnosis and six of the seven patients were hospitalized; one patient refused hospital admission. Pancreatitis resolved in all seven patients and none of these individuals had recurrent pancreatitis during a median follow-up of 18.0 months (range, 3.0-27.0 months). In conclusion, IFN and RBV combination therapy is a potential cause of drug-induced pancreatitis in patients with chronic HCV. In these individuals, pancreatitis is often severe enough to warrant hospital admission, although symptoms resolve promptly after discontinuation of antiviral therapy.
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PMID:Acute pancreatitis associated with interferon and ribavirin therapy in patients with chronic hepatitis C. 1530 91

Serum antibody to carbonic anhydrase II (CA II) has been reported in patients with autoimmune pancreatitis and its related autoimmune liver diseases. To evaluate its diagnostic significance, we studied serum antibodies to CA II and also CA I in patients with chronic viral hepatitis by enzyme-linked immunosorbent assay and reviewed its prevalence previously reported in patients with liver diseases. Anti-CA II antibody was detected in 5 of 20 patients with chronic hepatitis type C (25%, p<0.05 versus normal controls), 2 of 10 patients with chronic hepatitis type B (20%, not significant versus normal controls), and 1 of 30 normal controls (3%). Anti-CA I antibody was detected in 3 of 20 patients with chronic hepatitis type C (15%, not significant versus normal controls). Anti-CA II antibody has previously been reported as being associated with a variety of liver diseases, including primary biliary cirrhosis with or without anti-mitochondrial antibody, autoimmune hepatitis and chronic hepatitis type C. These findings suggest less significance of anti-CA II antibody for the diagnosis of autoimmune pancreatitis and its hepatic involvements than as having been reported. However, the pathogenetic role of the antibody remains uncertain.
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PMID:Serum antibody to carbonic anhydrase II in patients with chronic viral hepatitis: a review of its prevalence in liver diseases. 1558 28

Black Tea Extract (BTE), a phytocompound has been attributed with a plethora of health-promoting actions. We have previously demonstrated that BTE inhibits chronic hepatitis in a rat model induced with high-fat and ethanol (EtOH). This study reports that BTE prevents altered pancreatic acinar cell functions, oxidative stress, inflammatory changes and DNA damage in the EtOH+cholecystokinin (CCK)-induced model of pancreatitis. The EtOH+CCK model rats were administered with BTE, and were examined the activity of pancreatic digestive enzymes (amylase and lipase), proinflammatory cytokines (IL-6 and TNF-alpha), oxidative and antioxidative enzymes (nitric oxide, NO; malondialdehyde, MDA; superoxide dismutase, SOD; catalase, CAT), antioxidant level (glutathione, GSH), histopathological changes and the integrity of genomic DNA. Results show that because of chronic EtOH treatment, serum level of amylase and lipase (two biomarkers for pancreatitis) and pancreatic levels of MDA and NO (two biomarkers of oxidative stress) increased significantly, which could be effectively blunted by BTE. BTE could normalize EtOH+CCK-induced suppressed activities of SOD and CAT, and GSH content of pancreatic tissue. Also, histopathological and inflammatory changes during EtOH+CCK-induced pancreatitis could be blunted by BTE. Furthermore, BTE could effectively reduce EtOH+CCK-induced increase in DNA fragmentation and damage. These findings suggest that BTE prevents pancreatitis caused by chronic EtOH+CCK toxicity presumably by enhancing antioxidant, anti-inflammatory and antiapoptotic activity in rats.
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PMID:Aqueous extract of black tea (Camellia sinensis) prevents ethanol+cholecystokinin-induced pancreatitis in a rat model. 1628 61

HIV-infected patients are living longer since the introduction of highly active antiretroviral therapy. However, coinfection with the hepatitis C virus (HCV) leads to increased morbidity from liver disease and higher overall mortality. The prevalence of chronic hepatitis C among patients with HIV/AIDS ranges from 7% (sexual transmission of HIV) to >90% (injection drug use). Uncontrolled HIV infection seems to accelerate the progression of HCV-induced liver fibrosis. Forty-eight weeks of combination therapy with pegylated interferon alpha (2a or 2b) plus ribavirin achieves a sustained viral response in coinfected individuals in up to 38% with HCV genotype 1 and up to 73% with genotypes 2 or 3. The safety profile of this treatment is similar to therapy in HCV-monoinfected patients with influenza-like symptoms, cytopenia and neuropsychiatric symptoms dominating. However, HIV/HCV-coinfected patients who also take zidovudine develop more profound anaemia than those on other HIV nucleoside analogue therapy. Didanosine and stavudine are associated with rare but serious mitochondrial toxicity, such as pancreatitis or lactic acidosis. It does not appear that the addition of ribavirin increases that risk. There is currently no evidence that in HIV/HCV coinfection one pegylated interferon product is superior to the other. Contrary to common perception, it is also unproven that HIV/HCV-coinfected patients respond less well to therapy with peginterferon alpha plus ribavirin than HCV-monoinfected patients. Given the safety and efficacy of combination therapy with peginterferon plus ribavirin and the deleterious effects of chronic hepatitis C, all HIV/HCV-coinfected patients should be evaluated for therapy.
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PMID:Chronic hepatitis C in patients with HIV/AIDS: a new challenge in antiviral therapy. 1630 19

While classical opportunistic infections have decreased as the main cause of hospital admission of HIV-infected patients, other conditions including drug-related toxicities seem to have increased. We assessed the proportion of patients with hospital admission due to antiretroviral (ARV)-related toxicities over the last 7 years at a single HIV/AIDS reference institution located in Madrid. A total of 1981 consecutive hospital admissions in 1581 different HIV-infected patients were analyzed. Nearly half of them (45%) were on ARV therapy. Overall, ARV-related toxicities were the main or secondary reason for hospital admission in 141 patients (7%). Liver toxicity was the most frequent complication (n = 42; 30%), of which one-third were associated with NVP use and 80% occurred in subjects with underlying chronic hepatitis C virus (HCV) infection. Other main ARV-related toxicities were bone marrow toxicity due to zidovudine (17%), pancreatitis (13%), and indinavirassociated nephrolithiasis (6%). Eight patients presented with symptomatic hyperlactatemia, two of them with lactic acidosis. All subjects with ARV-related toxicities had a favorable outcome, except one with prior HCVrelated end-stage liver disease, who died after experiencing hepatic decompensation following initiation of a protease inhibitor-based regimen.
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PMID:Impact of antiretroviral treatment-related toxicities on hospital admissions in HIV-infected patients. 1698 5

A patient who developed necrotizing pancreatitis after transcatheter arterial chemoembolization (TACE) for hepatocellular carcinoma (HCC) is presented. A 55- year-old man had been followed for chronic hepatitis B infection for 10 years at another institution. He presented with multiple masses in the right lobe of the liver and a metastasis in the left adrenal gland. He was referred after a percutaneous liver biopsy which revealed a moderately differentiated HCC. He was treated by TACE. At the third session of TACE, the right hepatic artery was found to be thrombosed; however, angiography also demonstrated collateral feeder vessels (arising from the pancreaticoduodenal artery) which were used for treatment. He developed necrotizing pancreatitis, possibly due to regurgitation of the chemotherapeutic agents to the pancreas. He recovered without complications with imipenem-cilastatin prophylaxis. Acute pancreatitis is a rare but severe complication of TACE. Selective catheterization of the tumor vessels is the established standard in TACE. A careful risk-benefit analysis is mandatory in patients with abnormal collateral vessels. Treatment of acute necrotizing pancreatitis (ANP) after TACE is the same as the accepted approach to ANP due to other causes.
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PMID:Necrotizing pancreatitis after transcatheter arterial chemoembolization for hepatocellular carcinoma. 1926 72


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