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

To understand recent temporal trends in acquired immunodeficiency syndrome (AIDS) mortality in the era of highly active antiretroviral therapy (HAART), trends in causes of death among persons with AIDS in San Francisco who died between 1994 and 1998 were analyzed. Among 5234 deaths, the mortality rate for human immunodeficiency virus (HIV)-related or AIDS-related deaths declined after 1995 (P<.01), whereas the mortality rate for non-HIV- or non-AIDS-related deaths remained stable. The proportion of deaths of persons with AIDS associated with septicemia, non-AIDS-defining malignancy, chronic liver disease, viral hepatitis, overdose, obstructive lung disease, coronary artery disease, and pancreatitis increased (P<.05). The standardized mortality ratio was high for these causes in both pre- and post-HAART periods, except for pancreatitis, a possible complication of HAART, which demonstrated an increasing standardized mortality ratio trend after 1996. With increasing AIDS survival, prevention of chronic diseases, assessment of long-term toxicity from HAART, and surveillance for additional causes of mortality will become increasingly important.
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PMID:Trends in causes of death among persons with acquired immunodeficiency syndrome in the era of highly active antiretroviral therapy, San Francisco, 1994-1998. 1223 45

As a result of extensive clinical and basic research, the pivotal role of tumour necrosis factor (TNF) in the pathogenesis of chronic inflammatory diseases such as inflammatory bowel disease (IBD) has now generally been acknowledged. This has led to promising clinically effective anti-TNF-strategies. Of note, there is more and more evidence that TNF seems to play a key role in other gastrointestinal diseases including Helicobacter pylori infection, pancreatitis, viral hepatitis and toxic liver damage, too. The action of TNF at the cellular level is mediated by two cell surface receptors, TNF-R1 (p60) and TNF-R2 (p80). The function of these receptors and the downstream intracellular signal transduction pathway have been extensively studied in vitro and it can be expected, that there are critically important steps in TNF-signal transduction that might be dysregulated in these disease states. Their elucidation could lead to a better understanding of the pathogenesis of these diseases, in particular IBD and potentially reveal new, more specific therapeutic targets. Objective of this review is to give an overview about the current knowledge on TNF signal transduction in relationship to selected examples of important gastrointestinal disorders with special focus on IBD. Finally, the implications for future research efforts will be discussed.
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PMID:Functional relevance of soluble TNF-alpha, transmembrane TNF-alpha and TNF-signal transduction in gastrointestinal diseases with special reference to inflammatory bowel diseases. 1229 83

The commonest causes of acute pancreatitis are cholelithiasis and alcohol. Rare causes include various viral infections, among which mumps is the commonest. Hepatitis A, hepatitis B and, recently, hepatitis E have been reported to cause acute but mild pancreatitis in patients with acute viral hepatitis. This report describes a case of severe acute pancreatitis caused by hepatitis A.
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PMID:Severe acute pancreatitis due to hepatitis A virus infection in a patient of acute viral hepatitis. 1297 11

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

The coincidence of viral hepatitis and acute pancreatitis is well described. Most of the cases are related to acute hepatitis A or B. Hepatitis E virus (HEV) infections are rare in Europe, and very few reports describe HEV as a causative agent of acute pancreatitis in areas of endemic hepatitis E prevalence. We report a case of acute pancreatitis in the course of acute hepatitis E in a 28-year-old male patient. The majority of reported cases, including our case, show several common epidemiological and clinical features: young age, male predominance, onset of acute pancreatitis at the early stage of acute hepatitis, and favorable outcome. Acute pancreatitis should be considered in acute hepatitis E, especially in young, male patients presenting with severe epigastric pain early in the course of disease. The pancreatitis in these patients usually runs a benign course. The patients should be closely monitored because life-threatening complications have been reported.
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PMID:Acute hepatitis E complicated by acute pancreatitis: a case report and literature review. 1584 Oct 52

More and more HIV-infected patients are treated for viral hepatitis, increasing interactions. HEPATITIS C: The concomitant use of didanosine and ribavirin increases the risk of mitochondrial toxicity, responsible for pancreatitis and/or lactic acidosis. Lactic acidosis is characterized by a high mortality rate. Thus, didanosine, but also stavudine, should not be co-administered with ribavirin. Cases of hepatic decompensation have been reported in cirrhotics concomitantly receiving ribavirin and didanosine. Thus, this co-admininistration should be contraindicated in patients with advanced liver fibrosis. Anemia is a frequent side effect of ribavirin. In patients with zidovudine-related anemia, this drug should be discontinued before prescribing ribavirin. Erythropoietin may help to improve the haemoglobin level. HEPATITIS B: Adefovir significantly decreases the plasma levels of saquinavir. Pancreatitis may occur with the co-administration of didanosine and tenofovir. Thus this co-administration should be avoided. Atazanavir concentrations are decreased when tenofovir is co-administered. Thus, atazanavir should be boosted with ritonavir, when combined with tenofovir. Atazanavir increases the concentrations of tenofovir, with the potential risk of increasing the adverse events of tenofovir, including renal disorders. Tenofovir area under the curve is increased if lopinavir-ritonavir are co-administered. The main interactions, with a fatal risk, are observed with didanosine, when co-administered with ribavirin (hepatitis C) or with tenofovir (hepatitis B). Anemia is frequent, but usually moderate, when zidovudine is co-administered with ribavirin. Other interactions are usually easy to manage.
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PMID:Antiviral hepatitis and antiretroviral drug interactions. 1636 Feb 31

Autoimmune pancreatitis (AIP) is characterized by high serum immunoglobin (Ig) G4 concentrations, lymphoplasmacytic inflammation, and a favorable response to corticosteroid treatment. Since liver dysfunction is frequently seen in AIP patients, we investigated hepatic histopathology and its clinical significance in patients with AIP. We examined the clinical features, histology, and immunoglobin G (IgG)4-bearing plasma cell infiltration of liver biopsies from 17 patients with AIP and 63 patients with either autoimmune hepatitis, primary biliary cirrhosis, primary sclerosing cholangitis, or chronic viral hepatitis and histological changes in the 7 of 17 livers before and after glucocorticoid therapy. The liver histology of AIP was classified into 5 patterns: evident portal inflammation with or without interface hepatitis (6 cases), large bile-duct obstructive features (8 cases), portal sclerosis (8 cases), lobular hepatitis (5 cases), and canalicular cholestasis (4 cases); some of the histological features coexisted in the same liver. The number of IgG4-bearing plasma cells was significantly higher in AIP patients than controls (P < 0.01), and was significantly correlated with serum IgG4 concentration (P = 0.0014, r = 0.709). Glucocorticoid therapy reduced IgG4-bearing plasma cell infiltration in the liver (P = 0.031) and ameliorated other histological findings. In conclusion, virtually all AIP liver biopsies showed evidence of various pathological changes and infiltration of IgG4-bearing plasma cells. These features were ameliorated by steroid therapy, suggesting that the liver is concurrently affected in AIP, and that liver biopsies can provide significant information in the clinical evaluation and diagnosis of AIP.
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PMID:Immunoglobin G4-hepatopathy: association of immunoglobin G4-bearing plasma cells in liver with autoimmune pancreatitis. 1763 63

The association of viral hepatitis and acute pancreatitis is well described in the literature. Most of the cases occur in conjunction with fulminant hepatitis A and hepatitis B virus infections. The recent literature reports increasing number of cases of this complication secondary to hepatitis E virus (HEV) infection, mostly in young adults in regions endemic for the virus. Till date, to the authors' knowledge, there are 14 well-documented cases of HEV-associated acute pancreatitis in the literature. This study reports on a 7-year-old boy from India deficient in glucose 6 phosphate dehydrogenase (G6PD) with moderately severe pancreatitis, manifesting during the course of nonfulminant acute HEV infection. He developed extremely high serum bilirubin levels, probably attributed to the concomitant viral infection and his G6PD status. He recovered completely with conservative therapy. The present child is the youngest ever reported case till date with this complication secondary to HEV infection.
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PMID:Acute pancreatitis--complicating hepatitis E virus infection in a 7-year-old boy with glucose 6 phosphate dehydrogenase deficiency. 1912 25

Heme oxygenase (HO)-1 is the inducible isoform of the first and rate-limiting enzyme of heme degradation. HO-1 not only protects against oxidative stress and apoptosis, but has received a great deal of attention in recent years because of its potent anti-inflammatory functions. Studies with HO-1 knockout animal models have led to major advances in the understanding of how HO-1 might regulate inflammatory immune responses, although little is known on the underlying mechanisms. Due to its beneficial effects the targeted induction of this enzyme is considered to have major therapeutic potential for the treatment of inflammatory disorders. This review discusses current knowledge on the mechanisms that mediate anti-inflammatory protection by HO-1. More specifically, the article deals with the role of HO-1 in the pathophysiology of viral hepatitis, inflammatory bowel disease, and pancreatitis. The effects of specific HO-1 modulation as a potential therapeutic strategy in experimental cell culture and animal models of these gastrointestinal disorders are summarized. In conclusion, targeted regulation of HO-1 holds major promise for future clinical interventions in inflammatory diseases of the gastrointestinal tract.
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PMID:Heme oxygenase-1 as a therapeutic target in inflammatory disorders of the gastrointestinal tract. 2059 96

Autoimmune pancreatitis (AIP) is a rare form of chronic pancreatitis, characterised by elevated serum IgG4 levels. AIP is associated with many other diseases, including retroperitoneal fibrosis, sclerosing cholangitis, and sialoadenitis. Here, we report an interesting case of a 45-year-old male who presented with haematemesis, melena, and fever, accompanied by hepatosplenomegaly, systemic lymphadenopathy, diffuse swelling of the pancreas, portal hypertension, and multiple enlarged retroperitoneal lymph nodes on abdominal computed tomography (CT). The patient did not have a history of viral hepatitis or cirrhosis. Laboratory testing revealed an elevated IgG (3000 mg/dL). He underwent surgery for uncontrolled active upper gastrointestinal bleeding. We found splenomegaly, with a plump pancreas and involved peripheral lymph nodes, so a splenectomy was performed, and the pancreatic tail and some of the lymph nodes were biopsied. All of the resected tissues were infiltrated by large numbers of IgG4-positive plasma cells. Therefore, this patient was diagnosed with AIP associated with portal hypertension, systemic lymphadenopathy, and splenomegaly. The patient received no other treatment after the splenectomy. By the 6-month follow-up, the patient had recovered, the serum IgG had decreased to normal, and enhanced CT showed a normal pancreas. We speculate that splenectomy may be a new method of treating AIP.
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PMID:Regional portal hypertension, systemic lymphadenopathy, and splenomegaly associated with autoimmune pancreatitis. 2333 30


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