Home About us Contact
|
Home About us Contact | ||
|
|
||
Disease Secondary (disease + secondary)
Selected AbstractsSeasonal variation of enteric infections and inflammatory bowel diseaseINFLAMMATORY BOWEL DISEASES, Issue 7 2008Amnon Sonnenberg MD Abstract Background: The time trends of inflammatory bowel disease are characterized by short-term variations that affect Crohn's disease and ulcerative colitis alike. The aim of the present study was to test whether these variations might be related to exacerbations of inflammatory bowel disease secondary to superimposed gastrointestinal infection. Methods: The Hospital Episode Statistics (HES) comprises a data set of all patients admitted to hospitals throughout England, which includes inpatients and day cases. This data set was used to analyze the monthly variations in all hospital admissions for Crohn's disease (ICD10 code K50), ulcerative colitis (K51), bacterial intestinal infections (A04), viral intestinal infections (A08), diarrhea and infectious gastroenteritis (A09), upper respiratory infections (J06), pneumonia secondary to unspecified organism (J18), and unspecified acute lower respiratory infection (J22). Results: The temporal analysis revealed similar monthly fluctuations of hospital admissions for Crohn's disease, ulcerative colitis, and bacterial intestinal infections. Viral intestinal infections and infectious gastroenteritis were characterized by different seasonal variations that showed no relationship with any of the fluctuations of inflammatory bowel disease or bacterial intestinal infections. Similarly, respiratory infections resulted in marked cyclical variations in hospital admissions unrelated to any changes in inflammatory bowel disease or enteric infections. Conclusions: The similarity in the time trends of Crohn's disease, ulcerative colitis, and bacterial intestinal infections suggests that superinfection by intestinal bacteria are responsible for the fluctuations in hospital admissions for inflammatory bowel disease. (Inflamm Bowel Dis 2008) [source] Risk factors for recurrence of autoimmune hepatitis after liver transplantation,,LIVER TRANSPLANTATION, Issue 10 2009Aldo J. Montano-Loza Autoimmune hepatitis has been reported to recur after liver transplantation. The aim of our study was to evaluate the risk factors associated with recurrence of autoimmune hepatitis. Forty-six patients that underwent liver transplantation because of end-stage liver disease secondary to autoimmune hepatitis were studied. Recurrence of autoimmune hepatitis was diagnosed in 11 of the 46 (24%) patients, and the overall 5-year probability of recurrence was 18%. By univariate Cox analysis, the features before liver transplantation associated with a higher risk of recurrence were concomitant autoimmune disease [hazard ratio (HR), 3.74; 95% confidence interval (CI), 1.05,13.36; P = 0.04], high aspartate aminotransferase (HR, 1.09; 95% CI, 1.03,1.14; P = 0.002), high alanine aminotransferase (HR, 1.09; 95% CI, 1.03,1.20; P = 0.003), and high immunoglobulin G (IgG; HR, 1.25; 95% CI, 1.11,1.41; P = 0.0003). Moreover, patients with recurrence had a higher frequency of moderate to severe inflammatory activity (HR, 5.3; 95% CI, 1.55,18.79; P = 0.008) and plasma cell infiltration in the liver explant (HR, 5.8; 95% CI, 1.52,22.43; P = 0.01). In the multivariate Cox analysis, only the presence of moderate to severe inflammation (HR, 6.9; 95% CI, 1.76,26.96; P = 0.006) and high IgG levels before liver transplantation (HR, 7.5; 95% CI, 1.45,38.45; P = 0.02) were independently associated with the risk of autoimmune hepatitis recurrence. In conclusion, patients with concomitant autoimmune disease, high aspartate aminotransferase, alanine aminotransferase, and IgG before the transplant, or moderate to severe inflammatory activity or plasma cell infiltration in the liver explant have a higher risk of recurrent disease. These findings suggest that recurrence of autoimmune hepatitis may reflect incomplete suppression of disease activity prior to liver transplantation. Liver Transpl 15:1254,1261, 2009. © 2009 AASLD. [source] E2 quasispecies specificity of hepatitis C virus association with allografts immediately after liver transplantationLIVER TRANSPLANTATION, Issue 2 2004Michael G. Hughes Jr. It is unknown whether all hepatitis C virus (HCV) quasispecies variants found within patient serum have equal capacity to associate with the liver after transplantation; however, in vitro models of HCV infection suggest that variations in the hypervariable region 1 (HVR1) of the second envelope protein (E2) may be important in infectivity. The hypothesis of the current study is that the two hypervariable regions (HVR1 and HVR2) within E2 are important in the initial virus,liver interaction, and, therefore, certain HCV quasispecies variants will be isolated from the liver after reperfusion. In 8 patients with end-stage liver disease secondary to HCV infection, HCV envelope quasispecies were determined from intraoperative serum samples obtained before the anhepatic phase of transplantation and from liver biopsies 1.5 to 2.5 hours after the transplanted liver was perfused. Explanted (native) liver biopsies were taken as a control. Sequence analysis was performed on clones of specific HCV reverse transcriptase-polymerase chain reaction products spanning HVR1 and HVR2 of the E2 protein. HVR1 was more variable than HVR2 for all samples. Quasispecies isolated from postperfusion liver differed more from serum than did explanted liver quasispecies at HVR1 (P = 0.03) but not at HVR2 (P = 0.2). Comparison of HVR1 sequences from postperfusion liver versus serum revealed significantly less HVR1 genetic complexity and diversity (P = 0.02 and P = 0.04, respectively). Immediately after transplantation but before actual infection, liver allografts select out from the infecting serum inoculum a less heterogeneous, more closely related population of quasispecies variants. (Liver Transpl 2004;10:208,216.) [source] Approach to eradication of initial Pseudomonas aeruginosa infection in children with cystic fibrosisPEDIATRIC PULMONOLOGY, Issue 9 2007Miriam M. Treggiari MD Abstract The primary cause of morbidity and mortality in children with cystic fibrosis (CF) is the progression of obstructive lung disease secondary to chronic endobronchial infection, mainly caused by Pseudomonas aeruginosa (Pa). Initial Pa isolates are typically non-mucoid, usually susceptible to most anti-pseudomonal antibiotics, and potentially amenable to eradication. Preliminary studies of early intervention suggest a "window of opportunity" with anti-pseudomonal antibiotics to eradicate Pa from upper and lower airways. Several large trials in young children with CF are currently ongoing with the goals of (1) investigating if early intervention at the time of initial Pa acquisition is effective and safe and (2) identifying the least invasive and safest treatment regimen to achieve both microbiologic and clinical benefits. Pediatr Pulmonol. 2007; 42:751,756. © 2007 Wiley-Liss, Inc. [source] Simultaneous Pancreas-Kidney Transplantation Utilizing a Common Arterial Conduit: Early Experience and Potential ApplicationsAMERICAN JOURNAL OF TRANSPLANTATION, Issue 11 2003Paul L. Tso Simultaneous pancreas-kidney transplantation has gained acceptance as a therapeutic modality for patients with end-stage renal disease secondary to diabetes mellitus. In some instances, performing the procedure as conventionally described with renal revascularization from the left iliac vessels and pancreatic arterial inflow from the right iliac vessels may be difficult or undesirable. We describe our experience with an alternate operative technique utilizing a single arterial conduit to vascularize both organs. We believe that this technique may be of use in certain patients undergoing simultaneous pancreas-kidney transplantation. [source] Randomized, prospective, placebo-controlled trial of bosentan in interstitial lung disease secondary to systemic sclerosis,ARTHRITIS & RHEUMATISM, Issue 7 2010J. R. Seibold Objective Endothelin is implicated as a participatory pathway in systemic sclerosis (SSc). We tested this hypothesis in a 12-month trial of bosentan, a nonselective endothelin receptor antagonist, as a therapy for SSc-related interstitial lung disease (ILD). Method Patients with SSc and significant ILD were recruited to this prospective, double-blind, randomized, placebo-controlled, parallel group study. The inclusion criteria were designed to select a cohort enriched for patients with active and progressive disease. Exclusion factors included significant pulmonary hypertension. Patients with a diffusing capacity for carbon monoxide of <80% predicted and a 6-minute walk distance of 150,500 meters or a 6-minute walk distance of ,500 meters with a decrease in oxygen saturation received bosentan or placebo. The primary efficacy end point was a change in the 6-minute walk distance from baseline up to month 12. Secondary end points included time to death or worsening results of pulmonary function tests (PFTs). The safety and tolerability of bosentan were also assessed. Results Among the 163 patients, 77 were randomized to receive bosentan, and 86 were randomized to receive placebo. No significant difference between treatment groups was observed for change in the 6-minute walk distance up to month 12. No deaths occurred in this study group. Forced vital capacity and diffusing capacity for carbon monoxide remained stable in the majority of patients in both groups. Significant worsening of PFT results occurred in 25.6% of patients receiving placebo and 22.5% of those receiving bosentan (P not significant). Conclusion No improvement in exercise capacity was observed in the bosentan-treated group compared with the placebo group, and no significant treatment effect was observed for the other end points. Although many outcome variables were stable, bosentan did not reduce the frequency of clinically important worsening. These data do not support the use of endothelin receptor antagonists as therapy for ILD secondary to SSc. [source] | ||||||||||