49 research outputs found
AM3 (InmunoferĂłnÂź) as an adjuvant to hepatitis B vaccination in hemodialysis patients
AM3 (InmunoferĂłnÂź) as an adjuvant to hepatitis B vaccination in hemodialysis patients.BackgroundPatients with end-stage renal disease (ESRD) undergoing hemodialysis have severe alterations in cell-mediated immunity (CMI) that increases their risk of contracting chronic hepatitis B virus (HBV) infection and decreases their protective responses to HBV vaccine. In an effort to improve the humoral response to an accelerated HBV vaccine protocol in these patients, the ability of an immunomodulator, AM3, to improve seroconversion was investigated.MethodsA total of 269 patients were enrolled in a multicenter trial. All patients received a DNA recombinant vaccine (40 ÎŒg HBsAg/dose/day) on days 0, 10, 21, and 90. AM3 or placebo (3 g/day) was given orally for 30 consecutive days beginning 15 days prior to the first vaccine dose. Anti-HBsAg titers were measured on days 120 and 270 after the beginning of the trial.ResultsAfter one month, 207 patients could be evaluated and 132 patients after six months. The placebo and AM3-treated groups had comparable seroconversion and protective response rates one month after the final vaccine dose. The AM3 treatment group, but not the placebo group, maintained these protective titers up to six months after the final vaccine dose. At this time, the percentage of high responders (anti-HBsAg>100 IU/L) and mean anti-HBsAg titers in the AM3 group was significantly higher than in the placebo group.ConclusionsAM3 is a safe and easily tolerated oral agent that potentiates long-term serological immunity to hepatitis B in hemodialysis patients after vaccination
Cardiovascular Function in a Chronic Peritoneal Dialysis Pediatric Population on Recombinant Human Erythropoietin Treatment
The neurotoxicity and safety of treatment with cefepime in patients with renal failure. Nephrol Dial Transplant 2008
Abstract Background: Cases of cefepime neurotoxicity have been Sporadically reported in patients with renal failure. The neurotoxicity of cefepime might be underestimated and the frequency of its neurotoxic effects may be insufficiently recognized. Methods: We retrospectively reviewed the files of patients with renal failure who were treated with cefepime and who developed neurological complications. Results: All 8 patients developed decreased conscience, confusion, agitation, global aphasia, myoclonus, choreaathetosis, convulsions and coma. The latency, the period between the start of treatment and neurologicaldeterioration, was 4,75 ± 2,55 days (range: 1-10 days). All patients died 17 ± 14,7 days (range: 1-42 days) after becoming symptomatic. Three of them died shortly after neurological deterioration. Five patients developed a neurological "tableau" with global aphasia. Three patients showed clinical improvement after the discontinuation of cefepime. Electroencephalography revealed diffuse slow-wave activity (delta) and triphasic sharp wave activity. These findings confirm the possible neurotoxicity of treatment with cefepime in patients with renal failure. In none of the deceased patients have we been able to directly demonstrate a causal relationship between neurotoxicity and mortality. However, when a patient treated with cefepime develops neurological deterioration or aphasia, one must be aware of cefepime's potential neurotoxicity and treatment should be stopped. Conclusion: We recommend that, in view of the high and unexplained mortality, the use of cefepime in patients with kidney failure should be carefully considered
The neurotoxicity and safety of treatment with cefepime in patients with renal failure
Background: Cases of cefepime neurotoxicity have been Sporadically reported in patients with renal failure. The neurotoxicity of cefepime might be underestimated and the frequency of its neurotoxic effects may be insufficiently recognized.
Methods: We retrospectively reviewed the files of patients with renal failure who were treated with cefepime and who developed neurological complications.
Results: All 8 patients developed decreased conscience, confusion, agitation, global aphasia, myoclonus, chorea-athetosis, convulsions and coma. The latency, the period between the start of treatment and neurologicaldeterioration, was 4,75 +/- 2,55 days (range: 1-10 days). All patients died 17 +/- 14,7 days (range: 1-42 days) after becoming symptomatic. Three of them died shortly after neurological deterioration. Five patients developed a neurological "tableau" with global aphasia. Three patients showed clinical improvement after the discontinuation of cefepime. Electroencephalography revealed diffuse slow-wave activity (delta) and triphasic sharp wave activity. These findings confirm the possible neurotoxicity of treatment with cefepime in patients with renal failure. In none of the deceased patients have we been able to directly demonstrate a causal relationship between neurotoxicity and mortality. However, when a patient treated with cefepime develops neurological deterioration or aphasia, one must be aware of cefepime's potential neurotoxicity and treatment should be stopped.
Conclusion: We recommend that, in view of the high and unexplained mortality, the use of cefepime in patients with kidney failure should be carefully considered