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Cytomegalovirus Disease (cytomegalovirus + disease)

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Medical Sciences	100%

Selected Abstracts

Clinical Predictors of Relapse after Treatment of Primary Gastrointestinal Cytomegalovirus Disease in Solid Organ Transplant Recipients

AMERICAN JOURNAL OF TRANSPLANTATION, Issue 1 2010
A. J. Eid
Primary gastrointestinal cytomegalovirus (CMV) disease after solid organ transplantation (SOT) is difficult to treat and may relapse. Herein, we reviewed the clinical records of CMV D+/R, SOT recipients with biopsy-proven gastrointestinal CMV disease to determine predictors of relapse. The population consisted of 26 kidney (13 [50%]), liver (10 [38%]) and heart (3 [12%]) transplant recipients who developed gastrointestinal CMV disease at a median of 54 (interquartile range [IQR]: 40,70) days after stopping antiviral prophylaxis. Except for one patient, all received induction intravenous ganciclovir (mean ± SD, 33.8 ± 19.3 days) followed by valganciclovir (27.5 ± 13.3 days) in 18 patients. Ten patients further received valganciclovir maintenance therapy (41.6 ± 28.6 days). The median times to CMV PCR negativity in blood was 22.5 days (IQR: 16.5,30.7) and to normal endoscopic findings was 27.0 days (IQR: 21.0,33.5). CMV relapse, which occurred in seven (27%) patients, was significantly associated with extensive disease (p = 0.03). CMV seroconversion, viral load, treatment duration, maintenance therapy and endoscopic findings at the end of therapy were not significantly associated with CMV relapse. In conclusion, an extensive involvement of the gastrointestinal tract was significantly associated with CMV relapse. However, endoscopic evidence of resolution of gastrointestinal disease did not necessarily translate into a lower risk of CMV relapse. [source]

Cell-Mediated Immunity to Predict Cytomegalovirus Disease in High-Risk Solid Organ Transplant Recipients

AMERICAN JOURNAL OF TRANSPLANTATION, Issue 5 2009
D. Kumar
Late-onset cytomegalovirus (CMV) disease commonly occurs after discontinuation of antiviral prophylaxis. We determined the utility of testing CD8+ T-cell response against CMV as a predictor of late-onset CMV disease after a standard course of antiviral prophylaxis. Transplant patients at high-risk for CMV disease were enrolled. CD8+ T-cell-mediated immunity (CMI) was tested using the QuantiFERON-CMV assay at baseline, 1, 2 and 3 months posttransplant by measurement of interferon-, response to whole blood stimulation with a 21-peptide pool. The primary outcome was the ability of CMI testing to predict CMV disease in the first 6 months posttransplant. There were 108 evaluable patients (D+/R+ n = 39; D-/R+ n = 34; D+/R- n = 35) of whom 18 (16.7%) developed symptomatic CMV disease. At the end of prophylaxis, CMI was detectable in 38/108 (35.2%) patients (cutoff 0.1 IU/mL interferon-,). CMV disease occurred in 2/38 (5.3%) patients with a detectable interferon-, response versus 16/70 (22.9%) patients with a negative response; p = 0.038. In the subgroup of D+/R- patients, CMV disease occurred in 1/10 (10.0%) patients with a detectable interferon-, response (cutoff 0.1 IU/mL) versus 10/25 (40.0%) patients with a negative CMI, p = 0.12. Monitoring of CMI may be useful for predicting late-onset CMV disease. [source]

Symptomatic infant characteristics of congenital cytomegalovirus disease in Australia

JOURNAL OF PAEDIATRICS AND CHILD HEALTH, Issue 8 2005
Sian C Munro
Background: Human cytomegalovirus (CMV) is the most common cause of viral intrauterine infection. In utero transmission can occur during primary maternal infection, reactivation or reinfection of seropositive mothers. Objective: To describe the aetiology and clinical features of infants diagnosed with congenital CMV and to document maternal factors that were presented. Methods: Active national surveillance was initiated in 1999 in collaboration with the Australian Paediatric Surveillance Unit. Results: Monthly notifications resulted in 70 cases of congenital CMV being identified between 1999 and 2003. Nearly all of the cases were symptomatic with the most common clinical sequelae reported in infected infants being jaundice, thrombocytopaenia, hepatomegaly, petechiae, purpura and splenomegaly. Almost half (43.5%) of the infants had central nervous system (CNS) complications, such as microcephaly, chorioretinitis, sensorineural hearing loss, intracranial calcifications, developmental delay or seizures, with over half presenting two or more CNS abnormalities. Maternal febrile illness was noted in 54.8% of the cases. The majority of mothers were primiparous (46.4%) or secundiparous (39.3%), indicating two different population groups at risk of primary CMV infection. Conclusion: This study documents symptomatic congenital CMV cases in Australia. [source]

Calcineurin-Inhibitor-Free Immunosuppression Based on the JAK Inhibitor CP-690,550: A Pilot Study in De Novo Kidney Allograft Recipients

AMERICAN JOURNAL OF TRANSPLANTATION, Issue 8 2009
S. Busque
This randomized, pilot study compared the Janus kinase inhibitor CP-690,550 (15 mg BID [CP15] and 30 mg BID [CP30], n = 20 each) with tacrolimus (n = 21) in de novo kidney allograft recipients. Patients received an IL-2 receptor antagonist, concomitant mycophenolate mofetil (MMF) and corticosteroids. CP-690,550 doses were reduced after 6 months. Due to a high incidence of BK virus nephropathy (BKN) in CP30, MMF was discontinued in this group. The 6-month biopsy-proven acute rejection rates were 1 of 20, 4 of 20 and 1 of 21 for CP15, CP30 and tacrolimus groups, respectively. BKN developed in 4 of 20 patients in CP30 group. The 6-month rates of cytomegalovirus disease were 2 of 20, 4 of 20 and none of 21 for CP15, CP30 and tacrolimus groups, respectively. Estimated glomerular filtration rate was >70 mL/min at 6 and 12 months (all groups). NK cells were reduced by ,77% in CP-690,550-treated patients. In the CP-690,550 arms, there were modest lipid elevations and a trend toward more frequent anemia and neutropenia during the first 6 months. These data suggest that coadministration of CP-690,550 30 mg BID with MMF is associated with overimmunosuppression. At 15 mg BID, the efficacy/safety profile was comparable to the tacrolimus control group, excepting a higher rate of viral infection. Further dose-ranging evaluation of CP-690,550 is warranted. [source]