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• W2004705424 abstract "Chronic rejection is a serious limitation to long-term survival of all solid-organ allografts. The common pathologic feature of chronic rejection seen across all allografts is transplant arteriosclerosis (TA), an obliterative and fibrotic process involving the vasculature and other hollow structures. These changes are most apparent in cardiothoracic organ transplants, in which the majority of grafts are lost as a result of TA affecting the coronary artery disease after heart transplantation, and obliterative bronchiolitis (OB) after lung transplantation. Recently, considerable evidence has emerged supporting an important role for microorganisms in the disease process of vascular injury leading to chronic rejection. This evidence is based on epidemiologic and observational data from transplant recipients, as well as native organs, experimental models, and therapeutic trials. The organisms that have been implicated in the pathophysiology of arteriosclerosis, include Helicobacter pylori , chlamydia, and herpes viruses, most notably, cytomegalovirus (CMV). CMV infection has been reported as a risk factor for TA and OB, and patients who develop CMV disease after heart transplantation have been shown to have a higher incidence of TA and death from TA compared with those who remain free from the disease. Endomyocardial biopsies from patients during CMV viremia show endothelial and vascular smooth muscle cell proliferation, as well as endothelialitis, independent of acute rejection. These changes, which are consistent with vascular injury induced by CMV, have been shown to be markers of subsequent diffuse TA. Rodent models of heterotopic heart transplantation infected with rat CMV develop TA at an accelerated rate, and this process is partially inhibited by early, prophylactic treatment with the antiviral drug, ganciclovir. Similarly, patients treated prophylactically with ganciclovir during the initial 28 days after heart transplantation had a lower incidence of TA compared with placebo. However, this benefit was not seen in seronegative patients receiving hearts from seropositive donors, consistent with the high-risk nature of this group (D+/R−) for developing acute CMV disease. Recent studies have addressed the question of whether improved prophylaxis could be achieved with the addition of CMV hyperimmune globulin (CMVIG) in high-risk patients, including all donor or recipient seropositivity at lung transplantation. Using historical controls, these studies suggest that a combined regimen of ganciclovir plus CMVIG reduces the incidence of acute CMV disease, TA, OB, and death from OB. These observations emphasize the need for future, randomized, controlled trials to confirm a causal role for CMV (and other pathogens) in the disease process of TA and chronic rejection." @default.
• W2004705424 created "2016-06-24" @default.
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• W2004705424 date "2001-04-01" @default.
• W2004705424 modified "2023-09-27" @default.
• W2004705424 title "Role of cytomegalovirus infection in transplant arteriosclerosis and chronic rejection" @default.
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• W2004705424 doi "https://doi.org/10.1016/s0955-470x(05)80004-7" @default.
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