PubMed · 186149
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H W Murray. 1976-10-30. CMV retinitis.. https://doi.org/10.1136/bmj.2.6043.1071-c
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BACKGROUND: Transplant vasculopathy (TVP) is the most common cause of death and retransplantation after heart transplantation. Human cytomegalovirus (HCMV) infection has been linked to atherosclerosis and to the development of TVP. A prospective study evaluating the relation between CMV infection and progression of TVP is lacking thus far. The purpose of the present study was to investigate the influence of CMV infection status on the progression of TVP within 1 year. METHODS: We enrolled 103 consecutive heart-transplant recipients who underwent routine cardiac catheterization and intracoronary ultrasound examination at study entry and after 1 year. Plaque progression determined by quantitative intracoronary ultrasound was used to define the severity of disease at baseline and at 1-year follow-up. At study entry, HCMV infection status was evaluated by immunological assays and reverse-transcriptase polymerase chain reaction (RT-PCR). RESULTS: HCMV immunoglobulin (Ig)G/IgM seropositivity was found in 34 (33%) of transplant recipients, 11 of whom were HCMV PCR positive. The HCMV-positive group showed more advanced, calcified lesions (64.7% vs. 27.5%, P=0.002), and the maximal plaque thickness was significantly different from the HCMV IgG/IgM-negative group (median [quartile] 1.36 [0.85, 1.88] vs. 1.05 [0.58, 1.34], P=0.02). In a logistic regression model, we demonstrate that HCMV IgG/IgM positivity is a predictor for the progression of TVP independent of cardiovascular risk factors, inflammatory markers, and platelet activation (P=0.038). In addition, HCMV PCR positivity even increases the risk for accelerated TVP (P=0.017) and, consecutively, transplant failure. CONCLUSIONS: HCMV infection status in transplant patients detects patients with increased risk for transplant failure caused by TVP.
The syndrome of multiple intestinal atresia with immunodeficiency is a rare, invariably fatal congenital disorder. At 16 months of age, a child with this syndrome underwent liver-small bowel transplantation from a 1-of-6 HLA-matched donor. He acquired full enteral tolerance and normal liver function and has never shown evidence of allograft rejection. After mild graft-versus-host disease developed, studies revealed that more than 99% of his CD3(+) lymphocytes and 50% of his CD19(+) lymphocytes were of donor origin, whereas granulocytes and monocytes remained of recipient origin. He synthesizes polyclonal immunoglobulin G (IgG), IgA, and IgM and has developed antibodies to cytomegalovirus (CMV) and parainfluenza 3. His T lymphocytes are predominately CD3(+)CD4(-)CD8(-) with T-cell receptor gammadelta heterodimers and CD3(+)CD4(-)CD8(+) with CD8alphaalpha homodimers, populations consistent with an intraepithelial lymphocyte phenotypic profile. We postulate that he has engrafted a donor intestine-derived immune system and is incapable of rejecting his engrafted organs.