Seminars in respiratory and critical care medicine
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Human metapneumovirus (hMPV) is a common pathogen that can cause both upper and lower respiratory tract infections, particularly in children, elderly adults, and immunocompromised hosts. Since its initial identification in 2001, hMPV has been isolated from individuals with acute respiratory tract infections (ARTIs) in virtually every continent. Serological studies indicate that it has caused human infection since 1958 or earlier. ⋯ Ribavirin has similar activity in vitro and in animal models against hRSV and hMPV, but its efficacy in vivo is unproven. Monoclonal antibodies have activity in murine models but are not available in humans. Several vaccines are promising in animal models, but their safety and efficacy have not yet been evaluated in humans.
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The human Herpesviridae family consists of eight members: cytomegalovirus (CMV), Epstein-Barr virus (EBV), herpes simplex virus 1 and 2 (HSV-1, -2), varicella-zoster virus (VZV), and human herpesvirus 6, 7, and 8 (HHV-6, -7, -8). Lifelong latency may develop in the host with reactivation during periods of relative immunosuppression that occurs in transplant recipients. These are pleiotropic viruses: in addition to their direct effects of tissue injury and clinical illness, they exhibit several indirect effects, including immunomodulation and effects on angiogenesis and tumorigenesis, which may result in long-term adverse sequelae in the lung allograft. ⋯ EBV and HHV-8 have proven oncogenic potential. HSV-1 and -2 and VZV are neurotropic, causing perioral fever blisters, genital ulcerations, and, rarely, encephalitis. This article discusses the individual pathogens, preventive strategies in the era of potent treatment regimens for established viral infection or disease and their potential impact on the indirect effects of these viruses on long-term allograft function, and the incidence, risk factors for, and impact of antiviral resistance.
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Semin Respir Crit Care Med · Jun 2011
ReviewPulmonary: renal syndrome with a focus on anti-GBM disease.
Pulmonary-renal syndrome is a potentially life-threatening combination of pulmonary hemorrhage and acute renal failure. Several pathological entities can cause this syndrome. ⋯ Rapid serological testing and appropriate interpretation can be of great additive diagnostic value. Also discussed are the pathogenesis, therapy, and outcome of anti-glomerular basement membrane disease, one of the pathological entities that can cause pulmonary-renal syndrome.
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Semin Respir Crit Care Med · Jun 2011
ReviewImmunosuppressive and cytotoxic therapy: pharmacology, toxicities, and monitoring.
Treatment strategies for anti-neutrophil cytoplasmic antibody (ANCA)-associated vasculitis (AAV) are evolving. Cyclophosphamide (CYC) plus corticosteroids (CSs) is the mainstay of therapy for generalized, multisystemic AAV. Historically, the combination of CYC plus CS was used for a minimum of 12 months, but concern about late toxicities associated with CYC has led to novel treatment approaches. ⋯ Further, methotrexate combined with CS may be adequate for limited, non-life-threatening AAV. Recent studies suggest that rituximab may be useful for induction therapy or for CYC-refractory AAV. This article reviews the key agents used to treat AAV, with a focus on pharmacology, toxicities, and monitoring.
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The possible link between pulmonary fibrosis, anti-neutrophil cytoplasmic autoantibody (ANCA) positivity, and vasculitis is poorly understood. During the past 6 years, five retrospective case-control studies have been published. These studies suggest that pulmonary fibrosis (PF) is an underestimated manifestation of ANCA-associated vasculitis. ⋯ The diagnosis of PF often predates the development of vasculitis. There are no significant differences of pulmonary function parameters, bronchoalveolar lavage analysis, or high-resolution computed tomographic (HRCT) findings between ANCA-associated PF and idiopathic pulmonary fibrosis (IPF). The high mortality rate of ANCA-associated PF indicates that a search for ANCAs should be performed at diagnosis in every patient with PF because the presence of ANCAs increases the risk of development of vasculitis and should promote specific monitoring of patients with positive MPO-ANCA.