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      Virus y vasculitis sistémicas Translated title: Virus and systemic vasculitis

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          Abstract

          En la patogenia de las enfermedades autoinmunes sistémicas, incluyendo las vasculitis, siempre se ha invocado la participación de factores genéticos y factores ambientales. Entre los ambientales, las infecciones, fundamentalmente de naturaleza vírica, han sido siempre un foco de atención, máxime tras el descubrimiento de la estrecha relación existente entre la poliarteritis nudosa y el virus de la hepatitis B, por una parte, y la crioglobulinemia mixta esencial y el virus de la hepatitis C, por otra.

          La presente revisión pretende actualizar los conocimientos recogidos en la literatura más reciente sobre el binomio virus y vasculitis sistémicas, siguiendo la clasificación de vasculitis de Chapel-Hill.

          Translated abstract

          The participation of genetic and environmental factors has always been invoked in the pathogenesis of the autoimmune systemic diseases, including the primary vasculitides. Among the environmental factors, infections, fundamentally those having a viral nature, have always been focused on, especially after the discovery of the close existing relationship between the polyarteritis nodosa and the hepatitis B virus, on the one hand, and mixed cryoglobulinemia and the hepatitis C virus, on the other. The present review summarizes data from the most recent literature related to associations between virus infections and primary vasculitides, following the Chapel-Hill vasculitis classification.

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          Most cited references28

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          Hepatitis B virus-associated polyarteritis nodosa: clinical characteristics, outcome, and impact of treatment in 115 patients.

          Hepatitis B virus-associated polyarteritis nodosa (HBV-PAN) is a typical form of classic PAN whose pathogenesis has been attributed to immune-complex deposition with antigen excess. We conducted the current study to 1) analyze the frequency of HBV infection in patients with PAN, in light of the classification systems described since 1990; 2) describe the clinical characteristics of HBV-PAN; 3) compare the evolution according to conventional or antiviral treatment; and 4) evaluate long-term outcome. One hundred fifteen patients were included in therapeutic trials organized by the French Vasculitis Study Group and/or referred to our department for HBV-PAN between 1972 and 2002. To determine the frequency of HBV-PAN during the 30-year period, we analyzed a control group of patients with PAN without HBV infection, followed during the same period and diagnosed on the same bases. Depending on the year of diagnosis, different treatments were prescribed. Before the antiviral strategy was established, some patients were given corticosteroids (CS) with or without cyclophosphamide (CY). Since 1983, treatment for patients with HBV markers has combined 2 weeks of CS followed by an antiviral agent (successively, vidarabine, interferon-alpha, and lamivudine) combined with plasma exchanges (PE).Ninety-three (80.9%) patients entered remission during this period and 9 (9.7%) of them relapsed; 41 (35.7%) patients died. For the 80 patients given the antiviral strategy as intention-to-treat, 4 (5%) relapsed and 24 (30%) died vs 5 (14.3%) relapses (not significant [NS]) and 17 (48.6%) deaths (NS) among the 35 patients treated with CS alone or with CY or PE. HBe-anti-HBe seroconversion rates for the 2 groups, respectively, were: 49.3% vs 14.7% (p < 0.001). Patients who seroconverted obtained complete remission and did not relapse.Thus, HBV-PAN, a typical form of classic PAN, can be characterized as follows: when renal involvement is present, so is renal vasculitis; glomerulonephritis due to vasculitis is never found; antineutrophil cytoplasmic antibodies (ANCA) are not detected; relapses are rare, and never occur once viral replication has stopped and seroconversion has been obtained. Combining an antiviral drug with PE facilitates seroconversion and prevents the development of long-term hepatic complications of HBV infection. The major cause of death is gastrointestinal tract involvement. Importantly, the frequency of HBV-PAN has decreased in relation to improved blood safety and vaccination campaigns.
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            The incidence of giant cell arteritis in Olmsted County, Minnesota: apparent fluctuations in a cyclic pattern.

            To investigate trends in the incidence of giant cell arteritis over a 42-year period in Olmsted County, Minnesota. Population-based incidence study. Olmsted County, Minnesota. All incidence cases of giant cell arteritis first diagnosed between 1950 and 1991 were identified using the unified record system at Mayo Clinic. Age- and sex-specific incidence rates were calculated using the number of incidence cases as the numerator and population estimates as the denominator. Overall rates were age- and sex-adjusted to the 1980 United States white population. The annual incidence rates were graphically illustrated using a 3-year centered moving average. Between 1950 and 1991, 125 Olmsted County residents (103 women and 22 men) were diagnosed with giant cell arteritis. The age- and sex-adjusted incidence per 100,000 persons 50 years of age or older was 17.8 (95% CI, 14.7 to 21.0); incidence was significantly higher in women (24.2 [CI, 19.5 to 28.9]) than in men (8.2 [CI, 4.8 to 11.6]). Age-specific incidence rates increased with age (P < 0.0001). The annual incidence rates increased significantly over the study period (P = 0.002) and appear to have clustered in five peak periods, which occurred about every 7 years. A significant calendar-time effect was identified; it predicted an increase in incidence of 2.6% (CI, 0.9% to 4.3%) every 5 years. Our observation of a regular cyclic pattern in incidence rates over time supports the hypothesis of an infectious cause for giant cell arteritis. Similar studies in other populations are needed to confirm our findings.
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              Kawasaki Disease and Human Coronavirus

              To the Editor—Esper et al. [1] recently reported the possible causal association between a novel human coronavirus (HCoV) and Kawasaki disease (KD). They reported that respiratory secretions from 72.7% of 11 patients with KD but from only 4.5% of 22 age-matched control subjects tested positive for an HCoV designated by Esper et al. as the “New Haven coronavirus” (HCoV-NH). This virus was reported to be closely related to HCoV-NL and HCoV-NL63, which were identified by 2 independent groups from The Netherlands [2, 3] To determine if HCoV might be consistently associated with KD, we analyzed nasopharyngeal and oropharyngeal swab samples collected in 1999 as part of an etiologic investigation of KD in San Diego. The 1999 investigation focused on exploring the possible causal link between KD and Chlamydia pneumoniae and the details of the investigation and case-control design are described by Schrag et al. [4]. After the 1999 investigation was completed, the pharyngeal swab samples were stored at −70°C. Pharyngeal swab samples were available for analysis from 10 patients with KD and from 6 control subjects. The patients, who had onset of KD between 9 February and 20 March 1999, had a median age of 3.6 years (range, 0.6–8.6 years). The patients met the epidemiologic case definition for KD: they had fever lasting for ⩾5 days and had at least 4 of the 5 clinical features of KD [4]. The median age for the control subjects was 3.3 years (range, 1.3–8.3 years). Pharyngeal swab samples were obtained within 10 days of the onset of illness in 6 of the patients with KD and on days 11, 15, 16, and 37 after the onset of illness in the remaining 4 patients All pharyngeal swab samples from the patients with KD and from the control subjects tested negative for HCoV by use of 2 different primer sets. Nucleic acid was extracted from 200 μL of the pharyngeal swab samples by use of the automated NucliSens Extractor (bioMérieux). Twenty-five-microliter reactions containing 5 μL of the extracted nucleic acid were prepared with the 1-step Access RT-PCR System (Promega). The first primer set used for amplification was an HCoV-NH/HCoV-NL63–specific primer described by Esper et al. [1] that had the following modification: a single nucleotide degeneracy was introduced into the sense-strand primer, 5′-GCGCTATGAGGGTGGTTGYAAC-3′, to accommodate a sequence variation among published sequences of HCoV-NH/HCoV-NL63 strains (the underlining indicates the modification). The amplification program consisted of a reverse-transcription (RT) step of 45 min at 45°C and 2 min at 94°C, to denature the reverse transcriptase; 40 cycles of 1 min at 94°C, 1 min at 55°C, and 1 min at 72°C; and 10 min at 72°C, for final amplicon extension. The second RT–polymerase chain reaction (PCR) primer set had broadly reactive primers designed to target highly conserved regions of the HCoV RNA polymerase gene: sense-strand primer 5′-GGTTGGGATTATCCTAARTGTGA-3′ and antisense strand primer 5′-TATAACACACAACACCYTCATCA-3′. Amplification reactions were performed as described above, and the following program settings were used: an RT step of 45 min at 45°C and 2 min at 94°C, to denature the reverse transcriptase; 40 cycles of 1 min at 94°C, 1 min at 54°C, and 1 min at 72°C; and 5 min at 72°C, for final amplicon extension The sense-strand primers for both sets were labeled with Cy5 fluorescent dye at the 5′ end to facilitate amplicon detection (the predicted sizes for the first and second primer sets were 215 and 454 bp, respectively) using the CEQ 8000 Genetic Analysis System (Beckman Coulter). Assays were performed using standard viral nucleic acid extracts (HCoV 229E and OC43) and nuclease-free water for positive and negative controls, respectively. All pharyngeal swab samples tested positive by RT-PCR for human glyceraldehyde-3–phosphate dehydrogenase enzyme, which indicated that there was adequate recovery of RNA from the samples and that RT-PCR inhibitors were absent Our findings do not support those of Esper et al. [1]. Methodologic differences in the type and timing of sample collection; in sample handling, storage, and processing; and in the selection of case patients and control subjects may explain our different findings. Alternatively, different etiologic agents could have been associated with KD in the 2 study populations. Further studies that include serologic testing and prospectively collected high-quality pharyngeal swab samples may be needed to determine the role, if any, that HCoVs play in the etiology of KD
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                Author and article information

                Contributors
                Journal
                Rev Clin Esp
                Rev Clin Esp
                Revista Clinica Espanola
                Elsevier España S.L.
                0014-2565
                1578-1860
                6 January 2009
                November 2006
                6 January 2009
                : 206
                : 10
                : 507-509
                Affiliations
                Unidad de Enfermedades Autoinmunes Sistémicas. Hospital Clínico San Cecilio. Granada. España
                Author notes
                [* ]Correspondencia: N. Ortego Centeno. Unidad de Enfermedades Autoinmunes Sistémicas. Hospital Clínico San Cecilio. Avda. Dr. Oloriz, s/n. 18012. Granada. España. nortego@ 123456telefonica.net
                Article
                S0014-2565(06)72878-8
                10.1157/13094901
                7130152
                17129519
                6b9cd652-7d24-4e6e-b2bd-0ace99afa37e
                Copyright © 2006 Elsevier España S.L. All rights reserved.

                Since January 2020 Elsevier has created a COVID-19 resource centre with free information in English and Mandarin on the novel coronavirus COVID-19. The COVID-19 resource centre is hosted on Elsevier Connect, the company's public news and information website. Elsevier hereby grants permission to make all its COVID-19-related research that is available on the COVID-19 resource centre - including this research content - immediately available in PubMed Central and other publicly funded repositories, such as the WHO COVID database with rights for unrestricted research re-use and analyses in any form or by any means with acknowledgement of the original source. These permissions are granted for free by Elsevier for as long as the COVID-19 resource centre remains active.

                History
                : 10 April 2006
                Categories
                Article

                virus,vasculitis,viruses
                virus, vasculitis, viruses

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