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Rita A. Gangwani Jacky W.Y. Lee H.Y. Mo Rita Sum Alfred S.K. Kwong Jenny H.L. Wang Wendy W.S. Tsui Jonathan C.H. Chan Jimmy S.M. Lai 《Medicine》2015,94(23)
To investigate the association between retinal nerve fiber layer (RNFL) thickness and blood pressure (BP) in subjects with systemic hypertension.Subjects with systemic hypertension on anti-hypertensive medications were screened by fundus photography and referred for glaucoma work-up if there was enlarged vertical cup-to-disc (VCDR) ratio ≥0.6, VCDR asymmetry ≥0.2, or optic disc hemorrhage. Workup included a complete ophthalmological examination, Humphrey visual field test, and RNFL thickness measurement by optical coherence tomography. The intraocular pressure (IOP) and RNFL thicknesses (global and quadrant) were averaged from both eyes and the means were correlated with: the systolic BP (SBP), diastolic BP (DBP), and mean arterial pressure (MAP) using Pearson correlation.Among 4000 screened hypertensive subjects, 133 were referred for glaucoma workup and 110 completed the workup. Of the 4000 screened subjects, 1.3% had glaucoma (0.9% had normal tension glaucoma [NTG], 0.2% had primary open angle glaucoma, and 0.2% had primary angle closure glaucoma), whereas 0.3% were NTG suspects. The SBP was negatively correlated with the mean superior RNFL thickness (P = 0.01). The DBP was negatively correlated with the mean global (P = 0.03), superior (P = 0.02), and nasal (P = 0.003) RNFL thickness. The MAP was negatively correlated with the mean global (P = 0.01), superior (P = 0.002), and nasal (P = 0.004) RNFL thickness while positively correlated with the mean IOP (P = 0.02).In medically treated hypertensive subjects, glaucoma was present in 1.3%, with NTG being most prevalent. MAP control may help with IOP lowering and RNFL preservation, although future prospective studies will be needed.Glaucoma is a chronic, progressive and irreversible optic neuropathy with characteristic anatomical and structural defects due to loss of the retinal ganglion cells. Loss of the retinal nerve fiber layer (RNFL) may precede visual field changes.1,2 Various studies have demonstrated that up to 40–50% of the retinal ganglion cells need to be lost before visual field defects are observed in standard automated perimetry, which is still considered to be one of the gold standard investigations for glaucoma.3,4 Assessment of RNFL thickness, on the other hand, is an objective test that has a high degree of correlation with visual field defects but at the same time able to detect earlier, pre-perimetric disease.5,6Intraocular pressure (IOP) is still the most important modifiable risk factor of glaucoma progression. Vascular risk factors such as systemic hypertension, ocular perfusion pressure, hypercoagulability, carotid artery disease, and vasospasm have been extensively studied and it has been demonstrated that ocular hypoperfusion and systemic blood pressure play a vital role in the pathogenesis of glaucoma.7–13 Some studies have demonstrated a positive association between systemic hypertension (HT) and glaucoma,14–18 whereas others have demonstrated no significant association between the 2 entities.19,20To our knowledge, very few studies have examined the association between RNFL thickness and BP.21,22 The purpose of our study was to determine association between RNFL thickness with systolic blood pressure (SBP), diastolic blood pressure (DBP), and mean arterial pressure (MAP) in subjects with medically treated systemic HT. 相似文献
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Hélène Bauer Cécile Luxembourger Jacques-Eric Gottenberg Sophie Fournier Florence Abravanel Alain Cantagrel Emmanuel Chatelus Pascal Claudepierre Christophe Hudry Jacques Izopet Sylvie Fabre Guillaume Lefevre Laurent Marguerie Antoine Martin Laurent Messer Anna Molto Béatrice Pallot-Prades Yves-Marie Pers Anne-Marie Roque-Afonso Christian Roux Christelle Sordet Martin Soubrier Claire Veissier Daniel Wendling Jean-Marie Péron Jean Sibilia 《Medicine》2015,94(14)
The clinical presentation and outcome of hepatitis E virus (HEV) infection in inflammatory rheumatic diseases are unknown. We aimed to investigate the severity of acute HEV infection and the risk of chronic viral replication in patients with inflammatory arthritides treated with immunosuppressive drugs.All rheumatology and internal medicine practitioners belonging to the Club Rhumatismes et Inflammation in France were sent newsletters asking for reports of HEV infection and inflammatory arthritides. Baseline characteristics of patients and the course of HEV infection were retrospectively assessed by use of a standardized questionnaire.From January 2010 to August 2013, we obtained reports of 23 cases of HEV infection in patients with rheumatoid arthritis (n = 11), axial spondyloarthritis (n = 5), psoriatic arthritis (n = 4), other types of arthritides (n = 3). Patients received methotrexate (n = 16), antitumor necrosis factor α agents (n = 10), rituximab (n = 4), abatacept (n = 2), tocilizumab (n = 2), and corticosteroids (n = 10, median dose 6 mg/d, range 2–20). All had acute hepatitis: median aspartate and alanine aminotransferase levels were 679 and 1300 U/L, respectively. Eleven patients were asymptomatic, 4 had jaundice. The HEV infection diagnosis relied on positive PCR results for HEV RNA (n = 14 patients) or anti-HEV IgM positivity (n = 9). Median follow-up was 29 months (range 3–55). Treatment included discontinuation of immunosuppressants for 20 patients and ribavirin treatment for 5. Liver enzyme levels normalized and immunosuppressant therapy could be reinitiated in all patients. No chronic infection was observed.Acute HEV infection should be considered in patients with inflammatory rheumatism and elevated liver enzyme values. The outcome of HEV infection seems favorable, with no evolution to chronic hepatitis or fulminant liver failure.Hepatitis E virus (HEV) infection is ubiquitous and is due to a small nonenveloped virus with a positive-sense, single-stranded RNA genome. The virus was discovered in the 1980s. Four major genotypes representing a single serotype have been recognized: HEV1 and HEV2 are restricted to humans and transmitted via contaminated water in developing countries; HEV3 and HEV4 infect humans, pigs, and other mammalian species and are responsible for sporadic cases of autochthonous HEV infection in Western countries. In this setting, HEV infection causes acute disease, mainly in middle-aged and older men. Such an infection might be mistaken for drug-induced liver injury.1 Acute HEV infection might range in severity from subclinical to fulminant, in particular in the risk group of pregnant women, whose death rate in the course of HEV infection could approach 15% to 20%.2,3 However, in the rest of the population and in immunosuppressed patients,4 acute HEV infection is usually asymptomatic. Thus, in a French study of kidney transplant recipients, acute HEV infection was asymptomatic in 14 of 16 patients (87.5%).5 Some extrahepatic manifestations of HEV infection were reported. Kamar et al6 reported neurologic disorders among 126 patients with HEV infection: inflammatory polyradiculopathy (n = 3), Guillain-Barre syndrome (n = 1), bilateral brachial neuritis (n = 1), encephalitis (n = 1), and ataxia/proximal myopathy (n = 1). Hematological disorders, notably acute immune thrombocytopenia,7 were also reported.Recent efforts to develop and standardize the HEV serology led to data showing increasingly recognized cases of HEV infection. HEV infection might correspond to about 10% of cases of non-A–D acute viral hepatitis in Western countries among nontravelers.8Another feature of HEV is its ability to cause chronic infection, defined as a persistent infection lasting >6 months, usually in severely immunocompromised patients.9 In 3 well-known circumstances of immunodeficiency—AIDS, kidney or liver transplantation, and haematological malignancies—HEV infection can develop into chronic infection.10,11 In liver transplant recipients,12 chronic infection with HEV can result in HEV-related cirrhosis.13 However, little is known about the incidence and severity of acute and chronic HEV infection in patients with inflammatory rheumatic diseases. We therefore addressed this issue of HEV infection in patients receiving treatment for inflammatory arthritides. 相似文献
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Jason A. Bailey Jozelyn Pablo Amadou Niangaly Mark A. Travassos Amed Ouattara Drissa Coulibaly Matthew B. Laurens Shannon L. Takala-Harrison Kirsten E. Lyke Jeff Skinner Andrea A. Berry Algis Jasinskas Rie Nakajima-Sasaki Bourema Kouriba Mahamadou A. Thera Philip L. Felgner Ogobara K. Doumbo Christopher V. Plowe 《The American journal of tropical medicine and hygiene》2015,92(1):9-12
Parasite antigen diversity poses an obstacle to developing an effective malaria vaccine. A protein microarray containing Plasmodium falciparum apical membrane antigen 1 (AMA1, n = 57) and merozoite surface protein 1 19-kD (MSP119, n = 10) variants prevalent at a malaria vaccine testing site in Bandiagara, Mali, was used to assess changes in seroreactivity caused by seasonal and lifetime exposure to malaria. Malian adults had significantly higher magnitude and breadth of seroreactivity to variants of both antigens than did Malian children. Seroreactivity increased over the course of the malaria season in children and adults, but the difference was more dramatic in children. These results help to validate diversity-covering protein microarrays as a promising tool for measuring the breadth of antibody responses to highly variant proteins, and demonstrate the potential of this new tool to help guide the development of malaria vaccines with strain-transcending efficacy.Plasmodium falciparum uses antigenic variation to evade host immunity, including vaccine-induced immunity.1,2 The protective immunity against P. falciparum malaria disease that is acquired after years of exposure is believed to reflect, in part, the gradual acquisition of allele-specific immune responses against a repertoire of parasite antigens, and, importantly, against diverse variants of these antigens.3 Apical membrane antigen 1 (AMA1) and merozoite surface protein 1 (MSP1) are immunogenic parasite surface antigens considered vital for erythrocyte attachment and invasion. Antibodies against these proteins are associated with protection against malaria, and several subunit AMA1 and MSP1 vaccines have been developed and tested.1,4–6 Both AMA1 and MSP119, the C-terminus portion of the MSP1 protein used in subunit vaccines, are highly variable, with sequence diversity encoded by single nucleotide polymorphisms.7,8 The highest prevalence of any one of the 440 AMA1 haplotypes observed from sequencing the ama1 gene among more than 1,400 field infections diagnosed during prospective incidence studies and vaccine trials was less than 4%.1,8,9Although less extreme, MSP119 also has substantial diversity, with 17 haplotypes detected among more than 1,300 infections.7 Because vaccines that include dozens or hundreds of antigen variants are not feasible, malaria vaccine development would be aided by the identification of a manageable number of serodominant, cross-protective haplotypes among AMA1 and MSP119 variants. Developing such strain-transcending vaccines is hindered by the limited availability of diverse parasite antigens and the low throughput of standard assays such as enzyme-linked immunosorbent assay for measuring antibody responses.Protein microarrays offer the possibility of overcoming these obstacles to enable high throughput evaluations of seroreactivity to large numbers of antigen variants. Plasmodium falciparum proteins expressed in a cell-free Escherichia coli translation system and spotted onto microarrays are recognized by serum antibodies of persons exposed to malaria.10–12 To date, this platform has been used to measure seroreactivity to large numbers of proteins derived from the genome of the P. falciparum reference strain 3D7.10,12–14 To examine antibody responses to diverse variants of highly polymorphic P. falciparum antigens, we amplified, expressed and printed dozens of field-derived variants of AMA1 and MSP119 on a protein microarray.Antigen genes were amplified by polymerase chain reaction from DNA extracted from dried blood spots collected in a cohort study and an AMA1 vaccine trial in Mali, Africa. The resulting amplicons were analyzed by using the BigDye® Terminator v3.1 Cycle Direct Sequencing Kit (Applied Biosciences, Foster City, CA).4,8,15 Sequence contigs were compiled by using Sequencher software (Gene Codes, Ann Arbor, MI).9,16 Sixty of the most prevalent AMA1 ectodomain haplotypes and 10 MSP119 haplotypes were selected for inclusion on the prototype protein microarray. Microarray construction has been described.17Serum samples were obtained from 18 adults 18–55 years of age enrolled in the control arm of a phase 1 trial of an AMA1-based vaccine conducted during 2004–2005 in Bandiagara, Mali.18 Similarly, serum samples were randomly obtained from 24 children 1–6 years of age enrolled in the control arm of a phase 1 trial of an AMA1-based malaria vaccine during 2006–2007 at the same site.6,19 Bandiagara, Mali has high seasonal malaria transmission coinciding with the June–November rainy season, with entomologic inoculation rates of 50–150 infected bites/person/season.8 For each participant, paired serum samples from two time points corresponding to the pre-malaria (May–June) and post-malaria (December–January) seasons were probed in random order to eliminate batch and slide effects.Two microliters of serum from individual participant samples was diluted 1:200 with 10% E. coli lysate in blocking buffer and hybridized onto separate protein arrays overnight. Arrays were stained, washed, and scanned by using a Perkin-Elmer (Waltham, MA) ScanArray Express HT microarray scanner. Probing protocols have been described.10,12,17 Fluorescence was quantified by using the ScanArray Express Suite (Perkin-Elmer). Median fluorescent intensities (MFIs) were calculated by using an adaptive capture feature to account for varying spot size, and the per-spot local background was subtracted.Raw MFIs were asinh-transformed to convert the MFI values to a Gaussian (normal) distribution, and biological variance contributed by seroreactivity to the E. coli components included in the translation protocol was subtracted by taking the average of eight empty vector, translated, negative controls (i.e., the no DNA controls). Residual non-biological variance between slides, batches, and individual arrays was corrected by using robust linear modeling (RLM) with respect to the negative and positive controls.20 Asinh-transformed, RLM-scaled data were reverted to fluorescent intensities by sinh reverse-transformation and plotted on a heat map to show global trends (Figure 1).Open in a separate windowFigure 1.Heat map of seroreactivity to Plasmodium falciparum apical membrane antigen 1 (AMA1) and merozoite surface protein 1–19 (MSP119) variants. Each column represents serum from an individual Malian child or adult, or a malaria-naive North American adult, and each row represents an antigen variant. Gray, black, and red indicate low, moderate and high seroreactivity, respectively, to probed antigens. Four serial dilutions of IgG peptide were printed and probed as positive probing controls and used as a standardization parameter for robust linear model scaling as a measurement of total IgG. MFI = median fluorescent intensity.Parametric statistical hypotheses were tested on asinh-transformed, RLM-scaled data by using BioconductR (http://www.bioconductor.org/index.html, Excel (Microsoft, Redmond, WA), and SAS/STAT software (SAS Institute, Cary, NC). The magnitude of seroreactivity was measured by mean MFI using matched pair Student''s t tests (Antigen Cohort Mean MFI (95% CI) Serorecognition (%, 95% CI) Pre-season Post-season Pre-season Post-season AMA1 Children 296 (226–365) 434 (348–522) 13.1 (5.8–20.4) 18.6 (11.1– 26.1) Adults 1,506 (1,324–1,687) 1,428 (1,271–1,585) 49.3 (37.0–61.6) 53.2 (42.7–63.7) Controls 8.78 (5.22–12.4) – – – MSP119 Children 20.9 (4.40–37.5) 191 (110–273) 2.5 (–0.9 to 5.9) 9.4 (3.5–15.4) Adults 627 (345–909) 940 (474–1,406) 21.1 (11.4–30.9) 18.9 (6.3–31.4) Controls 21.4 (16.8–26.05) – – –