Database : MEDLINE
Search on : Vasculitis [Words]
References found : 33053 [refine]
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[PMID]: 25829955
[Au] Autor:Blaes F
[Ad] Address:Department of Neurology, KKH Gummersbach, Wilhelm-Breckow-Allee 20, 51643 Gummersbach, Germany.
[Ti] Title:Diagnosis and therapeutic options for peripheral vasculitic neuropathy.
[So] Source:Ther Adv Musculoskelet Dis;7(2):45-55, 2015 Apr.
[Is] ISSN:1759-720X
[Cp] Country of publication:England
[La] Language:eng
[Ab] Abstract:Vasculitis can affect the peripheral nervous system alone (nonsystemic vasculitic neuropathy) or can be a part of primary or secondary systemic vasculitis. In cases of pre-existing systemic vasculitis, the diagnosis can easily be made, whereas suspected vasculitic neuropathy as initial or only manifestation of vasculitis requires careful clinical, neurophysiological, laboratory and histopathological workout. The typical clinical syndrome is mononeuropathia multiplex or asymmetric neuropathy, but distal-symmetric neuropathy can frequently be seen. Standard treatments include steroids, azathioprine, methotrexate and cyclophosphamide. More recently the B-cell antibody rituximab and intravenous immunoglobulins have shown to be effective in some vasculitic neuropathy types.
[Pt] Publication type:JOURNAL ARTICLE; REVIEW
[Em] Entry month:1504
[Cu] Class update date: 150404
[Lr] Last revision date:150404
[Da] Date of entry for processing:150401
[St] Status:PubMed-not-MEDLINE
[do] DOI:10.1177/1759720X14566617

  2 / 33053 MEDLINE  
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[PMID]: 25829891
[Au] Autor:Lazar DB; Lemor D; Brown A; Nussdorf JD
[Ad] Address:Department of Ophthalmology, Louisiana State University Health Sciences Center, New Orleans, LA....
[Ti] Title:Simultaneous bilateral nonarteritic anterior ischemic optic neuropathy in a patient with a history of diffuse large B-cell lymphoma.
[So] Source:Ochsner J;15(1):106-9, 2015.
[Is] ISSN:1524-5012
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:BACKGROUND: Nonarteritic anterior ischemic optic neuropathy (NAAION) has a poorly understood etiology, and the onset of simultaneous bilateral NAAION in a patient <50 years without identifiable systemic risk factors is rare. CASE REPORT: We present the case of a patient with acute painless monocular vision loss and bilateral optic disc edema who subsequently developed painless vision loss in the fellow eye. The patient's history was significant for diffuse large B-cell lymphoma, and our pressing diagnostic concern was to determine if his vision loss and bilateral optic disc changes represented lymphomatous infiltrates. A complete ocular exam demonstrated findings consistent with simultaneous bilateral NAAION. After an extensive systemic workup for malignancy with central nervous system involvement, vasculitis, and other entities associated with NAAION, we determined that the patient's primary risk factor for developing bilateral ischemic optic neuropathies was his crowded optic discs. CONCLUSION: This case supports the hypothesis that a crowded optic disc is a sufficient primary risk factor for developing NAAION.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1504
[Cu] Class update date: 150404
[Lr] Last revision date:150404
[Da] Date of entry for processing:150401
[St] Status:PubMed-not-MEDLINE

  3 / 33053 MEDLINE  
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[PMID]: 25829554
[Au] Autor:Nobles IJ; Khan S
[Ad] Address:BluePearl Veterinary Partners - ER/CC, 3000 Busch Lake Blvd, Tampa, Florida 33614, USA (Nobles); ASPCA - Animal Poison Control Center, Urbana, Illinois, USA (Khan).
[Ti] Title:Multiorgan dysfunction syndrome secondary to joint supplement overdosage in a dog.
[So] Source:Can Vet J;56(4):361-4, 2015 Apr.
[Is] ISSN:0008-5286
[Cp] Country of publication:Canada
[La] Language:eng
[Ab] Abstract:A 5-year-old spayed female Bernese mountain dog, with a chief complaint of vomiting and melena ingested approximately 200 nutritional joint supplement tablets. Despite aggressive therapy, the patient developed a coagulopathy, pancreatitis, peritonitis, acute kidney injury, and was euthanized. Postmortem examination revealed myocardial necrosis, pneumonia, centrilobular hemorrhage and necrosis of the liver, vasculitis, and acute tubular necrosis.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1504
[Cu] Class update date: 150404
[Lr] Last revision date:150404
[Js] Journal subset:IM
[St] Status:In-Data-Review

  4 / 33053 MEDLINE  
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[PMID]: 25829553
[Au] Autor:Wobeser BK
[Ad] Address:Department of Veterinary Pathology, Western College of Veterinary Medicine, University of Saskatchewan, 52 Campus Drive, Saskatoon, Saskatchewan S7N 5B4.
[Ti] Title:Anthrax vaccine associated deaths in miniature horses.
[So] Source:Can Vet J;56(4):359-60, 2015 Apr.
[Is] ISSN:0008-5286
[Cp] Country of publication:Canada
[La] Language:eng
[Ab] Abstract:During a widespread anthrax outbreak in Canada, miniature horses were vaccinated using a live spore anthrax vaccine. Several of these horses died from an apparent immune-mediated vasculitis temporally associated with this vaccination. During the course of the outbreak, other miniature horses from different regions with a similar vaccination history, clinical signs, and necropsy findings were found.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1504
[Cu] Class update date: 150404
[Lr] Last revision date:150404
[Js] Journal subset:IM
[St] Status:In-Data-Review

  5 / 33053 MEDLINE  
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[PMID]: 25825636
[Au] Autor:Prathiba Rajalakshmi P; Srinivasan K
[Ad] Address:Parameswaran Prathiba Rajalakshmi, Department of Radiology, Sree Balaji Medical College and Hospital, Chromepet, Chennai 600044, Tamil Nadu, India.
[Ti] Title:Gastrointestinal manifestations of Henoch-Schonlein purpura: A report of two cases.
[So] Source:World J Radiol;7(3):66-9, 2015 Mar 28.
[Is] ISSN:1949-8470
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:Henoch-Schonlein purpura (HSP) is a small vessel vasculitis mediated by type III hypersensitivity with deposition of IgA immune complex in the walls of vessels. It is a multi-system disorder characterized by palpable purpura, arthritis, glomerulonephritis and gastrointestinal manifestations and commonly occurs in children and young adults. The patients with gastrointestinal involvement usually present with colicky abdominal pain, vomiting and melena. The imaging findings include multifocal bowel thickening with mucosal hyperenhancement, presence of skip areas, mesenteric vascular engorgement, with involvement of unusual sites like stomach, duodenum and rectum. These imaging findings in a child or young adult with appropriate clinical findings could suggest HSP.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1503
[Cu] Class update date: 150404
[Lr] Last revision date:150404
[Da] Date of entry for processing:150331
[St] Status:PubMed-not-MEDLINE
[do] DOI:10.4329/wjr.v7.i3.66

  6 / 33053 MEDLINE  
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[PMID]: 25604658
[Au] Autor:Crow YJ; Chase DS; Lowenstein Schmidt J; Szynkiewicz M; Forte GM; Gornall HL; Oojageer A; Anderson B; Pizzino A; Helman G; Abdel-Hamid MS; Abdel-Salam GM; Ackroyd S; Aeby A; Agosta G; Albin C; Allon-Shalev S; Arellano M; Ariaudo G; Aswani V; Babul-Hirji R; Baildam EM; Bahi-Buisson N; Bailey KM; Barnerias C; Barth M; Battini R; Beresford MW; Bernard G; Bianchi M; Billette de Villemeur T; Blair EM; Bloom M; Burlina AB; Carpanelli ML; Carvalho DR; Castro-Gago M; Cavallini A; Cereda C; Chandler KE; Chitayat DA; Collins AE; Sierra Corcoles C; Cordeiro NJ; Crichiutti G; Dabydeen L; Dale RC; D'Arrigo S; De Goede CG; De Laet C
[Ad] Address:INSERM UMR 1163, Laboratory of Neurogenetics and Neuroinflammation, Paris Descartes - Sorbonne Paris Cité University, Institut Imagine, Hôpital Necker, Paris, France; Manchester Centre for Genomic Medicine, Institute of Human Development, Faculty of Medical and Human Sciences, Manchester Academic Health Sciences Centre, University of Manchester, Manchester, UK.
[Ti] Title:Characterization of human disease phenotypes associated with mutations in TREX1, RNASEH2A, RNASEH2B, RNASEH2C, SAMHD1, ADAR, and IFIH1.
[So] Source:Am J Med Genet A;167A(2):296-312, 2015 Feb.
[Is] ISSN:1552-4833
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:Aicardi-Goutières syndrome is an inflammatory disease occurring due to mutations in any of TREX1, RNASEH2A, RNASEH2B, RNASEH2C, SAMHD1, ADAR or IFIH1. We report on 374 patients from 299 families with mutations in these seven genes. Most patients conformed to one of two fairly stereotyped clinical profiles; either exhibiting an in utero disease-onset (74 patients; 22.8% of all patients where data were available), or a post-natal presentation, usually within the first year of life (223 patients; 68.6%), characterized by a sub-acute encephalopathy and a loss of previously acquired skills. Other clinically distinct phenotypes were also observed; particularly, bilateral striatal necrosis (13 patients; 3.6%) and non-syndromic spastic paraparesis (12 patients; 3.4%). We recorded 69 deaths (19.3% of patients with follow-up data). Of 285 patients for whom data were available, 210 (73.7%) were profoundly disabled, with no useful motor, speech and intellectual function. Chilblains, glaucoma, hypothyroidism, cardiomyopathy, intracerebral vasculitis, peripheral neuropathy, bowel inflammation and systemic lupus erythematosus were seen frequently enough to be confirmed as real associations with the Aicardi-Goutieres syndrome phenotype. We observed a robust relationship between mutations in all seven genes with increased type I interferon activity in cerebrospinal fluid and serum, and the increased expression of interferon-stimulated gene transcripts in peripheral blood. We recorded a positive correlation between the level of cerebrospinal fluid interferon activity assayed within one year of disease presentation and the degree of subsequent disability. Interferon-stimulated gene transcripts remained high in most patients, indicating an ongoing disease process. On the basis of substantial morbidity and mortality, our data highlight the urgent need to define coherent treatment strategies for the phenotypes associated with mutations in the Aicardi-Goutières syndrome-related genes. Our findings also make it clear that a window of therapeutic opportunity exists relevant to the majority of affected patients and indicate that the assessment of type I interferon activity might serve as a useful biomarker in future clinical trials.
[Pt] Publication type:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Em] Entry month:1501
[Cu] Class update date: 150404
[Lr] Last revision date:150404
[Js] Journal subset:IM
[St] Status:In-Process
[do] DOI:10.1002/ajmg.a.36887

  7 / 33053 MEDLINE  
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[PMID]: 25440712
[Au] Autor:Azevedo FV; Albuquerque Jde D; Gonçalves DP
[Ad] Address:Hospital Geral Dr. Waldemar Alcântara, Fortaleza, CE, Brasil. Electronic address: vileimar@yahoo.com.br.
[Ti] Title:Policondrite recidivante com perda auditiva severa. [Relapsing polychondritis with severe hearing loss].
[So] Source:Rev Bras Reumatol;55(2):174-6, 2015 Mar-Apr.
[Is] ISSN:1809-4570
[Cp] Country of publication:Brazil
[La] Language:por
[Ab] Abstract:Relapsing polychondritis is an uncommon, immune-mediated condition characterized by episodes of inflammation of cartilaginous structures, especially the ears, nose, joints and respiratory tract. RP also affects proteoglycan-rich structures such as the eyes, heart, blood vessels and inner ear. Around one third of cases are associated with other diseases such as vasculitides, connective tissue diseases or myelodysplastic syndrome. Disorders of the inner ear occur in 40-50% of patients. Profound hearing loss is rare. The aim of this study was to describe the case of a patient with relapsing polychondritis associated with severe bilateral hearing loss and clinical manifestations of systemic vasculitis. This study reinforces the importance of an early diagnosis and immediate treatment in case of severe manifestations of the disease.
[Pt] Publication type:ENGLISH ABSTRACT; JOURNAL ARTICLE
[Em] Entry month:1504
[Js] Journal subset:IM
[St] Status:In-Data-Review

  8 / 33053 MEDLINE  
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[PMID]: 25839768
[Au] Autor:Yu HH; Liu PH; Yang YH; Lee JH; Wang LC; Chen WJ; Chiang BL
[Ad] Address:Department of Pediatrics, National Taiwan University Hospital, Taipei, Taiwan, ROC....
[Ti] Title:Chemokine MCP1/CCL2 and RANTES/CCL5 gene polymorphisms influence Henoch-Schönlein purpura susceptibility and severity.
[So] Source:J Formos Med Assoc;114(4):347-52, 2015 Apr.
[Is] ISSN:0929-6646
[Cp] Country of publication:China (Republic : 1949- )
[La] Language:eng
[Ab] Abstract:BACKGROUND/PURPOSE: Henoch-Schönlein purpura (HSP) is the most common small vessel vasculitis in children. It is considered to be an IgA-containing immune complex-mediated disease. Chemokines are small secreted proteins that attract leukocytes during inflammation. Our aim was to determine the serum levels of chemokines and investigate the association of chemokine gene polymorphisms with childhood HSP. METHODS: Serum levels of chemokines (interleukin-8/CXCL8, MCP-1/CCL2, RANTES/CCL5, MIG/CXCL9, and IP-10/CXCL10) were determined using cytometric beads arrays. We investigated the association of three single-nucleotide polymorphisms (SNPs) MCP1/CCL2 -2518C/T, RANTES/CCL5 -403C/T, and RANTES/CCL5 -28C/G with HSP in 85 HSP patients and 136 healthy controls. RESULTS: Five serum chemokine levels were significantly elevated in patients with the acute stage of HSP compared to the normal controls (p < 0.05). MCP1/CCL2 -2518 TT genotype and T allele were associated with the risk for HSP with OR (95% CI) 3.32 (1.45-7.59) and 1.78 (1.20-2.64), respectively. The RANTES/CCL5 -28 GG genotype was associated with a significantly lower percentage of corticosteroid usage and lower corticosteroid accumulative dose in HSP patients. RANTES/CCL5 -403 TC and TT genotype were significantly associated with renal manifestations with an OR (95% CI) of 4.33 (1.44-12.99), adjusted for sex and age and the other two SNP genotypes. CONCLUSION: Our results support the fact that chemokines play important roles in the pathogenesis of HSP. MCP1/CCL2 gene polymorphisms were associated with susceptibility for HSP. RANTES/CCL5 gene polymorphisms may be related to disease severity and HSP nephritis.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1504
[Js] Journal subset:IM
[St] Status:In-Data-Review

  9 / 33053 MEDLINE  
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[PMID]: 25714389
[Au] Autor:Lokhov PG; Balashova EE
[Ad] Address:a Institute of Biomedical Chemistry ; Moscow , Russia.
[Ti] Title:Design of universal cancer vaccines using natural tumor vessel-specific antigens (SANTAVAC).
[So] Source:Hum Vaccin Immunother;11(3):689-98, 2015 Mar 4.
[Is] ISSN:2164-554X
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:Vaccination against endothelial cells (ECs) lining the tumor vasculature represents one of the most attractive potential cancer immunotherapy options due to its ability to prevent solid tumor growth. Using this approach, target antigens can be derived from ECs and used to develop a universal cancer vaccine. Unfortunately, direct immunization with EC preparations can elicit autoimmune vasculitis in normal tissues. Recently, tumor-induced changes to the human EC surface were described that provided a basis for designing efficient EC-based vaccines capable of eliciting immune responses that targeted the tumor endothelium directly. This review examines these data from the perspective of designing EC-based cancer vaccines for the treatment of all solid tumors, including the antigen composition of vaccine formulations, the selection ECs for antigen derivation, the production and control of antigens, and the method for estimating vaccine efficacy and safety. As the vaccine preparation requires a specifically derived set of natural cell surface antigens, a new vaccine preparation concept was formulated. Antigen compositions prepared according to this concept were named SANTAVAC (Set of All Natural Target Antigens for Vaccination Against Cancer).
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1504
[Js] Journal subset:IM
[St] Status:In-Data-Review
[do] DOI:10.1080/21645515.2015.1011022

  10 / 33053 MEDLINE  
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[PMID]: 25817017
[Au] Autor:Carmona FD; Mackie SL; Martín JE; Taylor JC; Vaglio A; Eyre S; Bossini-Castillo L; Castañeda S; Cid MC; Hernández-Rodríguez J; Prieto-González S; Solans R; Ramentol-Sintas M; González-Escribano MF; Ortiz-Fernández L; Morado IC; Narváez J; Miranda-Filloy JA; Beretta L; Lunardi C; Cimmino MA; Gianfreda D; Santilli D; Ramirez GA; Soriano A; Muratore F; Pazzola G; Addimanda O; Wijmenga C; Witte T; Schirmer JH; Moosig F; Schönau V; Franke A; Palm Ø; Molberg Ø; Diamantopoulos AP; Carette S; Cuthbertson D; Forbess LJ; Hoffman GS; Khalidi NA; Koening CL; Langford CA; McAlear CA; Moreland L; Monach PA; Pagnoux C; Seo P; Spiera R; Spanish GCA Group
[Ad] Address:Instituto de Parasitología y Biomedicina "López-Neyra," CSIC, PTS Granada, Granada 18016, Spain. Electronic address: dcarmona@ipb.csic.es....
[Ti] Title:A Large-Scale Genetic Analysis Reveals a Strong Contribution of the HLA Class II Region to Giant Cell Arteritis Susceptibility.
[So] Source:Am J Hum Genet;96(4):565-80, 2015 Apr 2.
[Is] ISSN:1537-6605
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:We conducted a large-scale genetic analysis on giant cell arteritis (GCA), a polygenic immune-mediated vasculitis. A case-control cohort, comprising 1,651 case subjects with GCA and 15,306 unrelated control subjects from six different countries of European ancestry, was genotyped by the Immunochip array. We also imputed HLA data with a previously validated imputation method to perform a more comprehensive analysis of this genomic region. The strongest association signals were observed in the HLA region, with rs477515 representing the highest peak (p = 4.05 × 10(-40), OR = 1.73). A multivariate model including class II amino acids of HLA-DRß1 and HLA-DQα1 and one class I amino acid of HLA-B explained most of the HLA association with GCA, consistent with previously reported associations of classical HLA alleles like HLA-DRB1(∗)04. An omnibus test on polymorphic amino acid positions highlighted DRß1 13 (p = 4.08 × 10(-43)) and HLA-DQα1 47 (p = 4.02 × 10(-46)), 56, and 76 (both p = 1.84 × 10(-45)) as relevant positions for disease susceptibility. Outside the HLA region, the most significant loci included PTPN22 (rs2476601, p = 1.73 × 10(-6), OR = 1.38), LRRC32 (rs10160518, p = 4.39 × 10(-6), OR = 1.20), and REL (rs115674477, p = 1.10 × 10(-5), OR = 1.63). Our study provides evidence of a strong contribution of HLA class I and II molecules to susceptibility to GCA. In the non-HLA region, we confirmed a key role for the functional PTPN22 rs2476601 variant and proposed other putative risk loci for GCA involved in Th1, Th17, and Treg cell function.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1504
[Js] Journal subset:IM
[St] Status:In-Data-Review


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