10 research outputs found
miRNA-31 Improves Cognition and Abolishes Amyloid-beta Pathology by Targeting APP and BACE1 in an Animal Model of Alzheimer's Disease
Alzheimer's disease (AD) is the most common form of dementia worldwide, characterized by progressive memory impairment, behavioral changes, and, ultimately, loss of consciousness and death. Recently, microRNA (miRNA) dysfunction has been associated with increased production and impaired clearance of amyloid-ÎČ (AÎČ) peptides, whose accumulation is one of the most well-known pathophysiological markers of this disease. In this study, we identified several miRNAs capable of targeting key proteins of the amyloidogenic pathway. The expression of one of these miRNAs, miR-31, previously found to be decreased in AD patients, was able to simultaneously reduce the levels of APP and Bace1 mRNA in the hippocampus of 17-month-old AD triple-transgenic (3xTg-AD) female mice, leading to a significant improvement of memory deficits and a reduction in anxiety and cognitive inflexibility. In addition, lentiviral-mediated miR-31 expression significantly ameliorated AD neuropathology in this model, drastically reducing AÎČ deposition in both the hippocampus and subiculum. Furthermore, the increase of miR-31 levels was enough to reduce the accumulation of glutamate vesicles in the hippocampus to levels found in non-transgenic age-matched animals. Overall, our results suggest that miR-31-mediated modulation of APP and BACE1 can become a therapeutic option in the treatment of AD.This work was financed by the European Regional Development Fund (ERDF), through the Centro 2020 Regional Operational Programme under the project CENTRO-01-0145-FEDER-000008: BrainHealth 2020 and through the COMPETE 2020 - Operational Programme for Competitiveness and Internationalisation and Portuguese national funds via FCT - Fundação para a CiĂȘncia e a Tecnologia, under the project POCI- 01-0145-FEDER-007440 (reference UID/NEU/04539/2013). This work was also supported by the FCT Investigator Programme (IF/ 00694/2013 to J.P.), the Marie Curie Carrier Integration Grant (PCIG13-GA-2013-618525 to J.P.), HEALTHYAGING 2020 (CENTRO-01-0145-FEDER-000012 to A.T.B.-V.), and Bial Foundation Grant 264/16. A.T.B.-V., J.G., and A.L.C. are recipients of fellowships from the FCT (Grants PTDC/BIM-MEC/0651/2012, SFRH/ BPD/120611/2016, and SFRH/BPD/108312/2015)
Pervasive gaps in Amazonian ecological research
Biodiversity loss is one of the main challenges of our time,1,2 and attempts to address it require a clear un derstanding of how ecological communities respond to environmental change across time and space.3,4
While the increasing availability of global databases on ecological communities has advanced our knowledge
of biodiversity sensitivity to environmental changes,5â7 vast areas of the tropics remain understudied.8â11 In
the American tropics, Amazonia stands out as the worldâs most diverse rainforest and the primary source of
Neotropical biodiversity,12 but it remains among the least known forests in America and is often underrepre sented in biodiversity databases.13â15 To worsen this situation, human-induced modifications16,17 may elim inate pieces of the Amazonâs biodiversity puzzle before we can use them to understand how ecological com munities are responding. To increase generalization and applicability of biodiversity knowledge,18,19 it is thus
crucial to reduce biases in ecological research, particularly in regions projected to face the most pronounced
environmental changes. We integrate ecological community metadata of 7,694 sampling sites for multiple or ganism groups in a machine learning model framework to map the research probability across the Brazilian
Amazonia, while identifying the regionâs vulnerability to environmental change. 15%â18% of the most ne glected areas in ecological research are expected to experience severe climate or land use changes by
2050. This means that unless we take immediate action, we will not be able to establish their current status,
much less monitor how it is changing and what is being lostinfo:eu-repo/semantics/publishedVersio
Pervasive gaps in Amazonian ecological research
Biodiversity loss is one of the main challenges of our time,1,2 and attempts to address it require a clear understanding of how ecological communities respond to environmental change across time and space.3,4 While the increasing availability of global databases on ecological communities has advanced our knowledge of biodiversity sensitivity to environmental changes,5,6,7 vast areas of the tropics remain understudied.8,9,10,11 In the American tropics, Amazonia stands out as the world's most diverse rainforest and the primary source of Neotropical biodiversity,12 but it remains among the least known forests in America and is often underrepresented in biodiversity databases.13,14,15 To worsen this situation, human-induced modifications16,17 may eliminate pieces of the Amazon's biodiversity puzzle before we can use them to understand how ecological communities are responding. To increase generalization and applicability of biodiversity knowledge,18,19 it is thus crucial to reduce biases in ecological research, particularly in regions projected to face the most pronounced environmental changes. We integrate ecological community metadata of 7,694 sampling sites for multiple organism groups in a machine learning model framework to map the research probability across the Brazilian Amazonia, while identifying the region's vulnerability to environmental change. 15%â18% of the most neglected areas in ecological research are expected to experience severe climate or land use changes by 2050. This means that unless we take immediate action, we will not be able to establish their current status, much less monitor how it is changing and what is being lost
Genetic analysis of SURF gene in patients with isolated complex IV deficiency
A mitocĂŽndria Ă© um organelo subcelular com um papel preponderante no
metabolismo energético, em particular, relacionado com a fosforilação oxidativa
(OXPHOS). Encontra-se presente em maior nĂșmero em tecidos e ĂłrgĂŁos que requerem
elevados nĂveis de energia, como por exemplo, cĂ©rebro e mĂșsculo.
A produção de ATP (energia) ocorre pelo processo de OXPHOS, num sistema
multienzimĂĄtico, constituĂdo por cinco complexos proteicos e dois transportadores
intermediårios de electrÔes que formam o sistema da cadeia respiratória mitocondrial.
As doenças mitocondriais são caracterizadas por defeitos na OXPHOS,
constituindo um grupo designado por Doenças da Cadeia Respiratória Mitocondrial
(MRCD).
Diversos estudos tĂȘm comprovado que o sistema de OXPHOS Ă© codificado pelo
genoma mitocondrial (mtDNA) e nuclear (nDNA), o que leva a que a função
mitocondrial esteja dependente da coordenação e interacção entre os dois genomas.
Assim, mutaçÔes em qualquer um dos genomas podem originar uma disfunção
mitocondrial. Consequentemente, as DCRM sĂŁo caracterizadas por uma enorme
variedade de sintomas e encontram-se associadas a todos os tipos de hereditariedade,
podendo-se manifestar em qualquer idade, desde a infùncia até à idade adulta, o que
torna o seu diagnĂłstico complexo.
Qualquer alteração num dos cinco complexos pode afectar o funcionamento do
sistema de OXPHOS. Contudo, os défices dos complexos enzimåticos I e IV são os
mais frequentemente observados.
A citocromo c oxidase (COX) â complexo IV - Ă© o componente terminal da
cadeia de transporte de electrÔes, que são transferidos do citocromo c para o oxigénio
molecular, reduzindo-o a ĂĄgua. Este complexo Ă© constituĂdo por trĂȘs subunidades
codificadas pelo genoma mitocondrial (COX I, COX II e COX III) e dez subunidades
codificadas pelo genoma nuclear (COX4, COX5A, COX5B, COX6A, COX6B,
COX6C, COX7A, COX7B, COX7C e COX8). Alguns estudos tĂȘm referido que estas
subunidades conferem estabilidade estrutural e modulam a actividade da enzima,
estando envolvidas na produção de energia em diferentes tecidos, bem como no
desenvolvimento ontogenético.
A biogénese e o assembly do complexo IV mitocondrial ocorrem de acordo com
uma sequĂȘncia temporizada de diversos passos de incorporação das treze subunidades.
Este processo resulta na formação de intermediårios (S1-S4) e depende de um elevado
nĂșmero de genes especĂficos, tanto no genoma nuclear como no genoma mitocondrial.
AlteraçÔes nesses genes podem levar a falhas na actividade daquele complexo.
A sĂndrome de Leigh (LS) Ă© a doença neurodegenerativa mitocondrial
progressiva, podendo ocorrer na infĂąncia ou na idade adulta e Ă© caracterizada pela
presença de lesĂ”es neurolĂłgicas especĂficas. Esta doença tem sido relacionada com o
dĂ©fice da actividade da COX em dois grupos de doentes diferentes: LS tĂpico, associado
ao dĂ©fice isolado grave; e LS atĂpico, com dĂ©fice parcial da COX. Os doentes do
primeiro grupo tĂȘm sido frequentemente diagnosticados com mutaçÔes no gene SURF1,
correspondendo a 10-15% dos casos.
O gene Surfeit-1 (ou SURF1) é um gene nuclear que contém 4.696bp e encontrase
localizado na posição do cromossoma 9q34.2. Este codifica um polipeptĂdeo
hidrofĂłbico (Surfeit locus protein 1 â Surf1p), que se encontra na membrana interna
mitocondrial e que estĂĄ envolvido no assembly da COX. Este gene pertence a um
cluster de genes housekeeping, cuja extremidade 5â Ă© extremamente rica em GC.
Diversos estudos mostraram que a Surf1p estĂĄ envolvida no assembly da COX,
ao nĂvel dos intermediĂĄrios S2 e S3, relativamente Ă inserção da subunidade COX II no
subcomplexo COX I + COX 4 + COX5A. Assim, o dĂ©fice isolado da COX, devido Ă
ausĂȘncia/disfunção da Surf1p, estĂĄ associado a uma falha no assembly do complexo,
mais especificamente, antes da inserção das subunidades II e III no subcomplexo
anteriormente formado, o que leva a uma diminuição da incorporação das subunidades
da COX e, consequentemente, menor quantidade da holoenzima COX. Esta redução foi
demonstrada, por vårios autores, em doentes com LS portadores de mutaçÔes no
SURF1, apoiando esta hipótese. Actualmente, existem mais de 40 mutaçÔes descritas
neste gene nuclear.
O presente trabalho tem como objectivo identificar alteraçÔes no gene SURF1
em doentes com défice isolado da COX. Com este propósito, a anålise genética foi
realizada através das técnicas de sequenciação automåtica e RFLP, tendo sido também
utilizadas ferramentas de anålise in silico para previsão da patogenicidade das alteraçÔes
identificadas. Para este trabalho, foram usadas amostras de DNA, previamente extraĂdas no
LaboratĂłrio de BioquĂmica GenĂ©tica, a partir de tecido proveniente de 24 doentes com
défice isolado da COX (<40% que o normal), identificado por espectofotometria.
A anĂĄlise genĂ©tica do gene SURF1 (exĂ”es 3 â 9) na amostragem estudada,
permitiu identificar oito alteraçÔes diferentes, das quais quatro ainda não se encontram
descritas, em 24 doentes. Das oito variaçÔes de sequĂȘncia, todas ocorrem em zonas
conservadas ao longo da evolução, e quatro ocorrem em zonas não codificantes,
enquanto que as restantes surgem em exÔes; contudo, apenas duas alteram o aminoåcido
(missense). A anĂĄlise in silico das variaçÔes de sequĂȘncia sugere que Ă© pouco provĂĄvel
que as alteraçÔes nos intrÔes afectem o processo de splicing; no entanto, as duas
variaçÔes missense (c.574C>T e c.883C>T) são provavelmente patogénicas.
A alteração c.574C>T, no exão 6, leva à substituição de arginina por triptofano e
foi identificada em homozigotia no doente 6, com LS, o que estĂĄ de acordo com estudos
anteriormente realizados, que associam a presença desta alteração à doença. A alteração
c.883C>T, no exĂŁo 9, foi identificada em heterozigotia no doente 16 e origina a
substituição de arginina por cisteĂna num doente com menos de cinco anos de idade, que
apresenta sĂndrome malformativo, atraso do desenvolvimento psicomotor e fĂĄcies
grosseira. Esta variação de sequĂȘncia ainda nĂŁo se encontra descrita e poderĂĄ ser
importante na identificação das causas do fenĂłtipo clĂnico.
Como perspectiva futura e no sentido de complementar este estudo, pretende-se
analisar os exĂ”es 1 e 2 do gene, de modo a verificar a existĂȘncia de mutaçÔes
responsåveis pela doença e realizar estudos funcionais que comprovem a associação das
alteraçÔes identificadas com o fenĂłtipo clĂnico. Seria ainda Ăștil analisar controlos
normais para esclarecer melhor a existĂȘncia das alteraçÔes apenas em doentes.
Este trabalho representa uma contribuição positiva para o diagnóstico genético
dos doentes com défice isolado da COX no laboratório de acolhimento, com um
impacto importante no aconselhamento genético
Artes da Fala
Decorreu nos dias 27, 28 e 29 de Junho de 1996, na vila de Portel, o colĂłquio intitulado Artes da Fala e subordinado ao tema da oralidade a sul do rio Tejo numa perspectiva antropolĂłgica. Organizado pela CĂąmara Municipal de Portel e pelo Centro de TradiçÔes Populares Portuguesas (Universidade de Lisboa), tendo o professor Manuel Viegas Guerreiro assegurado a respectiva coordenação cientĂfica. A realização do evento traduz a congregação de esforços entre uma unidade cientĂfica e uma entidade autĂĄrquica para que durante as jornadas referidas se criasse um ambiente de estĂmulos mĂștuos. Durante as sessĂ”es do ColĂłquio de Portel foram debatidas questĂ”es relacionadas com a abordagem da oralidade no Sul de Portugal. Este tema tem um significado duplo. Se, por um lado, fornece matĂ©ria para a construção de memĂłria, por outro, caracteriza realidades presentes. Distinguir estas questĂ”es implicou interrogar a noção de cultura popular. Ao fazĂȘ-lo, somos obrigados a desfazer dicotomias no nosso modo de pensar
7th drug hypersensitivity meeting: part one
Table of contents
Oral Abstracts
O1 Functionally distinct HMGB1 isoforms correlate with physiological processes in drug-induced SJS/TEN
Daniel F. Carr, Wen-Hung Chung, Rosalind E. Jenkiins, Mas Chaponda, Gospel Nwikue, Elena M. Cornejo Castro, Daniel J. Antoine, Munir Pirmohamed
O2 Hypersensitivity reactions to beta-lactams, does the t cell recognition pattern influence the clinical picture?
Natascha Wuillemin, Dolores Dina, Klara K. Eriksson, Daniel Yerly
O3 Specific binding characteristics of HLA alleles associated with nevirapine hypersensitivity
Rebecca Pavlos, Elizabeth Mckinnin, David Ostrov, Bjoern Peters, Soren Buus, David Koelle, Abha Chopra, Craig Rive, Alec Redwood, Susana Restrepo, Austin Bracey, Jing Yuan, Silvana Gaudieri, Mary Carrington, David Haas, Simon Mallal, Elizabeth Phillips
O4 Do we need to measure total ige for the interpretation of analytical results of ImmunoCAP dnd 3gAllergy specific IgE?
Douwe De Boer, Paul Menheere, Chris Nieuwhof, Judith Bons
O5 Neutrophil activation in systemic anaphylaxis: results from the multicentric NASA study
Friederike Jonsson, Luc De Chaisemartin, Vanessa Granger, Caitlin Gillis, Aurelie Gouel, Catherine Neukirch, Fadia Dib, Pascale Roland Nicaise, Dan Longrois, Florence Tubach, Sylvie Martin, Pierre Bruhns, NASA Study Group
O6 Purpuric drug eruptions due to epidermal growth factor receptor tyrosine kinase inhibitors (EGFR-TKIs) for non-small-cell lung cancer (NSCLC): a clinic-pathological study of 32 cases
Kai-Lung Chen, Shu-Ling Liao, Yi-Shuan Sheen, Yung-Tsu Cho, Che-Wen Yang, Jau-Yu Liau, Chia-Yu Chu
Poster presentations: Poster Walk 1âAnaphylaxis (P01âP09)
P1 Anaphylactic reactions during anaesthesia and the perioperative period
Rita Aguiar, Anabela Lopes, NatĂĄlia Fernandes, Leonor Viegas, M. A. Pereira-Barbosa
P2 Anaphylaxis to chlorhexidine: is there a cross-reactivity to alexidine?
Antonia BĂŒnter, Nisha Gupta, Tatjana Pecaric Petkovic, Nicole Wirth, Werner J. Pichler, Oliver Hausmann
P3 Cefotaxime-induced severe anaphylaxis in a neonate
Mehtap Yazicioglu, Pinar G. Ozdemir, Gokce Ciplak, Ozkan Kaya
P4 Clinical features and diagnosis of anaphylaxis resulting from exposure to chlorhexidine
Peter John Cooke
P5 Drug-induced anaphylaxis: five-year single-center survey
InĂȘs Mota, Ăngela Gaspar, Filipe Benito-Garcia, Marta Chambel, MĂĄrio Morais-Almeida
P6 Intraoperative severe anaphylactic reaction due to patent blue v dye
Luis Marques, Eva Alcoceba, Silvia Lara
P7 Kounis syndrome in the setting of anaphylaxis to diclofenac
Leonor Carneiro-LeĂŁo, Carmen Botelho, Eunice Dias-Castro, Josefina Cernadas
P8 Perioperative anaphylaxis audit: Royal Melbourne Hospital
Katherine Nicholls, William Lay, Olivia Smith, Christine Collins, Gary Unglik, Kymble Spriggs, Priscilla Auyeung, Jeremy McComish, Jo A. Douglass
P9 Recurrent peri-operative anaphylaxis: a perfect storm
Jonny G. Peter, Paul Potter
Poster Walk 2: DH regions and patient groups (P10âP19)
P10 A rare presentation of amoxicillin allergy in a young child
FabrĂcia Carolino, Eunice Dias De Castro, Josefina R. Cernadas
P11 Adverse drug reactions in children: antibiotics or virus?
Ana Sofia Moreira, Carmo Abreu, Eva Gomes
P12 Allergic reactions in invasive medical procedures
BĂĄrbara Kong Cardoso, Elza Tomaz, Sara Correia, Filipe InĂĄcio
P13 Antibiotic allergy in children: room for improvement
Annabelle Arnold, Natasha Bear, Kristina Rueter, Grace Gong, Michael OâSullivan, Saravanan Muthusamy, Valerie Noble, Michaela Lucas
P14 Drug hypersensitivity reactions in children and results of diagnostic evaluation
Neringa Buterleviciute, Odilija Rudzeviciene
P15 Nonimmediate cutaneous drug reactions in children: are skin tests required?
Ana Sofia Moreira, Carmo Abreu, Eva Gomes
P16 Pediatric patients with a history of penicillin allergy and a positive penicillin skin test may not be at an increased risk for multiple drug allergies
Sara May, Thanai Pongdee, Miguel Park
P17 Proved hypersensitivity to drugs according data of Vilnius University Hospital Santariskiu Klinikos
Linas Griguola, Arturas Vinikovas, Simona KaĆĄinskaite, Violeta Kvedariene
P18 Self-reported prevalence of drug hypersensitivity reactions among students in Celal Bayar University, Turkey
Ayse Aktas, Suheyla Rahman, Huseyin Elbi, Beyhan Cengiz Ozyurt
P19 Severe drug hypersensitivity reactions in pediatric age
Ozlem Cavkaytar, Betul Karaatmaca, Pinar Gur Cetinkaya, Saliha Esenboga, Umit M. Sahiner, Bulent E. Sekerel, Ozge Soyer
Poster Walk 3: Desensitisation (P20âP28)
P20 A protocol for desensitisation to valaciclovir
Celia Zubrinich, Bianca Tong, Mittal Patel, Michelle Giles, Robyn OâHehir, Robert Puy
P21 A rare case of desensitization to modafinil
Josefina Cernadas, LuĂs Amaral, FabrĂcia Carolino
P22 A sixteen-day desensitization protocol in delayed type hypersensitivity reactions to oral drugs
Semra Demir, Asli Gelincik, Muge Olgac, Raif Caskun, Derya Unal, Bahauddin Colakoglu, Suna Buyukozturk
P23 Desensitization to intravenous etoposide using a 12 and a 13-step protocol. Two cases report
Olga Vega Matute, Amalia Bernad, Gabriel Gastaminza, Roselle Madamba, Carlos Lacasa, M. J. Goikoetxea, Carmen DâAmelio, Jose RifĂłn, Nicolas MartĂnez, Marta Ferrer
P24 Drug desensitisation in oncology: the experience of an immunoallergology department for 5Â years
Carmelita Ribeiro, EmĂlia Faria, Cristina Frutuoso, Anabela Barros, RosĂĄrio Lebre, Alice Pego, Ana Todo Bom
P25 Filgrastim anaphylaxis: a successful desensitization protocol
Luis Amaral, Josefina Cernadas
P26 Galsulfase hypersensitivity and desensitization of a mucopolysaccharidosis VI patient
Luis Felipe Ensina, Carolina Aranda, Ines Camelo Nunes, Ana Maria Martins, Dirceu Solé
P27 Rapid drug desensitization with biologicals: one-center experience with four biologicals
Sevim Bavbek, Resat Kendirlinan, Pamir Ăerçi, Seda Tutluer, Sadan Soyyigit, Zeynep Ăelebi Sözener, ĂmĂŒr Aydin, Reyhan GĂŒmĂŒsburun
P28 Successful desensitization to a high dose of methotrexate in a delayed type hypersensitivity reaction
Josefina Cernadas, Leonor Carneiro-LeĂŁo, FabrĂcia Carolino, Marta Almeida
Poster Walk 4: SJS (P29âP38)
P29 Assessment of impact of infection on drug-induced severe cutaneous adverse reactions and rhabdomyolysis using the Japanese adverse drug event report database
Kimie Sai, Takuya Imatoh, Ryosuke Nakamura, Chisato Fukazawa, Yasushi Hinomura, Yoshiro Saito
P30 Characterization of erythema multiforme and severe cutaneous adverse reactions hospitalizations
Bernardo Sousa-Pinto, ClĂĄudia Correia, LĂdia Gomes, Sara Gil-Mata, LuĂs AraĂșjo, LuĂs Delgado
P31 Effects of infection on incidence/severity of SJS/TEN and myopathy in Japanese cases analyzed by voluntary case reports
Ryosuke Nakamura, Kimie Sai, Takuya Imatoh, Yoshimi Okamoto-Uchida, Koji Kajinami, Kayoko Matsunaga, Michiko Aihara, Yoshiro Saito
P32 Efficacy of tumor necrosis factorâa antagonists in StevensâJohnson syndrome and toxic epidermal necrolysis: a randomized controlled trial and immunosuppressive effects evaluation
Chuang-Wei Wang, Shih-Chi Su, Shuen-Iu Hung, Hsin-Chun Ho, Chih-Hsun Yang, Wen-Hung Chung
P33 Evolution of drug causality in StevensâJohnson syndrome and toxic epidermal necrolysis in Europe: analysis of 10Â years RegiSCAR-Study
Maren Paulmann, Ariane Dunant, Maja Mockenhaupt, Peggy Sekula, Martin Schumacher, Sylvia Kardaun, Luigi Naldi, Teresa Bellón, Daniel Creamer, Cynthia Haddad, Bruno Sassolas, Bénédicte Lebrun-Vignes, Laurence Valeyrie-Allanore, Jean-Claude Roujeau
P34 Long-term sequelae in patients with StevensâJohnson syndrome and toxic epidermal necrolysis: a 5-year analysis
Maren Paulmann, Carmen Kremmler, Peggy Sekula, Laurence Valeyrie-Allanore, Luigi Naldi, Sylvia Kardaun, Maja Mockenhaupt
P35 Major emotional complications and decreased health related quality of life among survivors of StevensâJohnson syndrome and toxic epidermal necrolysis
Roni P. Dodiuk-Gad, Cristina Olteanu, Anthony Feinstein, Rena Hashimoto, Raed Alhusayen, Sonia Whyte-Croasdaile, Yaron Finkelstein, Marjorie Burnett, Shachar Sade, Robert Cartotto, Marc Jeschke, Neil H. Shear
P36 Retrospective analysis of StevensâJohnson syndrome and toxic epidermal necrolysis in Japanese patients: treatment and outcome
Naoko Takamura, Yumiko Yamane, Setsuko Matsukura, Kazuko Nakamura, Yuko Watanabe, Yukie Yamaguchi, Takeshi Kambara, Zenro Ikezawa, Michiko Aihara
P37 Severe physical complications among survivors of StevensâJohnson syndrome and toxic epidermal necrolysis
Roni P. Dodiuk-Gad, Cristina Olteanu, Rena Hashimoto, Hall Chew, Raed Alhusayen, Sonia Whyte-Croasdaile, Yaron Finkelstein, Marjorie Burnett, Shachar Sade, Robert Cartotto, Marc Jeschke, Neil H. Shear
P38 StevensâJohnson syndrome/toxic epidermal necrolysis combined with haemophagocytic lymphohistiocytosis: a case report
Brittany Knezevic, Una Nic Ionmhain, Allison Barraclough, Michaela Lucas, Matthew Anstey
Poster Walk 5: Other organs/unexpected immune reactions (P39âP47)
P39 A case report of patient with anti-tuberculosis drug-related severe liver failure
Toru Usui, Xiaoli Meng, John Farrell, Paul Whitaker, John Watson, Neil French, Kevin Park, Dean Naisbitt
P40 Acute interstitial nephritis induced by ibuprofen
Ana Castro Neves, Susana Cadinha, Ana Moreira, J. P. Moreira Da Silva
P41 Cetuximab induced acneiform rashâtwo case reports
Daniela Ledic Drvar, Sandra Jerkovic Gulin, Suzana Ljubojevic Hadzavdic, Romana Ceovic
P42 Enteropathy associated with losartan
Ana Montoro De Francisco, TalĂa De Vicente JimĂ©nez, Amelia GarcĂa Luque, Natalia Rosado David, JosĂ© MÂȘ Mateos GalvĂĄn
P43 Granuloma annulare after therapy with canakinumab
Razvigor Darlenski
P44 Hypersensitivity eosinophilic myocarditis or acute coronary syndrome? Case report
Dario Gulin, Jozica Sikic, Jasna Cerkez Habek, Sandra Jerkovic Gulin, Edvard Galic
P45 Piperacillin-induced immune haemolytic anaemia: a severe and frequent complication of antibiotic treatment in patients with cystic fibrosis
Philip Specht, Doris Staab, Beate Mayer, Jobst Roehmel
P46 Progesterone triggered pemphigus foliaceus: case report
Sandra Jerkovic Gulin, Caius Solovan, Anca Chiriac
P47 Ramipril: triggered generalized pustular psoriasis
Paola Djurinec, Kresimir Kostovic, Mirna Bradamante, Sandra Jerkovic Gulin, Romana Ceovic
Poster Walk 6: NSAIDs (P48âP56)
P48 Aspirin desensitization in cardiovascular diseaseâPortuguese experience
Jose Pedro Almeida, Joana Caiado, Elisa Pedro, Pedro Canas Da Silva, Manuel Pereira Barbosa
P49 Asthma and/or rhinitis to NSAIDs with good tolerance to ASA
Gador Bogas, Natalia Blanca-LĂłpez, Diana PĂ©rez-Alzate, Inmaculada Doña, JosĂ© Augusto AgĂșndez, Elena GarcĂa-MartĂn, JosĂ© Antonio Cornejo-GarcĂa, Cristobalina Mayorga, MarĂa JosĂ© Torres, Gabriela Canto, Miguel Blanca
P50 Clinical characteristics of 196 patients with non-steroidal anti-inflammatory drug (NSAIDs) hypersensitivity
SengĂŒl Aksakal, AytĂŒl Zerrin Sin, Zeynep Peker Koç, Fatma DĂŒsĂŒnĂŒr GĂŒnsen, ĂmĂŒr Ardeniz, Emine Nihal Mete Gökmen, Okan GĂŒlbahar, Ali Kokuludag
P51 Development of immediate hypersensitivity to several NSAIDs maintaining good tolerance to ASA
Natalia PĂ©rez-SĂĄnchez, Natalia Blanca-LĂłpez, Diana PĂ©rez-Alzate, Gador Bogas, Inmaculada Doña, MarĂa Salas, MarĂa JosĂ© Torres, Miguel Blanca, Gabriela Canto
P52 Diagnosis of hypersensitivity reactions to paracetamol in a large series of cases
Inmaculada Doña, Maria Salas, Francisca Gomez, Natalia Blanca-Lopez, Diana Perez-Alzate, Gador Bogas, Esther Barrionuevo, Maria Jose Torres, Inmaculada Andreu, Miguel Ăngel Miranda, Gabriela Canto, Miguel Blanca
P53 Hypersensitivity to paracetamol according to the new classification of hypersensitivity to NSAIDs
Gabija DidĆŸiokaite, Olesia Gaidej, Simona KaĆĄinskaite, Violeta Kvedariene
P54 Ibuprofen and other aryl propionic derivates can induce immediate selective hypersensitivity responses
Diana Perez-Alzate, Natalia Blanca-López, Maria Isabel Garcimartin, Inmaculada Doña, Maria Luisa Somoza, Cristobalina Mayorga, Maria Jose Torres, Gador Bojas, Jose Antonio Cornejo-Garcia, Maria Gabriela Canto, Miguel Blanca
P55 Subjects developing immediate responses to several NSAIDs can be selective with good tolerance to ASA
Natalia Blanca-Lopez, Diana Pérez-Alzate, Francisco Javier Ruano Perez, Inmaculada Doña, Maria Luisa Somoza, Inmaculada Andreu, Miguel Angel Miranda, Cristobalina Mayorga, Maria Jose Torres, Jose Antonio Cornejo-Garcia, Miguel Blanca, Maria Gabriela Canto
P56 Utility of low-dose oral aspirin challenges for diagnosis of aspirin exacerbated respiratory disease
Elina Jerschow, Teresa Pelletier, Zhen Ren, Golda Hudes, Marek Sanak, Esperanza Morales, Victor Schuster, Simon D. Spivack, David Rosenstreich
Poster Walk 7: NSAID 2 (P57âP65)
P57 Alternate regulation of cyclooxygenase-2 (COX-2) MRNA expression may predispose patients to aspirin-induced exacerbations
Renato Erzen, Mira Silar, Nissera Bajrovic, Matija Rijavec, Mihaela Zidarn, Peter Korosec
P58 Anaphylaxis to diclofenac: what about the underlying mechanism?
Leonor Carneiro-LeĂŁo, FabrĂcia Carolino, LuĂs Amaral, Carmen Botelho, Eunice Dias-Castro, Josefina Cernadas
P59 COX-2 inhibitors: are they always a safe alternative in hypersensitivity to nonsteroidal anti-inflammatory drugs?
Luis Amaral, Fabricia Carolino, Eunice Castro, Josefina Cernadas
P60 Management of patients with history of NSAIDs reactions prior to coronary angioplasty
Mona Al-Ahmad, Tito Rodriguez
P61 Oral drug challenge with non-steroidal anti-inflammatory drug under spirometric control: clinical series of 110 patients
JoĂŁo Pedro Azevedo, EmĂlia Faria, Beatriz Tavares, Frederico Regateiro, Ana Todo-Bom
P62 Prevalence and incidence of analgesic hypersensitivity reactions in Colombia
Pablo Andrés Miranda, Bautista De La Cruz Hoyos
P63 Recent endoscopic sinus surgery lessens reactions during aspirin challenge in patients with aspirin exacerbated respiratory disease
Teresa Pelletier, Waleed Abuzeid, Nadeem Akbar, Marc Gibber, Marvin Fried, Weiguo Han, Taha Keskin, Robert Tamayev, Golda Hudes, Simon D. Spivack, David Rosenstreich, Elina Jerschow
P64 Safe use of imidazole salycilate in a case of multiple NSAIDs induced urticaria-angioedema
Elisa Boni, Marina Russello, Marina Mauro
P65 Selective hypersensitivity reactions to ibuprofenâseven years experience
Marta Ferreira Neto
Poster Walk 8: Epidemiological methods (P66âP72)
P66 Allopurinol hypersensitivity: a 7-year review
Lise Brosseron, Daniela Malheiro, Susana Cadinha, PatrĂcia Barreira, J. P. Moreira Da Silva
P67 Antibiotic allergy labelling is associated with increased hospital readmission rates in Australia
Brittany Knezevic, Dustin Sprigg, Michelle Trevenen, Jason Seet, Jason Trubiano, William Smith, Yogesh Jeelall, Sandra Vale, Richard Loh, Andrew Mclean-Tooke, Michaela Lucas
P68 Expertsâ opinions on severe cutaneous adverse drug reactions-report of a survey from the 9th international congress on cutaneous adverse drug reactions 2015
Roni P. Dodiuk-Gad, Cristina Olteanu, Wen-Hung Chung, Neil H. Shear
P69 HLA-A*31-positive AGEP with carbamazepine use and other severe cutaneous adverse drug reactions (SCARs) detected by electronic medical records screening
Sabine MĂŒller, Ursula Amstutz, Lukas Jörg, Nikhil Yawalkar, Stephan KrĂ€henbĂŒhl
P70 Patients with suspected drug allergy: a specific psychological profile?
Eunice Dias-Castro, Ana Leblanc, Laura Ribeiro, Josefina R. Cernadas
P71 Use of an electronic device and a computerized mathematic algorithm to detect the allergic drug reactions through the analysis of heart rate variability
Arantza Vega, Raquel Gutierrez Rivas, Ana Alonso, Juan Maria Beitia, Belén Mateo, Remedios Cårdenas, Juan Jesus Garcia-Dominguez
P72 Variation in ERAP influences risk for HLA-B*57:01 positive abacavir hypersensitivity
Rebecca Pavlos, Kaija Strautins, Ian James, Simon Mallal, Alec Redwood, Elizabeth Phillips
Poster Walk 9: DRESS/AGEP (P73âP81)
P73 A clinical case of DRESS syndrome in a child after administration of amoxicillin-clavulanic acid
Rita Aguiar, Anabela Lopes, Ana Neves, Maria Do CĂ©u Machado, M. A. Pereira-Barbosa
P74 Acute generalized exanthematous pustulosis (AGEP) induced by mesalazine, reliable and oftenly used drug to treat inflammatory bowel disease
Ceyda Tunakan Dalgiç, Emine Nihal Mete Gökmen, Fatma DĂŒsĂŒnĂŒr GĂŒnsen, Gökten Bulut, Fatma ĂmĂŒr Ardeniz, Okan GĂŒlbahar, Ali Kokuludag, AytĂŒl Zerrin Sin
P75 Changes of blood plasmacytoid dendritic cells, myeloid dendritic cells, and basophils during the acute stage of drug reaction with eosinophilia and systemic symptoms (DRESS) and other drug eruptions
Shao-Hsuan Hsu, Yung-Tsu Cho, Che-Wen Yang, Kai-Lung Chen, Chia-Yu Chu
P76 Characterization of isoniazid/rifampicin-specific t-cell responses in patients with DRESS syndrome
Young-Min Ye, Gyu-Young Hur, Hae-Sim Park, Seung-Hyun Kim
P77 DRESS syndrome secondary to sulfasalazine with delayed TEN: a case presentation
Syed Ali, Michaela Lucas, Peter N. Hollingsworth, Andrew P. C. Mclean-Tooke
P78 Drug rash with eosinophilia and systemic symptoms (DRESS) features according to the culprit drug
Zohra Chadly, Nadia Ben Fredj, Karim Aouam, Haifa Ben Romdhane, Naceur A. Boughattas, Amel Chaabane
P79 Drug reaction with eosinophilia and systemic symptoms induced by allopurinol: not always easy to diagnose
Marina Lluncor Salazar, Beatriz Pola, Ana Fiandor, Teresa BellĂłn, Elena RamĂrez, Javier DomĂnguez Ortega, Santiago Quirce, Rosario Cabañas
P80 Drug reaction with eosinophilia and systemic symptoms syndrome induced by two drugs simultaneously: a case report
Krasimira Baynova, Marina Labella, Manuel Prados
P81 The drug reaction with eosinophilia and systemic symptoms (DRESS) induced by the second-line antituberculosis drugs and EpsteinâBarr virus infection
Agne Ramonaite, Ieva Bajoriuniene, Brigita Sitkauskiene, Raimundas Sakalauskas
Poster Walk 10: Miscellaneous drug hypersensitivity (P82âP91)
P82 A case of cycloserine-induced lichenoid drug eruption confirmed with a lymphocatye transformation test
Jae-Woo Kwon, Shinyoung Park
P83 Allergic reaction to topical eye drops: 5Â yearsâ retrospective study in a drug allergy unit
Diana Silva, Leonor Carneiro LeĂŁo, Fabricia Carolino, Eunice Castro, Josefina Cernadas
P84 Allergy to heparins
Diana Perez-Alzate, Natalia Blanca-LĂłpez, Maria Luisa Somoza Alvarez, Maria Garcimartin, Maria Vazquez De La Torre, Francisco Javier Ruano PĂ©rez, Elisa Haroun, Gabriela Canto Diez
P85 Allopurinol-induced adverse drug reactions
Katinka Ănodi-Nagy, Ăgnes KinyĂł, Lajos KemĂ©ny, Zsuzsanna Bata-Csörgo
P86 Analysis of a population with immediate hypersensitivity to corticosteroids: an 11Â year review
Joana Sofia Pita, EmĂlia Faria, Rosa Anita Fernandes, Ana Moura, Nuno Sousa, Carmelita Ribeiro, Carlos Loureiro, Ana Todo Bom
P87 Anaphylaxis against mivacurium in a 12-months old boy at first-time exposure
Wolfgang PfĂŒtzner
P88 Antihistamine-exacerbated chronic spontaneous urticaria: a paradox?
Nadine Marrouche, Clive Grattan
P89 Anti-osteoporotic agents-induced cutaneous adverse drug reactions in Asians
Yu-En Chen, Chun-Bing Chen, Wen-Hung Chung, Yu-
International Nosocomial Infection Control Consortiu (INICC) report, data summary of 43 countries for 2007-2012. Device-associated module
We report the results of an International Nosocomial Infection Control Consortium (INICC) surveillance study from January 2007-December 2012 in 503 intensive care units (ICUs) in Latin America, Asia, Africa, and Europe. During the 6-year study using the Centers for Disease Control and Prevention's (CDC) U.S. National Healthcare Safety Network (NHSN) definitions for device-associated health careâassociated infection (DA-HAI), we collected prospective data from 605,310 patients hospitalized in the INICC's ICUs for an aggregate of 3,338,396Â days. Although device utilization in the INICC's ICUs was similar to that reported from ICUs in the U.S. in the CDC's NHSN, rates of device-associated nosocomial infection were higher in the ICUs of the INICC hospitals: the pooled rate of central lineâassociated bloodstream infection in the INICC's ICUs, 4.9 per 1,000 central line days, is nearly 5-fold higher than the 0.9 per 1,000 central line days reported from comparable U.S. ICUs. The overall rate of ventilator-associated pneumonia was also higher (16.8 vs 1.1 per 1,000 ventilator days) as was the rate of catheter-associated urinary tract infection (5.5 vs 1.3 per 1,000 catheter days). Frequencies of resistance of Pseudomonas isolates to amikacin (42.8% vs 10%) and imipenem (42.4% vs 26.1%) and Klebsiella pneumoniae isolates to ceftazidime (71.2% vs 28.8%) and imipenem (19.6% vs 12.8%) were also higher in the INICC's ICUs compared with the ICUs of the CDC's NHSN