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  1 / 20785 MEDLINE  
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[PMID]:29460640
[Au] Autor:Sullivan A; Watkinson J; Waddington J; Park BK; Naisbitt DJ
[Ad] Endereço:a MRC Centre for Drug Safety Science, Department of Molecular and Clinical Pharmacology , The University of Liverpool , Liverpool , England.
[Ti] Título:Implications of HLA-allele associations for the study of type IV drug hypersensitivity reactions.
[So] Source:Expert Opin Drug Metab Toxicol;14(3):261-274, 2018 Mar.
[Is] ISSN:1744-7607
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:INTRODUCTION: Type IV drug hypersensitivity remains an important clinical problem and an obstacle to the development of new drugs. Several forms of drug hypersensitivity are associated with expression of specific HLA alleles. Furthermore, drug-specific T-lymphocytes have been isolated from patients with reactions. Despite this, controversy remains as to how drugs interact with immune receptors to stimulate a T-cell response. Areas covered: This article reviews the pathways of T-cell activation by drugs and how the ever increasing number of associations between expression of HLA alleles and susceptibility to hypersensitivity is impacting on our research effort to understanding this form of iatrogenic disease. Expert opinion: For a drug to activate a T-cell, a complex is formed between HLA molecules, an HLA binding peptide, the drug and the T-cell receptor. T-cell responses can involve drugs and stable or reactive metabolites bound covalently or non-covalently to any component of this complex. Recent research has linked the HLA associations to the disease through the characterization of drug-specific T-cell responses restricted to specific alleles. However, there is now a need to identify the additional genetic or environment factors that determine susceptibility and use our increased knowledge to develop predictive immunogenicity tests that offer benefit to Pharma developing new drugs.
[Mh] Termos MeSH primário: Hipersensibilidade a Drogas/imunologia
Antígenos HLA/imunologia
Hipersensibilidade Tardia/induzido quimicamente
[Mh] Termos MeSH secundário: Alelos
Hipersensibilidade a Drogas/genética
Predisposição Genética para Doença
Seres Humanos
Hipersensibilidade Tardia/genética
Hipersensibilidade Tardia/imunologia
Ativação Linfocitária/efeitos dos fármacos
Ativação Linfocitária/imunologia
Linfócitos T/imunologia
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (HLA Antigens)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180309
[Lr] Data última revisão:
180309
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180221
[St] Status:MEDLINE
[do] DOI:10.1080/17425255.2018.1441285


  2 / 20785 MEDLINE  
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[PMID]:29361624
[Au] Autor:Matsuoka N; Yokoyama T; Fujimoto E; Sakai M; Okame S; Shiroyama Y; Yokoyama T; Takehara K
[Ad] Endereço:Dept. of Gynecologic Oncology, National Hospital Organization Shikoku Cancer Center.
[Ti] Título:[Safety and Efficacy of Cisplatin Treatment after Carboplatin Hypersensitivity Reactions in Gynecologic Malignancies].
[So] Source:Gan To Kagaku Ryoho;44(13):2091-2095, 2017 Dec.
[Is] ISSN:0385-0684
[Cp] País de publicação:Japan
[La] Idioma:jpn
[Ab] Resumo:To investigate the safety and efficacy of cisplatin(CDDP)treatment after carboplatin(CBDCA)hypersensitivity reactions (CHSR)in gynecologic malignancies, we retrospectively reviewed the clinical records of 544 patients who underwent paclitaxel and CBDCA therapy(TC therapy). CHSR was observed in 18 patients. Eight patients were administered weekly paclitaxel and CDDP therapy(wTP therapy)continuously, to confirm that there was no CDDP hypersensitivity followingintravenous administration of 10 mgCDDP. At the onset of CHSR, the patients had received a median of 9 TC therapy cycles, and the median number of CBDCA administrations was 14. The frequency of CHSR was significantly higher in patients who received 7 cycles or more of TC therapy and CBDCA administration(p<0.0001). The median number of wTP therapy administrations was 8. Although CDDP hypersensitivity reactions were observed in 2 patients, their symptoms were mild(Grade 2, CTCAE v4.0). Of the 6 patients who received wTP therapy and had evaluable disease sites, 1, 2, 2 and 1 patients showed CR, PR, SD, and PD, respectively. The median progression-free survival in these 6 patients was 9.5 months. For patients with the platinum- sensitive disease who have CHSR, CDDP could improve their prognosis.
[Mh] Termos MeSH primário: Antineoplásicos/uso terapêutico
Cisplatino/uso terapêutico
Hipersensibilidade a Drogas
Neoplasias dos Genitais Femininos/tratamento farmacológico
[Mh] Termos MeSH secundário: Adulto
Idoso
Idoso de 80 Anos ou mais
Antineoplásicos/efeitos adversos
Carboplatina/uso terapêutico
Cisplatino/efeitos adversos
Feminino
Seres Humanos
Meia-Idade
Estudos Retrospectivos
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antineoplastic Agents); BG3F62OND5 (Carboplatin); Q20Q21Q62J (Cisplatin)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180302
[Lr] Data última revisão:
180302
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180124
[St] Status:MEDLINE


  3 / 20785 MEDLINE  
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[PMID]:29386429
[Au] Autor:Uno K
[Ad] Endereço:Faculty of Pharmacy, Chiba Institute of Science.
[Ti] Título:[Pathogenic Mechanism and Diagnostic Testing for Drug Allergies].
[So] Source:Yakugaku Zasshi;138(2):151-167, 2018.
[Is] ISSN:1347-5231
[Cp] País de publicação:Japan
[La] Idioma:jpn
[Ab] Resumo: Three stages of the pathogenic mechanism of drug allergies can be considered: antigen formation, immune reaction and inflammation/disorder reaction. Drugs are thought to form 4 types of antigens: drug only, polymers, drug-carrier conjugates, and metabolite-carrier complexes. Antigens are recognized by B cell receptors and T cell receptors. Helper T cells (Th) are differentiated into four subsets, namely, Th1, Th2, Th17 and regulatory T cells (Treg). Th1 produces interleukin (IL)-2 and interferon (IFN)-γ, and activates macrophages and cytotoxic T cells (Tc). Macrophages induce type IV allergies, and Tc lead to serious type IV allergies. On the other hand, Th2 produces IL-4, IL-5, and IL-6, etc., and activates B cells. B cells produce IgE antibodies, and the IgE antibody affects mast cells and induces type I allergies. Activated eosinophil leads to the chronic state of type I allergy. Diagnostic testing for allergenic drugs is necessary for patients with drug allergies. Because in vivo diagnostic tests for allergenic drugs are associated with a risk and burden to the patient, in vitro allergy tests are recommended to identify allergenic drugs. In allergy tests performed in vitro, cytological tests are more effective than serological tests, and the leukocyte migration test (LMT) presently has the highest efficacy. An LMT-chamber is better than LMT-agarose in terms of usability and sensitivity, and it can detect about 80% of allergenic drugs.
[Mh] Termos MeSH primário: Ensaios de Migração de Leucócitos
Hipersensibilidade a Drogas/diagnóstico
Hipersensibilidade a Drogas/imunologia
[Mh] Termos MeSH secundário: Antígenos/imunologia
Linfócitos B/imunologia
Citocinas/metabolismo
Eosinófilos/imunologia
Seres Humanos
Imunoglobulina E
Macrófagos/imunologia
Mastócitos/imunologia
Receptores de Antígenos de Linfócitos B/imunologia
Receptores de Antígenos de Linfócitos T/imunologia
Sensibilidade e Especificidade
Subpopulações de Linfócitos T/imunologia
Linfócitos T Auxiliares-Indutores/imunologia
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (Antigens); 0 (Cytokines); 0 (Receptors, Antigen, B-Cell); 0 (Receptors, Antigen, T-Cell); 37341-29-0 (Immunoglobulin E)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180228
[Lr] Data última revisão:
180228
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180202
[St] Status:MEDLINE
[do] DOI:10.1248/yakushi.17-00174-1


  4 / 20785 MEDLINE  
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[PMID]:27779086
[Au] Autor:Cornejo-Garcia JA; Oussalah A; Blanca M; Gueant-Rodriguez RM; Mayorga C; Waton J; Barbaud A; Gaeta F; Romano A; Gueant JL
[Ti] Título:Genetic Predictors of Drug Hypersensitivity.
[So] Source:Curr Pharm Des;22(45):6725-6733, 2016.
[Is] ISSN:1873-4286
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:Our knowledge of genetic predisposing factors of drug hypersensitivity reactions (DHRs) is still scarce. The analysis of the genetic basis of these reactions may contribute to dissect the underlying mechanisms. We will outline current knowledge of the genetic predictors of most common DHRs, including reactions to betalactam antibiotics (BLs), nonsteroidal anti-inflammatory drugs (NSAIDs) and biological agents. The predictors of DHRs to BLs are mostly linked to IgE-class switching, IgE pathway and atopy (IL4R, NOD2, LGALS3) in replicated candidate gene studies, and to antigen presentation (HLA-DRA) in the single replicated GWAS performed so far. The HLA-DRA variants are predictors of allergy to penicillins, but not to cephalosporins and they influence also the sensitization against prevalent allergens. The predictors of DHRs against NSAIDs are mostly linked to metabolism of eicosanoids (ALOX5, ALOX5AP, TBXAS1, PTGDR, CYSLTR1). Single nucleotide polymorphisms (SNPs) in genes involved in histamine biosynthesis and antigen presentation, HLA, could also have a role in DHRs against NSAIDs. The intriguing association of DHRs to NSAIDs with atopy should deserve further attention. Predictors of DHRs against asparaginase and other biological agents relate to antigen presentation (HLA-DRB1 and HLA-A alleles, respectively). The potential relationship of genetic predictors of DHRs with pathomechanisms also involved in environmental exposure and atopy highlights the need to perform GWAS in contrasted populations, taking into account world-wide variations of allele frequencies and contrasted situations of environmental exposure.
[Mh] Termos MeSH primário: Hipersensibilidade a Drogas/genética
[Mh] Termos MeSH secundário: Antibacterianos/efeitos adversos
Antibacterianos/imunologia
Antibacterianos/uso terapêutico
Anti-Inflamatórios não Esteroides/efeitos adversos
Anti-Inflamatórios não Esteroides/imunologia
Anti-Inflamatórios não Esteroides/uso terapêutico
Hipersensibilidade a Drogas/tratamento farmacológico
Hipersensibilidade a Drogas/imunologia
Seres Humanos
Imunoglobulina E/imunologia
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Anti-Bacterial Agents); 0 (Anti-Inflammatory Agents, Non-Steroidal); 37341-29-0 (Immunoglobulin E)
[Em] Mês de entrada:1712
[Cu] Atualização por classe:180227
[Lr] Data última revisão:
180227
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161026
[St] Status:MEDLINE
[do] DOI:10.2174/1381612822666160927114941


  5 / 20785 MEDLINE  
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[PMID]:27779087
[Au] Autor:Gonzalez-Morena JM; Montanez MI; Aldini G; Sanchez-Gomez FJ; Perez-Sala D
[Ti] Título:Adduct Formation and Context Factors in Drug Hypersensitivity: Insight from Proteomic Studies.
[So] Source:Curr Pharm Des;22(45):6748-6758, 2016.
[Is] ISSN:1873-4286
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:Drug hypersensitivity reactions result from the activation of the immune system by drugs or their metabolites. The clinical presentations of drug hypersensitivity can range from relatively mild local manifestations to severe systemic syndromes that can be lifethreatening. As in other allergic reactions, the causes are multifactorial as genetic, metabolic and concomitant factors may influence the occurrence of drug hypersensitivity. Formation of drug protein adducts is considered a key step in drug adverse reactions, and in particular in the immunological recognition in drug hypersensitivity reactions. Nevertheless, noncovalent interactions of drugs with receptors in immune cells or with MHC clefts and/or exposed peptides can also play an important role. In recent years, development of proteomic approaches has allowed the identification and characterization of the protein targets for modification by drugs in vivo and in vitro, the nature of peptides exposed on MHC molecules, the changes in protein levels induced by drug treatment, and the concomitant modifications induced by danger signals, thus providing insight into context factors. Nevertheless, given the complexity and multifactorial nature of drug hypersensitivity reactions, understanding the underlying mechanisms also requires the integration of knowledge from genomic, metabolomic and clinical studies.
[Mh] Termos MeSH primário: Antibacterianos/efeitos adversos
Antibacterianos/imunologia
Hipersensibilidade a Drogas/imunologia
Proteômica
[Mh] Termos MeSH secundário: Hipersensibilidade a Drogas/metabolismo
Seres Humanos
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Anti-Bacterial Agents)
[Em] Mês de entrada:1712
[Cu] Atualização por classe:180227
[Lr] Data última revisão:
180227
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161026
[St] Status:MEDLINE
[do] DOI:10.2174/1381612822666160927113748


  6 / 20785 MEDLINE  
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[PMID]:27779084
[Au] Autor:Bonadonna P; Bonifacio M; Zanotti R
[Ad] Endereço:Allergy Unit, Azienda Ospedaliera Universitaria Integrata di Verona, Piazzale Stefani 1, 37126, Verona, Italy.
[Ti] Título:Mast Cell Disorders In Drug Hypersensitivity.
[So] Source:Curr Pharm Des;22(45):6862-6869, 2016.
[Is] ISSN:1873-4286
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:Mastocytosis is a clonal disease characterized by proliferation and accumulation of mast cells (MC) in different tissues, preferentially skin and bone marrow, leading to a wide variety of clinical manifestations, mainly caused by the inappropriate release of MC mediators. As a consequence, patients with mastocytosis may experience symptoms due to massive MC activation and release of mediators. Anaphylaxis is the most frequent manifestation of this phenomenon. Drugs are possible triggers of anaphylaxis in patients with mastocytosis, even though the association between mastocytosis and drug anaphylaxis does not appear to be as strong as anaphylaxis after hymenoptera sting; nevertheless, MC disorders might be ruled out in cases of severe systemic reactions to drugs. Moreover, the risk of perioperative anaphylaxis in adults appears high, mainly in patients with indolent systemic mastocytosis regardless of skin involvement. Such risk is probably lower in patients who have never experienced anaphylaxis and/or have tolerated previous general anaesthesia. However, data published about drug anaphylaxis in patients with MC disorders are scanty and currently it is not possible to provide clear recommendations.
[Mh] Termos MeSH primário: Anafilaxia/imunologia
Hipersensibilidade a Drogas/imunologia
Mastócitos/imunologia
Mastócitos/patologia
Mastocitose/patologia
[Mh] Termos MeSH secundário: Anafilaxia/diagnóstico
Anafilaxia/epidemiologia
Hipersensibilidade a Drogas/diagnóstico
Hipersensibilidade a Drogas/epidemiologia
Seres Humanos
Mastócitos/efeitos dos fármacos
Mastocitose/diagnóstico
Mastocitose/epidemiologia
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Em] Mês de entrada:1712
[Cu] Atualização por classe:180227
[Lr] Data última revisão:
180227
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161026
[St] Status:MEDLINE
[do] DOI:10.2174/1381612822666160928121857


  7 / 20785 MEDLINE  
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[PMID]:27779083
[Au] Autor:Paulmann M; Mockenhaupt M
[Ti] Título:Severe Drug Hypersensitivity Reactions: Clinical Pattern, Diagnosis, Etiology and Therapeutic Options.
[So] Source:Curr Pharm Des;22(45):6852-6861, 2016.
[Is] ISSN:1873-4286
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:Severe cutaneous adverse reactions (SCAR) are known for a high morbidity and mortality. They may be life-threatening for the affected patient and difficult to accomplish for the patient's family and the treating physician. Such conditions include not only bullous reactions like toxic epidermal necrolysis (TEN) and Stevens-Johnson syndrome (SJS), but also acute generalized exanthematous pustulosis (AGEP) and drug reaction with eosinophilia and systemic symptoms (DRESS). Since clinical pattern, etiology, prognosis and treatment differ among these severe skin reactions, a clear diagnosis based on a comprehensive clinical examination, skin biopsy, and specific laboratory tests is necessary. Because most of these reactions are caused by drug intake, a thorough history of medication use has to be obtained. However, there are cases with an infectious or idiopathic cause. In any case it is crucial to identify the most likely cause and rapidly discontinue the inducing agent, if a drug cause is suspected. This is associated with the patient`s prognosis which is often poor for bullous reaction. In addition, patient's age, underlying conditions, and the extent of skin detachment play a major role in terms of prognosis. Severe cutaneous adverse reactions are T-cell-mediated reactions, and certain alleles of human leukocyte antigens (HLA) are involved in the activation of T-cells with cytotoxic effect. The therapeutic options depend on the clinical diagnosis. For all reactions a symptomatic and adequate supportive therapy is necessary, in some cases a systemic immunomodulating therapy can be useful.
[Mh] Termos MeSH primário: Hipersensibilidade a Drogas
Síndrome de Stevens-Johnson
[Mh] Termos MeSH secundário: Hipersensibilidade a Drogas/diagnóstico
Hipersensibilidade a Drogas/etiologia
Hipersensibilidade a Drogas/terapia
Seres Humanos
Síndrome de Stevens-Johnson/diagnóstico
Síndrome de Stevens-Johnson/etiologia
Síndrome de Stevens-Johnson/terapia
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW; RESEARCH SUPPORT, NON-U.S. GOV'T
[Em] Mês de entrada:1712
[Cu] Atualização por classe:180227
[Lr] Data última revisão:
180227
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161026
[St] Status:MEDLINE
[do] DOI:10.2174/1381612822666160928125152


  8 / 20785 MEDLINE  
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[PMID]:27779082
[Au] Autor:Dona I; Salas M; Perkins JR; Barrionuevo E; Gaeta F; Cornejo-Garcia JA; Campo P; Torres MJ
[Ad] Endereço:Allergy Unit, pabellon 6, 1º planta, Hospital Regional Universitario de Malaga (Pabellon C), Plaza del Hospital Civil, 29009 Malaga, Spain.
[Ti] Título:Hypersensitivity Reactions to Non-Steroidal Anti-Inflammatory Drugs.
[So] Source:Curr Pharm Des;22(45):6784-6802, 2016.
[Is] ISSN:1873-4286
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:Non-steroidal anti-inflammatory drugs (NSAIDs) are one of the leading causes of hypersensitivity reactions to drugs, and they are classified in two groups: those induced by nonspecific immunological mechanisms (non-allergic or cross-intolerance (CI) reactions), or by specific immunological mechanisms (allergic or selective reactions (SR)). The pathogenesis of CI is associated with their pharmacological activity (COX-1 inhibition), with symptoms due to an imbalance in the arachidonic acid pathway, independently of their chemical structure. SRs are mediated by specific IgE- or by a T-cell response and can be induced by a single NSAID or a class of chemically related NSAIDs, with patients tolerating chemically unrelated compounds. NSAIDs hypersensitivity reactions have been classified in five main groups: i) NSAIDs-exacerbated respiratory disease (NERD); ii) NSAIDs-exacerbated cutaneous disease (NECD); iii) NSAIDs-induced urticaria/angioedema (NIUA); iv) Single NSAID-induced urticaria/angioedema or anaphylaxis (SNIUAA); v) Single NSAID-induced delayed reactions (SNIDRs). Although this classification described above is widely accepted by most authors some phenotypes such as blended reactions do not fit. Therefore more research is needed in this topic.
[Mh] Termos MeSH primário: Anti-Inflamatórios não Esteroides/efeitos adversos
Anti-Inflamatórios não Esteroides/imunologia
Hipersensibilidade a Drogas/imunologia
[Mh] Termos MeSH secundário: Anti-Inflamatórios não Esteroides/uso terapêutico
Seres Humanos
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Anti-Inflammatory Agents, Non-Steroidal)
[Em] Mês de entrada:1712
[Cu] Atualização por classe:180227
[Lr] Data última revisão:
180227
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161026
[St] Status:MEDLINE
[do] DOI:10.2174/1381612822666160928142814


  9 / 20785 MEDLINE  
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[PMID]:27777129
[Au] Autor:Coyle C; Cafferty FH; Rowley S; MacKenzie M; Berkman L; Gupta S; Pramesh CS; Gilbert D; Kynaston H; Cameron D; Wilson RH; Ring A; Langley RE; Add-Aspirin investigators
[Ad] Endereço:MRC Clinical Trials Unit, UCL, Aviation House, 125 Kingsway, London WC2B 6NH, UK.
[Ti] Título:ADD-ASPIRIN: A phase III, double-blind, placebo controlled, randomised trial assessing the effects of aspirin on disease recurrence and survival after primary therapy in common non-metastatic solid tumours.
[So] Source:Contemp Clin Trials;51:56-64, 2016 11.
[Is] ISSN:1559-2030
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: There is a considerable body of pre-clinical, epidemiological and randomised data to support the hypothesis that aspirin has the potential to be an effective adjuvant cancer therapy. METHODS: Add-Aspirin is a phase III, multi-centre, double-blind, placebo-controlled randomised trial with four parallel cohorts. Patients who have undergone potentially curative treatment for breast (n=3100), colorectal (n=2600), gastro-oesophageal (n=2100) or prostate cancer (n=2120) are registered into four tumour specific cohorts. All cohorts recruit in the United Kingdom, with the breast and gastro-oesophageal cohort also recruiting in India. Eligible participants first undertake an active run-in period where 100mg aspirin is taken daily for approximately eight weeks. Participants who are able to adhere and tolerate aspirin then undergo a double-blind randomisation and are allocated in a 1:1:1 ratio to either 100mg aspirin, 300mg aspirin or a matched placebo to be taken daily for at least five years. Those participants ≥75years old are only randomised to 100mg aspirin or placebo due to increased toxicity risk. RESULTS: The primary outcome measures are invasive disease-free survival for the breast cohort, disease-free survival for the colorectal cohort, overall survival for the gastro-oesophageal cohort, and biochemical recurrence-free survival for the prostate cohort, with a co-primary outcome of overall survival across all cohorts. Secondary outcomes include adherence, toxicity including serious haemorrhage, cardiovascular events and some cohort specific measures. CONCLUSIONS: The Add-Aspirin trial investigates whether regular aspirin use after standard therapy prevents recurrence and prolongs survival in participants with four non-metastatic common solid tumours.
[Mh] Termos MeSH primário: Anti-Inflamatórios não Esteroides/uso terapêutico
Aspirina/uso terapêutico
Recidiva Local de Neoplasia/epidemiologia
Neoplasias/tratamento farmacológico
Taxa de Sobrevida
[Mh] Termos MeSH secundário: Neoplasias da Mama/tratamento farmacológico
Quimioterapia Adjuvante
Neoplasias Colorretais/tratamento farmacológico
Intervalo Livre de Doença
Método Duplo-Cego
Hipersensibilidade a Drogas/etiologia
Neoplasias Esofágicas/tratamento farmacológico
Feminino
Hemorragia Gastrointestinal/induzido quimicamente
Seres Humanos
Índia/epidemiologia
Hemorragias Intracranianas/induzido quimicamente
Estudos Longitudinais
Degeneração Macular/induzido quimicamente
Masculino
Recidiva Local de Neoplasia/sangue
Úlcera Péptica/induzido quimicamente
Neoplasias da Próstata/sangue
Neoplasias da Próstata/tratamento farmacológico
Neoplasias Gástricas/tratamento farmacológico
Zumbido/induzido quimicamente
Reino Unido/epidemiologia
[Pt] Tipo de publicação:CLINICAL TRIAL, PHASE III; JOURNAL ARTICLE; MULTICENTER STUDY; RANDOMIZED CONTROLLED TRIAL; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Anti-Inflammatory Agents, Non-Steroidal); R16CO5Y76E (Aspirin)
[Em] Mês de entrada:1712
[Cu] Atualização por classe:180209
[Lr] Data última revisão:
180209
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161030
[St] Status:MEDLINE


  10 / 20785 MEDLINE  
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[PMID]:28461606
[Au] Autor:Ueki N; Kanasaki K; Kanasaki M; Takeda S; Koya D
[Ad] Endereço:From the Department of Obstetrics and Gynecology, Juntendo University, Tokyo, Japan (N.U., S.T.); and Department of Diabetology and Endocrinology (N.U., K.K., M.K., D.K.) and Division of Anticipatory Molecular Food Science and Technology, Medical Research Institute (K.K., D.K.), Kanazawa Medical Uni
[Ti] Título:Catechol-O-Methyltransferase Deficiency Leads to Hypersensitivity of the Pressor Response Against Angiotensin II.
[So] Source:Hypertension;69(6):1156-1164, 2017 06.
[Is] ISSN:1524-4563
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Catechol-O-methyltransferase (COMT) metabolizes 2-hydroxyestradiol into 2-methoxyestradiol (2-ME); COMT deficiency has shown to be associated with hypertension in men and preeclampsia, the disease associated with hypersensitivity of pressor response against angiotensin II (Ang II). Here, we found that COMT deficiency could explain the hypersensitivity of pressor response against Ang II in mice because of the lack of 2-ME-dependent suppression of angiotensin II receptor type 1 (AT1R). Male C57BL/6 mice were subjected to COMT inhibitor (COMTi: 25 mg/kg per day) or oil (control) for 4 weeks, with or without low-dose Ang II infusion (ANGII: 70 ng/kg per minute) for the last 3 weeks. The Ang II-infused mice were treated with 2-ME (10 ng/d) or vehicle for the last 1 week. We obtained the following experimental groups: control, ANGII, COMTi, COMTi+ANGII, and COMTi+ANGII+2-ME. We performed similar experiments using the in vivo administration of small interfering RNA of COMT instead of COMTi. Neither ANGII nor COMTi exhibited significant alterations in systolic blood pressure. Compared with ANGII or COMTi, COMTi+ANGII displayed significantly higher systolic blood pressure, albuminuria, and glomerular endotheliosis; 2-ME normalized such alterations. Similar phenotypes were observed in COMT small interfering RNA-treated mice. In the aorta of COMT-deficient mice, AT1R expression was increased; 2-ME suppressed AT1R expression. The 2-ME exhibited peroxisome proliferator-activated receptor γ agonistic activity in vitro and ex vivo plasma from pregnant female mice as well. In vitro, 2-ME suppressed both basal and Ang II-induced AT1R levels in a peroxisome proliferator-activated receptor γ-dependent manner. The 2-ME is relevant to combat COMT deficiency-associated hypertensive disorders via suppression of AT1R by its peroxisome proliferator-activated receptor γ activity.
[Mh] Termos MeSH primário: Angiotensina II/farmacologia
Catecol O-Metiltransferase/deficiência
Hipersensibilidade a Drogas/fisiopatologia
Pré-Eclâmpsia/fisiopatologia
Prenhez
Tiazolidinedionas/farmacologia
[Mh] Termos MeSH secundário: Animais
Feminino
Hipertensão/tratamento farmacológico
Hipertensão/fisiopatologia
Masculino
Camundongos
Camundongos Endogâmicos C57BL
Camundongos Knockout
PPAR gama/metabolismo
Pré-Eclâmpsia/tratamento farmacológico
Gravidez
Receptor Tipo 1 de Angiotensina/metabolismo
Valores de Referência
Vasoconstritores/farmacologia
[Pt] Tipo de publicação:COMPARATIVE STUDY; JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (PPAR gamma); 0 (Receptor, Angiotensin, Type 1); 0 (Thiazolidinediones); 0 (Vasoconstrictor Agents); 11128-99-7 (Angiotensin II); EC 2.1.1.6 (Catechol O-Methyltransferase); X4OV71U42S (pioglitazone)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:180113
[Lr] Data última revisão:
180113
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170503
[St] Status:MEDLINE
[do] DOI:10.1161/HYPERTENSIONAHA.117.09247



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