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[PMID]:29229629
[Au] Autor:Iacobucci G
[Ad] Endereço:The BMJ.
[Ti] Título:Student who died from anorexia was failed by NHS, review finds.
[So] Source:BMJ;359:j5731, 2017 12 11.
[Is] ISSN:1756-1833
[Cp] País de publicação:England
[La] Idioma:eng
[Mh] Termos MeSH primário: Anorexia/complicações
Falha da Terapia de Resgate/legislação & jurisprudência
Transtornos da Alimentação e da Ingestão de Alimentos/complicações
Medicina Estatal/ética
[Mh] Termos MeSH secundário: Causas de Morte/tendências
Inglaterra/epidemiologia
Falha da Terapia de Resgate/ética
Evolução Fatal
Transtornos da Alimentação e da Ingestão de Alimentos/diagnóstico
Feminino
Seres Humanos
Hipoglicemia/complicações
Pacientes Internados
Defesa do Paciente
Medicina Estatal/normas
Estudantes
Adulto Jovem
[Pt] Tipo de publicação:CASE REPORTS; NEWS
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180223
[Lr] Data última revisão:
180223
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:171213
[St] Status:MEDLINE
[do] DOI:10.1136/bmj.j5731


  2 / 4418 MEDLINE  
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[PMID]:29212654
[Ti] Título:I thought I wasn't thin enough to be anorexic.
[So] Source:BMJ;359:j5378, 2017 12 06.
[Is] ISSN:1756-1833
[Cp] País de publicação:England
[La] Idioma:eng
[Mh] Termos MeSH primário: Anorexia/psicologia
Conhecimentos, Atitudes e Prática em Saúde
Aceitação pelo Paciente de Cuidados de Saúde/psicologia
[Mh] Termos MeSH secundário: Adolescente
Anorexia/diagnóstico
Feminino
Seres Humanos
Relações Médico-Paciente
Mídias Sociais
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180222
[Lr] Data última revisão:
180222
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:171208
[St] Status:MEDLINE
[do] DOI:10.1136/bmj.j5378


  3 / 4418 MEDLINE  
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[PMID]:28452130
[Au] Autor:Morley JE
[Ad] Endereço:Division of Geriatric Medicine, Saint Louis University School of Medicine, 1402 S. Grand Blvd., M238, St. Louis, MO, 63104, USA.
[Ti] Título:Anorexia of ageing: a key component in the pathogenesis of both sarcopenia and cachexia.
[So] Source:J Cachexia Sarcopenia Muscle;8(4):523-526, 2017 Aug.
[Is] ISSN:2190-6009
[Cp] País de publicação:Germany
[La] Idioma:eng
[Ab] Resumo:The anorexia of aging was first recognized as a physiological syndrome 30 years ago. Its major causes are an alteration in fundal compliance with an increase in antral stretch and enhanced cholecystokinin activity leading to increased satiation.This anorexia leads to weight loss in aging persons and is one of the component causes of the aging related sarcopenia. This physiological anorexia also increases the risk of more severe anorexia when an older person has an increase in inflammatory cytokines such as occurs when they have an illness. This results in an increase in the anorexia due to cachexia in older persons.
[Mh] Termos MeSH primário: Envelhecimento/fisiologia
Anorexia/etiologia
Caquexia/etiologia
Sarcopenia/etiologia
[Mh] Termos MeSH secundário: Idoso
Anorexia/metabolismo
Seres Humanos
Saciação/fisiologia
Perda de Peso/fisiologia
[Pt] Tipo de publicação:EDITORIAL
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180206
[Lr] Data última revisão:
180206
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170429
[St] Status:MEDLINE
[do] DOI:10.1002/jcsm.12192


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[PMID]:28457120
[Au] Autor:Stolovy T; Linder M; Zipris P; Doron A; Dafna Y; Melamed Y
[Ad] Endereço:Lev Hasharon Mental Health Medical Center, affiliated with Sackler Faculty of Medicine, Tel Aviv University, Tel Aviv, Israel.
[Ti] Título:Fertility Treatments and Psychiatric Disorders: Ethical Considerations Regarding a Patient's Desire to Become a Mother.
[So] Source:Isr Med Assoc J;19(1):63-64, 2017 Jan.
[Is] ISSN:1565-1088
[Cp] País de publicação:Israel
[La] Idioma:eng
[Mh] Termos MeSH primário: Anorexia/psicologia
Transtorno da Personalidade Borderline/psicologia
Transtorno Obsessivo-Compulsivo/psicologia
Gravidez/psicologia
Técnicas de Reprodução Assistida/ética
[Mh] Termos MeSH secundário: Feminino
Seres Humanos
Meia-Idade
Autonomia Pessoal
[Pt] Tipo de publicação:CASE REPORTS; JOURNAL ARTICLE
[Em] Mês de entrada:1711
[Cu] Atualização por classe:171128
[Lr] Data última revisão:
171128
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170501
[St] Status:MEDLINE


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[PMID]:28964791
[Au] Autor:Zhang J; Liu S; Zhang H; Li Y; Wu W; Zhang H
[Ad] Endereço:College of Veterinary Medicine, Nanjing Agricultural University, Nanjing 210095, PR China.
[Ti] Título:Gut satiety hormones cholecystokinin and glucagon-like Peptide-1 amide mediate anorexia induction by trichothecenes T-2 toxin, HT-2 toxin, diacetoxyscirpenol and neosolaniol.
[So] Source:Toxicol Appl Pharmacol;335:49-55, 2017 Nov 15.
[Is] ISSN:1096-0333
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The food-borne trichothecene mycotoxins have been documented to cause human and animal food poisoning. Anorexia is a hallmark of the trichothecene mycotoxins-induced adverse effects. Type B trichothecenes have been previously demonstrated to elicit robust anorectic responses, and this response has been directly linked to secretion of the gut satiety hormones cholecystokinin (CCK) and glucagon-like peptide-1 amide (GLP-1). However, less is known about the anorectic effects and underlying mechanisms of the type A trichothecenes, including T-2 toxin (T-2), HT-2 toxin (HT-2), diacetoxyscirpenol (DAS), neosolaniol (NEO). The purpose of this study was to relate type A trichothecenes T-2, HT-2, DAS and NEO-induced anorectic response to changes plasma concentrations of CCK and GLP-1. Following both oral gavage and intraperitoneal (IP) administration of 1mg/kg bw T-2, HT-2, DAS and NEO evoked robust anorectic response and secretion of CCK and GLP-1. Elevations of plasma CCK markedly corresponded to anorexia induction by T-2, HT-2, DAS and NEO. Following oral exposure, plasma CCK was peaked at 6h, 6h, 2h, 2h and lasted up to 24h, 24h, > 6h, > 6h for T-2, HT-2, DAS and NEO, respectively. IP exposed to four toxins all induced elevation of CCK with peak point and duration at 6h and >24h, respectively. In contrast to CCK, GLP-1 was moderately elevated by these toxins. Following both oral and IP exposure, T-2 and HT-2 evoked plasma GLP-1 elevation with peak point and duration at 2h and 6h, respectively. Plasma GLP-1 was peaked at 2h and still increased at 6h for IP and oral administration with DAS and NEO, respectively. In conclusion, CCK plays a contributory role in anorexia induction but GLP-1 might play a lesser role in this response.
[Mh] Termos MeSH primário: Anorexia/prevenção & controle
Regulação do Apetite
Comportamento Animal
Colecistocinina/sangue
Comportamento Alimentar
Peptídeo 1 Semelhante ao Glucagon/sangue
Fragmentos de Peptídeos/sangue
Resposta de Saciedade
Toxina T-2/análogos & derivados
Tricotecenos
[Mh] Termos MeSH secundário: Animais
Anorexia/sangue
Anorexia/induzido quimicamente
Anorexia/psicologia
Modelos Animais de Doenças
Feminino
Camundongos
Transdução de Sinais
Fatores de Tempo
Regulação para Cima
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Peptide Fragments); 0 (Trichothecenes); 107444-51-9 (glucagon-like peptide 1 (7-36)); 65041-92-1 (neosolaniol); 89750-14-1 (Glucagon-Like Peptide 1); 9011-97-6 (Cholecystokinin); I3FL5NM3MO (T-2 Toxin); NC6C26RM46 (HT-2 toxin); UYL28I099N (diacetoxyscirpenol)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171002
[St] Status:MEDLINE


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[PMID]:28821663
[Au] Autor:Essner RA; Smith AG; Jamnik AA; Ryba AR; Trutner ZD; Carter ME
[Ad] Endereço:Department of Biology, Program in Neuroscience, Williams College, Williamstown, Massachusetts 01267.
[Ti] Título:AgRP Neurons Can Increase Food Intake during Conditions of Appetite Suppression and Inhibit Anorexigenic Parabrachial Neurons.
[So] Source:J Neurosci;37(36):8678-8687, 2017 Sep 06.
[Is] ISSN:1529-2401
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:To maintain energy homeostasis, orexigenic (appetite-inducing) and anorexigenic (appetite suppressing) brain systems functionally interact to regulate food intake. Within the hypothalamus, neurons that express agouti-related protein (AgRP) sense orexigenic factors and orchestrate an increase in food-seeking behavior. In contrast, calcitonin gene-related peptide (CGRP)-expressing neurons in the parabrachial nucleus (PBN) suppress feeding. PBN CGRP neurons become active in response to anorexigenic hormones released following a meal, including amylin, secreted by the pancreas, and cholecystokinin (CCK), secreted by the small intestine. Additionally, exogenous compounds, such as lithium chloride (LiCl), a salt that creates gastric discomfort, and lipopolysaccharide (LPS), a bacterial cell wall component that induces inflammation, exert appetite-suppressing effects and activate PBN CGRP neurons. The effects of increasing the homeostatic drive to eat on feeding behavior during appetite suppressing conditions are unknown. Here, we show in mice that food deprivation or optogenetic activation of AgRP neurons induces feeding to overcome the appetite suppressing effects of amylin, CCK, and LiCl, but not LPS. AgRP neuron photostimulation can also increase feeding during chemogenetic-mediated stimulation of PBN CGRP neurons. AgRP neuron stimulation reduces Fos expression in PBN CGRP neurons across all conditions. Finally, stimulation of projections from AgRP neurons to the PBN increases feeding following administration of amylin, CCK, and LiCl, but not LPS. These results demonstrate that AgRP neurons are sufficient to increase feeding during noninflammatory-based appetite suppression and to decrease activity in anorexigenic PBN CGRP neurons, thereby increasing food intake during homeostatic need. The motivation to eat depends on the relative balance of activity in distinct brain regions that induce or suppress appetite. An abnormal amount of activity in neurons that induce appetite can cause obesity, whereas an abnormal amount of activity in neurons that suppress appetite can cause malnutrition and a severe reduction in body weight. The purpose of this study was to determine whether a population of neurons known to induce appetite ("AgRP neurons") could induce food intake to overcome appetite-suppression following administration of various appetite-suppressing compounds. We found that stimulating AgRP neurons could overcome various forms of appetite suppression and decrease neural activity in a separate population of appetite-suppressing neurons, providing new insights into how the brain regulates food intake.
[Mh] Termos MeSH primário: Proteína Relacionada com Agouti/metabolismo
Anorexia/fisiopatologia
Regulação do Apetite
Ingestão de Alimentos
Inibição Neural
Neurônios/metabolismo
Núcleos Parabraquiais/fisiopatologia
[Mh] Termos MeSH secundário: Proteína Relacionada com Agouti/genética
Animais
Anorexia/patologia
Hipotálamo/metabolismo
Hipotálamo/patologia
Masculino
Camundongos
Camundongos Endogâmicos C57BL
Camundongos Transgênicos
Neurônios/patologia
Núcleos Parabraquiais/patologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Agouti-Related Protein); 0 (Agrp protein, mouse)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170925
[Lr] Data última revisão:
170925
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170820
[St] Status:MEDLINE
[do] DOI:10.1523/JNEUROSCI.0798-17.2017


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[PMID]:28763145
[Au] Autor:Li J; Xu R; Xu J; Denda T; Ikejiri K; Shen L; Toh Y; Shimada K; Kato T; Sakai K; Yamamoto M; Mishima H; Wang J; Baba H
[Ad] Endereço:Department of Oncology, Fudan University Shanghai Cancer Center, Shanghai, China.
[Ti] Título:Phase II study of S-1 plus leucovorin in patients with metastatic colorectal cancer: Regimen of 1 week on, 1 week off.
[So] Source:Cancer Sci;108(10):2045-2051, 2017 Oct.
[Is] ISSN:1349-7006
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:A phase II study of S-1 plus leucovorin (LV) given in a 4-week schedule (2 weeks' administration followed by 2 weeks' rest) for patients with untreated metastatic colorectal cancer (mCRC) showed that the combination was effective, but grade 3 toxicities (diarrhea, stomatitis and anorexia) occurred at a relatively high rate. In this phase II study, we evaluated the efficacy and safety of a 2-week schedule of S-1 plus LV. Patients with mCRC received oral S-1 (40-60 mg) and LV (25 mg) twice daily for 1 week, followed by 1 week's rest. Treatment was repeated until disease progression or unacceptable toxicity. The primary endpoint was response rate. The pharmacokinetics of S-1 and LV in Chinese patients were evaluated on day 1 of the first cycle. Seventy-three patients were enrolled in Japan and China. Of 71 eligible patients, the response rate was 53.5%, and the disease control rate was 83.1%. Median progression-free survival and median overall survival were 6.5 and 24.3 months, respectively. The incidences of grade 3 toxicities were diarrhea 8.3%, stomatitis 8.3%, anorexia 2.8% and neutropenia 9.7%. There were no treatment-related deaths. The pharmacokinetics profiles of S-1 plus LV in Chinese patients were similar to those in Japanese patients. This 2-week schedule of S-1 plus LV showed good efficacy and better tolerability than the 4-week schedule. This therapy will be the base regimen for mCRC to be added by other cytotoxic or molecular-targeted drugs. The optimized treatment schedule for S-1 plus LV was 1 week on and 1 week off.
[Mh] Termos MeSH primário: Protocolos de Quimioterapia Combinada Antineoplásica/administração & dosagem
Neoplasias Colorretais/tratamento farmacológico
Leucovorina/administração & dosagem
Ácido Oxônico/administração & dosagem
Tegafur/administração & dosagem
[Mh] Termos MeSH secundário: Adulto
Idoso
Idoso de 80 Anos ou mais
Anorexia/induzido quimicamente
Anorexia/epidemiologia
Protocolos de Quimioterapia Combinada Antineoplásica/uso terapêutico
China
Diarreia/induzido quimicamente
Diarreia/epidemiologia
Esquema de Medicação
Combinação de Medicamentos
Feminino
Seres Humanos
Japão
Leucovorina/efeitos adversos
Leucovorina/farmacocinética
Masculino
Meia-Idade
Metástase Neoplásica
Neutropenia/induzido quimicamente
Neutropenia/epidemiologia
Ácido Oxônico/efeitos adversos
Ácido Oxônico/farmacocinética
Estomatite/induzido quimicamente
Estomatite/epidemiologia
Análise de Sobrevida
Tegafur/efeitos adversos
Tegafur/farmacocinética
Resultado do Tratamento
[Pt] Tipo de publicação:CLINICAL TRIAL, PHASE II; JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Drug Combinations); 150863-82-4 (S 1 (combination)); 1548R74NSZ (Tegafur); 5VT6420TIG (Oxonic Acid); Q573I9DVLP (Leucovorin)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171005
[Lr] Data última revisão:
171005
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170802
[St] Status:MEDLINE
[do] DOI:10.1111/cas.13335


  8 / 4418 MEDLINE  
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[PMID]:28751550
[Au] Autor:Argilés JM; López-Soriano FJ; Stemmler B; Busquets S
[Ad] Endereço:Cancer Research Group, Departament de Bioquímica i Biomedicina Molecular, Facultat de Biologia, Universitat de Barcelona, Diagonal 643, Barcelona 08028, Spain jargiles@ub.edu.
[Ti] Título:Novel targeted therapies for cancer cachexia.
[So] Source:Biochem J;474(16):2663-2678, 2017 Jul 27.
[Is] ISSN:1470-8728
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Anorexia and metabolic alterations are the main components of the cachectic syndrome. Glucose intolerance, fat depletion, muscle protein catabolism and other alterations are involved in the development of cancer cachexia, a multi-organ syndrome. Nutritional approach strategies are not satisfactory in reversing the cachectic syndrome. The aim of the present review is to deal with the recent therapeutic targeted approaches that have been designed to fight and counteract wasting in cancer patients. Indeed, some promising targeted therapeutic approaches include ghrelin agonists, selective androgen receptor agonists, ß-blockers and antimyostatin peptides. However, a multi-targeted approach seems absolutely essential to treat patients affected by cancer cachexia. This approach should not only involve combinations of drugs but also nutrition and an adequate program of physical exercise, factors that may lead to a synergy, essential to overcome the syndrome. This may efficiently reverse the metabolic changes described above and, at the same time, ameliorate the anorexia. Defining this therapeutic combination of drugs/nutrients/exercise is an exciting project that will stimulate many scientific efforts. Other aspects that will, no doubt, be very important for successful treatment of cancer wasting will be an optimized design of future clinical trials, together with a protocol for staging cancer patients in relation to their degree of cachexia. This will permit that nutritional/metabolic/pharmacological support can be started early in the course of the disease, before severe weight loss occurs. Indeed, timing is crucial and has to be taken very seriously when applying the therapeutic approach.
[Mh] Termos MeSH primário: Caquexia/terapia
Neoplasias/terapia
[Mh] Termos MeSH secundário: Antagonistas Adrenérgicos beta/uso terapêutico
Antagonistas de Receptores de Andrógenos/uso terapêutico
Anorexia/metabolismo
Anorexia/patologia
Anorexia/terapia
Caquexia/metabolismo
Caquexia/patologia
Dietoterapia/métodos
Terapia por Exercício/métodos
Grelina/agonistas
Seres Humanos
Miostatina/antagonistas & inibidores
Miostatina/metabolismo
Neoplasias/metabolismo
Neoplasias/patologia
Peptídeos/uso terapêutico
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (Adrenergic beta-Antagonists); 0 (Androgen Receptor Antagonists); 0 (Ghrelin); 0 (MSTN protein, human); 0 (Myostatin); 0 (Peptides)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:170803
[Lr] Data última revisão:
170803
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170729
[St] Status:MEDLINE
[do] DOI:10.1042/BCJ20170032


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[PMID]:28651929
[Au] Autor:Harrington KJ; Ferris RL; Blumenschein G; Colevas AD; Fayette J; Licitra L; Kasper S; Even C; Vokes EE; Worden F; Saba NF; Kiyota N; Haddad R; Tahara M; Grünwald V; Shaw JW; Monga M; Lynch M; Taylor F; DeRosa M; Morrissey L; Cocks K; Gillison ML; Guigay J
[Ad] Endereço:Royal Marsden NHS Foundation Trust/The Institute of Cancer Research, London, UK. Electronic address: kevin.harrington@icr.ac.uk.
[Ti] Título:Nivolumab versus standard, single-agent therapy of investigator's choice in recurrent or metastatic squamous cell carcinoma of the head and neck (CheckMate 141): health-related quality-of-life results from a randomised, phase 3 trial.
[So] Source:Lancet Oncol;18(8):1104-1115, 2017 Aug.
[Is] ISSN:1474-5488
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Patients with platinum-refractory recurrent or metastatic squamous cell carcinoma of the head and neck have few treatment options and poor prognosis. Nivolumab significantly improved survival of this patient population when compared with standard single-agent therapy of investigator's choice in Checkmate 141; here we report the effect of nivolumab on patient-reported outcomes (PROs). METHODS: CheckMate 141 was a randomised, open-label, phase 3 trial in patients with recurrent or metastatic squamous cell carcinoma of the head and neck who progressed within 6 months after platinum-based chemotherapy. Patients were randomly assigned (2:1) to nivolumab 3 mg/kg every 2 weeks (n=240) or investigator's choice (n=121) of methotrexate (40-60 mg/m of body surface area), docetaxel (30-40 mg/m ), or cetuximab (250 mg/m after a loading dose of 400 mg/m ) until disease progression, intolerable toxicity, or withdrawal of consent. On Jan 26, 2016, the independent data monitoring committee reviewed the data at the planned interim analysis and declared overall survival superiority for nivolumab over investigator's choice therapy (primary endpoint; described previously). The protocol was amended to allow patients in the investigator's choice group to cross over to nivolumab. All patients not on active therapy are being followed for survival. As an exploratory endpoint, PROs were assessed at baseline, week 9, and every 6 weeks thereafter using the European Organisation for Research and Treatment of Cancer (EORTC) Quality of Life Questionnaire-Core 30 (QLQ-C30), the EORTC head and neck cancer-specific module (EORTC QLQ-H&N35), and the three-level European Quality of Life-5 Dimensions (EQ-5D) questionnaire. Differences within and between treatment groups in PROs were analysed by ANCOVA among patients with baseline and at least one other assessment. All randomised patients were included in the time to clinically meaningful deterioration analyses. Median time to clinically meaningful deterioration was analysed by Kaplan-Meier methods. CheckMate 141 was registered with ClinicalTrials.org, number NCT02105636. FINDINGS: Patients were enrolled between May 29, 2014, and July 31, 2015, and subsequently 361 patients were randomly assigned to receive nivolumab (n=240) or investigator's choice (n=121). Among them, 129 patients (93 in the nivolumab group and 36 in the investigator's choice group) completed any of the PRO questionnaires at baseline and at least one other assessment. Treatment with nivolumab resulted in adjusted mean changes from baseline to week 15 ranging from -2·1 to 5·4 across functional and symptom domains measured by the EORTC QLQ-C30, with no domains indicating clinically meaningful deterioration. By contrast, eight (53%) of the 15 domains in the investigator's choice group showed clinically meaningful deterioration (10 points or more) at week 15 (change from baseline range, -24·5 to 2·4). Similarly, on the EORTC QLQ-H&N35, clinically meaningful worsening at week 15 was seen in no domains in the nivolumab group and eight (44%) of 18 domains in the investigator's choice group. Patients in the nivolumab group had a clinically meaningful improvement (according to a difference of 7 points or greater) in adjusted mean change from baseline to week 15 on the EQ-5D visual analogue scale, in contrast to a clinically meaningful deterioration in the investigator's choice group (7·3 vs -7·8). Differences between groups were significant and clinically meaningful at weeks 9 and 15 in favour of nivolumab for role functioning, social functioning, fatigue, dyspnoea, and appetite loss on the EORTC QLQ-C30 and pain and sensory problems on the EORTC QLQ-H&N35. Median time to deterioration was significantly longer with nivolumab versus investigator's choice for 13 (37%) of 35 domains assessed across the three questionnaires. INTERPRETATION: In this exploratory analysis of CheckMate 141, nivolumab stabilised symptoms and functioning from baseline to weeks 9 and 15, whereas investigator's choice led to clinically meaningful deterioration. Nivolumab delayed time to deterioration of patient-reported quality-of-life outcomes compared with single-agent therapy of investigator's choice in patients with platinum-refractory recurrent or metastatic squamous cell carcinoma of the head and neck. In view of the major unmet need in this population and the importance of maintaining or improving quality of life for patients with recurrent or metastatic squamous cell carcinoma of the head and neck, these data support nivolumab as a new standard-of-care option in this setting. FUNDING: Bristol-Myers Squibb.
[Mh] Termos MeSH primário: Anticorpos Monoclonais/uso terapêutico
Antineoplásicos/uso terapêutico
Carcinoma de Células Escamosas/tratamento farmacológico
Neoplasias de Cabeça e Pescoço/tratamento farmacológico
Recidiva Local de Neoplasia/tratamento farmacológico
Qualidade de Vida
[Mh] Termos MeSH secundário: Anorexia/etiologia
Carcinoma de Células Escamosas/complicações
Carcinoma de Células Escamosas/secundário
Cetuximab/uso terapêutico
Progressão da Doença
Dispneia/etiologia
Fadiga/etiologia
Neoplasias de Cabeça e Pescoço/complicações
Neoplasias de Cabeça e Pescoço/patologia
Seres Humanos
Estimativa de Kaplan-Meier
Metotrexato/uso terapêutico
Recidiva Local de Neoplasia/complicações
Dor/etiologia
Medidas de Resultados Relatados pelo Paciente
Transtornos das Sensações/etiologia
Participação Social
Taxoides/uso terapêutico
[Pt] Tipo de publicação:CLINICAL TRIAL, PHASE III; COMPARATIVE STUDY; JOURNAL ARTICLE; MULTICENTER STUDY; RANDOMIZED CONTROLLED TRIAL
[Nm] Nome de substância:
0 (Antibodies, Monoclonal); 0 (Antineoplastic Agents); 0 (Taxoids); 15H5577CQD (docetaxel); 31YO63LBSN (nivolumab); PQX0D8J21J (Cetuximab); YL5FZ2Y5U1 (Methotrexate)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170919
[Lr] Data última revisão:
170919
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170628
[St] Status:MEDLINE


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[PMID]:28645611
[Au] Autor:Akiyama Y; Yoshimura M; Nishimura K; Nishimura H; Sonoda S; Ueno H; Mitojima Y; Saito R; Maruyama T; Nonaka Y; Hashimoto H; Uezono Y; Hirata K; Ueta Y
[Ad] Endereço:Department of Surgery 1, School of Medicine, University of Occupational and Environmental Health, Kitakyushu 807-8555, Japan.
[Ti] Título:Activation of central nesfatin-1/NucB2 after intraperitoneally administered cisplatin in rats.
[So] Source:Biochem Biophys Res Commun;490(3):794-799, 2017 Aug 26.
[Is] ISSN:1090-2104
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Cisplatin, known as an anticancer drug, has been widely used; however, diverse disadvantageous side effects, including appetite loss, afflict patients. Nesfatin-1/NucB2, discovered as an anorexic neuropeptide, is broadly expressed in the central nervous system (CNS) and peripheral organ. In the present study, we examined the effects of intraperitoneally (i.p.) administered cisplatin on central nesfatin-1/NucB2. Saline, as control, or cisplatin (6 mg/kg dissolved in saline) was i.p. administered in adult male Wistar rats (180-220 g). Cumulative food intake was remarkably suppressed for at least 24 h and body weight was significantly smaller at 24 h after i.p. administration of cisplatin compared to control group. At 90 min after i.p. administration, they were perfused, followed by carrying out double-immunohistochemistry for Fos and nesfatin-1/NucB2. The percentage of nesfatin-1/NucB2 immunoreactive neurons expressing Fos was marked increased in the hypothalamus and brainstem after i.p. administration of cisplatin. Intracerebroventricularlly administered nesfatin-1/NucB2-antisense resulted in a significant attenuation of decreased food intake for 2 h after i.p. administration of cisplatin compared to nesfatin-1/NucB2-missense treated group. These results suggest that i.p. administration of cisplatin activated, at least in part, nesfatin-1/NucB2 neuron in the CNS and may exert anorexigenic effects in rats.
[Mh] Termos MeSH primário: Anorexia/induzido quimicamente
Antineoplásicos/efeitos adversos
Proteínas de Ligação ao Cálcio/metabolismo
Cisplatino/efeitos adversos
Proteínas de Ligação a DNA/metabolismo
Ingestão de Alimentos/efeitos dos fármacos
Proteínas do Tecido Nervoso/metabolismo
Neurônios/efeitos dos fármacos
Ganho de Peso/efeitos dos fármacos
[Mh] Termos MeSH secundário: Animais
Anorexia/metabolismo
Anorexia/patologia
Antineoplásicos/administração & dosagem
Proteínas de Ligação ao Cálcio/análise
Cisplatino/administração & dosagem
Proteínas de Ligação a DNA/análise
Injeções Intraperitoneais
Masculino
Proteínas do Tecido Nervoso/análise
Neurônios/metabolismo
Neurônios/patologia
Ratos
Ratos Wistar
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antineoplastic Agents); 0 (Calcium-Binding Proteins); 0 (DNA-Binding Proteins); 0 (Nerve Tissue Proteins); 0 (nucleobindin); Q20Q21Q62J (Cisplatin)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:170814
[Lr] Data última revisão:
170814
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170625
[St] Status:MEDLINE



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