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1.
BMC Emerg Med ; 22(1): 120, 2022 07 06.
Artigo em Inglês | MEDLINE | ID: mdl-35794516

RESUMO

BACKGROUND: The risk of choking increases with aging, and the number of cases of choking-induced cardiac arrest is increasing. However, few studies have examined the prognosis of choking-induced cardiac arrest. The aim of this study was to reveal the rates of survival and dependence on devices in the long term after choking-induced cardiac arrest. METHODS: We analyzed data from the Shizuoka Kokuho Database, which consists of claims data of approximately 2.2 million people, from April 2012 to September 2018. We selected patients with choking-induced cardiac arrest who received cardiopulmonary resuscitation in the hospital. Patients were excluded if they were less than 20 years old, had an upper airway tumor, received ventilation assistance, or received enteral nutrition in the month prior to cardiac arrest. The primary outcome was death, and the secondary outcomes were the rates of survival at 3-months and independence on devices. Descriptive statistics are presented and compared among age groups (20-64 years, 65-74 years, 75-84 years, 85 years and older), and survival time analysis (Kaplan-Meier method) was performed. RESULTS: In total, 268 patients were analyzed, including 26 patients in the 20-64 age group, 33 patients in the 65-74 age group, 70 patients in the 75-84 age group, and 139 patients in the ≥85 age group. The overall 3-month survival rate was 5.6% (15/268). The 3-month survival rates were 3.8% (1/26) in the 20-64 age group, 15.2% (5/33) in the 65-74 age group, 8.6% (6/70) in the 75-84 age group, and 2.2% (3/139) in the ≥85 age group. The overall 12-month survival rate was 2.6% (7/268). Of the 7 patients who survived for 12 months, 3 received ventilation management and 5 received tube or intravenous feedings at 3 months. These survivors were still receiving ventilation assistance and tube feedings in the hospital and had not been discharged at 12 months. CONCLUSIONS: The prognosis of choking-induced cardiac arrest was extremely poor when patients were not resuscitated before hospital arrival. Those who survived were mostly dependent on assistive devices. Additionally, none of the survivors dependent on assistive devices had discontinued the use of the devices at the long-term follow-up.


Assuntos
Obstrução das Vias Respiratórias , Retorno da Circulação Espontânea , Adulto , Obstrução das Vias Respiratórias/epidemiologia , Obstrução das Vias Respiratórias/etiologia , Parada Cardíaca Induzida , Hospitais , Humanos , Pessoa de Meia-Idade , Prognóstico , Adulto Jovem
2.
Endocr Pract ; 27(6): 586-593, 2021 Jun.
Artigo em Inglês | MEDLINE | ID: mdl-34057406

RESUMO

OBJECTIVE: The incidence of type 1 diabetes mellitus (T1DM) and hypothyroidism as immune-related adverse events (irAEs) after programmed cell death-1 inhibitor (PD-1i) administration has not yet been sufficiently evaluated in a real clinical setting. To assess the incidence of T1DM and hypothyroidism among PD-1is and to identify the risk factors associated with hypothyroidism using a large claims database. METHODS: This cohort study used the Shizuoka Kokuho database in Japan from 2012 to 2018, including approximately 2.2 million people. We enrolled 695 PD-1i-treated patients. T1DM and hypothyroidism as irAEs were identified using International Classification of Diseases 10th Revision and Anatomical Therapeutic Chemical classification codes. Risk factors for hypothyroidism were explored using the multivariable Fine and Gray regression model after adjusting for age group and sex, treating death as a competing risk. RESULTS: The cumulative incidences of T1DM and hypothyroidism were 0.3% and 8.3%, respectively. We described the detailed onset timing of irAEs in patients with T1DM and hypothyroidism; hypothyroidism was observed evenly within 1 year of the PD-1i prescription. Sex and certain cancer types, such as lung and urothelial cancers, were significantly associated with subdistribution hazard ratio (sHR) (female: sHR, 2.04 [95% CI, 1.20-3.47]; lung cancer: sHR, 0.55 [95% CI, 0.32-0.95]; and urothelial carcinoma: sHR, 2.40 [95% CI, 1.05-5.49]). CONCLUSION: The incidence of T1DM and hypothyroidism as irAEs and associated risk factors identified in this analysis were comparable to those found in previous studies. The use of a large claims database to detect irAEs, such as T1DM and hypothyroidism, may lead to safer use of PD-1is.


Assuntos
Diabetes Mellitus Tipo 1 , Hipotireoidismo , Apoptose , Estudos de Coortes , Diabetes Mellitus Tipo 1/epidemiologia , Feminino , Humanos , Hipotireoidismo/induzido quimicamente , Hipotireoidismo/epidemiologia , Incidência , Japão/epidemiologia , Receptor de Morte Celular Programada 1 , Estudos Retrospectivos , Fatores de Risco
3.
Eur J Pharmacol ; 820: 31-38, 2018 Feb 05.
Artigo em Inglês | MEDLINE | ID: mdl-29221950

RESUMO

Nonalcoholic steatohepatitis (NASH) is one of the most common liver diseases involving chronic accumulation of fat and inflammation, often leading to advanced fibrosis, cirrhosis and carcinoma. However, the pathological mechanism for this is unknown. GPR120/FFAR4 has been recognized as a functional fatty acid receptor and an attractive therapeutic target for metabolic diseases. In this study, we investigated the involvement of GPR120/FFAR4 in the pathogenesis of NASH. Mice fed with a 0.1% methionine and choline deficient high-fat (CDAHF) diet showed a significant increase in plasma aspartate transaminase and alanine transaminase levels, fatty deposition, inflammatory cell infiltration, and mild fibrosis. Docosahexaenoic acid (DHA, GPR120/FFAR4 agonist) suppressed the inflammatory cytokines in the liver tissues and prevented fibrosis in the wild type (WT) mice fed CDAHF diet, but not GPR120/FFAR4 deficient (GPR120KO) mice. GPR120KO mice fed CDAHF diet showed increment of the number of crown like structures and the immunoreactivity for F4/80 positive cells, and increased TNF-α mRNA in the liver compared to WT mice fed CDAHF diet. GPR120 KO mice fed CDAHF diet showed more severe liver inflammation than that of WT mice fed CDAHF diet, but not fibrosis. Our findings suggest that DHA supplementation could be prevented the development of NASH via GPR120/FFAR4 signaling. Furthermore, decrease of GPR120/FFAR4 signaling could be facilitated an inflammatory response in the process of NASH progression.


Assuntos
Suplementos Nutricionais , Progressão da Doença , Ácidos Docosa-Hexaenoicos/farmacologia , Hepatopatia Gordurosa não Alcoólica/patologia , Receptores Acoplados a Proteínas G/metabolismo , Transdução de Sinais/efeitos dos fármacos , Animais , Biomarcadores/metabolismo , Peso Corporal/efeitos dos fármacos , Dieta Hiperlipídica/efeitos adversos , Fibrose , Técnicas de Inativação de Genes , Fígado/efeitos dos fármacos , Fígado/lesões , Fígado/metabolismo , Fígado/patologia , Masculino , Camundongos , Hepatopatia Gordurosa não Alcoólica/metabolismo , Fenótipo , Receptores Acoplados a Proteínas G/deficiência , Receptores Acoplados a Proteínas G/genética
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