Insulin resistance reduction after sustained virological response with direct acting antiviral: Not every population improves

Detalhes bibliográficos
Autor(a) principal: de Andrade, Vanessa Gutierrez [UNESP]
Data de Publicação: 2018
Outros Autores: Yamashiro, Fábio da Silva [UNESP], Oliveira, Cássio Vieira [UNESP], Moreira, Alecsandro [UNESP], Winckler, Fernanda Cristina [UNESP], Silva, Giovanni Faria [UNESP]
Tipo de documento: Artigo
Idioma: eng
Título da fonte: Repositório Institucional da UNESP
Texto Completo: http://dx.doi.org/10.1590/s0004-2803.201800000-69
http://hdl.handle.net/11449/188489
Resumo: Background – Hepatitis C virus (HCV) infection is a serious public health problem, that affects approximately 170 million people worldwide. Chronic HCV infection is associated with hepatic insulin resistance and an increased risk of diabetes HCV-infected patients has been well documented. Objective – To assess the homeostasis model assessment of insulin resistance (HOMA-IR) index in patients treated with direct acting antiviral (DAAs) medication in the sustained virological response (SVR), categorized by the presence or absence of cirrhosis. Methods – A prospective study was conducted. Data were collected at the beginning of treatment (t-base) and in the twelfth week after the completion of treatment (t-SVR12). The inclusion criteria were presence of: HCV infection (RNA-HCV positive), age ≥18 years, completion of DAAs’ therapy, and presence of diabetes with use of oral hypoglycemic agents. All samples were collected during the study period. The exclusion criteria were: presence of HBV/HIV co-infection, hepatocellular carcinoma at baseline, diabetic patients taking insulin and transplanted patients (liver/kidney). Fibrosis was assessed by hepatic elastog-raphy or biopsy (METAVIR). Cirrhosis was determined by clinical results or imaging. HOMA-IR was calculated as fasting insulin (μU/mL) × fasting glucose (mmol/L)/22.5) The patients were divided into two groups: the general study population (all patients, including the diabetic patients) and the special population (patients with normal values of HOMA-IR, which is >2.5, and without diabetes). The delta HOMA-IR value was calculated as: HOMA-IR at t-base – HOMA-IR at t-SVR12. For the descriptive statistical analysis, the paired t-test and generalized linear model assuming the log binding function were performed. A P value of < 0.05 was considered significant. Results – We included 150 patients, and 75 were cirrhotic. The mean age was 55.3±9.97 and body mass index was 27.4±5.18. Twenty-two (14.67%) were diabetic patients using oral hypoglycemic agents, and 17 (11%) were cirrhotic. In the general study population, the mean glucose and HOMA-IR values increased at t-SVR12, but insulin decreased. Delta HOMA-IR was negative at t-SVR12, but there was no significant difference. Excluding diabetic patients and those with normal HOMA-IR values (<2.5), mean glucose, insulin and HOMA-IR decreased at t-SVR12. Delta HOMA-IR decreased significantly at t-SVR12 (P: 0.02). Conclusion – In the general population, glucose and HOMA-IR values increased at t-SVR12, but insulin decreased. In the special population, glucose, insulin, HOMA-IR and Delta HOMA-IR decreased at t-SVR12.
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spelling Insulin resistance reduction after sustained virological response with direct acting antiviral: Not every population improvesRedução da resistência à insulina após resposta virológica sustentada com agentes antivirais diretos: Nem toda população melhoraAntiviral agentsHepatitis CInsulin resistanceBackground – Hepatitis C virus (HCV) infection is a serious public health problem, that affects approximately 170 million people worldwide. Chronic HCV infection is associated with hepatic insulin resistance and an increased risk of diabetes HCV-infected patients has been well documented. Objective – To assess the homeostasis model assessment of insulin resistance (HOMA-IR) index in patients treated with direct acting antiviral (DAAs) medication in the sustained virological response (SVR), categorized by the presence or absence of cirrhosis. Methods – A prospective study was conducted. Data were collected at the beginning of treatment (t-base) and in the twelfth week after the completion of treatment (t-SVR12). The inclusion criteria were presence of: HCV infection (RNA-HCV positive), age ≥18 years, completion of DAAs’ therapy, and presence of diabetes with use of oral hypoglycemic agents. All samples were collected during the study period. The exclusion criteria were: presence of HBV/HIV co-infection, hepatocellular carcinoma at baseline, diabetic patients taking insulin and transplanted patients (liver/kidney). Fibrosis was assessed by hepatic elastog-raphy or biopsy (METAVIR). Cirrhosis was determined by clinical results or imaging. HOMA-IR was calculated as fasting insulin (μU/mL) × fasting glucose (mmol/L)/22.5) The patients were divided into two groups: the general study population (all patients, including the diabetic patients) and the special population (patients with normal values of HOMA-IR, which is >2.5, and without diabetes). The delta HOMA-IR value was calculated as: HOMA-IR at t-base – HOMA-IR at t-SVR12. For the descriptive statistical analysis, the paired t-test and generalized linear model assuming the log binding function were performed. A P value of < 0.05 was considered significant. Results – We included 150 patients, and 75 were cirrhotic. The mean age was 55.3±9.97 and body mass index was 27.4±5.18. Twenty-two (14.67%) were diabetic patients using oral hypoglycemic agents, and 17 (11%) were cirrhotic. In the general study population, the mean glucose and HOMA-IR values increased at t-SVR12, but insulin decreased. Delta HOMA-IR was negative at t-SVR12, but there was no significant difference. Excluding diabetic patients and those with normal HOMA-IR values (<2.5), mean glucose, insulin and HOMA-IR decreased at t-SVR12. Delta HOMA-IR decreased significantly at t-SVR12 (P: 0.02). Conclusion – In the general population, glucose and HOMA-IR values increased at t-SVR12, but insulin decreased. In the special population, glucose, insulin, HOMA-IR and Delta HOMA-IR decreased at t-SVR12.Universidade Estadual Paulista (UNESP) Faculdade de Medicina Departamento de Clínica MédicaUniversidade Estadual Paulista (UNESP) Faculdade de Medicina Departamento de Clínica MédicaUniversidade Estadual Paulista (Unesp)de Andrade, Vanessa Gutierrez [UNESP]Yamashiro, Fábio da Silva [UNESP]Oliveira, Cássio Vieira [UNESP]Moreira, Alecsandro [UNESP]Winckler, Fernanda Cristina [UNESP]Silva, Giovanni Faria [UNESP]2019-10-06T16:09:49Z2019-10-06T16:09:49Z2018-07-01info:eu-repo/semantics/publishedVersioninfo:eu-repo/semantics/article274-278application/pdfhttp://dx.doi.org/10.1590/s0004-2803.201800000-69Arquivos de Gastroenterologia, v. 55, n. 3, p. 274-278, 2018.1678-42190004-2803http://hdl.handle.net/11449/18848910.1590/s0004-2803.201800000-69S0004-280320180023002742-s2.0-85058402536S0004-28032018002300274.pdfScopusreponame:Repositório Institucional da UNESPinstname:Universidade Estadual Paulista (UNESP)instacron:UNESPengArquivos de Gastroenterologiainfo:eu-repo/semantics/openAccess2023-12-04T06:12:02Zoai:repositorio.unesp.br:11449/188489Repositório InstitucionalPUBhttp://repositorio.unesp.br/oai/requestopendoar:29462023-12-04T06:12:02Repositório Institucional da UNESP - Universidade Estadual Paulista (UNESP)false
dc.title.none.fl_str_mv Insulin resistance reduction after sustained virological response with direct acting antiviral: Not every population improves
Redução da resistência à insulina após resposta virológica sustentada com agentes antivirais diretos: Nem toda população melhora
title Insulin resistance reduction after sustained virological response with direct acting antiviral: Not every population improves
spellingShingle Insulin resistance reduction after sustained virological response with direct acting antiviral: Not every population improves
de Andrade, Vanessa Gutierrez [UNESP]
Antiviral agents
Hepatitis C
Insulin resistance
title_short Insulin resistance reduction after sustained virological response with direct acting antiviral: Not every population improves
title_full Insulin resistance reduction after sustained virological response with direct acting antiviral: Not every population improves
title_fullStr Insulin resistance reduction after sustained virological response with direct acting antiviral: Not every population improves
title_full_unstemmed Insulin resistance reduction after sustained virological response with direct acting antiviral: Not every population improves
title_sort Insulin resistance reduction after sustained virological response with direct acting antiviral: Not every population improves
author de Andrade, Vanessa Gutierrez [UNESP]
author_facet de Andrade, Vanessa Gutierrez [UNESP]
Yamashiro, Fábio da Silva [UNESP]
Oliveira, Cássio Vieira [UNESP]
Moreira, Alecsandro [UNESP]
Winckler, Fernanda Cristina [UNESP]
Silva, Giovanni Faria [UNESP]
author_role author
author2 Yamashiro, Fábio da Silva [UNESP]
Oliveira, Cássio Vieira [UNESP]
Moreira, Alecsandro [UNESP]
Winckler, Fernanda Cristina [UNESP]
Silva, Giovanni Faria [UNESP]
author2_role author
author
author
author
author
dc.contributor.none.fl_str_mv Universidade Estadual Paulista (Unesp)
dc.contributor.author.fl_str_mv de Andrade, Vanessa Gutierrez [UNESP]
Yamashiro, Fábio da Silva [UNESP]
Oliveira, Cássio Vieira [UNESP]
Moreira, Alecsandro [UNESP]
Winckler, Fernanda Cristina [UNESP]
Silva, Giovanni Faria [UNESP]
dc.subject.por.fl_str_mv Antiviral agents
Hepatitis C
Insulin resistance
topic Antiviral agents
Hepatitis C
Insulin resistance
description Background – Hepatitis C virus (HCV) infection is a serious public health problem, that affects approximately 170 million people worldwide. Chronic HCV infection is associated with hepatic insulin resistance and an increased risk of diabetes HCV-infected patients has been well documented. Objective – To assess the homeostasis model assessment of insulin resistance (HOMA-IR) index in patients treated with direct acting antiviral (DAAs) medication in the sustained virological response (SVR), categorized by the presence or absence of cirrhosis. Methods – A prospective study was conducted. Data were collected at the beginning of treatment (t-base) and in the twelfth week after the completion of treatment (t-SVR12). The inclusion criteria were presence of: HCV infection (RNA-HCV positive), age ≥18 years, completion of DAAs’ therapy, and presence of diabetes with use of oral hypoglycemic agents. All samples were collected during the study period. The exclusion criteria were: presence of HBV/HIV co-infection, hepatocellular carcinoma at baseline, diabetic patients taking insulin and transplanted patients (liver/kidney). Fibrosis was assessed by hepatic elastog-raphy or biopsy (METAVIR). Cirrhosis was determined by clinical results or imaging. HOMA-IR was calculated as fasting insulin (μU/mL) × fasting glucose (mmol/L)/22.5) The patients were divided into two groups: the general study population (all patients, including the diabetic patients) and the special population (patients with normal values of HOMA-IR, which is >2.5, and without diabetes). The delta HOMA-IR value was calculated as: HOMA-IR at t-base – HOMA-IR at t-SVR12. For the descriptive statistical analysis, the paired t-test and generalized linear model assuming the log binding function were performed. A P value of < 0.05 was considered significant. Results – We included 150 patients, and 75 were cirrhotic. The mean age was 55.3±9.97 and body mass index was 27.4±5.18. Twenty-two (14.67%) were diabetic patients using oral hypoglycemic agents, and 17 (11%) were cirrhotic. In the general study population, the mean glucose and HOMA-IR values increased at t-SVR12, but insulin decreased. Delta HOMA-IR was negative at t-SVR12, but there was no significant difference. Excluding diabetic patients and those with normal HOMA-IR values (<2.5), mean glucose, insulin and HOMA-IR decreased at t-SVR12. Delta HOMA-IR decreased significantly at t-SVR12 (P: 0.02). Conclusion – In the general population, glucose and HOMA-IR values increased at t-SVR12, but insulin decreased. In the special population, glucose, insulin, HOMA-IR and Delta HOMA-IR decreased at t-SVR12.
publishDate 2018
dc.date.none.fl_str_mv 2018-07-01
2019-10-06T16:09:49Z
2019-10-06T16:09:49Z
dc.type.status.fl_str_mv info:eu-repo/semantics/publishedVersion
dc.type.driver.fl_str_mv info:eu-repo/semantics/article
format article
status_str publishedVersion
dc.identifier.uri.fl_str_mv http://dx.doi.org/10.1590/s0004-2803.201800000-69
Arquivos de Gastroenterologia, v. 55, n. 3, p. 274-278, 2018.
1678-4219
0004-2803
http://hdl.handle.net/11449/188489
10.1590/s0004-2803.201800000-69
S0004-28032018002300274
2-s2.0-85058402536
S0004-28032018002300274.pdf
url http://dx.doi.org/10.1590/s0004-2803.201800000-69
http://hdl.handle.net/11449/188489
identifier_str_mv Arquivos de Gastroenterologia, v. 55, n. 3, p. 274-278, 2018.
1678-4219
0004-2803
10.1590/s0004-2803.201800000-69
S0004-28032018002300274
2-s2.0-85058402536
S0004-28032018002300274.pdf
dc.language.iso.fl_str_mv eng
language eng
dc.relation.none.fl_str_mv Arquivos de Gastroenterologia
dc.rights.driver.fl_str_mv info:eu-repo/semantics/openAccess
eu_rights_str_mv openAccess
dc.format.none.fl_str_mv 274-278
application/pdf
dc.source.none.fl_str_mv Scopus
reponame:Repositório Institucional da UNESP
instname:Universidade Estadual Paulista (UNESP)
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instname_str Universidade Estadual Paulista (UNESP)
instacron_str UNESP
institution UNESP
reponame_str Repositório Institucional da UNESP
collection Repositório Institucional da UNESP
repository.name.fl_str_mv Repositório Institucional da UNESP - Universidade Estadual Paulista (UNESP)
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