Impact of Anti-GPIIb/IIIa Antibody-Producing B Cells as a Predictor of the Response to Lusutrombopag in Thrombocytopenic Patients with Liver Disease.


Journal

Digestive diseases (Basel, Switzerland)
ISSN: 1421-9875
Titre abrégé: Dig Dis
Pays: Switzerland
ID NLM: 8701186

Informations de publication

Date de publication:
2021
Historique:
received: 09 05 2020
accepted: 15 07 2020
pubmed: 8 8 2020
medline: 22 5 2021
entrez: 8 8 2020
Statut: ppublish

Résumé

To make an accurate estimate of the response to thrombopoietin (TPO) receptor agonists for thrombocytopenia associated with chronic liver disease, we evaluated the influence of antiplatelet autoantibodies on the response to lusutrombopag in thrombocytopenic patients with liver disease. A prospective study was conducted at 2 hospitals. Thrombocytopenic patients with liver disease received oral lusutrombopag 3.0 mg once daily for up to 7 days. We analyzed changes in platelet counts from baseline to the maximum platelet count on days 9-14. The definition of clinical response was a platelet count of ≥5 × 104/μL with an increased platelet count of ≥2 × 104/μL from baseline. We assessed the correlation between the response to treatment drug and antiplatelet autoantibodies measured by anti-GPIIb/IIIa antibody-producing B cells. Thirty patients received the trial drug. There were 25 responders and 5 nonresponders. The median change in platelet counts was 3.9 × 104/μL (95% CI 2.8-4.6, p < 0.0001). The correlation between change in platelet counts and the frequency of the anti-glycoprotein IIb/IIIa antibody-producing B cells was moderate (r = 0.414, 95% CI 0.064-0.674, p = 0.023). In multivariate analysis of factors affecting the change in platelet counts, the anti-GPIIb/IIIa antibody-producing B cells were identified as an independent factor (regression coefficient [B] = 0.089; CI 0.021-0.157, p = 0.013). Anti-GPIIb/IIIa antibody-producing B cells may be a predictor for TPO receptor agonists in patients with chronic liver disease.

Sections du résumé

BACKGROUND BACKGROUND
To make an accurate estimate of the response to thrombopoietin (TPO) receptor agonists for thrombocytopenia associated with chronic liver disease, we evaluated the influence of antiplatelet autoantibodies on the response to lusutrombopag in thrombocytopenic patients with liver disease.
METHODS METHODS
A prospective study was conducted at 2 hospitals. Thrombocytopenic patients with liver disease received oral lusutrombopag 3.0 mg once daily for up to 7 days. We analyzed changes in platelet counts from baseline to the maximum platelet count on days 9-14. The definition of clinical response was a platelet count of ≥5 × 104/μL with an increased platelet count of ≥2 × 104/μL from baseline. We assessed the correlation between the response to treatment drug and antiplatelet autoantibodies measured by anti-GPIIb/IIIa antibody-producing B cells.
RESULTS RESULTS
Thirty patients received the trial drug. There were 25 responders and 5 nonresponders. The median change in platelet counts was 3.9 × 104/μL (95% CI 2.8-4.6, p < 0.0001). The correlation between change in platelet counts and the frequency of the anti-glycoprotein IIb/IIIa antibody-producing B cells was moderate (r = 0.414, 95% CI 0.064-0.674, p = 0.023). In multivariate analysis of factors affecting the change in platelet counts, the anti-GPIIb/IIIa antibody-producing B cells were identified as an independent factor (regression coefficient [B] = 0.089; CI 0.021-0.157, p = 0.013).
CONCLUSION CONCLUSIONS
Anti-GPIIb/IIIa antibody-producing B cells may be a predictor for TPO receptor agonists in patients with chronic liver disease.

Identifiants

pubmed: 32759604
pii: 000510692
doi: 10.1159/000510692
pmc: PMC8220915
doi:

Substances chimiques

Autoantibodies 0
Cinnamates 0
Platelet Glycoprotein GPIIb-IIIa Complex 0
Thiazoles 0
lusutrombopag 6LL5JFU42F

Types de publication

Clinical Trial Journal Article

Langues

eng

Sous-ensembles de citation

IM

Pagination

234-242

Informations de copyright

© 2020 The Author(s). Published by S. Karger AG, Basel.

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Auteurs

Naohisa Wada (N)

Department of Gastroenterology, Internal Medicine, Kitasato University School of Medicine, Sagamihara, Japan.

Haruki Uojima (H)

Department of Gastroenterology, Internal Medicine, Kitasato University School of Medicine, Sagamihara, Japan, kiruha@kitasato-u.ac.jp.

Takashi Satoh (T)

Division of Hematology, Department of Medical Laboratory Sciences, Kitasato University School of Allied Health Sciences, Sagamihara, Japan.
Division of Molecular Hematology, Kitasato University Graduate School of Medical Sciences, Sagamihara, Japan.

Sosei Okina (S)

Department of Hematology, Internal Medicine, Kitasato University School of Medicine, Sagamihara, Japan.

Shuichiro Iwasaki (S)

Department of Gastroenterology, Internal Medicine, Kitasato University School of Medicine, Sagamihara, Japan.

Xue Shao (X)

Department of Gastroenterology, Internal Medicine, Kitasato University School of Medicine, Sagamihara, Japan.

Hayato Takiguchi (H)

Division of Molecular Hematology, Kitasato University Graduate School of Medical Sciences, Sagamihara, Japan.

Yoshitaka Arase (Y)

Division of Gastroenterology and Hepatology, Department of Internal Medicine, Tokai University School of Medicine, Sagamihara, Japan.

Norio Itokawa (N)

Department of Internal Medicine, Division of Gastroenterology, Nippon Medical School Chiba Hokusoh Hospital, Chiba, Japan.

Masanori Atsukawa (M)

Department of Internal Medicine, Division of Gastroenterology and Hepatology, Nippon Medical School, Tokyo, Japan.

Koji Miyazaki (K)

Department of Transfusion and Cell Transplantation, Kitasato University School of Medicine, Sagamihara, Japan.

Hisashi Hidaka (H)

Department of Gastroenterology, Internal Medicine, Kitasato University School of Medicine, Sagamihara, Japan.

Makoto Kako (M)

Department of Gastroenterology, Shonan Kamakura General Hospital, Kamakura, Japan.

Tatehiro Kagawa (T)

Division of Gastroenterology and Hepatology, Department of Internal Medicine, Tokai University School of Medicine, Sagamihara, Japan.

Katsuhiko Iwakiri (K)

Department of Internal Medicine, Division of Gastroenterology, Nippon Medical School Chiba Hokusoh Hospital, Chiba, Japan.

Ryouichi Horie (R)

Division of Hematology, Department of Medical Laboratory Sciences, Kitasato University School of Allied Health Sciences, Sagamihara, Japan.
Division of Molecular Hematology, Kitasato University Graduate School of Medical Sciences, Sagamihara, Japan.

Takahiro Suzuki (T)

Department of Hematology, Internal Medicine, Kitasato University School of Medicine, Sagamihara, Japan.

Wasaburo Koizumi (W)

Department of Gastroenterology, Internal Medicine, Kitasato University School of Medicine, Sagamihara, Japan.

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Classifications MeSH