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40978

Platelets Accumulation In The Liver : A novel Mechanism Of Thrombocytopenia In Chronic Hepatic C Patients

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Last updated: 24 Dec 2024

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Abstract

Background and aim: Thrombocytopenia is a common complication of chronicliver diseases and is due to various causes.The effect of thrombocytopenia on liver damage and the exact mechanisms that lead to thrombocytopenia in chronic liver disease and cirrhosis are still unclear. As Platelets Derived Growth Factor ß (PDGF-ß) is released from platelets (PLTs) upon activation. We tried to identify PLTs and PDGFR- ß in the liver to shed some light on the pathophysiology of thrombocytopenia and liver fibrosis in chronic hepatic C patients.
Patients and Methods: Analytical cross-sectional study was conducted on fiftypatients with proven chronic hepatitis C. All patients were referred to Tropical Medicine and Gastroenterology Department, Sohag University Hospital. Patients were categorized into two groups. Group 1 includes patients with PLT count less than 150000/µL (thrombocytopenia). Group 2 includes patients with normal PLT count (150000-450000/µL). All patients were subjected to full history taking, complete clinical examination, complete blood count, liver function tests. Liver biopsy was obtained for histological staging and grading. Immunohistochemical study of PLTs and PDGFR- ß were done using monoclonal antibodies against PLT's surface marker CD41 and PDGFR- ß.
Results: The included patients were 80 % males and 20 % females. Their mean agewas 44.42± 11.17 years. The mean average weighted score (AWS) of Imunohisto-chemical expression of CD41was significantly higher in thrombocytopenic group compared to normal PLTs group (5.8±2.86 vs 3.43±3.03; P<0.001). There was a significant negative correlation between CD41 expression and peripheral PLT count (r=-0.4; P=0.007). PDGFR- ß expression was significantly stronger in thrombocytopenic patients than patients with normal PLT count (6.9±3.6 vs 5.27±3.92; P=0.001). It showed also a significant negative correlation with peripheral PLT count (r=-0.34, P=0.045). Both CD41 and PDGFR- ß expression were significantly elevated in patients with advanced stage of fibrosis than in those
with earlier stages (7.26±5.23 vs 5.88±3.24; P=0.04 &9.2±2.7 vs 6.7±3.6; P Conclusion: The accumulation of PLTs in the liver in patients with chronic hepatitisC may be involved in thrombocytopenia and liver fibrosis.

DOI

10.21608/smj.2018.40978

Keywords

Chronic hepatitis C, thrombocytopenia, CD41, PDGFR- ß

Authors

First Name

Ghada

Last Name

Galal

MiddleName

Moustafa

Affiliation

Department of Tropical Medicine and Gastroenterology, Faculty of Medicine, Sohag University.

Email

ghada_galal@med.sohag.edu.eg

City

Sohag

Orcid

-

First Name

Mahmoud

Last Name

Abd-El-Fatah

MiddleName

Saif-Al-Islam

Affiliation

Department of Tropical Medicine and Gastroenterology, Faculty of Medicine, Sohag University.

Email

mahmoud_elislam@med.sohag.edu.eg

City

Sohag

Orcid

0000-0003-3311-3354

First Name

Zeinab

Last Name

Al- Badawi

MiddleName

Hamdi

Affiliation

Department of, Pathology Department, Faculty of Medicine, Sohag University.

Email

zainab_elbadawi@med.sohag.edu.eg

City

Sohag

Orcid

-

First Name

Yasser

Last Name

Mohamed

MiddleName

Abo Daif

Affiliation

Department of, Tropical Medicine, and Gastroenterology Department, Faculty of Medicine, Sohag University.

Email

-

City

Sohag

Orcid

-

Volume

22

Article Issue

2

Related Issue

4798

Issue Date

2018-07-01

Receive Date

2018-05-07

Publish Date

2018-07-01

Page Start

313

Page End

322

Print ISSN

1687-8353

Online ISSN

2682-4159

Link

https://smj.journals.ekb.eg/article_40978.html

Detail API

https://smj.journals.ekb.eg/service?article_code=40978

Order

38

Type

Original Article

Type Code

785

Publication Type

Journal

Publication Title

Sohag Medical Journal

Publication Link

https://smj.journals.ekb.eg/

MainTitle

Platelets Accumulation In The Liver : A novel Mechanism Of Thrombocytopenia In Chronic Hepatic C Patients

Details

Type

Article

Created At

22 Jan 2023