Thromb Haemost 1996; 76(04): 545-548
DOI: 10.1055/s-0038-1650620
Original Article
Schattauer GmbH Stuttgart

Serum Thrombopoietin (c-MpI Ligand) Levels in Patients with Liver Cirrhosis

Shigetaka Shimodaira
The Second Department of Internal Medicine, Shinshu University School of Medicine, Matsumoto, Japan
,
Fumihiro Ishida
The Second Department of Internal Medicine, Shinshu University School of Medicine, Matsumoto, Japan
,
Naoaki Ichikawa
The Second Department of Internal Medicine, Shinshu University School of Medicine, Matsumoto, Japan
,
Tomoyuki Tahara
1   The Pharmaceutical Research Laboratory, Kirin Brewery Co., Ltd., Maebashi, Japan
,
Takashi Kato
The Second Department of Internal Medicine, Shinshu University School of Medicine, Matsumoto, Japan
,
Hiroshi Kodaira
The Second Department of Internal Medicine, Shinshu University School of Medicine, Matsumoto, Japan
,
Toshiro Ito
The Second Department of Internal Medicine, Shinshu University School of Medicine, Matsumoto, Japan
,
Eiji Tanaka
The Second Department of Internal Medicine, Shinshu University School of Medicine, Matsumoto, Japan
,
Takeshi Sodeyama
1   The Pharmaceutical Research Laboratory, Kirin Brewery Co., Ltd., Maebashi, Japan
,
Kendo Kiyosawa
The Second Department of Internal Medicine, Shinshu University School of Medicine, Matsumoto, Japan
,
Kiyoshi Kitano
The Second Department of Internal Medicine, Shinshu University School of Medicine, Matsumoto, Japan
› Author Affiliations
Further Information

Publication History

Received 22 January 1996

Accepted after resubmission 28 June 1996

Publication Date:
10 July 2018 (online)

Summary

To clarify the role of c-Mpl ligand (thrombopoietin: TPO) in liver cirrhosis (LC), we examined serum TPO levels (sTPO) in patients with LG (N = 44), chronic hepatitis (CH; N = 13) and healthy controls (N = 41) by an enzyme-linked immunosorbent assay. Although platelet counts of all LC patients (89 ± 59 × 109/1; mean ± SD) were lower than those of controls and CH patients, sTPO levels in LC patients (1.23 ± 0.51 fmol/ml) were the same as those in controls (1.22 ± 0.37) and CH patients (1.18 ± 0.36). Platelet counts were significantly higher in splenectomized patients than in unsplenectomized patients, but the sTPO level did not differ between these two groups. In LC patients, the sTPO level was not correlated with the platelet count, but was correlated with prothrombin time, activated partial thromboplastin time, and total bilirubin, indicating that production of TPO in the liver decreases slightly with the development of liver dysfunction. Our findings suggest that production of TPO is maintained in LC patients and their thrombocytopenia is not due to a defect in platelet production.

 
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