๐”– Bobbio Scriptorium
โœฆ   LIBER   โœฆ

Disordered hemostasis in extrahepatic portal hypertension

โœ Scribed by Dr. Simon C. Robson; Delawir Kahn; J. Kruskal; Arthur R. Bird; Ralph E. Kirsch


Publisher
John Wiley and Sons
Year
1993
Tongue
English
Weight
556 KB
Volume
18
Category
Article
ISSN
0270-9139

No coin nor oath required. For personal study only.

โœฆ Synopsis


To assess the contribution of naturally occurring portal-systemic shunts to the coagulopathy of patients with liver disease, we studied laboratory parameters of hemostasis in 20 adult patients with extrahepatic portal hypertension, secondary to portal vein thrombosis, that had resulted in variceal bleeding. All extrahepatic portal hypertension patients had normal liver function and histological appearance. None had any evidence of preexisting coagulation disorders, and none had bled or undergone sclerotherapy in the 6 mo before study. Age- and gender-matched groups of 20 healthy individuals and 20 stable patients with cirrhosis and portal hypertension who had a history of variceal bleeding served as controls. Both patient groups had thrombocytopenia consistent with hypersplenism and portal hypertension. Prothrombin international normalized ratio (extrahepatic portal hypertension, 1.3 +/- 0.12; cirrhosis, 1.7 +/- 0.2; control, 1.02 +/- 0.06; p < 0.05) and partial thromboplastin time ratios (extrahepatic portal hypertension, 1.12 +/- 0.1; cirrhosis, 1.26 +/- 0.2; controls, 1.01 +/- 0.03; p < 0.05) were significantly prolonged in both patient groups. Extrahepatic portal hypertension and cirrhotic patient groups had significantly increased levels of serum total fibrin(ogen)-related antigen (extrahepatic portal hypertension, 818 +/- 150 ng/ml; cirrhosis, 454 +/- 52 ng/ml; controls, 124 +/- 7.3 ng/ml; p < 0.05), fibrin monomer (extrahepatic portal hypertension, 168.8 +/- 16.9 ng/ml; cirrhosis, 115.6 +/- 11.1 ng/ml; controls, 19.7 +/- 0.4 ng/ml; p < 0.05) and D-dimer (extrahepatic portal hypertension, 118 +/- 9.6 ng/ml; cirrhosis, 129 +/- 10 ng/ml; controls, 53.2 +/- 1.6 ng/ml; p < 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)


๐Ÿ“œ SIMILAR VOLUMES


Pregnancy and extrahepatic portal hypert
โœ W. F. Hendry; W. A. Mackey ๐Ÿ“‚ Article ๐Ÿ“… 1969 ๐Ÿ› John Wiley and Sons ๐ŸŒ English โš– 442 KB ๐Ÿ‘ 2 views

EXTRAHEPATIC obstruction of the portal venous system frequently affects children and young people, some at least of whom may be expected to survive to adult life. Gibson, Johnstone, Fulton, and Rodgers (1965) suggested that the minimum objective of treatment should be to enable these patients to lea

Primary Pulmonary Hypertension: An Unusu
โœ Mark D. Cohen; Lewis J. Rubin; Wayne E. Taylor; Jennifer A. Cuthbert ๐Ÿ“‚ Article ๐Ÿ“… 2007 ๐Ÿ› John Wiley and Sons ๐ŸŒ English โš– 616 KB

A patient with both extrahepatic portal hypertension and primary pulmonary hypertension is reported. The pulmonary hypertension developed without a surgical portal-systemic shunt, and at autopsy there was no evidence of a large spontaneous shunt. This association of pulmonary arterial hypertension a

Haematemesis in portal hypertension
โœ Sheila Sherlock ๐Ÿ“‚ Article ๐Ÿ“… 1964 ๐Ÿ› John Wiley and Sons ๐ŸŒ English โš– 448 KB
Haematemesis in portal hypertension
โœ Alan H. Hunt ๐Ÿ“‚ Article ๐Ÿ“… 1964 ๐Ÿ› John Wiley and Sons ๐ŸŒ English โš– 485 KB
Role of prostacyclin in hemodynamic alte
โœ Frederic Oberti; Philippe Sogni; Stephane Cailmail; Richard Moreau; Bernard Pipy ๐Ÿ“‚ Article ๐Ÿ“… 1993 ๐Ÿ› John Wiley and Sons ๐ŸŒ English โš– 673 KB

Although prostaglandins are thought to be involved in the hyperdynamic circulation of portal hypertension, the role of this substance has not been elucidated. Dose-response curves, the hemodynamic effects of prostacyclin (20 k e g ) and its inhibitor indomethacin and measurements of plasma and urina

Portal hypertension in lymphoproliferati
โœ Alain Dubois; Dr. Michel Dauzat; Christine Pignodel; Gilles Pomier-Layrargues; C ๐Ÿ“‚ Article ๐Ÿ“… 1993 ๐Ÿ› John Wiley and Sons ๐ŸŒ English โš– 460 KB

The pathogenesis of portal hypertension in patients with lymphoproliferative and myeloproliferative disorders is not fully understood. We investigated 20 patients with myeloproliferative disease and 47 patients with lymphoproliferative disease. Transvenous liver biopsies and hepatic vein pressure gr