1,721,158 research outputs found
Spleen and liver cirrhosis: relationship between spleen enlargement and portal hypertension in patients with cirrhosis.
No full textSplenomegaly is a common finding in patients with liver cirrhosis, but its relationship with portal hypertension has not been clarified yet. Indeed, in portal hypertension, spleen enlargement is not only caused by portal and splenic vein congestion, but it is mainly due to tissue hyperplasia and fibrosis. The increase in spleen size is followed by an increase in splenic blood flow, which actively congests the portal system. The increased splenic blood flow takes part in the increased splanchnic inflow of the hyperdynamic circulatory syndrome that characterizes patients with cirrhosis and portal hypertension.
Splenomegaly is often associated with hypersplenism, a clinical syndrome characterized by anemia and a decrease in neutrophil granulocytes and platelets counts. Splenectomy is the traditional surgical therapy for hypersplenism, but it is not commonly recommended in patients with cirrhosis and portal hypertension, because in these patients the surgical procedure is affected by a higher incidence of complications. Recently, a few studies have suggested a new role of the spleen in the pathogenesis of portal hypertension, as they demonstrated an active splenic production of endothelin and carbon monoxide, which are two substances involved in the pathogenesis of this condition
Clinical role of non-invasive assessment of portal hypertension
Full text linkMeasurement of portal pressure is pivotal in the evaluation of patients with liver cirrhosis. The measurement of the hepatic venous pressure gradient represents the reference method by which portal pressure is estimated. However, it is an invasive procedure that requires significant hospital resources, including experienced staff, and is associated with considerable cost. Non-invasive methods that can be reliably used to estimate the presence and the degree of portal hypertension are urgently needed in clinical practice. Biochemical and morphological parameters have been proposed for this purpose, but have shown disappointing results overall. Splanchnic Doppler ultrasonography and the analysis of microbubble contrast agent kinetics with contrast-enhanced ultrasonography have shown better accuracy for the evaluation of patients with portal hypertension. A key advancement in the non-invasive evaluation of portal hypertension has been the introduction in clinical practice of methods able to measure stiffness in the liver, as well as stiffness/congestion in the spleen. According to the data published to date, it appears to be possible to rule out clinically significant portal hypertension in patients with cirrhosis (i.e., hepatic venous pressure gradient ≥ 10 mmHg) with a level of clinically-acceptable accuracy by combining measurements of liver stiffness and spleen stiffness along with Doppler ultrasound evaluation. It is probable that the combination of these methods may also allow for the identification of patients with the most serious degree of portal hypertension, and ongoing research is helping to ensure progress in this field
Vasoactive factors and hemodynamic mechanisms in the pathophysiology of portal hypertension in cirrhosis
Full text linkPortal hypertension is primarily caused by the increase in resistance to portal outflow and secondly by an increase in splanchnic blood flow, which worsens and maintains the increased portal pressure. Increased portal inflow plays a role in the hyperdynamic circulatory syndrome, a characteristic feature of portal hypertensive patients. Almost all the known vasoactive systems/substances are activated in portal hypertension, but most authors stress the pathogenetic role of endothelial factors, such as COX-derivatives, nitric oxide, carbon monoxide. Endothelial dysfunction is differentially involved in different vascular beds and consists in alteration in response both to vasodilators and to vasoconstrictors. Understanding the pathogenesis of portal hypertension could be of great utility in preventing and curing the complications of portal hypertension, such as esophageal varices, hepatic encephalopathy, ascites
Paraumbilical vein patency in cirrhosis: effects on hepatic hemodynamics evaluated by Doppler sonography.
No full textAbstract
Doppler sonographic portal vein parameters are used for the noninvasive evaluation of portal hypertension in cirrhosis. The patency of a paraumbilical vein is a rather frequent finding in cirrhosis, which may affect hepatic hemodynamics and function. We evaluated portal and hepatic arterial parameters in 184 cirrhotic patients with and without a patent paraumbilical vein and the relationships with paraumbilical blood flow. A patent paraumbilical vein was found in 33.7% of patients. The prevalence was higher (56.8%) in Child C patients. Portal blood flow velocity (PBV) (10.8 +/- 2.2 vs. 9.8 +/- 2.4 cm/sec; P < .01) and volume (PBF) (995.0 +/- 383.8 vs. 811.6 +/- 318.7 mL/min; P < .001) was significantly higher, and effective portal liver perfusion (PLP) (portal blood flow--paraumbilical blood flow) (621.3 +/- 420.8 vs. 811.6 +/- 318.7 mL/min; P < .001) was significantly lower in patients with a patent paraumbilical vein than in those without. These differences were more evident in Child C patients (10.7 +/- 2.0 vs. 8.3 +/- 2.3 cm/sec; 935.7 +/- 378.3 vs. 680.6 +/- 239.4 mL/min; 369.0 +/- 282.0 vs. 680.6 +/- 239.4 mL/min). Portal vein diameter, the congestion index (CI) of the portal vein, hepatic arterial resistance indexes, and the severity of esophageal varices did not differ between the two groups. In patients with a patent paraumbilical vein, the Child-Pugh score and the prevalence of ascites were significantly higher than in those without. In conclusion, the evaluation of PBV and PBF in cirrhotic patients can provide misleading results if a paraumbilical vein is patent, underestimating the degree of portal hypertension
The use of human albumin millimicrospheres tagged with 99mTc in the evaluation of the removal capacity of the reticuloendothelial system.
No full textLiver uptake kinetics of 99mTc labelled millimicrospheres of human serum albumin (MM) was studied in 16 subjects. Every subject received four doses of MM intravenously. The uptake constant decreased progressively with increasing dose. The maximum liver removal capacity, a parameter which is independent of liver blood flow, was calculated according to the method of Iio and Wagner (1963). From these data we conclude that MM are taken up by the reticuloendothelial system (RES) with saturable kinetics, and they are suitable for clinical use to evaluate RES function in man
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