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  • 1
    ISSN: 1432-2277
    Keywords: Key words Liver transplantation ; Rejection ; ICAM-1 ; Immunohistochemistry
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Acute rejection (AR) is a frequent complication following liver transplantation (LT). ICAM-1 may be involved in its pathogenesis. High doses of glucocorticoids are the standard treatment in these patients. The aim of this study was to describe corticoid effects on ICAM-1 tissue expression in liver biopsies of patients with LT and AR. The study included liver biopsies performed before and after treatment in 12 patients with LT and proven AR. In 10 patients AR was reversible and in 2, was steroid resistant. For immunohistochemistry, an indirect immunoperoxidase technique was used. Each histology section was semiquantitatively evaluated as follows: 0: 〈 10 % staining, 1: 10–25 %, 2: 25–50 %, 3: 〉 50 %. The control group comprised nine patients with LT and normal liver biopsies. In pre-treatment liver biopsy samples, ICAM-1 was markedly expressed on sinusoidal cells (2.41 ± 0.66), and there was also expression on periportal (0.66 ± 0.65) and perivenular hepatocytes (0.83 ± 0.57). By contrast, in the liver tissue from the control group, sinusoidal ICAM-1 reactivity was significantly lower (0.88 ± 0.33; P 〈 0.05), and hepatocytes showed no reliable ICAM-1 expression. After steroid treatment the intensity of ICAM-1 decreased significantly in sinusoids (1.5 ± 0.67; P 〈 0.05) and in perivenular hepatocytes (0.25 ± 0.86; P 〈 0.05). Additionally, we also observed a decreased ICAM-1 reactivity in portal hepatocytes (0.25 ± 0.62), but these differences did not reach statistical significance. Remarkably, after treatment, hepatocytes did not show ICAM-1 reactivity in resolved AR, but in corticoid-resistant patients AR did not change or increase. In conclusion, in patients with LT and AR, ICAM-1 was expressed in hepatocytes and with more intensity in sinusoid cells. Additionally, a down-regulation of the ICAM-1 tissue expression after corticoid treatment may exist, although in corticoid-resistant AR no modulation on ICAM-1 tissue expression was observed.
    Type of Medium: Electronic Resource
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  • 2
    ISSN: 1573-2568
    Keywords: TIPS ; portal hypertension ; systemic hemodynamics ; splanchnic hemodynamics ; hepatic function
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract The purpose of this study was to evaluate the short-term splanchnic and systemic hemodynamics and hepatic function after TIPS creation. Fifteen cirrhotics with portal hypertension underwent TIPS placement for treatment of variceal hemorrhage, and extensive hemodynamic studies including right heart catheterization, portal pressure measurement, hepatic blood flow, and indocyanine green (ICG) clearance were performed before and 1 month after the procedure. Self-expandable metal stents (Strecker 11 mm diameter) were placed in all cases. Portasystemic gradient significantly diminished (18.3±4.2 vs 8±2.8; 54%±18 mm Hg) after the technique, mainly due to a decrease in portal pressure, and remained stable in the final study. Cardiac output and mean arterial pressure increased (6.2±1.4 vs 8.2±1.8 liters/min, 80.1±10.1 vs 91±11.2 mm Hg, respectively), and a decrease in systemic vascular resistance was registered (1018±211 vs 872±168 dyne/sec/cm5); the hepatic blood flow and ICG clearance also decreased significantly (1.5±0.7 vs 0.68±0.2 liters/min, 0.4±0.2 vs 0.24 ±0.06 liters/min, respectively). There was an increase in the preload at the final study, as evidenced by a marked increase in right atrial (3.1±1.6 vs 4.35±2.2 mm Hg, +15%,P〈0.05), pulmonary arterial (12.2±2.4 vs 15.9±3.2 mm hg, +31.8%,P〈0.001), and wedge pulmonary arterial pressures (6.9±2.4 vs 9.8±3.1 mm Hg, +53%,P〈0.001). These results suggest that TIPS worsens the hyperdynamic syndrome associated to portal hypertension. Therefore, in patients with cardiac insufficiency, this procedure should be evaluated. TIPS also decreases the hepatic blood flow, inducing a mild worsening in liver function.
    Type of Medium: Electronic Resource
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