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Biomedical subjects

F Y Lee

Publications and source records attributed to F Y Lee.

At least 127 records · Page 7Linked to original sources

Clinical evaluation of primary biliary cirrhosis in Chinese patients without serum anti-mitochondrial antibody.

BACKGROUND: Primary biliary cirrhosis (PBC), a chronic, progressive, cholestatic liver disease characterized by frequent presence of the anti-mitochondrial antibody (AMA), is rarely seen in the Asian population. Whether or not the presence of AMA alters the clinical, serological and histological features of the disease remains unclear. METHODS: During the 25-year period from 1972 to 1996, 71 Chinese patients with PBC who were diagnosed clinically and/or histologically were reviewed. Seventeen (24%) of them repeatedly tested negative for serum AMA. Clinical, biochemical, immunological, histological data and treatment response to ursodeoxycholic acid were compared between PBC patients with positive and negative serum AMA. RESULTS: Mean serum immunoglobulin M (IgM) level was significantly lower in AMA-negative PBC patients when compared with AMA-positive PBC patients (422 +/- 163 vs. 651 +/- 412 mg/dL, p = 0.042). Serum anti-nuclear antibodies (ANA) were positive in 93% of the AMA-negative PBC patients, a significantly higher percentage when compared with the 66% of AMA-positive patients (p = 0.048). There were no significant differences with regard to age, sex, clinical manifestations, liver biochemistries, histological findings, survival and response to 1-year ursodeoxycholic acid treatment between the AMA-negative and AMA-positive patients. Univariate logistic regression analysis showed relatively lower serum IgM levels, positive serum ANA and anti-centromere type ANA were significant predictive factors to negative serum AMA in PBC patients (p = 0.035, 0.044 and 0.029, respectively). Multi-variate analysis revealed relatively lower serum IgM levels were the only independent significant predictor to negative serum AMA in PBC patients (p = 0.015). CONCLUSIONS: Twenty-four percent of Chinese patients with PBC were negative for serum AMA. AMA-negative PBC patients were characterized by relatively lower serum IgM levels and a higher rate of positive serum ANA.

Adult↗

Plasma substance P levels in patients with liver cirrhosis: relationship to systemic and portal hemodynamics.

OBJECTIVES: Nitric oxide has been proposed as being responsible for the hyperdynamic circulation observed in portal hypertensive states. Substance P, a neuropeptide partly cleared by liver, induces vasodilation through the activation of the endothelial nitric oxide pathway. This study investigated the plasma levels of substance P in cirrhotic patients and the relationship of these levels to systemic and portal hemodynamics. METHODS: Sixty-four patients with cirrhosis and 53 healthy controls had blood samples taken for determining plasma values of substance P by ELISA. Systemic and portal hemodynamics were measured on the same day of blood sampling using a Swan-Ganz catheterization and thermodilution technique. RESULTS: Plasma levels of substance P were higher in cirrhotic patients than in healthy controls (45.7 +/- 2.0 vs 32.9 +/- 1.0 pg/ml, p < 0.001) and directly correlated with Child-Pugh's score (r = 0.52, p < 0.0001). Compared with compensated cirrhotic patients, decompensated cirrhotic patients had higher plasma levels of substance P accompanied by a lower systemic vascular resistance and higher hepatic venous pressure gradient. There was no significant correlation between plasma levels of substance P and systemic vascular resistance and hepatic venous pressure gradient. In addition, no significant difference in plasma levels of substance P was observed between cirrhotic patients with and cirrhotic patients without a hepatic venous pressure gradient > 12 mm Hg or between patients with and patients without large esophageal varices. CONCLUSIONS: Plasma levels of substance P are increased in patients with cirrhosis and may contribute to the pathogenesis and/or maintenance of hyperdynamic circulation in decompensated patients. The severity of cirrhosis is more important than portal hypertension and the severity of esophageal varices for the development of increased plasma substance P levels.

Female↗

Sequential changes of esophageal motility after endoscopic injection sclerotherapy or variceal ligation for esophageal variceal bleeding: a scintigraphic study.

OBJECTIVE: Endoscopic injection sclerotherapy and variceal ligation are two popular endoscopic methods used to treat esophageal variceal hemorrhage. These two methods have not been compared with regard to esophageal dysfunction after treatment. This is a prospective investigation of esophageal dysmotility after endoscopic injection sclerotherapy and variceal ligation. METHODS: Sequential changes of esophageal motility after endoscopic injection sclerotherapy (n = 25) and variceal ligation (n = 25) were investigated in 50 cirrhotic patients with recent variceal bleeding. Another 22 cirrhotics without esophageal varices were included as controls. Radionuclide esophageal transit tests were performed before initial endoscopic treatment, and 1 and 3 months after variceal eradication. RESULTS: The baseline esophageal transit time was longer in both the sclerotherapy (n = 25, 7.8 +/- 1.4 s) and ligation groups (n = 25, 8.2 +/- 1.8 s) than in controls (n = 22, 6.7 +/- 0.7 s, p < 0.005). The transit time was longer in patients with large varices than in those with small varices (8.3 +/- 1.7 vs. 7.2 +/- 0.7 s, p < 0.05). In the sclerotherapy group, the transit time was prolonged 1 month after variceal eradication, compared with its pretreatment state (n = 20, 7.6 +/- 1.5 vs. 10.0 +/- 2.2 s, p < 0.0001) but was shortened at 3 months compared with 1 month after variceal eradication (n = 12, 10.7 +/- 1.5 vs. 8.6 +/- 2.2 s, p < 0.05). Multiple regression analysis showed that the number of treatment sessions required to eradicate varices was the only significant factor associated with prolonged transit time (p < 0.05). In the ligation group, the transit time changed little at 1 month or 3 months after variceal eradication. CONCLUSIONS: Impairment of esophageal motility can be significant with endoscopic injection sclerotherapy but is reversible. However, endoscopic variceal ligation exerts no significant impact on esophageal motility.

Esophageal and Gastric Varices↗

Development of highly potent inhibitors of Ras farnesyltransferase possessing cellular and in vivo activity.

Analogs of CVFM (a known nonsubstrate farnesyltransferase (FT) inhibitor derived from a CA1A2X sequence where C is cysteine, A is an aliphatic residue, and X is any residue) were prepared where phenylalanine was replaced by (Z)-dehydrophenylalanine, 2-aminoindan-2-carboxylate, 1,2,3,4-tetrahydroisoquinoline-3-carboxylate (Tic), and indoline-2-carboxylate. The greatest improvement in FT inhibitory potency was observed for the Tic derivative (IC50 = 1 nM); however, this compound was ineffective in blocking oncogenic Ras-induced transformation of NIH-3T3 fibroblast cells. A compound was prepared in which both the Cys-Val methyleneamine isostere and the Tic replacement were incorporated. This derivative inhibited FT with an IC50 of 0.6 nM and inhibited anchorage-independent growth of stably transformed NIH-3T3 fibroblast cells by 50% at 5 microM. Replacing the A1 side chain of this derivative with a tert-butyl group and replacing the X position with glutamine led to a derivative with an IC50 of 2.8 nM and an EC50 of 0.19 microM, a 26-fold improvement over (S*,R*)-N-[[2-[N-(2-amino-3-mercaptopropyl)-L-valyl]-1,2,3,4- tetrahydro-3-isoquinolinyl]carbonyl]-L-methionine. This derivative, (S*,R*)-N-[[2-[N-(2-amino-3-mercaptopropyl)-L-tert-leucyl]-1,2,3,4 - tetrahydro-3-isoquinolinyl]-carbonyl]-L-glutamine, was evaluated in vivo along with (S*,R*)-N-[[2-[N-(2-amino-3- mercaptopropyl)-L-tert-leucyl]-1,2,3,4-tetrahydro-3- isoquinolinyl]carbonyl]-L-methionine methyl ester for antitumor activity in an athymic mouse model implanted ip with H-ras-transformed rat-1 tumor cells. When administered by injection twice a day at 45 mg/kg for 11 consecutive days, both compounds showed prolonged survival time (T/C = 142-145%), thus demonstrating efficacy against ras oncogene-containing tumors in vivo.

3T3 Cells↗

Long-term octreotide treatment prevents vascular hyporeactivity in portal-hypertensive rats.

Chronically portal-hypertensive rats show in vitro vascular hyporeactivity in large part mediated by the endothelium-derived vasodilator nitric oxide. We tested whether long-term octreotide treatment (15 micrograms/kg subcutaneously in 5% D/W, 8-hourly) corrects the in vitro vascular hyporeactivity. Increases in perfusion pressures (delta mm Hg) to potassium chloride (30-300 mmol/L) of in vitro perfused superior mesenteric arterial vascular beds of partial portal vein-ligated (PVL) rats were significantly (P < .05) higher in octreotide (n = 9) compared with placebo (n = 10, 5% D/W) treated animals. Octreotide significantly (P < .05) increased mean arterial pressure compared with placebo, the values being 129 +/- 3 and 117 +/- 4 mm Hg, respectively. Furthermore, a significant (P < .001) correlation was observed between in vitro vascular reactivity and mean arterial pressure. Incubation of separate vascular beds (n = 7 for both PVL and sham-operated rats) with octreotide (10(-6) mol/L) did not enhance pressure responses to 125 mmol/L potassium chloride, and failed to increase perfusion pressures in preconstricted vessel preparations (n = 6), excluding a direct inhibitory effect on NO. In summary, long-term octreotide treatment prevents in vitro vascular hyporeactivity in prehepatic portal-hypertensive rats, and octreotide does not exert its action through direct effects on endothelium-derived NO.

Animals↗

Hypoxic-ischaemic injury of the spinal cord in systemic shock: MRI.

The imaging characteristics of concurrent spinal cord injury in children with hypoxic-ischaemic injury of the brain have not been described. We present the MRI findings of hypoxic-ischaemic injury of the brain and spinal cord following hypovolaemic shock in a 2-year-old girl.

Child, Preschool↗

Natural history of bleeding peptic ulcers with a tightly adherent blood clot: a prospective observation.

BACKGROUND: The natural history of a bleeding peptic ulcer with a tightly adherent blood clot remains uncertain. Controversy exists concerning removal of such blood clots at the bleeding ulcer base. This article presents the natural history of a bleeding peptic ulcer with a tightly adherent clot and defines the characteristics of those requiring aggressive management. METHODS: Clinical parameters were analyzed to determine the independent predictors of rebleeding in these patients. One hundred one patients with bleeding peptic ulcers and tightly adherent blood clots were enrolled during a period of 12 months. RESULTS: Twenty-five patients (25%) rebled within 1 month. With a multivariate analysis, we found comorbid illness (odds ratio, 3.41), shock (odds ratio, 3.65), and initial hemoglobin at or below 10 gm/dL (odds ratio, 2.99) to be independent predictors of rebleeding. CONCLUSIONS: Most patients with a tightly adherent clot in an ulcer have an uneventful course. However, endoscopic therapy may prove to be beneficial in the subset of patients with independent predictors of rebleeding.

Blood Coagulation↗

Decreased vascular reactivity of portal vein in rats with portal hypertension.

BACKGROUND/AIMS: Vascular hyporesponsiveness in portal hypertension is well documented in the arterial tissue. The present study aimed to investigate the possible changes in the portal vein from portal hypertensive rats. METHODS: Portal hypertension was induced by partial portal vein ligation. Fourteen days after surgery, portal veins were removed for contractile study and measurement of cAMP, cGMP and [Ca2+]i. RESULTS: In vitro tension preparation showed a decreased maximum response to norepinephrine in portal vein of portal vein ligated rats (38.3 +/- 4.1 vs. 23.4 +/- 1.5 mN/mm2). The pA2 values of WB4101 and yohimbine (alpha1- and alpha2-adrenoceptor antagonist, respectively) were not different between the two groups. Tissue cAMP (14.4 +/- 0.9 vs. 12.2 +/- 0.7 pmol/mg protein), but not cGMP, content was increased and intracellular calcium [Ca2+]i levels (247 +/- 9 vs. 281 +/- 13 nM) were decreased in portal vein ligated rats. CONCLUSIONS: These results showed that in portal vein from portal vein ligated rats, vascular hyporesponsiveness and an increase in basal cAMP content and a decrease in basal [Ca2+]i were observed.

Animals↗

Utility of lentil lectin affinity of alpha-fetoprotein in the diagnosis of hepatocellular carcinoma.

AIMS/METHODS: Frozen sera obtained from 70 patients (35 with hepatocellular carcinoma and 35 with benign chronic liver disease) with serum alpha-fetoprotein > 20 ng/ml were studied to evaluate the diagnostic indices of lentil lectin affinity of alpha-fetoprotein in detecting hepatocellular carcinoma. RESULTS: The proportion of alpha-fetoprotein-L3 was significantly higher in patients with hepatocellular carcinoma than in those with benign chronic liver disease (41.0 +/- 33.6% vs. 16.4 +/- 15.3%, p < 0.001). This difference led to a sensitivity, specificity, positive predictive value, negative predictive value and accuracy of 57, 89, 83, 67 and 73%, respectively, in detecting hepatocellular carcinoma using the proportion of alpha-fetoprotein-L3 > 35% as a parameter. Within a 1-year period, 1500 high-risk persons were collaborating, leading to 22 cases with serum total alpha-fetoprotein > 20 ng/ml. These 22 cases included six pregnant women. The parameter, alpha-fetoprotein-L3 > 35% was used along with sonography to detect hepatocellular carcinoma for the remaining 16 cases. The sensitivity, specificity, positive predictive value, negative predictive value and accuracy were 75, 83, 60, 91 and 81%, respectively, by the proportion of alpha-fetoprotein-L3 > 35%; and 100, 92, 80, 100 and 94%, respectively, by sonography. CONCLUSIONS: Lentil lectin affinity of alpha-fetoprotein provides a moderately high sensitivity and a high specificity in the detection of hepatocellular carcinoma for persons with high alpha-fetoprotein levels. It may be a useful adjuvant tool of sonography and total alpha-fetoprotein level in a mass survey of hepatocellular carcinoma for a high-risk population.

Aged↗

Effect of octreotide on total effective vascular compliance in patients with posthepatitic cirrhosis.

BACKGROUND/AIMS: This study aimed to evaluate the effect of octreotide on total effective vascular compliance, measured during rapid volume expansion, in patients with posthepatitic cirrhosis. METHODS: Twenty-nine patients with posthepatitic cirrhosis were randomly assigned to receive a 100-micrograms/h infusion of octreotide after a 100-micrograms bolus (n = 15), or a placebo (n = 14). Hemodynamic measurements were recorded before and 30 min after drug administration. Thereafter, rapid volume expansion was performed in each patient and hemodynamic measurements were repeated immediately after volume expansion. RESULTS: Before volume expansion, placebo administration did not affect any of the hemodynamic values, while the hepatic blood flow was significantly decreased following octreotide administration. After volume expansion, the hemodynamic changes were similar between patients receiving octreotide and the placebo. However, the increase in right atrial pressure from the beginning to the end of volume expansion was higher and the total effective vascular compliance was lower in patients receiving octreotide (+3.5 +/- 0.3 mmHg, p = 0.05 and 1.69 +/- 0.16 ml.mmHg-1.kg-1, p < 0.05) compared to patients receiving placebo (+2.5 +/- 0.3 mmHg, 2.60 +/- 0.34 ml.mmHg-1.kg-1). CONCLUSIONS: The present study suggests that octreotide decreased total effective vascular compliance in patients with posthepatitic cirrhosis. It is possible that, in patients with posthepatitic cirrhosis, venoconstriction was induced following octreotide administration.

Aged↗

Loss of normal p53 function confers sensitization to Taxol by increasing G2/M arrest and apoptosis.

The anticancer agent paclitaxel (Taxol) stabilizes tubulin polymerization resulting in arrest in mitosis and apoptotic cell death. Normal human fibroblasts depleted of functional p53 by SV40 T antigen or HPV-16 E6, and primary embryo fibroblasts from p53 null mice showed seven- to ninefold increased cytotoxicity by paclitaxel. Reduced levels of p53 correlated with increased G2/M phase arrest, micronucleation, and p53-independent paclitaxel-induced apoptosis. Surviving cells with intact p53 progressed through mitosis and transiently accumulated in the subsequent G1 phase, coincident with increased p53 and p21cip1,waf1 protein levels. These results are in contrast to studies linking p53 loss with resistance to DNA damaging anticancer agents.

Animals↗

Effect of buthionine sulfoximine, a synthesis inhibitor of the antioxidant glutathione, on the murine nigrostriatal neurons.

This study analyzed the effects of acute systemic treatment with buthionine sulfoximine (BSO), a synthesis inhibitor of the antioxidant reduced glutathione (GSH), on dopaminergic neurons of the murine nigrostriatal pathway. Part 1 of the study established a dose-response curve and the temporal pattern of GSH loss and recovery in the substantia nigra and striatum following acute BSO treatment. Part 2 of the study determined the effect of acute BSO treatment on the morphology and biochemistry of nigrostriatal neurons. We found that decreases in GSH levels had profound morphological effects, including decreased catecholamine fluorescence per cell, increased levels of lipid peroxidation and lipofuscin accumulation, and increased numbers of dystrophic axons in dopaminergic neurons of the nigrostriatal pathway. However, no measurable effects were observed in biochemical levels of either dopamine or its metabolites. These changes mimic those that have been reported to occur in the nigrostriatal system of rodents with advancing age. Our data suggest that reduction of GSH via BSO treatment results in the same types of nigrostriatal degenerative effects that occur during the aging process and consequently is a good model system for examining the role of GSH in protecting this area of the brain against the harmful effects of age-related oxidative stress.

3,4-Dihydroxyphenylacetic Acid↗

Early or delayed endoscopy for patients with peptic ulcer bleeding. A prospective randomized study.

The benefit of early endoscopy in the management of peptic ulcer bleeding remains controversial. In this study we looked at the role of early endoscopy in bleeding peptic ulcer patients with clear, "coffee grounds," or bloody nasogastric aspirate. A consecutive series of 325 patients with peptic ulcer bleeding were included (218 patients with clear aspirate, 77 patients with coffee-grounds aspirate, and 30 patients with bloody aspirate). They were randomized to receive early endoscopy (within 12 h of arrival at the emergency room) or delayed endoscopy (12 h after arrival at the emergency room). Early endoscopy did not benefit patients with clear or coffee-grounds aspirate. However, combined with endoscopic therapy, it did significantly benefit patients with bloody aspirate in reducing the need for blood transfusion (mean, 450 ml vs. 666 ml; p < 0.001) and hospital stay (mean, 4 vs. 14.5 days, p < 0.001). Early endoscopy and endoscopic therapy are not needed in bleeding peptic ulcer patients with clear or coffee-grounds nasogastric aspirate. However, early endoscopy and endoscopic therapy benefit patients with bloody nasogastric aspirate.

Aged↗

Gastric secretion in Chinese patients with cirrhosis.

The role of gastric secretion has been controversial in patients with cirrhosis. Except for studies of gastric secretion in cirrhotic patients who underwent a shunt operation, there is no report correlating gastric secretion with portal pressure in patients with cirrhosis. In this study, we evaluated gastric secretion in cirrhotic patients and correlated it with hemodynamic parameters. Within 12 months, 20 normal volunteers and 16 cirrhotic patients were enrolled. Gastric secretion was assessed in all patients, but portal pressure hemodynamic studies were performed only in cirrhotic patients. We found that the median basal acid output, maximal acid output, and basal pepsin output in the controls (1.41 mmol/h, 9.2 mmol/h, and 0.02 mg/h, respectively) and in the cirrhotic patients (0.6 mmol/h, 7.84 mmol/h, and 1.5 mg/h, respectively) were not statistically different. However, maximal pepsin output was lower in the cirrhotic patients (1.5 mg/h) than in the normal subjects (5.14 mg/h) (p < 0.05). Gastric secretion correlated poorly with hepatic venous pressure gradient (HVPG) and the presence of congestive gastropathy in cirrhotic patients. The severity of congestive gastropathy correlated poorly with HVPG. Helicobacter pylori has difficulty replicating in the stomach when HVPG is > 14 mm Hg. We conclude that patients with cirrhosis have a lower maximal pepsin output than that of the healthy subjects. Gastric secretion correlates poorly with HVPG and the presence of congestive gastropathy in patients with cirrhosis.

Aged↗

Prevalence of gastric ulcer in cirrhotic patients and its relation to portal hypertension.

The prevalence of gastric ulcer and its relationship to the severity of cirrhosis and degree of portal hypertension was evaluated in 245 cirrhotic patients, and compared with 245 age- and sex-matched healthy subjects. Portal and systemic haemodynamic studies were performed in cirrhotic patients. The prevalence of gastric ulcer in cirrhotic patients was 20.8%, which was significantly higher than the 4.0% found in healthy controls. Using a multivariate logistic regression model, the hepatic venous pressure gradient was found to be the only predictor of the prevalence of gastric ulcer in cirrhotic patients to present with gastric ulcer. The hepatic venous pressure gradient was significantly higher in cirrhotic patients with gastric ulcer than in those without (17.3 +/- 4.4 vs 15.5 +/- 5.0 mmHg, P = 0.01). Other variables, including sex, smoking, cardiac output and severity or aetiology of cirrhosis did not show significant differences between the two patient groups. The prevalence of gastric ulcer in cirrhotic patients whose hepatic venous pressure gradient was below 12 mmHg (4.5%) was similar to that observed in the healthy controls (4.0%). However, when the hepatic venous pressure gradient was > 12 mmHg, the prevalence of gastric ulcer (24.4%) was significantly higher than that in control subjects. However, the incidence of gastric ulcer was not related to the degree of portal hypertension. In conclusion, the prevalence of gastric ulcer in cirrhotic patients was found to be significantly higher than in the age- and sex-matched healthy subjects. Portal hypertension with a hepatic venous pressure gradient > 12 mmHg may be an important factor contributing to the increased prevalence of gastric ulcer observed in patients with liver cirrhosis.

Case-Control Studies↗

Role of endotoxaemia in hyperdynamic circulation in rats with extrahepatic or intrahepatic portal hypertension.

This study investigated the role of endotoxaemia in the development of hyperdynamic circulation observed in rats with extrahepatic (high collateralization) or intrahepatic (low collateralization) portal hypertension. Compared with sham-operated rats, decreased mean arterial pressure and systemic vascular resistance were detected on days 1, 4, and 14 following partial portal vein ligation. By day 1, the cardiac index of portal vein-ligated rats was similar to that of sham-operated rats and progressively increased, thereafter, reaching statistically higher values days 4 and 14. No differences in plasma endotoxin levels were found between portal vein-ligated and sham-operated rats throughout the observation period. Both carbon tetrachloride-induced cirrhotic rats with and without ascites had a higher cardiac index and lower systemic vascular resistance. Plasma endotoxin levels were higher in cirrhotic rats with ascites (8.6 +/- 2.0 pg/mL; P < 0.01) than those of control rats (2.2 +/- 0.3 pg/mL) and cirrhotic rats without ascites (2.4 +/- 0.6 pg/mL). These results suggest that factors other than endotoxaemia play a role in the development of hyperdynamic circulation observed in rats with extrahepatic portal hypertension and cirrhotic rats without ascites, but that endotoxaemia may contribute to the maintenance of hyperdynamic circulation found in cirrhotic rats with ascites. The severity of liver disease may be a more important factor than the presence of portosystemic shunting for the development of endotoxaemia in portal hypertensive states.

Animals↗

Hyperglucagonaemia in cirrhotic patients and its relationship to the severity of cirrhosis and haemodynamic values.

Plasma glucagon concentrations were measured in 160 cirrhotic patients (Pugh's grade A in 52 patients, Pugh's grade B in 64 patients and Pugh's grade C in 44 patients). These values were compared with plasma glucagon concentrations in 57 age and sex-matched healthy subjects. Systemic and portal haemodynamic measurements, effective renal plasma flow and creatinine clearance were recorded for each patient. Plasma glucagon levels were significantly increased in cirrhotic patients compared with healthy subjects. In addition, plasma glucagon levels were higher in cirrhotic patients with ascites than in those without ascites and were increased in relation to the severity of cirrhosis as assessed by Pugh's score. Multiple linear regression found that only Child-Pugh's score was estimated to be an independent predictor of hyperglucagonaemia in cirrhotic patients. However, in patients with different degrees of oesophageal varices and in patients without oesophageal varices, plasma glucagon concentrations were no different among the different groups of patients, but were still higher than plasma glucagon concentrations in healthy subjects. In contrast, plasma glucagon levels were negatively correlated with mean arterial pressure and systemic vascular resistance. The results of the present study suggest that impairment of liver function plays, in part, a role in increased plasma glucagon levels observed in patients with cirrhosis. In addition, these data support the hypothesis that hyperglucagonaemia may contribute, at least in part, to the pathogenesis of peripheral arterial vasodilatation in cirrhosis with portal hypertension.

Adult↗

Plasma interleukin-8 levels in patients with post-hepatitic cirrhosis: relationship to severity of liver disease, portal hypertension and hyperdynamic circulation.

The present study investigated plasma levels of interleukin-8 (IL-8) in patients with post-hepatitic cirrhosis and correlated it with the severity of liver diseases and haemodynamic parameters. Plasma IL-8 levels were significantly higher in 57 post-hepatitic cirrhotic patients (7.5 +/- 1.8 pg/mL; P < 0.005) than those in 41 healthy subjects (2.0 +/- 0.2 pg/mL). Elevated (> 5 pg/mL) plasma IL-8 levels were found in up to 30% of cirrhotic patients. In cirrhotic patients, plasma IL-8 levels progressively increased in relation to the severity of liver dysfunction (4.5 +/- 1.0, 4.9 +/- 1.4 and 20.5 +/- 8.3 pg/mL for Pugh's class A, B and C, respectively; P < 0.005). A significant correlation was observed between plasma IL-8 levels and serum bilirubin levels (r = 0.72; P < 0.001). There were no differences in the hepatic venous pressure gradient (15.4 +/- 1.1 vs 15.1 +/- 0.9 mmHg; P > 0.05) and systemic vascular resistance (1119 +/- 118 vs 1199 +/- 54 dyn.s/cm5; P > 0.05) between cirrhotic patients with and without elevated plasma IL-8 levels. In addition, plasma IL-8 levels did not correlate with hepatic venous pressure gradient (r = 0.26; P > 0.05) and systemic vascular resistance (r = -0.24; P > 0.05). These results demonstrate that plasma IL-8 levels are increased in patients with post-hepatitic cirrhosis. The severity of liver cirrhosis is an important factor for the occurrence of enhanced IL-8 levels. IL-8 does not play a role in the hyperdynamic circulation observed in patients with post-hepatitic cirrhosis.

Bilirubin↗