[Preventing colorectal cancer]. / Prevence kolorektálního karcinomu.

Colorectal cancer is one the most frequently diagnosed cancer at the presence. The mortality can be reduced by early investigations. Screening tests are able to detect both early adenomatous polyps and cancers soon (immunochemical tests, colonoscopy and other methods virtual colonoscopy etc.).

Osteopontin: A non-invasive parameter of portal hypertension and prognostic marker of cirrhosis.

AIM: To investigate the relationship between osteopontin plasma concentrations and the severity of portal hypertension and to assess osteopontin prognostic value. METHODS: A cohort of 154 patients with confirmed liver cirrhosis (112 ethylic, 108 men, age 34-72 years) were enrolled in the study. Hepatic venous pressure gradient (HVPG) measurement and laboratory and ultrasound examinations were carried out for all patients. HVPG was measured using a standard catheterization method with the balloon wedge technique. Osteopontin was measured using the enzyme-linked immunosorbent assay (ELISA) method in plasma. Patients were followed up with a specific focus on mortality. The control group consisted of 137 healthy age- and sex- matched individuals. RESULTS: The mean value of HVPG was 16.18 ± 5.6 mmHg. Compared to controls, the plasma levels of osteopontin in cirrhotic patients were significantly higher (P < 0.001). The plasma levels of osteopontin were positively related to HVPG (P = 0.0022, r = 0.25) and differed among the individual Child-Pugh groups of patients. The cut-off value of 80 ng/mL osteopontin distinguished patients with significant portal hypertension (HVPG above 10 mmHg) at 75% sensitivity and 63% specificity. The mean follow-up of patients was 3.7 ± 2.6 years. The probability of cumulative survival was 39% for patients with HVPG > 10 mmHg and 65% for those with HVPG ≤ 10 mmHg (P = 0.0086, odds ratio (OR), 2.92, 95% confidence interval (CI): 1.09-7.76). Osteopontin showed a similar prognostic value to HVPG. Patients with osteopontin values above 80 ng/mL had significantly lower cumulative survival compared to those with osteopontin ≤ 80 ng/mL (37% vs 56%, P = 0.00035; OR = 2.23, 95%CI: 1.06-4.68). CONCLUSION: Osteopontin is a non-invasive parameter of portal hypertension that distinguishes patients with clinically significant portal hypertension. It is a strong prognostic factor for survival.

The prevalence of nonalcoholic liver steatosis in patients with type 2 diabetes mellitus in the Czech Republic.

AIMS: Nonalcoholic fatty liver disease (NAFLD) is associated with components of the metabolic syndrome (MS) but the prevalence of NAFLD in the Czech Republic is unknown. The aim of this study was to assess the latter in patients with type 2 diabetes (DM2) and to compare the noninvasive fibrosis scores with ultrasound findings in those patients. METHODS: 180 consecutive patients with DM2 (mean age 64.2±9.3 years, 63% men) were examined for liver biochemistry, MS parameters and had liver ultrasound. MS was diagnosed according to the International Diabetes Federation. The diagnosis of NAFLD was based on liver ultrasound. Other aetiology of liver lesion was ruled out. Additionally, AST/ALT ratio, APRI, NAFLD fibrosis score, FIB4 and BARD scores were calculated. RESULTS: 93% of patients met the MS criteria, 79% had NAFLD and 13% had ultrasound signs of fibrosis/cirrhosis. NAFLD patients had greater weight (96.9±19.3 vs 84.7±14.7 kg; P=0.003), BMI (32.6±5.2 vs 29.4±5.4 kg/m(2); P=0.007), waist circumference (113.8±12.8 vs 107.1±10.3 cm; P=0.033), ALT (0.73±0.57 vs 0.55±0.53 µkat/L, P=0.007) and triglyceridaemia (1.9±1.4 vs 1.4±1 mmol/L; P=0.005) than patients without NAFLD. There were no significant differences in age, sex, cholesterol, fasting glycaemia or glycated haemoglobin. Of calculated scores only the NAFLD fibrosis score revealed significant differences between patients with and without ultrasound signs of fibrosis/cirrhosis (1.027±2.228 vs -0.118±1.402, P=0.026). CONCLUSION: Patients with DM2 had in the majority of cases NAFLD which was related to weight, BMI, waist circumference and serum triglycerides. The validity of the liver fibrosis scoring system has to be assessed in those patients in the future.

Effect of carvedilol on portal hypertension depends on the degree of endothelial activation and inflammatory changes.

OBJECTIVE: Bleeding from esophageal varices is a major complication of liver cirrhosis. Non-selective beta-blockers exert an influence on the functional part of portal hypertension, thereby reducing the risk of bleeding. Direct measurement of this functional part is not possible; nevertheless, pro-inflammatory markers as well as parameters of endothelial dysfunction might serve as surrogate markers. The aim of study was to assess the correlation between the therapeutic efficacy of carvedilol and markers of endothelial dysfunction and systemic inflammation in patients with liver cirrhosis and portal hypertension. MATERIAL AND METHODS: Thirty-six patients with cirrhosis and portal hypertension were given carvedilol, 25 mg q.i.d. for 30 days. Hepatic venous pressure gradient (HVPG) and biochemical determinations were performed prior to and after the treatment. Eight healthy individuals served as controls for comparison of biochemical markers. RESULTS: In the whole group of cirrhotic patients, HVPG decreased from 17.7+/-3.8 to 14.9+/-4.8 mmHg (p<0.001). Complete response was seen in 15 patients (42%). Baseline serum levels of E-selectin were significantly higher in responders than in non-responders (119.8+/-70.6 versus 52.6+/-25.7 ng/ml; p=0.023) and in controls (28.8+/-22.2 ng/ml; p=0.004). Furthermore, baseline TNF-alpha levels were significantly higher in responders than in non-responders (22.8+/-15.7 versus 7+/-8.9; p=0.047) and in controls (5.5+/-5.9 pg/ml; p=0.005). Serum levels of ICAM-1 showed the same trend (4360+/-2870 versus 2861+/-1577 versus 651+/-196 ng/ml), although differences did not reach statistical significance. CONCLUSIONS: Markers of systemic inflammation and endothelial dysfunction seem to predict the hypotensive effect of carvedilol on portal hypertension in patients with liver cirrhosis and may be useful in the assessment of the efficacy of the therapy.

Hepatic vein stenosis and inferior vena cava stenosis in a patient with chronic obstructive pulmonary disease.

The case is presented of a patient with stenosis of the intrahepatic portion of the inferior vena cava and the terminal part of hepatic veins, a state manifesting itself in ascites resistant to treatment. The case was originally seen as decompensated cirrhosis of the liver. Once properly diagnosed, it was successfully treated with angioplasty and subsequent anticoagulation. After all the relevant hypercoagulation states potentially leading to IVC and hepatic vein stenosis were ruled out, the cause of the patient's stenosis could be traced to: 1. secondary polycythemia concomitant to severe pulmonary obstruction disease and 2. simultaneous corticosteroid therapy. This cause has not been described in literature before.