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Aim: The liver is an important reference organ for positron emission tomography/ computed tomography (PET-CT) examination using 18F-fluorodeoxyglucose (18F-FDG). However, 18F-FDG uptake by the liver is affected by many factors. We therefore investigated the effect of hepatic function on 18F-FDG uptake in the liver., Methods: A retrospective analysis of data on the hepatic function and the mean liver standardized up-take value (SUV) of 18F-FDG uptake in the liver during PET-CT examination of 500 (381 males, 119 females, aged 27-71) physical examinees., Results: The mean liver SUV was 1.88 ± 0.20. The correlation coefficient and partial correlation coefficient for age, the levels of conjugated bilirubin, globulin, AST and the mean liver SUV were statistically significant (r' = 0.119, -0.197, -0.089 and 0.151, all p < 0.05). Multiple linear regression analysis showed that age and the levels of conjugated bilirubin, globulin and aspartate amino-transferase (AST) were independent factors that influenced changes in the mean liver SUV (β = 0.008, -0.025, -0.151 and 0.005, all p < 0.05). The globulin level had the biggest predictive ability (β' = -0.151, p < 0.05)., Conclusions: The uptake of 18F-FDG in the liver was influenced by some liver function indexes. The levels of conjugated bilirubin, globulin and AST were independent factors for predicting changes in the uptake of 18F-FDG in the liver. Liver function test results should be combined with an evaluation of the metabolic activity of the liver., Competing Interests: Disclosure The authors report no conflicts of interest in this work., (Schattauer GmbH.)

Platelets tests, acute phase reactants and serum lipids were measured in patients with diabetes mellitus and patients with peripheral vascular disease. Patients frequently had abnormal platelet tests and significantly increased acute phase reactants and serum lipids, compared to young healthy control subjects. These differences were compared with multidiscriminant analysis. Patients could be separated in part from the control subjects with variables derived from the measurement of acute phase proteins and serum lipids. Platelet test results improved the separation between diabetics and control subjects, but not between patients with peripheral vascular disease and control subjects. Diabetic patients with severe retinopathy frequently had evidence of platelet activation. They also had increased acute phase reactants and serum lipids compared to diabetics with absent or non-proliferative retinopathy. In patients with peripheral vascular disease, only the fibrinogen concentration was related to the degree of vessel damage by arteriography.

We studied human platelet aggregation and beta-TG/PF4 release induced by heparin and related GAGs in vitro both in normal PRP and in PRP after aspirin. In our experimental conditions, heparin and related GAGs always caused PF4 release in vitro from normal platelets, whether or not there was measurable platelet aggregation in the aggregometer. Significant beta-TG release was induced only by the mucosal heparin preparation (which also induced platelet aggregation in some citrated PRP). Therefore, while beta-TG release in vitro seems to correlate with platelet aggregating activity of heparin, the selective PF4 release, caused by heparin and related GAGs also in conditions in which neither platelet aggregation nor beta-TG are measurable, is probably associated with the high affinity of PF4 for heparin. The degree of affinity of GAGs for PF4 (heparin greater than DeS greater than HS) seems to correlate with PF4 release. Moreover, the significant reduction in PF4 release in vitro after aspirin suggests that GAGs-induced PF4 release is related to a cyclooxygenase-dependent activation process.

Plasma levels of betathromboglobulin (BTG), fibrinopeptide A (FPA) and B beta 15-42 fragment, indices of platelet release, thrombin generation and plasmin activity respectively, were measured in 32 high risk patients during a double blind study of a single dose of the anabolic steroid stanozolol (50 mg IM) in the prevention of DVT after major gastro-intestinal surgery. The prevalence of malignancy and the incidence of DVT (125I fibrinogen scan) were similar in the two treatment groups. On the first postoperative day, BTG, FPA and B beta 15-42 levels were increased in most patients. Plasma BTG levels were significantly increased on the first post-operative day in patients who developed a DVT (n = 14) compared to those patients who did not (n = 18). A significant increase in FPA levels was found in the DVT group, 7 days after surgery. On the morning before surgery, plasma B beta 15-42 levels were significantly increased in patients who developed a DVT. In patients undergoing surgery for early malignancy (n = 17), we observed a pre-operative increase in FPA levels when compared to patients without malignancy. At post-operative day 7, B beta 15-42 levels were significantly increased in patients who received stanozolol (n = 15), when compared to the placebo group, suggesting that intramuscular stanozolol increases fibrinolysis in vivo.

At the end of a diagnostic right heart catheterization ten patients received an intravenous infusion of l-adrenaline which gradually increased the arterial plasma adrenaline concentration from resting physiological values to high values as seen during myocardial infarction, pheochromocytoma and hypoglycemia. Blood was sampled from the brachial artery, femoral vein and hepatic vein. During the adrenaline infusion venous beta-thromboglobulin concentrations increased 23% from 61 +/- 5 to 80 +/- 7 micrograms/l (mean +/- SE), arterial platelet counts 20% from 212 +/- 17 to 253 +/- 25 X 10(9)/l and arterial platelet volume 4% from 7.25 +/- 0.20 to 7.56 +/- 0.21 femtoliter. All changes were significant at the 5% level. Thus, acute increments of arterial plasma adrenaline significantly stimulated the blood platelet parameters studied.

Plasma beta-thromboglobulin (beta TG) and platelet factor 4 (PF4) were significantly higher in a group of 116 hypertensive men than in a normotensive group of 142 men. They increased with the stage of hypertension but the level did not correlate with the age of the subjects. Platelet aggregation was similar in the two groups and positively correlated with the age of the subjects in the normotensive group but not in the hypertensive group. A strong positive correlation was observed between the levels of plasma beta TG and PF4 and between platelet aggregation to ADP and that to epinephrine in both the hypertensive and normotensive groups. However, there was no correlation between the level of plasma beta TG or PF4 and platelet aggregation. Plasma antithrombin III was lower in the hypertensive group than in the normotensive group. These studies suggest that plasma levels of beta TG and PF4 are closely related to the stage of hypertension and are better indicators than aggregation of in vivo platelet activation in hypertensive subjects. Enhanced platelet activation may be involved in the acceleration of hypertensive arteriovascular damage and atherosclerosis.

The purpose of this study was to assess the usefulness of plasma fibrinopeptide A and beta-thromboglobulin concentrations for the diagnosis of acute venous thromboembolism in patients with a major bacterial infection. In 80 controls the mean plasma fibrinopeptide A concentration was 0.72 +/- 0.47 (ng/ml +/- SD) and the mean plasma beta-thromboglobulin concentration 28.2 +/- 10.1 (ng/ml +/- SD). On admission the mean fibrinopeptide A concentration was significantly raised (5.42 ng/ml) in these patients and 17 of them had a raised fibrinopeptide A concentration. However, the mean beta-thromboglobulin concentration was not significantly different from that of the healthy individuals (35.4 ng/ml) and only three patients had an increased beta-thromboglobulin concentration. Our data show that patients with major bacterial infections tend to have increased fibrinopeptide A and normal beta-thromboglobulin concentrations. Consequently, the measuring of plasma fibrinopeptide A concentration is useless for the diagnosis of acute venous thromboembolism in these patients. However, the determination of plasma beta-thromboglobulin concentration can still be used for this purpose, since a normal beta-thromboglobulin concentration excludes the presence of acute venous thrombosis.