Risk for post-thrombotic syndrome after lower-limb deep vein thrombosis: location of the thrombus or residual thrombi? / Risk razvitiia posttromboflebiticheskogo sindroma posle tromboza glubokikh ven nizhnikh konechnostei: lokalizatsiia tromba ili rezidual'nyi tromboz?

BACKGROUND: Many works aimed to determine factors that influence the onset of postthrombotic syndrome after an acute episode of deep venous thrombosis. We aimed to compare the prognostic value of the most proximal extent of thrombus (proximal and distal DVT) versus the residual thrombosis as identified by venous ultrasonography performed during follow-up. METHOD: We conducted a retrospective study of prospectively collected 1183 consecutive cohort patients in the RIETE registry after a first episode of deep venous thrombosis and assessed for postthrombotic syndrome after 12 months. RESULTS: Multivariate analysis revealed that: residual thrombosis (OR 1.40; 95% CI 0,88-2,21), the presence of cancer (OR 1.38; 95% CI: 0,64-2,97), immobility (OR 1.31; 95% CI 0,70-2,43) and estrogen-containing drugs use (OR 2.08, 95% CI 0,63-6,83), all had a predictive value for the occurrence of PTS. CONCLUSION: Our study results revealed that ultrasound finding of residual thrombosis is more predictive than proximal location of thrombus for postthrombotic syndrome after episode of deep venous thrombosis. Real life data from a large group of patients from the RIETE registry substantiates that.

Liver lipocalin 2 expression in severely obese women with non alcoholic fatty liver disease.

BACKGROUND: Lipocalin 2 (LCN2) has been related to obesity, insulin resistance and metabolic disturbance. However, its relation with non alcoholic fatty liver disease (NAFLD) has hardly been studied. METHODS: We examined LCN2 circulating levels and its protein and gene expression in liver from women with severe obesity and NAFLD. We analyzed the liver histology of 59 white severely obese women (BMI ≥40 Kg/m²): 15 subjects presented normal liver histology or non-significant liver disease (NL), 18 simple steatosis (SS) and 26 non alcoholic steatohepatitis (NASH). We determined the anthropometric and metabolic features of the women. LCN2 levels were determined by an ELISA and liver mRNA expression by real time RT-PCR. We also studied LCN2 expression in HepG2 liver cells under various inflammatory stimuli. RESULTS: Liver LCN2 protein and gene expression were higher in NAFLD than in obese with NL. Liver LCN2 gene expression correlated with SS (r=0.351, p=0.016), and its protein expression correlated with NASH (r=0.705, p=0.003). LCN2 expression was detected in HepG2 cells after the administration of TNFα, IL6, resistin or adiponectin. LCN2 expression was induced by TNFα, IL6 and resistin. CONCLUSIONS: Liver LCN2 is related to NAFLD in severely obese women. Up-regulation of LCN2 expression is detected in HepG2 cells after exposure to TNFα, IL6 and resistin. These results suggest that LCN2 expression is induced under liver harmful conditions.

[Evaluation of serum adenosine deaminase as a prognostic marker in the treatment of human immunodeficiency virus infection with zidovudine]. / Evaluación de la adenosina desaminasa sérica como marcador pronóstico en el tratamiento de la infección por el virus de la immunodeficiencia humana con zidovudina.

BACKGROUND: Adenosine deaminase (ADA) is a key enzyme in cellular immunity. It catalyses the reaction 2'deoxyadenosine to 2'deoxiinosine, a critical step in the production of essential metabolites for the synthesis of nucleic acids. Its main physiological activity occurs in T cells of lymphoid tissue. The advanced HIV infection is characterized by a severe and progressive cellular immunity compromise. Partial positive results have been obtained with Zidovudine (AZT), a drug which Serum adenosine deaminase has been proposed as a useful marker for the assessment of the therapy response in these patients. METHODS: Serum ADA activity was determined in patients infected with HIV in stage II, before and after four months of therapy with AZT, regarding variations in its activity with improvements in biological parameters--CD4 and CD8 lymphocytes. RESULTS: Patients infected with HIV showed a significant increase in ADA activity compared with patients in the control group: 21.6 +/- 5.4 vs. 10.4 +/- 2.3 U/l (p < 0.001). Therapy with AZT decreased ADA activity: 21.6 +/- 5.4 vs. 15.2 +/- 4.3 U/l (p < 0.001) and correlated with an increase in CD4 counts: 187 +/- 105 vs. 353 +/- 145/mm3 (p < 0.001) and in CD4/CD8 ratio: 0.188 +/- 0.10 vs. 0.382 +/- 0.18 (p < 0.001). CONCLUSIONS: The detection of a decrease in ADA correlates significantly with a favourable outcome in immunological parameters in individuals infected with HIV in stage II of disease treated with AZT.