Predicting portal thrombosis in cirrhosis: A prospective study of clinical, ultrasonographic and hemostatic factors.

BACKGROUND & AIMS: Portal vein thrombosis (PVT) is a relatively frequent event in patients with cirrhosis. While different risk factors for PVT have been reported, such as decreased portal blood flow velocity (PBFV) and parameters related with severity of portal hypertension, these are based on retrospective studies assessing only a discrete number of parameters. The aim of the current study was to evaluate the incidence and risks factors for non-tumoral PVT development in a large prospective cohort of patients with cirrhosis. METHODS: We performed an exhaustive evaluation of clinical, biochemical, inflammatory and acquired/hereditary hemostatic profiles in 369 patients with cirrhosis without PVT who were prospectively followed-up. Doppler ultrasound was performed at baseline and every 6 months or whenever clinically indicated. PVT development was always confirmed by computed tomography. RESULTS: Twenty-nine patients developed non-tumoral PVT, with an incidence of 1.6%, 6% and 8.4% at 1, 3 and 5 years, respectively. Low platelet count, PBFV <15 cm/sec and history of variceal bleeding were factors independently associated with a high PVT risk. No relationship between PVT development and any other clinical biochemical, inflammatory and acquired or hereditary hemostatic parameter was found. CONCLUSIONS: In patients with cirrhosis, the factors predictive of PVT development were mainly those related to the severity of portal hypertension. Our results do not support the role of hemostatic alterations (inherited or acquired) and inflammatory markers in the prediction of PVT in patients with cirrhosis. LAY SUMMARY: Patients with cirrhosis and more severe portal hypertension are at higher risk of non-tumoral portal vein thrombosis development. Acquired or inherited hemostatic disorders, as well as inflammatory status, do not seem to predict the development of portal vein thrombosis in patients with cirrhosis.

Inflammation is correlated with severity and outcome of cerebral venous thrombosis.

BACKGROUND: Few studies have suggested a relationship between inflammation and cerebral venous thrombosis (CVT). This retrospective study aimed to explore the changes in inflammation in different CVT stages and the correlation between inflammation and severity and outcome of CVT. METHODS: In total, 95 suitable patients with CVT and 41 controls were compared. Patients with CVT were divided into three groups. The inflammatory factors studied included hypersensitive C-reactive protein (Hs-CRP), interleukin-6 (IL-6), and neutrophil-to-lymphocyte ratio (NLR) in the peripheral blood and immunoglobulin A (IgA), immunoglobulin M (IgM), and immunoglobulin G (IgG) in the cerebrospinal fluid (CSF). The severity of CVT was evaluated with the modified Rankin Scale (mRS), the National Institutes of Health Stroke Scale (NIHSS), fundus condition, intracranial pressure (ICP), and complications on admission. The short-term outcome was evaluated with the mRS at discharge. RESULTS: The following results were obtained: (1) Inflammatory factor levels in patients with CVT were higher than those in the controls. (2) Inflammatory factor levels in the acute and subacute stages were significantly higher than those in the chronic stage (all P < 0.05). (3) Serum NLR and CSF IgM levels were positively related to baseline degree of disability (odds ratio [OR], 1.279, 95% confidence interval [CI] 1.009-1.621, P = 0.042; OR 1.402, 95% CI 1.036-1.896, P = 0.028). The Hs-CRP level was positively correlated with the baseline occurrence of seizure (OR 1.040, 95% CI 1.001-1.080, P = 0.043). The baseline serum NLR (r = 0.244, P = 0.017), CSF IgA (r = 0.615, P < 0.001), CSF IgM (r = 0.752, P < 0.001), and CSF IgG (r = 0.248, P = 0.015) levels were positively associated with NIHSS. (4) The baseline NLR was significantly associated with high risk of poor outcome at discharge (OR 1.339, 95% CI 1.097-1.784, P = 0.007). Moreover, the ROC showed that NLR ≥ 4.205 could better predict the poor outcome at discharge. The data were analyzed using SPSS. CONCLUSIONS: Inflammation may develop after CVT and gradually decrease during the course. Inflammation was significantly correlated with severity on admission and short-term poor outcome at discharge in CVT.

URGENT DIAGNOSTICS OF CEREBRAL VENOUS TROMBOSIS.

Investigations were carried out in 24 patients in order to evaluate information value of the data of clinical, laboratory, neuroradiological methods of research and develop the diagnostic algorithm in case of cerebral venous thrombosis (CVT). The main group consisted of 11 patients (7 male, 4 female, average age 49,1±4,3) with CVT. The comparison group included 13 patients (6 male, 7 female; average age 68,1±9,5) with ischemic stroke (IS) of moderate severity. There were revealed changes in blood and cerebrospinal fluid (CSF) as form of leukocytosis of blood and moderately increased cell count with elevated protein in CSF and blood in case of CTV. The authors noted an elevated protein in CSF and blood and leukocytosis with predominant lymphopenia in blood and neurophilic predominance in CSF within the reference range of CSF in patient with ischemic stroke. The epileptic attacks, meningeal syndromes, headaches were more often among clinical syndromes at CTV than in case of ischemic stroke. The algorithm of neuroimaging research methods and modes of MRI were determined and allowed an effective diagnostics of damages of venous sinuses, superficial and deep cerebral veins in case of urgent hospitalization of patients. It was possible to suggest the venous pathology in 7 (63,6%) cases due to SKT (without contrast) and in case of application of MR venography (2D TOFmode), there were revealed 100% of cases.