No abstract

Twenty patients with tuberculous pleural effusions were studied with ultrasonography. In 18 patients, ultrasonography demonstrated regular pleural thickening which was less than 1 cm except in 1 case. In 4 cases there were a few pleural nodules, whereas in 2 cases the pleural surface showed small nodularity. The latter finding may be diagnostic for a tuberculous etiology. Eighteen patients had multiple, delicate, mobile septations in the effusions, and a lattice-like appearance had formed in 6 cases. Computed tomography was obtained in 7 cases, and pleural thickening was demonstrated in 6 of them. Ultrasonography is a useful imaging modality in the diagnosis of tuberculous pleurisy.

Intrahepatic portosystemic venous shunt, considered to be a rare disease, can lead to hepatic encephalopathy. With recent advances in diagnostic imaging techniques, the number of reports of intrahepatic portosystemic venous shunts identified incidentally in patients without symptoms are increasing. We report an intrahepatic portosystemic venous shunt that was diagnosed incidentally by real-time ultrasound and colour Doppler imaging, including the use of three-dimensional ultrasound using minimum intensity projections and power Doppler.

In this prospective study, it seems that CHF is not a pure liver disease but rather a multiorgan disorder involving the brain, portal vein, kidneys, and bile ducts. In most cases, the clinical picture includes other organ involvement, rather than purely the liver parenchyma.

In a retrospective cohort, we investigated the presence of the JAK2V617F mutation in chronic non-cirrhotic portal vein thrombosis (PVT) patients, irrespective of the presence or absence of myeloproliferative diseases (MPDs). We identified 25 patients in whom thrombophilia workup was completed. The diagnoses of MPDs were made according to the World Health Organization (WHO) criteria. JAK2V617F mutation analysis was performed by allele-specific polymerase chain reaction (PCR). There were 9 male and 16 female patients. Prior to JAK2V617F analysis, there were one or more thrombophilic risk factors in 19 patients (76%). The JAK2V617F mutation analysis revealed the presence of this mutation (all in the heterozygote state) in six patients (24%; two male, four female). Five of the six cases with prior clinical diagnosis of MPDs were found to have wild-type JAK2. We found that the addition of JAK2V617F analysis into the thrombophilia workup in patients with chronic PVT contributes to a 4% increase in the diagnosis of thrombophilic conditions.