Biomedical subjects
Publications and source records attributed to Gurpreet Gulati.
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BACKGROUND: Assessment of disease activity in patients with Takayasu's arteritis (TA) is difficult due to absence of definitive tests. Presence of carotid intima-medial thickening has been suggested as a possible marker of inflammation and disease activity. METHODS: We evaluated common carotid artery carotid intima-medial thickness (CCA-IMT) in 56 common carotid arteries (CCAs) in 28 healthy controls and 74 CCAs in 37 patients of TA. We correlated these findings with the presence of activity as assessed by the National Institutes of Health (NIH) criteria. RESULTS: CCA-IMT was increased (>0.8 mm) in 59% of the patients with TA. In patients with disease activity, the CCA-IMT was more than in those without activity (1.5+/-0.16 vs. 0.9+/-0.2 mm, P<0.005). This is presumably because of ongoing inflammation causing abnormal thickening. Even among patients without active disease, CCA-IMT was more than in controls (0.9+/-0.2 vs. 0.6+/-0.1 mm, P<0.05) possibly due to a milder degree of inflammation or healing with fibrosis. All patients with angiographic carotid obstruction had increased CCA-IMT irrespective of whether they were active or not. However, in patients with angiographically normal carotid arteries, CCA-IMT was increased only among the patients who were active (1.4+/-0.2 vs. 0.7+/-0.04, P<0.05). Abnormal CCA-IMT as marker of disease activity had a sensitivity of 82% and specificity of 60%. On excluding patients with increased CCA-IMT who had angiographic carotid stenosis (because the increase in CCA-IMT cannot be attributed entirely to activity alone in these patients), the specificity increased to 70%. CONCLUSION: Increased CCA-IMT is a reliable marker of active disease, especially in the absence of angiographically visible carotid disease.
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Biliary abnormalities in extrahepatic portal vein obstruction (EHPVO) have been described in detail on endoscopic retrograde cholangiopancreaticography (ERCP), but have never before been reported on colour Doppler flow imaging (CDFI). These changes occur either due to extrinsic compression of the bile ducts or due to ischaemic biliary stenosis. The aim of this study was to evaluate the role of CDFI in demonstrating the biliary changes in patients with EHPVO. Three out of 46 patients with EHPVO (7%), who presented clinically with obstructive jaundice, were subjected to a detailed CDFI study of the abdomen, followed by ERCP and splenoportovenography (SPV). One of the patients also underwent a repeat CDFI examination at 8 weeks following a lienorenal shunt. In all 3 cases, CDFI easily distinguished the anechoeic structures seen on ultrasound at the porta hepatis as periportal collaterals, the hepatic artery and dilated bile ducts. It revealed the actual indentation made on the common bile duct (CBD) by the collaterals besides showing the presence of biliary calculi. Gallbladder varices were also well demonstrated in all the cases. ERCP confirmed the presence of portal biliopathy besides showing other changes, such as angulation, displacement and stricture of the CBD. SPV confirmed the presence of EHPVO. One patient who underwent shunt surgery showed persistent dilatation of the CBD with calculi. CDFI is a rapid, non-invasive and widely available modality which can be used to demonstrate the biliary changes in patients with EHPVO with obstructive jaundice. It may thus help screen patients who require a further by ERCP examination for the planning of treatment.