Introduction: We present the CT scan-derived turricephaly index (TI) as a quotient of the maximal occipito-frontal length of the skull to the distance from the centre of the sella to the highest point on the vertex as a validated tool for assessing turricephaly and evaluating surgical techniques.Materials and Methods: TI measurements were taken from CTs from non-operated children with Apert syndrome and age-matched controls and analysed using Centricity PACS system (from the lateral scout image) and Osirix (the thick-sliced Osirix tool).CTs from non-operated children with Apert syndrome were used to investigate the natural history of turricephaly.Results: There was statistically significant agreement between measurements taken from the CT scout and Osirix for 42 control children (R 2 =0.97) and 42 children with Apert syndrome (R 2 = 0.98) and between two separate observers. There was a statistically significant difference (p<0.001) between CT scout-derived TI value between controls (1.730.12, range 1.46 -1.99) and Apert children (1.420.15, range 1.13 -1.73).Analysis of 113 CTs of 65 non-operated children with Apert syndrome showed a decrease in turricephaly with age (positive spearman correlation: r = 0.50, p<0.001).Analysis of 37 CTs of those with multiple (>2) CT's showed a decrease in turricephaly in the individual child (p<0.001).
BackgroundChronic hepatitis C is the most common cause of cirrhosis in industrialized countries. Successful treatment of chronic hepatitis C in patients with advanced fibrosis or cirrhosis has significant benefits, including improvements in inflammation, fibrosis, and portal hypertension, with prevention of esophageal varices and clinical decompensation.CaseIn this report, we present two patients with well-compensated hepatitis C cirrhosis who achieved an end-of-treatment response on a direct-acting antiviral therapy-based triple regimen for hepatitis C virus, but subsequently presented with new-onset ascites associated with virologic relapse.ConclusionWe propose that the development of ascites in this setting is due to the adverse impact of inflammation of the virologic relapse on portal hypertension. Our observation that ascites formation can be a manifestation of virologic relapse has potentially important clinical implications, as it highlights not only the importance of close monitoring of cirrhotic patients after achieving end-of-treatment response but also the impact of active inflammation on the severity of portal hypertension.
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