Objective. To assess the diagnostic performance of a T1-independent, T2*-corrected multiecho magnetic resonance imaging (MRI) technique for the quantification of hepatic steatosis in a cohort of patients affected by chronic viral C hepatitis, using liver biopsy as gold standard. Methods. Eighty-one untreated patients with chronic viral C hepatitis were prospectively enrolled. All included patients underwent MRI, transient elastography, and liver biopsy within a time interval <10 days. Results. Our cohort of 77 patients included 43/77 (55.8%) males and 34/77 (44.2%) females with a mean age of 51.31 ± 11.27 (18–81) years. The median MRI PDFF showed a strong correlation with the histological fat fraction (FF) (r = 0.754, 95% CI 0.637 to 0.836, P < 0.0001), and the correlation was influenced by neither the liver stiffness nor the T2* decay. The median MRI PDFF result was significantly lower in the F4 subgroup (P < 0.05). The diagnostic accuracy of MRI PDFF evaluated by AUC-ROC analysis was 0.926 (95% CI 0.843 to 0.973) for S ≥ 1 and 0.929 (95% CI 0.847 to 0.975) for S = 2. Conclusions. Our MRI technique of PDFF estimation allowed discriminating with a good diagnostic accuracy between different grades of hepatic steatosis.
e14605 Background: Cetuximab and panitumumab are monoclonal antibodies that target EGFR, approved for the treatment of KRAS WT MCRC. Few data describe the activity of panitumumabafter cetuximab-irinotecan based regimen failure. Methods: The aim of this study is to assess if panitumumab has some activity in pts with KRAS WT MCRC that has progressed on prior cetuximab. Results: We retrospectively analysed 25 pts with KRAS WT MCRC who received from 07/2009 to 01/2013 panitumumab after progression on cetuximab. Median age: 63 yrs (40-78), primary site tumor: colon 64%, rectum 36%; synchronous metastases 36%, metachronous 64%. Sites of metastases: liver 44%, liver and lung 8%, other sites 48%. All pts had previously received cetuximab associated with irinotecan (20 pts) or oxaliplatin (5 pts) and subsequently received panitumumab. We withdrew cetuximab because of intolerance in 4 pts (16%), while 21 pts (84%) with ECOG PS 0-1 who had previously responded to cetuximab (ORR plus SD lasting more than 5 months) received panitumumab “off-label” after progression on cetuximab because strongly motivated to continue treatment. Median cycles of panitumumab were 7 (1-54). Only eighteen pts were evaluable for ORR (4 pts received 1-2 cycles and then died, 3 pts too early). We observed one PR (5%); five pts (28%) had SD, median duration 9 months. Median PFS was 5 months (3-28) and median OS 8 months (5-41). All pts were evaluable for toxicity. No pts developed anemia, nor neutropenia. One patient (4%) developed grade 2 CTCAE version 4.03 thrombocytopenia. Eight pts (32%) developed grade 2-3 CTCAE version 4.03 dry skin or rash, 2 pts (8%) grade 2 CTCAE version 4.03 nausea-vomiting. Conclusions: Panitumumab has minimal benefit in pts with KRAS WT MCRC who have progressed on prior cetuximab andthis approach up to date should not be adopted in the clinical practice. Our data anyway show a longer PFS and OS as compared to other few series in the same setting. Further confirmatory prospective studies with larger series of pts would be necessary.
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