The authors demonstrated that these glycans were differentially expressed in HCC patients compared with healthy controls; both G2890 (m/z value, 2,890.052) and G3560 (m/z value, 3,560.295)

were recurrent and prognostic factors, respectively. To determine whether these two serum glycans could be clinical markers for advanced HCC patients Doxorubicin order and their levels in patients with chronic hepatitis (CH), we investigated serum N-glycan profiles using the same method used by Kamiyama et al. in 85 consecutive HCC patients treated with sorafenib, 41 patients with CH B or C, and 459 healthy volunteers. Mean serum levels (SDs) of G2890 were 2.60 (1.50), 0.85 (0.60), and 1.04 (0.41) pmol/mL (P < 0.0001), and the levels of G3560 were 0.42 (0.37), 0.05 (0.06), and 0.09 (0.06) pmol/mL (P < 0.0001) in HCC, CH, and healthy volunteers, respectively. Changes in the levels of the two glycans did not correlate with CH virus infection but with

the presence of HCC. Of the 61 glycans detected, 15 glycans, including G2890 and G3560, were elevated in patients with progressive disease 6 weeks after starting sorafenib. Comparing overall survival (OS) between patients with high and low values of these 15 glycans, only G2890 correlated with poor OS in univariate analysis using Cox’s proportional hazard model, while G3560 showed a borderline correlation (Table 1). Multivariate analysis with selleck chemicals known prognostic factors revealed that high levels of G2890 (hazard ratio, 1.88; 95% confidence interval, 1.04-3.48), as well as Eastern

Cooperative Oncology Group performance status (ECOG PS)[1, 2] and Child-Pugh (B), were identified as independent risk factors for survival. We have yet to identify the ligands of G2890 and the biological effects in HCC patients; however, our findings support and expand the results by Kamiyama et al.: serum G2890 is a novel diagnostic and prognostic factor in HCC patients treated with sorafenib, as was observed in surgically treated patients. Koji Miyahara, M.D.1 “
“A 49-year-old male presented with a 1-year history of combined bulbar and pseudobulbar dysarthria, involuntary movements, and gait instability. Laboratory evaluation showed a decreased serum ceruloplasmin of <0.06 g/L. Despite mild elevation of aspartate aminotransferase (54 E/L) and alanine aminotransferase Meloxicam (101 E/L), liver function (international normalized ratio, albumin, and bilirubin) was preserved. Magnetic resonance imaging (MRI) showed an abnormal attenuation of bilateral basal ganglia and cerebellar atrophy (Fig. 1). A brain computed tomography scan revealed hyperdensity of the basal ganglia and dentate nucleus. Because these findings were strongly suggestive of Wilson’s disease (WD), our workup continued to focus on further establishing this diagnosis. The ophthalmologist did not see Kayser-Fleischer (KF) rings, and 24-hour urine collection demonstrated a 0.6-umol copper loss per day (normal, 0.0-1.2 umol/day).