Avantika Chenna

Microvessel density analysis in patients with viral hepatitis-related hepatocellular carcinoma.

AimThe aim of this study is to compare tumoral microvessel density (MVD) and overall survival in two different groups of hepatocellular carcinoma (HCC), namely, viral hepatitis-related HCC (VHr-HCC) versus non-hepatitis-related HCC (NHr-HCC).MethodsSeventy-eight consecutive cases of HCC (47 hepatitis and 31 non-hepatitis cases) were studied. Microvessel numbers were assessed by staining for the antigens CD31, CD34, and CD240. The highest number of microvessel density and number of vessels were counted in the tumor, and the mean value represented the final MVD. Overall survival (OS) was analyzed between the two groups.ResultsVHr-HCC and NHr-HCC were observed in 47 and 31 cases, respectively. No significant differences were seen between the VHr-HCC and NHr-HCC groups with respect to age, gender, or Child-Pugh class distribution. Mean number of vessels was significantly higher in Hr-HCC using CD31 (97.7 vs 83.7) and CD34 (82.4 vs 71.9) (p value 0.025 and 0.039, respectively). Higher MVD was detected in Hr-HCC compared to NHr-HCC using CD31 (4.9 vs 4.4) and CD34 (4.7 vs 4.3) (p value 0.0095 and 0.0190, respectively). No significant difference was observed between VHr-HCC and NHr-HCC using CD240 immunostaining for MVD (p value 0.0945 and 0.906, respectively). Overall survival was not statistically significantly different between VHr-HCC and NHr-HCC groups (p value 0.104).ConclusionsHCC due to viral hepatitis has higher tumor microvessel formation and higher MVD values. This observation may explain the higher response of agents that target vascular endothelial growth factor (such as sorafenib) in patients with VHr-HCC.

738: ASSOCIATION BETWEEN SERUM C-REACTIVE PROTEIN LEVELS AND PULMONARY ARTERIAL HYPERTENSION

Learning Objectives: Accumulating evidence implicates the role of systemic inflammation in the pathogenesis of pulmonary arterial hypertension (PAH). C reactive protein (CRP) is an established marker of inflammation that is active in the physiopathology of the vascular wall. It is hypothesized that the proinflammatory properties of CRP contribute to pulmonary vascular remodeling via modulation of the nuclear factor–kappa B pathway. The association between CRP and PAH is unclear. We conducted a meta-analysis to evaluate the relationship between serum CRP levels and PAH. Methods: We searched MEDLINE, CINAHL and COCHRANE databases for studies reporting serum CRP levels in the PAH and non PAH study population. We included case controls, cohort and cross-sectional studies. We calculated the weighted standardized mean difference (SMD) in serum CRP levels between the PAH and control groups. Results: Our search strategy yielded 124 articles. We included eight studies enrolling 861 participants. PAH was diagnosed either by doppler echocardiography (52%) or right heart catheterization (48%). The median age of the PAH group was 55 yr. (IQR 41 61) vs 48 yr. (IQR 34 56) in the control group. The median body mass index in the PAH group was 25.6 kg/m2 (IQR 24.7–26.4) vs 25.9 kg/m2 (IQR 25.1–27.3) in the control group. The unweighted median serum CRP levels in the PAH group were 6.75 mg/l (IQR 3.912.5) vs 3.15 mg/l (IQR 2 – 6.9) in the control group. The SMD of CRP level was 0.75 (95% CI 0.31 – 1.18) p<0.001 comparing the PAH group vs the control group. Conclusions: An elevated serum CRP level is significantly associated with the presence of PAH. Given the significance of elevated CRP levels in PAH, directing further studies in understanding the role or CRP in the etio-pathogenesis of PAH would help determine newer modalities of therapeutic options and prognostic indicators.