Rationale GlycA, an emerging inflammatory biomarker, predicted cardiovascular events in population-based studies. Psoriasis, an inflammatory disease associated with increased cardiovascular risk, provides a model to study inflammatory biomarkers in cardiovascular disease (CVD). Whether GlycA associates with psoriasis and how it predicts subclinical CVD beyond hsCRP in psoriasis is unknown. Objective To investigate the relationships between GlycA and psoriasis, and between GlycA and subclinical CVD. Methods and Results Psoriasis patients and controls (n=412) participated in a two-stage study. We measured GlycA by NMR spectroscopy. NIH participants underwent 18-FDG PET/CT scans to assess vascular inflammation (VI) and coronary CT angiography to quantify coronary artery disease (CAD) burden. Psoriasis cohorts were young (mean age=47.9), with low cardiovascular risk and moderate skin disease. HsCRP and GlycA were increased in psoriasis compared to controls [GlycA: (PENN: 408.8±75.4 vs. 289.4±60.2, p<0.0001, NIH: 415.8±63.2 vs. 346.2±46, p<0.0001)] and demonstrated a dose-response with psoriasis severity. In stage 2, VI (β=0.36, p<0.001) and CAD (β=0.29, p=0.004) associated with GlycA beyond CV risk factors in psoriasis. In ROC analysis, GlycA added value in predicting VI (p=0.01) and CAD (p<0.01). Finally, initiating anti-TNF therapy (n=16) reduced psoriasis severity (p<0.001), GlycA (463.7±92.5 vs. 370.1±78.5; p<0.001) and VI (1.93±0.36 vs. 1.76±0.19; p<0.001), while GlycA remained associated with VI (β=0.56, p<0.001) post-treatment. Conclusions GlycA associated with psoriasis severity and subclinical CVD beyond traditional CV risk and hsCRP. Moreover, psoriasis treatment reduced GlycA and VI. These findings support the potential utility of GlycA in subclinical CVD risk assessment in psoriasis and potentially other inflammatory diseases.

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Concordance between mutations in the primary papillary thyroid carcinoma (PTC) and the paired x lymph node metastasis may elucidate the potential role of molecular targeted therapy in advanced stages. BRAF and NRAS mutations in primary PTC (n = 253) with corresponding metastatic lymph node (n = 46) were analyzed utilizing StripAssays (ViennaLab Diagnostics). Statistical analysis was performed using (SPSS, Inc.), version 24.0 with a p-value of <0.05, and concordance via kappa agreement. BRAF mutation frequency in conventional PTC (cPTC): 56.8%, papillary thyroid microcarcinoma (PTMC): 36.5%, PTMC-FV: 2.7% and PTC-FV: 4.1%. NRAS mutation frequency in PTC-FV: 28.6%, PTMC: 28.6%, PTMC-FV: 23.8%, and cPTC: 19.0%. BRAF mutation correlation with older age in cPTC (42.6 versus 33.6) years (p < 0.001) was the only significant clinicopathologic parameter. BRAF mutations were concordant in the primary and its corresponding lymph node deposits in PTC with a kappa of 0.77 (p-value < 0.0001). BRAF mutations are predominant in cPTC and PTMC while NRAS mutations in PTC-FV. BRAF mutation is conserved in metastatic lymph node deposits, thus BRAF is an early mutational pathogenetic driver. Therefore, targeted therapy is potential in recurrent and advanced stage disease.

Hepatoid adenocarcinoma of the stomach (HAS) is a rare aggressive tumor with hepatocellular differentiation. HAS often produces alpha fetoprotein (AFP) and metastasizes to the lymph nodes and the liver. Molecular studies revealed Her2 amplification and overexpression, association with p53 mutations, but no association with KRAS mutations. EGFR and BRAF mutations have not yet been evaluated in hepatoid carcinoma of the stomach so far. Hereby, we present a case of a 41-year-old female patient with HAS with high AFP level and liver metastases. Molecular analysis revealed Her2 overexpression by immunohistochemistry (IHC), but no EGFR, KRAS, or BRAF mutations were detected. The patient underwent chemotherapy type DCX (docetaxel, cisplatinum, and capecitabine) every 3 weeks with partial response after two cycles, maintained for eight cycles, and then was on maintenance therapy with trastuzumab for 7 months before relapsing and dying 18 months from the day of diagnosis. Conclusively, HAS may be misdiagnosed as hepatocellular carcinoma; therefore, it should be considered in the differential diagnosis of multiple hepatic nodules with high AFP and no history of hepatitis, liver fibrosis or cirrhosis.