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Elevated serum Ang-2 levels on admission are associated with and may be a useful biomarker of predicting persistent organ failure and ongoing endothelial cell activation in AP.

While well received, well tolerated, nontoxic, and noninvasive, ginger aromatherapy did not significantly decrease nausea in patients enrolled in this study. Among 21 patients who indicated feeling nausea prechemotherapy, 67% reported improvement, 5% worsening, and 28% no change in their postinfusion PeNAT score. We failed to detect a statistical significant difference in the change in PeNAT scores among the three groups.

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Background/Objectives Acute pancreatitis (AP) is a complex inflammatory syndrome with unpredictable progression to systemic inflammation and multi-organ dysfunction syndrome (MODS). Tumor necrosis factor alpha (TNF–α) is a cytokine that may link inflammation to the systemic inflammatory response syndrome (SIRS), which usually precedes MODS. Small genetic cohort studies of the TNFA promoter in AP produced ambiguous results. We performed a comprehensive evaluation of TNFA promoter variants to assess both susceptibility to AP and risk of progression to MODS. Methods We prospectively ascertained 401 controls and 211 patients with AP that were assessed for persistent SIRS (>48 hours) and MODS. MODS was defined as failure of ≥2 organ systems (cardiovascular, pulmonary, and/or renal) persisting more than 48 hours. Subjects were genotyped by DNA sequencing and analyzed for SNPs at −1031 C/T (rs1799964), −863 A/C (rs1800630), −857 C/T (rs1799724), −308 A/G (rs1800629), and −238 A/G (rs361525). Results Twenty-three of 211 AP patients (11%) developed MODS. TNFA promoter variants were not associated with susceptibility to AP, but progression to MODS was associated with the minor allele at −1031C (56.5% vs. 32.4% P=0.022, OR: 2.7; 95%CI: 1.12–6.51) and −863A (43.5% vs. 21.8% P=0.022, OR: 2.76; 95%CI: 1.12–6.74). Conclusion TNFA promoter variants do not alter susceptibility to AP, but rather the TNF–α expression-enhancing −1031C and −863A alleles significantly increased the risk of AP progression to MODS. These data, within the context of previous studies, clarify the risk of specific genetic variants in TNFA and therefore the role of TNF–α in the overall AP syndrome.