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Figure 1.

NO-ADMA-DDAH pathway.

Onset of infection in sepsis leads to an up-regulation of inducible nitric oxide synthase (NOS) in response to lipopolysaccharide and pro-inflammatory cytokines. This consequently increases nitric oxide (NO) production, which has a multitude of effects on endothelial, vascular, and immune function. Asymmetric dimethylarginine (ADMA) is produced by the methylation of arginine residues on proteins by the enzyme protein-arginine methyltransferase (PRMT) and metabolized by dimethylarginine dimethylaminohydrolase (DDAH). ADMA competitively inhibits NOS, thereby limiting NO production.

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Table 1.

Hemodynamic Shock Types.

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Table 1 Expand

Figure 2.

DDAH2 gene.

Schematic representation of DDAH2 gene (adopted from www.ncbi.nlm.nih.gov/gene/23564), including the upstream promoter, the ATG translation start site, and the −871 6g/7g and −449 G/C polymorphisms. Exons are numbered 1–7. Exon 1 is non-coding, but this area and intron 1 appear to contain a second promoter region.

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Figure 3.

Patient screening and study enrollment.

Flow diagram of patient screening and enrollment.

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Table 2.

Patient Characteristics.

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Table 2 Expand

Table 3.

DDAH2 Genotype Frequencies.

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Table 3 Expand

Figure 4.

Relationship between plasma ADMA concentration and the DDAH2 −449G/C genotype in septic patients.

Plasma ADMA concentrations differed according to −449G/C genotype on day 1 but not day 3. ADMA was highest in septic patients with −449CC homozygous genotype, intermediate in −449GC heterozygotes, and lowest in the GG homozygotes on day 1 (p = 0.01, panel A). While a similar trend in plasma ADMA was observed on day 3, the difference was not significant (p = 0.33, panel B).

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Table 4.

ADMA, type of shock, and vasoactive infusion requirements in septic patientsa.

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Table 4 Expand

Figure 5.

Plasma ADMA and shock type.

All of the septic shock patients with the −449CC homozygous genotype exhibited “warm” shock. While day 1 plasma ADMA concentration did not differ between “warm” and “cold” shock (p = 0.42), when compared with −449CC homozygous patients with shock, ADMA was significantly lower in those with the −449G allele for “cold” shock (p = 0.02) and trended lower for “warm” shock (p = 0.09).

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