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Objective Patients with incomplete lupus erythematosus (ILE) have lupus features but insufficient criteria for SLE classification. Some patients with ILE transition to SLE, but most avoid major organ involvement. This study tested whether the milder disease course in ILE is influenced by reduced SLE risk allele genetic load.Methods We calculated the genetic load based on 99 SLE-associated risk alleles in European American patients with SLE (≥4 American College of Rheumatology (ACR) 1997 criteria, n=170), patients with ILE (3 ACR 1997 criteria, n=169), a subset of patients with ILE not meeting Systemic Lupus International Collaborating Clinics (SLICC) classification (ILESLICC, n=119) and healthy controls (n=133). Unweighted genetic loads were calculated as the total sum of risk alleles for each individual, while weighted genetic loads were defined as the sum of risk alleles multiplied by the natural logarithm of the previously published OR of each risk allele for SLE susceptibility.Results The median unweighted and weighted SLE risk allele genetic load was significantly greater in patients with ILE (unweighted: 81, p value=0.01; weighted: 16.3, p value=0.001) and patients with SLE (80, p value=0.02; 16.29, p value=0.0006) compared with healthy controls (78, 15.76). Patients with ILESLICC trended towards an increased genetic load, although not statistically significant (unweighted: 80, p value=0.14; weighted: 16.05, p value=0.07). However, the median genetic load did not significantly differ between ILE and SLE, and genetic load did not differentiate patients with ILE and SLE (area under the curve=0.51, p=0.78) by receiver operator characteristic analysis.Conclusions Patients with ILE and SLE have comparable genetic loads of SLE risk loci, suggesting similar genetic predispositions between these conditions. Phenotypical differences between SLE and ILE may instead be influenced by ILE-specific variants and gene–environment interactions.

Previous research reported the role of nonenzymatic metmyoglobin (MetMb) and methemoglobin (MetHb) reduction in meat color; however, limited studies have characterized the cofactors involved in nonenzymatic reduction. The objective of this study was to characterize electron donors and carriers in nonenzymatic MetMb and MetHb reduction at various temperatures and postmortem muscle pHs in vitro. Methylene blue and cytochrome c (cyt-c) were evaluated as electron carriers and nicotinamide adenine dinucleotide, reduced form (NADH) and ascorbate were considered as electron donors. All combinations of electron donors and carriers were evaluated in the following order: NADH plus methylene blue, ascorbate plus methylene blue, NADH plus cyt-c, and ascorbate plus cyt-c. Spectrophotometry was utilized to monitor the rates of reduction. The results indicated that methylene blue was an effective electron carrier than cyt-c in the presence of NADH. Temperature and pH had cofactor-specific effects on nonenzymatic MetMb and MetHb reduction. Lower temperature resulted in an increased nonenzymatic MetMb reduction for methylene blue regardless of electron donor (ascorbate, P = 0.03, NADH, P = 0.04). As pH increased, MetHb reduction was enhanced in the presence of ascorbate plus cyt-c. Nonenzymatic MetHb reduction was numerically lower than nonenzymatic MetMb reduction in the presence of NADH plus methylene blue. In summary, in addition to NADH, the current in vitro research demonstrated that ascorbate plus cyt-c could contribute to nonenzymatic MetMb and MetHb reduction at meat-pH and storage temperature.