nicotinamide appears to be associated with the development of clinical symptoms of pellagra, principally dermatitis (Dillon et al., 1992).
In plasma the 2-pyridone derivative drops below detection limits after a low niacin intake (Jacob et al., 1989). With an oral niacin load (nicotinamide at 20 mg/70 kg body weight), postdose changes in 2-pyridone in both plasma and urine were more responsive to niacin status than changes seen in N1-methyl-nicotinamide. Plasma concentrations of other niacin metabolites and of niacin are not useful markers of niacin status.
Analysis of erythrocyte NAD concentration promises to be a sensitive indicator of niacin depletion. In an experimental study in which adult male subjects were fed low-niacin diets containing either 6 or 10 mg NE/day, the erythrocyte NAD concentration decreased by 70 percent, whereas the NADP concentration remained unchanged (Fu et al., 1989). An earlier study reported a similar decrease in NAD relative to NADP in fibroblasts grown in niacin-restricted culture (Jacobson et al., 1979). Erythrocyte NAD concentrations provided a marker of niacin depletion equally as sensitive and reliable as excretion of urine metabolites in a study of seven healthy young men (Fu et al., 1989) and in an experimental niacin depletion study of elderly subjects (Ribaya-Mercado et al., 1997).
A possible functional measure for niacin status could be polyadenosine diphosphate (ADP) ribosylation, because ADP ribosylation may contribute to gene stability (poly-ADP-ribose polymerase in the nucleus) and may function in deoxyribonucleic acid (DNA) replication and repair (Stierum et al., 1994). However, the assays have not been developed or refined well enough to be used to judge niacin status at present.
Clinical pellagra may represent various degrees of combined niacin and riboflavin deficiencies (Carpenter and Lewin, 1985).