Background: Zn (Zn) is an essential trace element with important roles in protein structure
and function. Labile Zn is the fraction available for regulatory functions through it loose binding
to albumin. As Zn deprivation reduces labile Zn levels and leads to an immune compromised state,
we investigated labile Zn levels in the context of systemic autoimmune disease.
Methods: Cross sectional case control study in patients with Systemic Lupus Erythematosus (SLE;
n= 45), primary Sjögren’s Syndrome (n= 53) and healthy controls (HC; n= 27). Serum labile Zn
levels were measured by an in-house assay using the UV-excitable fluorophore zinquin ethyl ester.
Associations between labile Zn levels and SLE manifestations were investigated by nonparametric
Results: None of the SLE or pSS patients was found to be Zn deficient. Labile Zn levels were significantly
higher in SLE (31.7 mcg/dl) than in pSS patients (22.3 mcg/dl) and HC (19.7 mcg/dl)
(p<0.001). Labile Zn levels did not associate with demographics, disease activity scores, or inflammatory
cytokine levels, but correlated inversely with lymphocyte counts (Rs -0.37, p<0.01), antidsDNA,
anticardiolipin (Rs -0.29, p=0.01), anti-rib P antibody levels (Rs -0.24, p=0.02) and with
circulating NK-cell numbers in SLE patients (Rs .27, p= 0.02).
Conclusions: There is no evidence of Zn deficiency in patients with pSS or SLE. Labile Zn levels
are unexpectedly high in SLE patients, independent of cytokine levels and may play a role in immune
modulation through increased NK numbers and autoantibody containment.