Scott, J., Havyarimana, E., Navarro-Gallinad, A., White, A. Wyse, J., van Geffen, J., van Weele, M., Buettner, A., Wanigasekera, T., Walsh, A., Aslett, L., Kelleher, J.D., Power, J., Ng, J., O'Sullivan, D., Hederman, L., Basu, N., Little, M.A. and Zgaga, L.: 2022,
Arthritis Research & Therapy 24, 147, 14 pp.
doi: 10.1186/s13075-022-02834-6
Background
The aetiology of ANCA-associated vasculitis (AAV) and triggers of relapse
are poorly understood. Vitamin D (vitD) is an important immunomodulator,
potentially responsible for the observed latitudinal differences between
granulomatous and non-granulomatous AAV phenotypes. A narrow ultraviolet B
spectrum induces vitD synthesis (vitD-UVB) via the skin. We hypothesised
that prolonged periods of low ambient UVB (and by extension vitD deficiency)
are associated with the granulomatous form of the disease and an increased
risk of AAV relapse.
Methods
Patients with AAV recruited to the Irish Rare Kidney Disease (RKD) (n = 439)
and UKIVAS (n = 1961) registries were studied. Exposure variables comprised
latitude and measures of ambient vitD-UVB, including cumulative weighted UVB
dose (CW-D-UVB), a well-validated vitD proxy. An n-of-1 study design was
used to examine the relapse risk using only the RKD dataset. Multi-level
models and logistic regression were used to examine the effect of predictors
on AAV relapse risk, phenotype and serotype.
Results
Residential latitude was positively correlated (OR 1.41, 95% CI 1.14-1.74, p
= 0.002) and average vitD-UVB negatively correlated (0.82, 0.70-0.99, p =
0.04) with relapse risk, with a stronger effect when restricting to winter
measurements (0.71, 0.57-0.89, p = 0.002). However, these associations were
not restricted to granulomatous phenotypes. We observed no clear
relationship between latitude, vitD-UVB or CW-D-UVB and AAV phenotype or
serotype.
Conclusion
Our findings suggest that low winter ambient UVB and prolonged vitD status
contribute to AAV relapse risk across all phenotypes. However, the
development of a granulomatous phenotype does not appear to be directly
vitD-mediated. Further research is needed to determine whether sufficient
vitD status would reduce relapse propensity in AAV.
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