Metabolic phenotype in Darier disease: a cross-sectional clinical study

Table 2 Metabolic parameters in Darier disease patients sub-grouped for acitretin treatment and mutation variant pathogenicity

	DD acitretin	DD no acitretin	p-value^#
n	14	11
Fasting plasma glucose (mmol/L)	5.3 ± 0.3	5.4 ± 0.4	0.12
2-h plasma glucose (mmol/L)	5.6 ± 2.2	5.6 ± 0.6	0.76
HbA1c (mmol/mol)	35 ± 3	37 ± 4	0.62
Proinsulin/insulin (ratio)	0.85 ± 0.28	0.94 ± 0.41	0.63
C-peptide (nmol/L)	0.9 ± 0.2	0.7±0.2	0.05*
HOMA2-%B	134.6 ± 29.2	107.6±14.1	< 0.01*

	Pathogenic mutation variant	Benign mutation variant	p-value^#
n	15	9
Fasting plasma glucose (mmol/L)	5.2 ± 0.3	5.5 ± 0.4	0.04*
2-h plasma glucose (mmol/L)	5.6 ± 2.1	5.8 ± 1.0	0.77
HbA1c (mmol/mol)	37 ± 4	34 ± 2	0.02*
Proinsulin/insulin (ratio)	0.87 ± 0.30	0.83 ± 0.35	0.62
C-peptide (nmol/L)	0.8 ± 0.2	0.8 ± 0.2	0.55
HOMA2-%B	128.1 ± 30.0	115.4 ± 21.0	0.40

Note that ATP2A2 mutation variant pathogenicity was previously determined by in silico prediction programmes [3]. Continuous variables were expressed as mean ± standard deviation (minimum–maximum)
n, number; DD, Darier disease; HbA1c, hemoglobin A1c
^#Mann–Whitney U Test, *insignificant differences after Benjamini–Hochberg correction for multiple comparisons (p ≥ 0.05)

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