Background
Sodium disulfite (SD), also known as sodium metabisulfite, is an increasingly recognized cause of allergic contact dermatitis.
Objectives
The objective of this work was to characterize individuals with positive patch test reactions to SD as well as analyse reaction strength, clinical relevance, and sources.
Methods
This is a retrospective analysis of patients patch tested with SD (1% petrolatum) by the North American Contact Dermatitis Group (NACDG), 2017 to 2018.
Results
Of 4885 patients patch tested with SD, 132 (2.7%) had a positive reaction. Common primary anatomic sites of dermatitis were face (28.8%), hands (20.5%), and a scattered/generalized distribution (13.6%). Compared with SD‐negative patients, SD‐positive patients were more likely male (odds ratio 2.81, 95% confidence interval 1.98‐4.00) and/or over 40 years (odds ratio 1.95, 95% confidence interval 1.30‐2.94). Reactions were most commonly + (50.4%) or ++ (34.1%); 65.2% were considered currently relevant. About 15.2% were definitively confirmed in sources, commonly personal care products (18.9%, especially hair dye), and drugs/medications/alcoholic beverages (9.1%). Only 2.3% of positive reactions were linked to occupation.
Conclusions
Positive reactions to SD occurred in 2.7% of tested patients. Reactions were often clinically relevant and linked to personal care products and drugs/medications/alcoholic beverages.
single-nucleotide polymorphism (c.2268G>A) according to sequenced mRNA, whereas Sanger sequencing of the patient's blood detected the single-nucleotide polymorphism in a heterozygous form. The allele carrying the missense mutation is successfully transcribed into mRNA, but no protein is detected in the epidermis or keratinocytes. We assume protein degradation due to potential conformational change of the protein, resulting in protein instability and/or failure of protein-protein interaction. For now, this remains unresolved.AP1B1 encodes the large b-subunit of the adaptor protein (AP)1 complexes, which play an important role in polarized vesicular transport in eukaryotic cells. AP1 is involved in the formation of clathrin-associated vesicles and the selection of cargo proteins in the trans-Golgi network and/or endosomes for basolateral transport. 5,6 The pathophysiological causes of KIDAR have not yet been clarified, but previous studies have indicated that cell-polarity defects may cause at least deafness and hyperproliferation, 2,7 whereas epidermal consequences remain to be investigated.In summary, we demonstrate that compound heterozygous mutations in AP1B1 can induce complete loss of protein in human epidermis and may cause the symptoms described in our index patient. In addition to expanding the extremely short list of diagnosed AP1B1-deficient patients and specification of the main clinical features of this new syndrome, we describe the molecular consequences of AP1B1 mutations at the mRNA and protein levels.
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