ABSTRACT
Vitiligo is a common skin disorder characterized by immune-mediated destruction of melanocytes. Non-segmental vitiligo, the most common clinical subtype, has usually a chronic course and often results in significant psychosocial consequences for the affected patient. Early recognition, awareness of comorbidity, precise assessment of disease extent and activity, evaluation of impairment of quality of life as well as rapid initiation of treatment based on currently available evidence-based therapies are crucial cornerstones in the management of vitiligo. This S1 guideline helps German dermatologists to better diagnose and treat vitiligo.
Subject(s)
Practice Guidelines as Topic , Vitiligo , Humans , Vitiligo/diagnosis , Vitiligo/therapyABSTRACT
We present the case of a 77-year-old female patient who suffered from severe anaphylaxis during wound care. Allergologic evaluation yielded specific IgE antibodies to chlorhexidine, but anaphylaxis to chlorhexidine was not congruent with the patient history and dermal provocation tests. However, skin prick tests provided evidence for a sensitization to polyhexanide that was further supported by the detection of specific IgE antibodies to polyhexanide, the results of basophil activation tests and IgE inhibition analysis. We presume cross-reactive IgE antibodies binding to both biguanide antiseptics and identified polyhexanide as the likely cause of the anaphylactic reaction. We recognize polyhexanide as an emerging allergen that has to be considered as a cause of anaphylaxis.
Subject(s)
Allergens/adverse effects , Anaphylaxis/chemically induced , Anti-Infective Agents, Local/immunology , Biguanides/adverse effects , Disinfectants/adverse effects , Drug Hypersensitivity/etiology , Aged , Allergens/immunology , Anaphylaxis/diagnosis , Anaphylaxis/immunology , Biguanides/immunology , Cross Reactions , Disinfectants/immunology , Drug Hypersensitivity/diagnosis , Drug Hypersensitivity/immunology , Female , Humans , Immunoglobulin E/immunology , Skin TestsSubject(s)
Erythema/diagnosis , Erythema/therapy , Giant Cell Arteritis/diagnosis , Giant Cell Arteritis/therapy , Leg Dermatoses/diagnosis , Leg Dermatoses/therapy , Anti-Inflammatory Agents/therapeutic use , Cerebrovascular Disorders/diagnosis , Cerebrovascular Disorders/therapy , Diagnosis, Differential , Female , Humans , Middle Aged , Treatment OutcomeABSTRACT
CONTEXT: Vitiligo frequently coincides with autoimmune endocrinopathies, particularly Hashimoto's thyroiditis (HT). Genetic susceptibility may underlie this coincident occurrence. One candidate region is the autoimmunity susceptibility locus on chromosome 1, which encompasses forkhead transcription factor D3 (FoxD3), a gene involved in embryonal melanogenesis. We identified a promotor variant (rs78645479) in an index case of vitiligo + HT + candidiasis and evaluated its clinical and functional relevance. DESIGN: We genotyped 281 patients with variable autoimmune endocrinopathies: HT, Graves' disease (GD), type 1 diabetes (T1D), Addison's disease (AD), autoimmune polyglandular syndrome (APS), and/or vitiligo and 1858 controls. Furthermore, we experimentally assessed the effect of the variant on promotor activity and assessed the expression of FoxD3 in human thyroid tissue samples. RESULTS: Patients with vitiligo had a higher frequency of the risk allele (30%) compared with healthy controls (18.2%). In addition, the variant was associated with the incidence of elevated anti-TPO antibodies and anti-Tg antibodies, but not with TSH, FT3, or FT4 levels and also not with GD, T1D, AD, or APS. Functionally, the variant increased transcriptional activity in Jurkat and in Hek293 cells. We confirmed gene expression of FoxD3 in human thyroid tissue, which seemed elevated in thyroid tissue samples of some patients with GD and nonautoimmune goiter but not in patients with HT. CONCLUSION: In addition to a possible association of rs78645479 in FoxD3 with vitiligo, our data on the association of this FoxD3 variant with thyroid autoantibodies suggest a potential involvement of FoxD3 in thyroid immunoregulation.
