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Extensive scalp angioedema following high-dose diphenylcyclopropenone for alopecia areata.

ABSTRACT: OBJECTIVE: To describe a case of an unusual adverse drug reaction to diphenylcyclopropenone for the treatment of alopecia areata. CASE SUMMARY: A 31-year-old Caucasian male presented with extensive angioedema to the head with neck involvement 10 days following treatment with diphenylcyclopropenone 2% solution in acetone topically on his scalp to treat alopecia areata. Findings on patient presentation included edema of the soft tissues (deeper dermis and subcutaneous tissue) of the head and face with mild neck involvement, acute inflammatory changes from chemical-induced irritation, scalp erythema, and serous fluid drainage from inflamed and fissured edematous scalp. Acute treatments used for control of the reaction included intravenous steroids and antihistamines during hospitalization followed by oral steroids and antihistamines for maintenance during outpatient treatment of the resolving condition. DISCUSSION: The role of topical diphenylcyclopropenone in this case of alopecia areata is probable according to the Naranjo criteria, with a score of 8. Diphenylcyclopropenone is not approved by the US Food and Drug Administration, but it has been used by many clinicians for the treatment of alopecia areata. Diphenylcyclopropenone causes an allergic contact dermatitis in the area of hair loss. In general, diphenylcyclopropenone is applied at a high concentration of 2% once and then at lower concentrations once weekly after the sensitization dose. This patient applied the 2% concentration on multiple consecutive days. CONCLUSION: Frequent use of topical diphenylcyclopropenone 2% applied to the scalp may cause scalp angioedema.

SUBMITTER: Buchanan R

PROVIDER: S-EPMC3887587 | biostudies-other | 2014 Jan

REPOSITORIES: biostudies-other

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Project description:BackgroundAlopecia areata (AA) is one of the most common autoimmune diseases and targets the hair follicles, with high impact on the quality of life and self-esteem of patients due to hair loss. Clinical management and outcomes are challenged by current limited immunosuppressive and immunomodulating regimens.MethodsWe have developed a Stem Cell Educator therapy in which a patient's blood is circulated through a closed-loop system that separates mononuclear cells from the whole blood, allows the cells to briefly interact with adherent human cord blood-derived multipotent stem cells (CB-SC), and returns the "educated" autologous cells to the patient's circulation. In an open-label, phase 1/phase 2 study, patients (N = 9) with severe AA received one treatment with the Stem Cell Educator therapy. The median age was 20 years (median alopecic duration, 5 years).ResultsClinical data demonstrated that patients with severe AA achieved improved hair regrowth and quality of life after receiving Stem Cell Educator therapy. Flow cytometry revealed the up-regulation of Th2 cytokines and restoration of balancing Th1/Th2/Th3 cytokine production in the peripheral blood of AA subjects. Immunohistochemistry indicated the formation of a "ring of transforming growth factor beta 1 (TGF-β1)" around the hair follicles, leading to the restoration of immune privilege of hair follicles and the protection of newly generated hair follicles against autoimmune destruction. Mechanistic studies revealed that co-culture with CB-SC may up-regulate the expression of coinhibitory molecules B and T lymphocyte attenuator (BTLA) and programmed death-1 receptor (PD-1) on CD8β(+)NKG2D(+) effector T cells and suppress their proliferation via herpesvirus entry mediator (HVEM) ligands and programmed death-1 ligand (PD-L1) on CB-SCs.ConclusionsCurrent clinical data demonstrated the safety and efficacy of the Stem Cell Educator therapy for the treatment of AA. This innovative approach produced lasting improvement in hair regrowth in subjects with moderate or severe AA.Trial registrationClinicalTrials.gov, NCT01673789, 21 August 2012.

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Extensive scalp angioedema following high-dose diphenylcyclopropenone for alopecia areata.

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