Serum level of IL-4 predicts response to topical immunotherapy with diphenylcyclopropenone in alopecia areata.

BACKGROUND: This study investigated predictors of response to topical diphenylyclopropenone (DPCP) immunotherapy in patients with alopecia areata (AA). OBJECTIVE: To identify predictors of response, or resistance, to treatment for AA through clinical observations and serum tests. METHODS: Eighty four AA patients were treated with DPCP. Serum cytokine levels were measured in 33 AA patients pre- and post-treatment, and in 18 healthy controls, using ELISA assays. RESULTS: Of patients, 56.1% responded to DPCP with satisfactory hair regrowth; the response rate was negatively correlated with hair loss extent. Before DPCP treatment, higher serum IFN-γ and IL-12 cytokine levels were observed in AA patients compared to healthy controls. Non-responders to DPCP had significantly elevated serum IL-4 pre-treatment (3.07 fold higher) and lower IL-12 levels compared with responders. After DPCP treatment, non-responders had persistently high IL-4, increased IL-12, negligible decrease in IFN-γ and decreased IL-10. Post-treatment DPCP responders exhibited significantly decreased IFN-γ and IL-12, and increased IL-4 and IL-10. Development of adverse side-effects was significantly associated with higher pre-treatment serum IgE levels. LIMITATIONS: A small number of subjects were evaluated. CONCLUSIONS: Potentially, elevated pre-treatment serum levels of IL-4 and IL-12 can be used as unfavorable and favorable predictors of DPCP therapeutic effect, respectively. In addition, pre-treatment elevated serum total IgE may predict increased risk for severe adverse side-effects to DPCP application. Whether serum cytokine expression levels can be used as predictors of response to other forms of treatment is unknown, but it may warrant investigation in the development of personalized treatments for AA.

Early stage alopecia areata is associated with inflammation in the upper dermis and damage to the hair follicle infundibulum.

BACKGROUND/OBJECTIVES: Alopecia areata (AA) is a non-scarring inflammatory hair loss disease. We investigated the early pathological changes of AA to identify possible factors participating in its pathogenesis. METHODS: Clinical, laboratory and pathological features of 87 AA patients were investigated. RESULTS: Anti-nuclear antibody was found in 11 of 85 patients tested (13%), with a higher percentage in women (21%) than men (5%) (P = 0.026). In early AA lesions, inflammatory infiltration in the upper dermis and epithelial cell damage of the hair follicle infundibulum, just above the sebaceous gland, was observed. Liquefaction and disarrangement of peripheral infundibular epithelial cells coexisted with T-lymphocytic invasion and regression of the lower follicle. The latter findings positively correlated with the presence of eosinophils and perivascular mononuclear cell infiltration in the upper dermis. Eosinophilic infiltration was found in 35 patients (40%) and was positively correlated to elevated serum IgE levels (r = 0.21, P = 0.044), a more severe perivascular lymphocytic inflammation in the upper dermis (r = 0.24, P = 0.026), as well as a prominent swarm of bees-like peri-follicular infiltration (r = 0.41, P < 0.001). Mast cells were abundant in the upper dermis, especially around blood vessels, and positively correlated with eosinophil presence (r = 0.30, P = 0.027). CONCLUSION: Damage to the hair follicle infundibulum in the upper dermis might be an important component of early changes in AA lesions, possibly caused by lymphocyte cell infiltration in the same area. AA may involve damage of the upper hair follicle as well as the bulb, possibly involving hypersensitivity and autoimmunity.

Diffuse alopecia areata is associated with intense inflammatory infiltration and CD8+ T cells in hair loss regions and an increase in serum IgE level.

BACKGROUND: Mechanism leading to an abrupt hair loss in diffuse alopecia areata (AA) remains unclear. AIMS: To explore the characteristics of diffuse AA and possible factors involved in its pathogenesis. METHODS: Clinical and laboratory data of 17 diffuse AA patients and 37 patchy AA patients were analyzed retrospectively. Serum IgE level was evaluated in all diffuse and patchy AA patients, as well as 27 healthy subjects without hair loss to serve as normal control. Univariate analysis was performed using Fisher's exact test and Wilcoxon rank-sum test. Associations between inflammatory cell infiltration and laboratory values were analyzed using Spearman rank correlation test. RESULTS: The mean age of patients with diffuse AA was 27 years with a mean disease duration of 1.77 months. All of them presented in spring or summer with an acute onset of diffuse hair loss preceded by higher incidence of scalp pruritus. Although no statistically significant difference on the incidence of atopic disease among three groups has been found, serum IgE level in diffuse AA was higher than that in healthy controls, but was comparable to that in patchy AA group. Histopathology of lesional scalp biopsies showed more intense infiltration comprising of mononuclear cells, eosinophils, CD3 + , and CD8 + T cells around hair bulbs in diffuse AA group than in patchy AA group. Moreover, IgE level in diffuse AA patients positively correlated with intensity of infiltration by mononuclear cells, eosinophils, and CD8 + T cells. CONCLUSIONS: Hypersensitivity may be involved in pathogenesis of diffuse AA. The acute onset of diffuse AA may be related to intense local inflammatory infiltration of hair loss region and an increase in serum IgE level.

Female pattern hair loss: clinico-laboratory findings and trichoscopy depending on disease severity.

BACKGROUND: Female pattern hair loss (FPHL) is a progressive hair loss disorder with unclear triggering and supporting factors. Trichoscopic features of each stage of FPHL have not been specifically elaborated previously. AIMS: To analyze characteristics and investigate associations of clinico-laboratory and trichoscopic features of female patients in regard to the severity of hair loss in FPHL and to facilitate its diagnosis using noninvasive scalp dermoscopy (trichoscopy) in Fitzpatrick skin type III patients. MATERIALS AND METHODS: Clinico-laboratory and trichoscopic data from 60 patients with FPHL were analyzed using Spearman's correlation test. RESULTS: Patients had mean age of 34.4±10.6 years and mean duration of hair loss of 4.49±3.76 years. Of all, 45% (27/60) had a family history of pattern hair loss (PHL) and had an earlier onset of hair loss. Stage of hair loss positively correlated with duration and age at presentation. No association was found between the severity of FPHL and laboratory values including anemic and gonadal hormone profiles. Characteristic trichoscopic features (at 10-fold magnification) of FPHL were peripilar signs (PPS) (brown, BPPS and white, WPPS), white dots, scalp pigmentation, and focal atrichia. WPPS, scalp pigmentation, and focal atrichia positively correlated with the stage and duration of hair loss. CONCLUSIONS: Family history of PHL causes an earlier onset of hair loss but does not influence its course or severity. The latter is also not affected by abnormal anemic profile or hormonal levels. PPS, scalp pigmentation, focal atrichia, and white dots are characteristic of PHL. WPPS, scalp pigmentation, and focal atrichia reflect advanced PHL.