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The ALLEGRO phase 2b/3 study investigated the efficacy and safety of ritlecitinib in patients with alopecia areata (AA). To describe the impact of ritlecitinib on patient-reported hair loss using the Alopecia Areata Patient Priority Outcomes (AAPPO) instrument and evaluate the relationship between clinically meaningful hair regrowth and improvements in patient-reported impacts. In ALLEGRO-2b/3, patients aged ≥ 12 years with AA and ≥ 50% scalp hair loss received once-daily ritlecitinib 50 or 30 mg (± 4-week 200-mg daily loading dose), 10 mg, or placebo for 24 weeks and then continued ritlecitinib or switched from placebo to ritlecitinib 200/50 or 50 mg for 24 weeks. The AAPPO instrument evaluated improvement in hair loss, emotional symptoms (ES), and activity limitations (AL) from weeks 4 to 48 (secondary endpoint). Mean changes in ES and AL domain scores and individual items at weeks 24 and 48 were calculated for Severity of Alopecia Tool (SALT) score ≤ 20 responders and nonresponders (exploratory endpoint). Overall, 718 patients were randomized. At week 24, 5-36% of patients receiving ritlecitinib 10-200/50 mg reported improvement in scalp hair loss versus 9% receiving placebo. The results for eyebrow, eyelash, and body hair loss were similar. Mean change from baseline in ES and AL scores at weeks 24 and 48 was small and similar between groups. Mean change was larger for individual hair loss and ES items at weeks 24 and 48 in SALT score ≤ 20 responders versus nonresponders. The AAPPO instrument demonstrated the beneficial impact of ritlecitinib on patient-reported hair growth, which was consistent with improvements in clinician-reported outcomes. NCT03732807. INFOGRAPHIC.

Alopecia areata (AA) is a common form of non-scarring hair loss. The pathogenesis of AA is believed to involve multiple inflammatory cytokines, including possibly IL-17A. To assess the efficacy and safety of the IL-17A antagonist secukinumab in AA, we conducted a double-blinded, randomized prospective pilot study in which 11 subjects were treated with either secukinumab ( n  = 7) or placebo ( n  = 4) subcutaneously at weeks 0, 1, 2, 3, 4 and every 4 weeks thereafter until (inclusive of) week 20. The primary endpoint for the study was the percentage of patients achieving SALT50 at 24 weeks. A total of three subjects out of 11 completed the study through the primary endpoint, and therefore, we used the last observation carried forward method to analyze the missing data. At the primary endpoint or last completed observation, 0% (0/7) of the secukinumab-treated subjects achieved a 50% reduction in SALT score (SALT50), and likewise, 0% (0/4) of the placebo-treated subjects achieved SALT50. In the secukinumab group, one (14.3%) subject had some hair regrowth, one (14.3%) subject had worsening hair loss, and five (71.4%) subjects had no change in response to treatment. No adverse events attributable to the study drug were observed. The lack of a treatment response to most of our treated patients suggests that the T H 17/IL-17 axis likely has no pathogenic role in AA and an alternative therapeutic approach should be considered for this disease. However, due to the low statistical power of this study, future studies may be required to corroborate these findings.

Alopecia areata is a chronic relapsing autoimmune inflammatory hair disorder with no novel therapy. The objectives of this study are to compare the efficacy of topical calcipotriol vs narrow band ultraviolet B phototherapy (NB-UVB) in the treatment of alopecia areata and its correlation with serum vitamin D 3 levels. A randomized-controlled trial has been conducted on 60 patients with scalp alopecia areata randomized into four groups; topical calcipotriol, NB-UVB, both and placebo. All patients were evaluated by assessment of severity of alopecia areata by severity of alopecia tool (SALT) score at baseline and 3 months after treatment and vitamin D 3 levels at baseline and after 3 months. SALT score and vitamin D 3 levels were significantly improved in all groups except placebo after treatment with ( P  = 0.026, P  = 0.005, P  = 0.004, P  = 0.140) and ( P  = 0.028, P  = 0.011, P  = 0.003, P  = 0.725), respectively. Combined therapy showed non-significant improvement in SALT score ( P  = 0.530, P  = 0.643), respectively, and significant improvement in serum vitamin D 3 levels than each line alone with ( P  = 0.021, P  = 0.044), respectively. Both topical calcipotriol and NB-UVB are effective therapies in the treatment of AA and associated with improvement of SALT score and vitamin D 3 levels.

Background Alopecia areata (AA) is an autoimmune pathology manifested by loss of hair. Objective To evaluate and compare the efficacy and safety of tofacitinib and azathioprine in patients with AA and variants. Methods In this double-blind randomized controlled trail (RCT) carried out at the Department of Dermatology, Medical Teaching Institute-Lady Reading Hospital (MTI-LRH), Peshawar, Pakistan, patients aged ≥ 12 years diagnosed with AA, alopecia totalis (AT) or alopecia universalis (AU) with minimum 50% scalp hair loss for a period ≥ 06 years were included. Patients were randomly assigned to receive oral tofacitinib 5 mg twice daily (Group I) or oral azathioprine 2 mg/kg body weight once daily (Group II). The primary endpoint was Severity of Alopecia Tool (SALT) score, evaluated at baseline and 06 months follow-up. Safety was consistently assessed during the study. Results A total of 104 patients underwent random allocation into either the tofacitinib group ( n  = 52) or the azathioprine group ( n  = 52). The mean (SD) age of patients was 20.23 (7.14) years and 22.26 (8.07) years, while the mean (SD) disease duration was 6.59 (4.01) years and 7.98 (4.40) years in in Group I and II, respectively. Overall, 40 (38.5%) patients were adolescents while 70 (67.3%) were male. 52 (50%) had AA, 37 (35.5%) had AT and 15 (14.5%) had AU. Mean baseline SALT score in tofacitinib group was 91.02 ± 10.21 and azathioprine group was 91.02 ± 10.63, which at 06 months follow-up improved to 14.1 ± 24.6 and 63.9 ± 33.9, respectively (difference, 11.5 points; 95% confidence interval, 38.3–61.3, p  < 0.0001). Overall, no major adverse effects and no difference among the minor adverse effects in the two groups (04 adverse events for tofacitinib group and 08 for azathioprine group: p  = 0.23) was observed. Conclusions Efficacy of tofacitinib was significantly higher than azathioprine, whilst both drugs were well-tolerated in patients with AA and variants.

Background Alopecia areata (AA) is a common non‐scarring hair loss disorder that affects children and adults with a great psychological burden because of its recurrent and sometimes treatment‐refractory nature. Objective To compare the efficacy of topical calcineurin inhibitor, topical potent steroid combined with vitamin D analogue versus topical superpotent steroid in treatment of localized AA. Patients and Methods Sixty subjects with chronic (>1 year) localized (SALT score < 25%) AA, confirmed clinically and dermoscopically, were randomized into three groups. Group I used topical 0.03% tacrolimus (Tarolimus®), group II used topical potent steroid combined with vitamin D analogue (Daivobet®). and group III used topical superpotent steroid (Dermovate®). All patients continued a daily therapy for three successive months and were followed up for three other months. Assessment was done using PULL test, SALT score, and dermoscopic comparison before and after therapy. Results Group II showed comparable statistical results to group III with lower values in a non‐statistically significant way. Group I achieved the least improvement among all groups. Conclusion Combined vitamin D analogues with potent steroid appears to be a more convenient treatment for localized AA than superpotent steroids because of less side effects and comparable efficacy. Tacrolimus needs further research or formula customization to be used as a topical therapy for AA.

Background Alopecia areata (AA) is an autoimmune condition resulting in hair loss, sometimes just in small patches but occasionally across larger areas like the entire scalp. For localized AA, treatments often involve injecting corticosteroids, such as triamcinolone acetonide (TrA), directly into the affected areas. Methotrexate (MTX), a drug known for its ability to suppress immune responses, has also been considered as an alternative. However, there has not been much research directly comparing these two treatments. Methods This study involved 40 individuals with localized AA. These patients were divided into two groups: one received TrA injections, and the other was given MTX. Both groups were treated once a month for 3 months. We tracked their progress using the Severity of Alopecia Tool (SALT) over 6 months. Their trichoscopic findings, adverse effects, and satisfaction with treatment were also documented. Results Cases receiving TrA showed strong improvements, with their SALT scores dropping by an average of 54.36%, which meant significant hair regrowth. In contrast, the MTX group saw their scores worsen by 54.6%, meaning losing more hair. For trichoscopic changes, both groups showed some progress, but only the reduction in black dots in the MTX group was statistically significant. Side effects like mild redness or pigmentation changes were uncommon and similar for both groups. When asked how satisfied they were, patients who received TrA gave a much higher score:7.1 out of 10 compared to 4.9 for MTX. Discussion According to our results, TrA outperformed MTX in treating localized AA, both in terms of hair regrowth and patient satisfaction. While MTX may have potential as a therapy, its inconsistent performance in this study suggests it is not ready to be a primary option for localized AA. Future research is needed to explore whether adjusting doses or combining it with other treatments could result in better outcomes.

Alopecia areata (AA) is a common chronic tissue-specific autoimmune disease, resulting in hair loss, that affects up to 2% of the general population. The exact pathobiology of AA has still remained elusive, while the common theory is the collapse of the immune privilege of the hair follicle caused by immunological mechanism. Multiple genetic and environment factors contribute to the pathogenesis of AA. There are several clinical treatments for AA, varying from one or multiple well-defined patches to more diffuse or total hair loss of the scalp (alopecia totalis) or hair loss of the entire body (alopecia universalis). The available treatments for AA, such as corticosteroids and other immunomodulators, minoxidil, and contact immunotherapy, are of limited efficacy with a high risk of adverse effects and high recurrence rates, especially for patients with severe AA. Recent insights into the pathogenesis of AA have led to the development of new treatment strategies, such as Janus kinase (JAK) inhibitors, biologics, and several small molecular agents. In addition, modern therapies for AA, including antihistamines, platelet-rich plasma (PRP) injection, and other novel therapies have been well explored. In this review, we discussed the recent advances in the pathogenesis, diagnosis, and treatment of AA.

This review article synthesizes relevant information about hair-follicle biology and pathobiology and summarizes the clinical presentation and management of this common condition. The impact of certain skin diseases on the lives of those affected tends to be underestimated or even dismissed as simply a “cosmetic problem.” Alopecia areata exemplifies such a condition, owing to its substantial disease burden and its often devastating effects on the patient's quality of life and self-esteem. 1 , 2 Although alopecia areata is one of the most common autoimmune diseases, the pathobiology of this chronic, relapsing hair-loss disorder is not fully understood, and the available therapies are disappointing. 3 – 6 This review summarizes the pathogenesis, clinical presentation, and management of alopecia areata and synthesizes relevant background information concerning the biologic . . .

Alopecia areata (AA) is an easy-recurring disease that presents huge challenges globally. An efficient clinical tool to predict AA onset would be valuable for timely intervention. We extracted six AA-related datasets from Gene Expression Omnibus (GEO). GO, KEGG, GSEA, GSVA and CIBERSORT algorithm were performed to elucidate the characteristics of AA. Feature genes were identified using LASSO regression and Random Forest algorithms. Five machine learning algorithms (Logistic Regression, K-nearest neighbors, Elastic Net, XGBoost and LightGBM) were employed to construct predictive models, with internal and external validation conducted to determine the optimal model. Additionally, SHapley Additive exPlanations (SHAP) analysis was applied to interpret the best-performing model and shiny framework was applied to establish an online predictive website. Five datasets (GSE45512, GSE68801, GSE80342, GSE58573, GSE74761) were integrated as train set and GSE148346 was defined as test set. Tissue regeneration and immune dysregulation were the key factors in AA pathogenesis. Three feature genes (KRT83, PPP1R1C, PIRT) were selected for model construction, with innate immune response, neural inflammatory and stress being a potential regulator for AA. The XGBoost model outperformed other algorithms, SHAP provided explanations for predictions and an online predictive website was established. Our study provides a potential “neuro-stress-immune” interplay insight into the pathogenesis of AA and establishes a clinically applicable predictive model for AA onset.