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Excimer light was reported to be effective in treating alopecia areata (AA), as it induces T-cell apoptosis, however its combination with topical steroids in the management of AA still needs to be investigated. The study objectives were to determine the efficacy and safety of combining 308 nm–Excimer light and topical steroid versus either Excimer light or topical steroid alone in treating AA. Thirty AA patients were included, each patient had at least three patches, patches in each patient were randomly classified in to 3 groups. Group I patch: was treated by topical steroid only. Group II patch: was treated by Excimer light only. Group III patch: was treated by topical steroid and Excimer light. The response for hair growth was assessed at the baseline, week 8, week 12 then at 3months after the last session using a hair regrowth scale and trichoscopy. Any encountered adverse effects were recorded. All treatment groups showed significant improvement at the end of the study compared to the baseline, although hair regrowth was significantly better in group III where 60% of patches showed > 50% hair regrowth. All treatment groups showed significant decrease in black dots (BD) (trichoscopic sign of activity), and increase in signs of improvement (upright growing and pigtail hairs). However, BD and exclamation mark hair (EMH) were significantly reduced in the mixed therapy group compared to the other two groups. We concluded that excimer light is an effective and safe treatment option for AA, particularly when combined with topical steroid.

Introduction Alopecia areata (AA) is a challenging disease with variable treatment outcomes. Hair follicles express vitamin D receptors. Therefore, vitamin D3 may be promising for AA treatment through immunomodulatory mechanisms. The efficacy of bimatoprost in scalp AA treatment was reported by few studies. Objective To evaluate the efficacy and safety of microneedling (MN) with topical vitamin D3 versus MN with bimatoprost in comparison with MN alone in the treatment of localized AA. Patients and Methods Seventy‐five patients with localized AA were divided into three groups. The first group: 25 patients were treated with MN alone. The second group: 25 patients treated with MN combined with topical vitamin D3. The third group: 25 patients treated with MN combined with bimatoprost solution. The response was evaluated clinically and dermoscopically. Results At the end of the study, all groups showed a statistically significant decrease in the SALT score compared to the baseline. The clinical response (regrowth scale): vitamin D and bimatoprost groups showed a statistically significant higher regrowth scale compared to MN alone group (p‐value = 0.000). After treatment, hair regrowth was significantly higher in MN combined with bimatoprost than in MN combined with topical vitamin D3. However, after 3 months of follow‐up, there was no statistically significant difference between both groups. Side effects were mild and transient in all groups. Conclusion Topical vitamin D3 and bimatoprost combined with MN are safe and effective therapeutic options for localized AA.

Alopecia areata is characterised by non-scarring loss of scalp, face, or body hair. We investigated the efficacy and safety of ritlecitinib, an oral, selective dual JAK3/TEC family kinase inhibitor, in patients with alopecia areata. In this randomised, double-blind, multicentre, phase 2b–3 trial done at 118 sites in 18 countries, patients aged 12 years and older with alopecia areata and at least 50% scalp hair loss were randomly assigned to oral ritlecitinib or placebo once-daily for 24 weeks, with or without a 4-week loading dose (50 mg, 30 mg, 10 mg, 200 mg loading dose followed by 50 mg, or 200 mg loading dose followed by 30 mg), followed by a 24-week extension period during which ritlecitinib groups continued their assigned doses and patients initially assigned to placebo switched to ritlecitinib 50 mg or 200 mg loading dose followed by 50 mg. Randomisation was done by use of an interactive response system and was stratified by baseline disease severity and age. The sponsor, patients, and investigators were masked to treatment, and all patients received the same number of tablets to maintain masking. The primary endpoint was Severity of Alopecia Tool (SALT) score 20 or less at week 24. The primary endpoint was assessed in all assigned patients, regardless of whether they received treatment. This study was registered with ClinicalTrials.gov, NCT03732807. Between Dec 3, 2018, and June 24, 2021, 1097 patients were screened and 718 were randomly assigned to receive ritlecitinib 200 mg + 50 mg (n=132), 200 mg + 30 mg (n=130), 50 mg (n=130), 30 mg (n=132), 10 mg (n=63), placebo to 50 mg (n=66), or placebo to 200 mg + 50 mg (n=65). 446 (62%) of 718 patients were female and 272 (38%) were male. 488 (68%) were White, 186 (26%) were Asian, and 27 (4%) were Black or African American. Of 718 patients randomly assigned, 104 patients discontinued treatment (34 withdrew, 19 adverse events [AEs], 12 physician decision, 12 lack of efficacy, 13 lost to follow up, five rolled over to long-term study transfer, four pregnancies, two protocol deviations, one declined to attend follow-up due to COVID-19, one attended last visit very late due to COVID-19, and one non-compliance). At week 24, 38 (31%) of 124 patients in the ritlecitinib 200 mg + 50 mg group, 27 (22%) of 121 patients in the 200 mg + 30 mg group, 29 (23%) of 124 patients in the 50 mg group, 17 (14%) of 119 patients in the 30 mg group, and two (2%) of 130 patients in the placebo group had a response based on SALT score 20 or less. The difference in response rate based on SALT score 20 or less between the placebo and the ritlecitinib 200 mg + 50 mg group was 29·1% (95% CI 21·2–37·9; p<0·0001), 20·8% (13·7–29·2; p<0·0001) for the 200 mg + 30 mg group, 21·9% (14·7–30·2; p<0·0001) for the 50 mg group, and 12·8% (6·7–20·4; p=0·0002) for the 30 mg group. Up to week 48 and including the follow-up period, AEs had been reported in 108 (82%) of 131 patients in the ritlecitinib 200 mg + 50 mg group, 105 (81%) of 129 patients in the 200 mg + 30 mg group, 110 (85%) of 130 patients in the 50 mg group, 106 (80%) of 132 patients in the 30 mg group, 47 (76%) of 62 patients in the 10 mg group, 54 (83%) of 65 patients placebo to ritlecitinib 200 mg + 50 mg in the extension period, and 57 (86%) of 66 patients in the placebo to 50 mg group. The incidence of each AE was similar between groups, and there were no deaths. Ritlecitinib was effective and well tolerated in patients aged 12 years and older with alopecia areata. Ritlecitinib might be a suitable treatment option for alopecia areata in patients who are candidates for systemic therapy. Pfizer.

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.

Alopecia areata is a distressing disorder of hair loss that is mediated partly by cytokines dependent on Janus kinases. The JAK1 and JAK2 inhibitor baricitinib reduced the extent of hair loss in two randomized trials over a period of 36 weeks.

The ALLEGRO phase 2a and 2b/3 studies demonstrated that ritlecitinib, an oral JAK3/TEC family kinase inhibitor, is efficacious at doses of ≥ 30 mg in patients aged ≥ 12 years with alopecia areata (AA). The objective of this study was to evaluate the safety of ritlecitinib in an integrated analysis of four studies in AA. Two cohorts were analyzed: a placebo-controlled and an all-exposure cohort. Proportions and study size-adjusted incidence rates (IRs) of adverse events (AEs) of interest and laboratory abnormalities are reported. In the placebo-controlled cohort (n = 881; median exposure: 169 days), the proportion of ritlecitinib-treated patients with AEs was 70.2-75.4% across doses versus 69.5% in the placebo group; serious AEs occurred in 0-3.2% versus 1.9% for the placebo. A total of 19 patients permanently discontinued due to AEs (5 while receiving the placebo). In the all-exposure cohort (n = 1294), median ritlecitinib exposure was 624 days [2091.7 total patient-years (PY)]. AEs were reported in 1094 patients (84.5%) and serious AEs in 57 (4.4%); 78 (6.0%) permanently discontinued due to AEs. The most common AEs were headache (17.7%; 11.9/100 PY), severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) positive test (15.5%; 9.8/100 PY), and nasopharyngitis (12.4%; 8.2/100 PY). There were two deaths (breast cancer and acute respiratory failure/cardiorespiratory arrest). Proportions (IRs) were < 0.1% (0.05/100 PY) for opportunistic infections, 1.5% (0.9/100 PY) for herpes zoster, 0.5% (0.3/100 PY) for malignancies (excluding nonmelanoma skin cancer), and 0.2% (0.1/100 PY) for major adverse cardiovascular events. Ritlecitinib is well tolerated with an acceptable safety profile up to 24 months in patients aged ≥ 12 years with AA (video abstract and graphical plain language summary available). ClinicalTrials.gov: NCT02974868 (date of registration: 11/29/2016), NCT04517864 (08/18/2020), NCT03732807 (11/07/2018), and NCT04006457 (07/05/2019).

Alopecia areata (AA) is a non-scarring inflammatory hair loss disorder characterized by a T-cell–mediated autoimmune disease that targets the hair follicles. In particular, Natural Killer Group 2 member D (NKG2D) + CD8 + T cells have been identified as central players in its pathogenesis. Current treatment options have limited efficacy and are often associated with adverse effects and high risk of relapse upon discontinuation, highlighting the need for targeted and durable therapeutic strategies. Janus kinase (JAK) inhibitors have emerged as representative therapies; however, they are limited by a high relapse rate after treatment cessation. Recently, novel therapeutic approaches such as neutralizing antibodies targeting cytokines and chemokines, and sphingosine-1-phosphate (S1P) receptor modulators have gained attention. Various molecular markers associated with AA have been identified as potential therapeutic targets. This review provides a comprehensive overview of the roles of immune cells in AA pathogenesis and introduces emerging immunomodulatory strategies and novel therapeutic targets.

The scalp microbiome represents an array of microorganisms important in maintaining scalp homeostasis and mediating inflammation. Scalp microbial dysregulation has been implicated in dermatologic conditions including alopecia areata (AA), dandruff/seborrheic dermatitis (D/SD), scalp psoriasis (SP) and folliculitis decalvans (FD). Understanding the impact of scalp microbial dysbiosis gives insight on disease pathophysiology and guides therapeutic decision making. Herein we review the scalp microbiome and its functional role in scalp conditions by analysis of metagenomic medical literature in alopecia, D/SD, SP, and other dermatologic disease. Increased abundance of Malassezia, Staphylococcus, and Brevibacterium was associated with SD compared to healthy controls. A higher proportion of Corynebacterium, actinobacteria , and firmicutes are present in AA patients, and lower proportions of Staphylococcus caprae are associated with worse clinical outcomes. Decreased prevalence of actinobacteria and Propionibacterium and increased firmicutes, staphylococcus, and streptococcus are associated with scalp psoriasis. Studies of central centrifugal cicatricial alopecia (CCCA) suggest scalp microbial composition contributes to CCCA’s pro-inflammatory status. The most common organisms associated with FD include methicillin-resistant S. aureus and S. lugdunensis . Antifungals have been a mainstay treatment for these diseases, while other alternatives including coconut oils and shampoos with heat-killed probiotics have shown considerable potential efficacy by replenishing the scalp microbiome.

Background The oral Janus kinase (JAK) inhibitor baricitinib has demonstrated efficacy for severe alopecia areata (AA) over 36 weeks. There are limited data on the longer-term treatment of AA. Objective The aim of this study was to evaluate the efficacy and safety of baricitinib for AA in adults with ≥50% scalp hair loss through 52 weeks of continuous therapy in two phase III trials (BRAVE-AA1 and BRAVE-AA2). Methods Patients randomized to baricitinib at baseline in BRAVE-AA1 ( N  = 465) and BRAVE-AA2 ( N  = 390) retained their treatment allocation through Week 52. Efficacy outcomes included the proportion of patients achieving a Severity of Alopecia Tool (SALT) score ≤ 20 (≤ 20% scalp hair loss). Data were censored after permanent treatment discontinuation or if collected remotely due to the coronavirus disease 2019 (COVID-19) pandemic. Results Response rates for hair regrowth increased over the 52-week period. Of patients treated with baricitinib 4 mg and 2 mg, respectively, 40.9% and 21.2% in BRAVE-AA1 and 36.8% and 24.4% in BRAVE-AA2 achieved a SALT score ≤ 20 at Week 52. The most frequent treatment-emergent adverse events included upper respiratory tract infection, headache, nasopharyngitis, acne, urinary tract infection, creatine phosphokinase elevation, and COVID-19 infection. Limitation There were no comparisons with placebo. Conclusion Efficacy of baricitinib for adults with severe AA continuously improved over 52 weeks, indicating that long-term treatment may be necessary to observe maximum clinical benefit. There were no new safety signals. ClinicalTrials Registration ClinicalTrials.gov NCT03570749 and NCT03899259. Video abstract 2xPMF6xnh1c2LanTTqiSp- Efficacy and Safety of Baricitinib in Patients with Severe Alopecia Areata: Week-52 Results from BRAVE-AA1 and BRAVE-AA2 Plain Language Summary Alopecia areata (AA) is an autoimmune disease that causes patchy hair loss on the scalp, face, and body. Baricitinib is a Janus kinase inhibitor that is approved to treat AA in several countries, based on results from two studies, BRAVE-AA1 and BRAVE-AA2. In these studies, adults with at least 50% scalp hair loss were treated with baricitinib for 36 weeks. Long-term therapy is important in AA, and hair regrowth can take longer in some patients with severe disease. Therefore, we assessed outcomes from a longer course of therapy. In this study, we report the results after 52 weeks of continuous treatment with baricitinib 4 mg or 2 mg in 465 patients in BRAVE-AA1 and 390 patients BRAVE-AA2. The goal was to reduce scalp hair loss to 20% or less by Week 52. In BRAVE-AA1, 40.9% of patients who took baricitinib 4 mg and 21.2% of patients who took baricitinib 2 mg had 20% or less missing scalp hair by Week 52. Similarly, in BRAVE-AA2, 36.8% of patients who took baricitinib 4 mg and 24.4% of patients who took baricitinib 2 mg had 20% or less missing scalp hair by Week 52. The most common adverse effects that were reported during the study period were upper respiratory tract infection, headache, nasopharyngitis, acne, urinary tract infection, creatine phosphokinase elevation, and coronavirus disease 2019 (COVID-19) infection. The results of longer-term treatment indicate that hair regrowth continues to improve without any new safety concerns for adults with severe AA taking baricitinib.

Alopecia areata (AA) is a prevalent autoimmune condition characterized by hair loss, with the collapse of hair follicle immune privilege being a pivotal event in its pathogenesis. This collapse involves intricate immunological disturbances, where CD8 + NKG2D + T cells, driven by inflammatory cytokines like IFN-γ, attack hair follicles. Additionally, various immune cell, including Th1, Th2, Th17 cells, γδT cells, NK cells, and mast cells, contribute to this pathological process. Defects in the function of Tregs, Bregs, and iNKT cells further compound the immune imbalance. At the molecular level, the JAK-STAT pathway emerges as a central regulatory node integrating multiple cytokine signals and presenting itself as a significant therapeutic target. JAK inhibitors have shown notable effectiveness in clinical settings, with some agents even gaining FDA approval for treating moderate-to-severe AA. However, the effectiveness of targeting IL-17, TNF-α, Th2 cytokines, PDE4, and other molecules remains debated. This review comprehensively explores the dynamic interactions among immune cell subsets, cytokine networks, and crucial signaling pathways in AA pathogenesis. It also summarizes the latest clinical progress and challenges in targeted therapies. Future studies should delve deeper into AA’s immune regulatory framework and devise tailored treatment approaches to enhance patient outcomes.