奥达帕替尼对日本瘙痒型特应性皮炎患者的疗效:四例报告

IF 1.1 Q4 ALLERGY
Keiji Kosaka MD, Akihiko Uchiyama MD, PhD, Mai Ishikawa MD, Sei-ichiro Motegi MD, PhD
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引用次数: 0

摘要

瘙痒型特应性皮炎(AD)是特应性皮炎的一种变异型,其特征为与 2 型细胞因子反应相关的剥脱性丘疹、硬化性结节和剧烈瘙痒。1 最近,在一项临床试验中发现,口服选择性 Janus 激酶(JAK)1 抑制剂达帕替尼(upadacitinib)在治疗 12 岁中重度 AD 患者方面具有良好的疗效和安全性。我们的病例包括两名男性和两名女性中重度 AD 患者(表 S1)。我们的病例包括两男两女中重度 AD 患者(表 S1),患者均符合 AD 标准。他们接受了 15 或 30 毫克达帕替尼、局部皮质类固醇激素和保湿剂的治疗,每天一次。病例 1:49 岁女性,腿部出现大面积红斑、结节和瘙痒(图 1A)。我们给她服用了 30 毫克的达帕替尼。8 周后,她的湿疹面积和严重程度指数(EASI)达到 90,并且不再瘙痒(图 1B)。病例 2:女性,50 岁。几十年来,她一直在难治性结节上涂抹皮质类固醇软膏(图 1C)。由于瘙痒导致失眠,她终生难以入眠。我们给她服用了30毫克的达帕替尼,2周后她的瘙痒症状消失,4周后达到EASI-90(图1D)。病例 3:64 岁男性,躯干和四肢有多个瘙痒性结节(图 1E)。我们首先给他服用了 30 毫克的达帕替尼,以缓解他的剧烈瘙痒。4 周后,他的皮损和瘙痒症状明显好转。因此,我们将达帕替尼的剂量降至 15 毫克。12 周后,他的皮损几乎消失(图 1F)。病例 4:66 岁男性。他的颈部和手臂上有多个结节,形成斑块(图 1G)。虽然我们诊断他患有严重的 AD,但考虑到他的年龄,我们给他开了 15 毫克的达达替尼。12 周后,他的 EASI 达到 90,皮损也几乎消失(图 1H)。图1I-K显示了EASI、以患者为导向的湿疹测量(POEM)和瘙痒数字评分量表(NRS)的变化情况。从基线到第4周,所有类别的数据都迅速下降,这种效果持续了12周。从基线到第 4 周,血清中胸腺和活化调节趋化因子及免疫球蛋白 E 均有所下降;但在第 12 周,部分病例有所上升(图 1L、M)、4 这些结果表明,在瘙痒型 AD 的治疗过程中,不仅要抑制 IL-4 和 IL-13,还要抑制其他细胞因子,包括 IL-31 和胸腺基质淋巴细胞生成素,因为它们会诱发瘙痒。6 我们的病例(图 1K)和之前关于巴利昔替尼的报道显示,巴利昔替尼可在 4 周内达到 NRS-Itch-50 的疗效。5 JAK 抑制剂可通过强烈抑制瘙痒,使瘙痒型 AD 早期得到改善:本研究未涉及人类参与者:注册表和注册号:不适用。动物研究:不适用:动物研究:不详。
本文章由计算机程序翻译,如有差异,请以英文原文为准。

Effectiveness of upadacitinib in Japanese patients with prurigo-type atopic dermatitis: Four cases report

Effectiveness of upadacitinib in Japanese patients with prurigo-type atopic dermatitis: Four cases report

Prurigo-type atopic dermatitis (AD) is an AD variant characterized by excoriated papules, indurated nodules, and intense itching associated with type 2 cytokine responses.1 Recently, upadacitinib, an oral selective Janus kinase (JAK) 1 inhibitor, was found to be efficacious and safe in treating moderate-to-severe AD in patients aged >12 years in a clinical trial.2 However, few reports have demonstrated evidence of upadacitinib in prurigo-type AD. Here, we present four Japanese patients with prurigo-type AD who received upadacitinib.

Our cases included two male and two female patients with moderate-to-severe AD (Table S1). The patients fulfilled the AD criteria.3 Cases 3 and 4 were also confirmed AD pathologically. They were treated with 15 or 30 mg upadacitinib, topical corticosteroid, and moisturizers once a day. Case 1: a 49-year-old female with widespread areas of erythema, nodules, and itching on her legs (Figure 1A). We initiated 30 mg of upadacitinib. After 8 weeks, she achieved Eczema Area and Severity Index (EASI)-90 and was itch-free (Figure 1B). Case 2: a 50-year-old female. She applied corticosteroid ointments on her refractory nodules for decades (Figure 1C). She had difficulty throughout her life due to insomnia caused by itching. We initiated 30 mg of upadacitinib; she was pruritus-free after 2 weeks, achieving EASI-90 after 4 weeks (Figure 1D). Case 3: a 64-year-old male with multiple pruritic nodules on his trunk and extremities (Figure 1E). We first initiated 30 mg of upadacitinib for his severe itchiness. After 4 weeks, his skin lesions and itching improved noticeably. Thus, we decreased the upadacitinib dose to 15 mg. After 12 weeks, his skin lesions almost disappeared (Figure 1F). Case 4: a 66-year-old male. He had multiple nodules on his neck and arms, forming plaque (Figure 1G). Although we diagnosed him with severe AD, we prescribed 15 mg of upadacitinib because of his age. After 12 weeks, he achieved EASI-90, and his skin lesions almost disappeared (Figure 1H). No adverse events were observed in the patients.

Figure 1I–K shows the transition of EASI, patient-oriented eczema measure (POEM), and pruritus numerical rating scale (NRS). A rapid decrease was seen in all categories from baseline to Week 4, and this effectiveness lasted for 12 weeks. Thymus and activation-regulated chemokine and immunoglobulin E in the serum were decreased from baseline to Week 4; however, some cases increased at Week 12 (Figure 1L,M).

The effectiveness of dupilumab and baricitinib against prurigo-type AD was recently reported.4, 5 Dupilumab showed a significantly lower achievement rate of EASI-50 at 2 months in the prurigo compared with the non-prurigo group.4 These results indicate the importance of suppressing not only IL-4 and IL-13 but also other cytokines, including IL-31 and thymic stromal lymphopoietin, which can induce itchiness during prurigo-type AD treatment. Chronic pruritus occurs due to neural sensitization to pruritus and the development of a pruritus-scratching cycle.6 Our cases (Figure 1K) and previous reports on baricitinib achieved NRS-Itch-50 in 4 weeks.5 JAK inhibitors can lead to the early improvement of prurigo-type AD by strongly suppressing itching.

The authors declare no conflict of interest.

Approval of the research protocol: No human participant was involved in this study.

Informed Consent: Informed consent was obtained from the patient.

Registry and the Registration No.: N/A.

Animal Studies: N/A.

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