化脓性汗腺炎携带金黄色葡萄球菌:对阿达木单抗反应的影响。

Dermatology (Basel, Switzerland) Pub Date : 2021-01-01 Epub Date: 2021-01-05 DOI:10.1159/000512617
Dimitra Stergianou, Vassiliki Tzanetakou, Maria Argyropoulou, Theodora Kanni, Pantelis G Bagos, Evangelos J Giamarellos-Bourboulis
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引用次数: 2

摘要

背景:一些化脓性汗腺炎(HS)患者在阿达木单抗(ADA)治疗期间出现急性发作,其原因尚不清楚。ADA是fda批准的唯一用于治疗中重度HS的生物制剂。本课组前期研究表明,金黄色葡萄球菌刺激全血可影响人β-防御素2的产生,调节HS的严重程度。因此,假设金黄色葡萄球菌的携带可能导致HS发作。目的:探讨金黄色葡萄球菌携带与ADA治疗反应丧失的关系。患者和方法:在ADA治疗开始时未携带金黄色葡萄球菌的中重度HS患者中,我们调查了急性发作时鼻腔携带金黄色葡萄球菌的情况。急性发作被预先定义为炎性病变(炎性结节和脓肿的总和)较基线增加至少25%。在完成12周的ADA治疗后,对所有未出现急性发作的患者进行采样。采用HS临床反应评分(HiSCR)评估ADA的临床反应。结果:39例患者纳入研究;24例赫尔利II期HS 15例赫尔利III期HS。29例患者在治疗12周后达到HiSCR,无任何突发;10例患者突发HiSCR失败。3例(10.3%)和5例(50%)患者鼻腔携带金黄色葡萄球菌(优势比8.67;95% ci 1.54-48.49;P = 0.014)。在随访第48周的32例患者中,20例患者达到HiSCR, 12例患者出现急性发作导致ADA失败;金黄色葡萄球菌培养阳性患者分别为2例(10%)和5例(41.7%)(优势比6.42;95% ci 1.00-41.20;P = 0.05)。结论:鼻腔携带金黄色葡萄球菌可能与ADA治疗反应丧失有关。研究结果需要在更大的患者系列中得到证实。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Staphylococcus aureus Carriage in Hidradenitis Suppurativa: Impact on Response to Adalimumab.

Background: Several patients with hidradenitis suppurativa (HS) present flare-ups during treatment with adalimumab (ADA), the cause of which is not clear. ADA is the only FDA-approved biologic for the therapy of moderate-to-severe HS. A previous study of our group has shown that Staphylococcus aureus stimulation of whole blood affects the production of human β-defensin 2 and modulates HS severity. It is, therefore, hypothesized, that carriage of S. aureus may drive HS flare-ups.

Objective: To explore the association between carriage of S. aureus and loss of response to ADA.

Patients and methods: Among patients with moderate-to-severe HS without carriage of S. aureus at start of treatment with ADA, we investigated for carriage of S. aureus from the nares when flare-ups occurred. Flare-ups were pre-defined as at least 25% increase of inflammatory lesions (sum of inflammatory nodules and abscesses) from baseline. Samplings were also done after completion of 12 weeks of ADA treatment from all patients who did not present flare-ups. Clinical response to ADA was assessed by the HS Clinical Response score (HiSCR).

Results: Thirty-nine patients were studied; 24 with Hurley II stage HS and 15 with Hurley III stage HS. Twenty-nine patients achieved HiSCR after 12 weeks of treatment without any flare-ups; 10 patients had flare-ups and failed HiSCR. Three (10.3%) and 5 (50%) patients, respectively, had nasal carriage of S. aureus (odds ratio 8.67; 95% CI 1.54-48.49; p = 0.014). Among 32 patients reaching follow-up week 48, 20 patients achieved HiSCR and 12 had flare-ups leading to ADA failure; 2 (10%) and 5 (41.7%) patients, respectively, had positive culture for S. aureus (odds ratio 6.42; 95% CI 1.00-41.20; p = 0.05).

Conclusion: Nasal carriage of S. aureus may be associated with loss of response to ADA. Findings need confirmation in larger series of patients.

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