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Chlamydia-induced reactive arthritis diagnosed during gout flares: A case report and cumulative effect of inflammatory cytokines on chronic arthritis

机译:衔接性诱导的肾斑型诱导的活性关节炎:炎症细胞因子对慢性关节炎的病例报告和累积效应

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Rationale: The pathology of gouty arthritis and reactive arthritis (ReA) partially overlaps, and both diseases are characterized by the production of inflammatory cytokines associated with the activation of monocytes and macrophages. However, the precise cytokine profile of cases with a coexistence of both diseases is unknown, and there are few reports on the course of treatment in patients with both gouty arthritis and ReA. Patient concerns: A 39-year-old man with a recurrent episode of gouty arthritis presented prednisolone-resistant polyarthritis with high level of C-reactive protein (CRP). He had the features of gouty arthritis such as active synovitis of the first manifestation of metatarsophalangeal (MTP) joints and the presence of monosodium urate (MSU) crystals from synovial fluid. But he also had the features of ReA such as the presence of tenosynovitis in the upper limb, the positivity of human leukocyte antigen (HLA)-B27, a history of sexual contact and positive findings of anti- Chlamydia trachomatis -specific IgA and IgG serum antibodies. Diagnoses: He was diagnosed with HLA-B27 associated Chlamydia-induced ReA accompanied by gout flares. Interventions: He was treated with 180 mg/day of loxoprofen, 1 mg/day of colchicine, and 10 mg/day of prednisolone for gout flares. However, his polyarthritis worsened with an increased level of CRP (23.16 mg/dL). Accordingly, we added 500 mg/day of salazosulfapyridine followed by adalimumab (ADA) 40 mg once every 2 weeks. Outcomes: After starting ADA, the patient's symptoms and laboratory findings showed rapid improvement and he achieved clinical remission 1 month after initiation of ADA treatment. As of this writing, the patient's clinical remission has been maintained for 1 year. Lessons: This case suggests that with exacerbation of arthritis during gouty arthritis, coexistence with other pathologies such as peripheral spondyloarthritis should be considered, and early intensive treatment including tumor necrosis factor inhibitors may be necessary.
机译:理由:痛风性关节炎和反应性关节炎(REA)部分重叠的病理学,并且两种疾病的特征在于产生与激活单核细胞和巨噬细胞的炎性细胞因子。然而,两种疾病共存的病例的精确细胞因子概况未知,少数关于痛风性关节炎和REA患者的治疗过程中少。患者担忧:一名39岁的男子,具有痛风性关节炎的反复发作,提出了具有高水平C-反应蛋白(CRP)的抗真菌抗性多关节炎。他具有痛风性关节炎的特征,例如跖骨膜(MTP)关节的第一个表现的活性滑膜炎以及来自滑膜液中的单钠尿剂(MSU)晶体的存在。但他还具有Rea的特征,例如腱鞘炎在上肢中的存在,人白细胞抗原(HLA)-B27的阳性,性接触史和抗衣原体的抗衣原体的阳性结果 - 特异性IgA和IgG血清抗体。诊断:他被诊断出患有HLA-B27相关的衣原体诱导的REA,伴随着痛风斑点。干预措施:他被含180毫克/天的洛洛芬,1毫克/天的血清序列治疗,以及10毫克/天的雷尼斯龙,用于痛风。然而,他的多组织炎随着CRP的增加而恶化(23.16mg / dl)。因此,我们加入了500毫克/天的Salazosulfapyridine,然后每2周每2周洗脱一次Adalimalab(Ada)40mg。结果:启动ADA后,患者的症状和实验室发现表现出快速改善,他在发起ADA治疗后1个月达到临床缓解。截至本文的撰写,患者的临床缓解已维持> 1年。课程:这种情况表明,在痛风关节炎期间随着关节炎的加剧,应考虑与外周脊椎炎等其他病理等的共存,并且可能需要具有肿瘤坏死因子抑制剂的早期密集治疗。

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