Ellis John, Lew Jeffrey, Brahmbhatt Sumir, Gordon Sarah, Denunzio Troy
Department of Medicine, Tripler Army Medical Center, Honolulu, HI, USA.
Nephrology Service, Tripler Army Medical Center, Honolulu, HI, USA.
Case Rep Med. 2019 Mar 28;2019:8165808. doi: 10.1155/2019/8165808. eCollection 2019.
Erythrodermic psoriasis is a rare and severe variant of psoriasis. It is characterized by widespread skin erythema, scaling, pustules, or exfoliation of more than 75% of the body's surface area. This condition has life-threatening complications to include hemodynamic, metabolic, immunologic, and thermoregulatory disturbances. One metabolic complication, hyperuricemia, occurs from rapid keratinocyte differentiation and infiltration of inflammatory cells into psoriatic lesions. Although renal injury caused by shunting of blood to the skin has been reported, there are no reports of erythrodermic psoriasis causing crystal-induced nephropathy. We present a case of erythrodermic psoriasis and hyperuricemia complicated by uric acid crystal nephropathy.
A 57-year-old male with long-standing psoriatic arthritis presented with diffuse scaling of his skin. He was being treated with adalimumab, leflunomide, and topical clobetasol, but had recently stopped taking his medications. Physical exam revealed yellow scaling covering his entire body with underlying erythema and tenderness without mucosal involvement. Labs were notable for a creatinine of 3.3 mg/dL, with no prior history of renal disease, and uric acid of 12.7 mg/dL. He was admitted to the intensive care unit given >80% of body surface area involvement and acute renal failure. Despite aggressive fluid resuscitation, renal function did not improve, and creatinine peaked at 4.61 mg/dL. Urine microscopy showed diffuse polymorphic uric acid crystals, consistent with uric acid crystal-induced nephropathy. He was started on rasburicase, urinary alkalinization, and fluids. His renal function improved dramatically; urine output, uric acid, and electrolytes normalized. He was discharged on topical clobetasol and leflunomide and started on secukinumab with little to no skin involvement.
This case presents the rare complication of crystal-induced nephropathy in a patient with erythrodermic psoriasis. Uric acid crystal nephropathy is well described in diseases with rapid cell turnover such as tumor lysis syndrome. It is thought that rapid keratinocyte differentiation and inflammatory infiltration of psoriatic lesions produced life-threatening electrolyte abnormalities similar to tumor lysis syndrome. Early recognition of this rare complication is critical, and aggressive fluid resuscitation, urine alkalinization, and uric acid lowering agents should be administered immediately.
红皮病型银屑病是银屑病的一种罕见且严重的类型。其特征为全身皮肤广泛红斑、脱屑、脓疱，或体表面积超过75%出现剥脱。这种情况会引发危及生命的并发症，包括血流动力学、代谢、免疫和体温调节紊乱。一种代谢并发症即高尿酸血症，是由角质形成细胞快速分化以及炎性细胞浸润银屑病皮损所致。虽然已有因血液分流至皮肤导致肾损伤的报道，但尚无红皮病型银屑病引发结晶性肾病的报道。我们报告一例红皮病型银屑病合并高尿酸血症并发尿酸结晶肾病的病例。
一名患有长期银屑病关节炎的57岁男性，出现皮肤弥漫性脱屑。他正在接受阿达木单抗、来氟米特和外用氯倍他索治疗，但最近停药了。体格检查发现全身覆盖黄色鳞屑，伴有皮下红斑和压痛，无黏膜受累。实验室检查结果显示肌酐为3.3mg/dL，既往无肾脏疾病史，尿酸为12.7mg/dL。鉴于体表面积受累>80%且存在急性肾衰竭，他被收入重症监护病房。尽管积极进行液体复苏，肾功能仍未改善，肌酐峰值达到4.61mg/dL。尿液显微镜检查显示弥漫性多形性尿酸结晶，符合尿酸结晶所致肾病。他开始接受拉布立酶治疗、尿液碱化及补液。其肾功能显著改善；尿量、尿酸和电解质恢复正常。他出院时使用外用氯倍他索和来氟米特，并开始使用司库奇尤单抗，皮肤受累情况轻微或基本无受累。
本病例呈现了红皮病型银屑病患者罕见的结晶性肾病并发症。尿酸结晶肾病在细胞更新迅速的疾病如肿瘤溶解综合征中已有充分描述。据认为，银屑病皮损中角质形成细胞的快速分化和炎性浸润产生了与肿瘤溶解综合征类似的危及生命的电解质异常。早期识别这种罕见并发症至关重要，应立即进行积极的液体复苏、尿液碱化及使用降尿酸药物。
