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蛋白酶抑制剂诱发的尿路结石症。

Protease inhibitor-induced urolithiasis.

作者信息

Gentle D L, Stoller M L, Jarrett T W, Ward J F, Geib K S, Wood A F

机构信息

Department of Urology, University of California School of Medicine, San Francisco 94143-0738, USA.

出版信息

Urology. 1997 Oct;50(4):508-11. doi: 10.1016/S0090-4295(97)00401-9.

Abstract

OBJECTIVES

To describe protease inhibitor-induced urinary stone disease in patients with human immunodeficiency virus (HIV) or acquired immunodeficiency syndrome (AIDS) who are taking indinavir sulfate (Crixivan), a protease inhibitor, for the treatment of AIDS.

METHODS

Patients with HIV/AIDS and symptomatic renal colic temporally related to the initiation of indinavir sulfate therapy were prospectively identified. Seven patients (mean age 42 years; all men) with HIV and renal colic who were taking indinavir were identified. Retrospective chart reviews and patient interviews were performed.

RESULTS

Indinavir therapy averaged 5.7 months prior to presentation with renal colic. All patients had microscopic hematuria. One patient presented with acute azotemia from bilateral urinary obstruction. Six patients had no history of urinary stones prior to initiating indinavir. The median number of symptomatic urinary stone episodes after initiating indinavir was two stones per patient. All patients had moderate- to high-grade urinary obstruction from radiolucent calculi. Abdominal computed tomography (CT) demonstrated hydronephrosis without urinary calcifications. Three patients spontaneously passed stones and 4 required intervention. Yellow debris and/or brown matrix-like material was seen endoscopically. Stone analysis revealed pure protease inhibitor. Six patients (86%) eventually discontinued protease inhibitor therapy.

CONCLUSIONS

Protease inhibitor-induced urinary stones are radiolucent and can cause high-grade ureteral obstruction. Protease inhibitor-induced urinary stones were not identified on unenhanced abdominal CT scans. The radiolucent gelatinous nature of such stones makes lithotripsy a poor choice of treatment. Ureteral stenting may allow spontaneous stone passage if symptomatic obstruction occurs. Urologists may encounter a greater number of patients with symptomatic protease inhibitor-induced urinary calculi as these medications become more popular.

摘要

目的

描述在感染人类免疫缺陷病毒(HIV)或获得性免疫缺陷综合征(AIDS)的患者中,因服用蛋白酶抑制剂硫酸茚地那韦(克力芝)治疗艾滋病而引发的蛋白酶抑制剂相关性尿路结石病。

方法

前瞻性地识别出HIV/AIDS患者以及与硫酸茚地那韦治疗起始时间存在时间关联且有症状性肾绞痛的患者。确定了7名服用茚地那韦且患有HIV和肾绞痛的患者(平均年龄42岁;均为男性)。进行了回顾性病历审查和患者访谈。

结果

出现肾绞痛前,茚地那韦治疗平均持续5.7个月。所有患者均有镜下血尿。1例患者因双侧尿路梗阻出现急性氮质血症。6例患者在开始服用茚地那韦之前无尿路结石病史。开始服用茚地那韦后,有症状性尿路结石发作的中位数为每位患者2块结石。所有患者均因透光结石出现中度至高度尿路梗阻。腹部计算机断层扫描(CT)显示肾盂积水但无尿路钙化。3例患者结石自行排出,4例需要干预。在内镜下可见黄色碎屑和/或棕色基质样物质。结石分析显示为纯蛋白酶抑制剂。6例患者(86%)最终停用蛋白酶抑制剂治疗。

结论

蛋白酶抑制剂引起的尿路结石是透光的,可导致高度输尿管梗阻。未增强的腹部CT扫描未发现蛋白酶抑制剂引起的尿路结石。此类结石的透光凝胶状性质使碎石术成为不佳的治疗选择。如果出现症状性梗阻,输尿管支架置入术可能会使结石自行排出。随着这些药物越来越普及,泌尿外科医生可能会遇到更多有症状的蛋白酶抑制剂引起的尿路结石患者。

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