他莫昔芬诱发高脂血症的临床特征、管理及结局：一项系统评价。
完整摘要 · 中文译文
背景：将他莫昔芬与高甘油三酯血症（HTG）相关联的证据主要来自病例报告。本研究旨在评估临床特征，并为改进识别和管理提供证据。 方法：检索了包括中国知网（CNKI）、万方、维普（VIP）、Web of Science、PubMed、Embase 和 Elsevier 在内的数据库，检索截止日期为2026年2月25日。收集他莫昔芬诱导的高甘油三酯血症（HTG）的病例报告和病例系列并进行描述性分析。 结果：共纳入49例患者（男性2例，女性47例），中位年龄49岁（范围34-74岁）。31例（63.3%）发生急性胰腺炎（AP）。甘油三酯（TG）水平中位数从治疗前的274 mg/dL升至他莫昔芬启动后的2,534 mg/dL。HTG发生的中位时间为6个月，出现AP症状的中位时间为9个月。与非AP组相比，AP组更年轻（中位47岁 vs. 50.5岁，p = 0.005），高血压患病率更高（25.6% vs. 0%，p = 0.029），治疗后TG水平更高（3,358 vs. 1,566 mg/dL，p = 0.051）。Logistic回归分析确定年龄较小是AP的独立危险因素，风险随年龄每增加1岁下降约15%（OR 0.849，95% CI 0.750-0.961，p = 0.01）。在接受再激发的3例患者中，HTG显著更快复发（中位17.5天）。大多数患者（39/49）停用了他莫昔芬，81.6%接受了降脂治疗。AP组的TG恢复正常时间较短（中位11.5天 vs. 60天，p = 0.003）。46例患者 患者改善。1例死于肝衰竭，1例因感染性休克自行离院，1例结局未报告。因果关系评定为“可能”者占85.7%（Naranjo量表）。结论：他莫昔芬诱导的高甘油三酯血症（HTG）是急性胰腺炎（AP）的重要且常见的危险因素，AP可能很严重。年龄较小与AP风险呈负相关。密切监测血脂，尤其是在治疗第一年和代谢紊乱患者中，至关重要。及时停药、积极降脂治疗和支持治疗是处理的关键。
完整摘要 · 英文原文
BACKGROUND: Evidence linking tamoxifen to hypertriglyceridemia (HTG) is mainly derived from case reports. This study aimed to evaluate clinical characteristics and provide evidence to improve identification and management. METHODS: Databases including China National Knowledge Infrastructure (CNKI), Wanfang, VIP, Web of Science, PubMed, Embase, and Elsevier were searched up to 25 February 2026. Case reports and case series on tamoxifen-induced hypertriglyceridemia (HTG) were collected and descriptively analyzed. RESULTS: A total of 49 patients (2 males, 47 females) were included, with a median age of 49 years (range 34-74). Acute pancreatitis (AP) occurred in 31 patients (63.3%). Median triglyceride (TG) levels increased from 274 mg/dL before treatment to 2,534 mg/dL after tamoxifen initiation. Median time to HTG onset was 6 months, and to AP symptoms 9 months. Compared with the non-AP group, the AP group was younger (median 47 vs. 50.5 years, (p = 0.005)), had a higher prevalence of hypertension (25.6% vs. 0%, (p = 0.029)), and had higher post-treatment TG levels (3,358 vs. 1,566 mg/dL, (p = 0.051)). Logistic regression identified younger age as an independent risk factor for AP, with risk decreasing by approximately 15% per year of age (OR 0.849, 95% CI 0.750-0.961, (p = 0.01)). In three patients who underwent rechallenge, HTG recurred significantly faster (median 17.5 days). Tamoxifen was discontinued in most patients (39/49), and 81.6% received lipid-lowering therapy. TG normalization time was shorter in the AP group (median 11.5 vs. 60 days, (p = 0.003)). Forty-six patients improved. One died of liver failure, one left the hospital voluntarily due to septic shock, and one had unreported outcome. Causality was judged "probable" in 85.7% (Naranjo scale). CONCLUSION: Tamoxifen-induced HTG is a significant and frequent risk factor for AP, which can be severe. Younger age is inversely correlated with AP risk. Close lipid monitoring, especially during the first year of treatment and in patients with metabolic disorders, is crucial. Prompt drug discontinuation, aggressive lipid-lowering therapy, and supportive care are key to management.