睾酮诱导的红细胞增多症:解决代谢综合征和广泛处方sglt2抑制剂药物的挑战。

IF 2.8 3区 医学 Q3 ENDOCRINOLOGY & METABOLISM
Endocrine Connections Pub Date : 2025-06-21 Print Date: 2025-06-01 DOI:10.1530/EC-24-0695
Federica Tramontana, Azmi Mohammed, Yaasir H Mamoojee, Richard Quinton
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引用次数: 0

摘要

睾酮是治疗男性性腺功能减退的基础药物,也可以通过促进红细胞生成来治疗任何相关的贫血。然而,过量的剂量会引起红细胞增多(红细胞增多),特别是在存在其他危险因素的情况下。在人群研究中,红细胞增多与动脉和静脉血栓形成有关。睾酮现在越来越多地用于功能性性腺功能减退、肥胖、高血压或2型糖尿病的老年男性;他们无论如何都有更高的红血病和血栓的风险。虽然这些男性中短期睾酮治疗与不良心血管结果无关,但有更多的肺栓塞病例。最初设想为纯口服降糖药,葡萄糖共转运蛋白2抑制剂钠(SGLT2i)现在越来越多地用于慢性肾病、缺血性心脏病和左心室损伤,而不考虑血糖,因此与睾酮共处方的可能性大大增加。至关重要的是,它们还通过促进造血来增加红细胞压积。这篇综述的重点是在肥胖和睾酮和SGLT2i处方更为普遍的背景下,目前管理红细胞增多症的最佳证据。它强调了平衡代谢和治疗益处与潜在风险的必要性。管理策略包括重新评估原来的治疗指征,处理可改变的危险因素,改用透皮睾酮和/或减少睾酮剂量。除克隆性红细胞增多症外,由于其潜在的促血栓作用,不推荐静脉切除。然而,睾酮和SGLT2s联合治疗晚期CKD贫血患者可以增加,甚至部分取代昂贵的传统促红细胞增生药物治疗。
本文章由计算机程序翻译,如有差异,请以英文原文为准。

Testosterone-induced erythrocytosis: addressing the challenge of metabolic syndrome and widely prescribed SGLT2-inhibitor drugs.

Testosterone-induced erythrocytosis: addressing the challenge of metabolic syndrome and widely prescribed SGLT2-inhibitor drugs.

Testosterone-induced erythrocytosis: addressing the challenge of metabolic syndrome and widely prescribed SGLT2-inhibitor drugs.

Testosterone-induced erythrocytosis: addressing the challenge of metabolic syndrome and widely prescribed SGLT2-inhibitor drugs.

Testosterone is the cornerstone therapy for men with hypogonadism, and also treats any associated anaemia by promoting erythropoiesis. However, excessive doses cause erythrocytosis (raised red cell mass), especially if other risk factors are present. Erythrocytosis is associated with arterial and venous thrombosis in population studies. Testosterone is now increasingly prescribed to older men with functional hypogonadism and obesity, hypertension or type 2 diabetes, who are anyway at higher risk of both erythrocytosis and thrombosis. Although short-medium term testosterone treatment in these men was not associated with adverse cardiovascular outcomes, there were more cases of pulmonary embolism. Originally envisaged as purely oral hypoglycaemic drugs, sodium-glucose cotransporter 2 inhibitors (SGLT2i) are now increasingly prescribed in chronic kidney disease (CKD), ischaemic heart disease and left ventricular impairment, irrespective of glycaemia, and the likelihood of co-prescription with testosterone is thus increased considerably. Crucially, they also increase haematocrit by promoting haematopoiesis. This review focuses on the current best evidence for managing erythrocytosis, in the context of more prevalent obesity and prescriptions of testosterone and SGLT2i in this population. It highlights the need to balance the metabolic and therapeutic benefits against the potential risks. Management strategies include re-evaluating the original treatment indication, addressing modifiable risk factors, switching to transdermal testosterone and/or reducing the testosterone dose. Venesection is not recommended, except for clonal erythrocytosis, due to its potential pro-thrombotic effects. However, combination therapy with testosterone and SGLT2s in men with anaemia of advanced CKD could augment, or even partly supersede, expensive treatment with conventional erythrocytosis-stimulating agents.

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来源期刊
Endocrine Connections
Endocrine Connections Medicine-Internal Medicine
CiteScore
5.00
自引率
3.40%
发文量
361
审稿时长
6 weeks
期刊介绍: Endocrine Connections publishes original quality research and reviews in all areas of endocrinology, including papers that deal with non-classical tissues as source or targets of hormones and endocrine papers that have relevance to endocrine-related and intersecting disciplines and the wider biomedical community.
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