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生长激素疗法在代谢功能障碍相关脂肪性肝病中的作用:一项系统评价和荟萃分析。

Role of Growth Hormone Therapy in Metabolic-Dysfunction-Associated Steatotic Liver Disease: A Systematic Review and Meta-Analysis.

作者信息

Dutta Deep, Nagendra Lakshmi, Mohindra Ritin, Bhattacharya Saptarshi, Joshi Ameya, Kamrul-Hasan Abm

机构信息

Department of Endocrinology, CEDAR Super-Speciality Healthcare, Dwarka, New Delhi, India.

Department of Endocrinology, JSS Medical College, JSS Academy of Higher Education and Research, Mysuru, Karnataka, India.

出版信息

Indian J Endocrinol Metab. 2024 Jul-Aug;28(4):336-342. doi: 10.4103/ijem.ijem_488_23. Epub 2024 Aug 28.

DOI:10.4103/ijem.ijem_488_23
PMID:39371653
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11451958/
Abstract

Multiple observation studies and meta-analysis have linked growth hormone (GH) deficiency with metabolic-dysfunction-associated steatotic liver disease (MASLD). No meta-analysis has analysed the efficacy and safety of GH therapy on different aspects of MASLD. We undertook this meta-analysis to address this gap in knowledge. Electronic databases were searched for RCTs involving patients with MASLD receiving GH therapy. Primary outcome was to evaluate changes in radiologic measures of MASLD (magnetic resonance spectroscopy (MRS) and ultrasonography) and liver enzymes. Secondary outcomes were to evaluate alterations in body composition parameters [dual-energy X-ray absorptiometry (DXA)], lipids, glycaemia and side effects. From initially searched 1047 articles, data from three RCTs (120 patients) which fulfilled all criteria were analysed. After 6 months of GH therapy in MASLD, the per cent reduction in intrahepatic lipid (MRS) was significantly higher with GH as compared to placebo [MD -5.85% (95%CI:-11.41- -0.30); = 0.04; I = 63%]. Visceral adipose tissue (VAT) area reduction (DXA) was significantly higher with GH [MD-9.94 cm (95%CI:-19.04- -0.84); = 0.03; I = 0%]. Serum insulin-like growth factor-1 (IGF-1) was significantly raised in MASLD patients receiving GH as compared to placebo [MD +166.86 ng/ml (95%CI: 79.19-254.53); < 0.0.001; I = 90%]. High-sensitivity C-reactive protein (hsCRP) was significantly lower in patients receiving GH [MD -0.89 mg/L (95%CI:-1.40--0.38); = 0.0.0006; I = 0%]. Patients receiving GH had similar changes in triglycerides [MD-1.06 mg/L (95%CI:-20.45-18.34); = 0.91; I = 15%] and fasting glucose [MD -0.56 mg/L (95%CI:-4.67-3.55); = 0.79; I = 39%]. Gamma-glutamyl transpeptidase was significantly lower in patients receiving GH [MD -7.86 U/L (95%CI:-12.46--3.27); = 0.0008; I = 0%]. No increase in new-onset hypothyroidism was noted [OR 5.49 (95%CI: 0.25-121.18); = 0.28]. Short-term 6-month GH therapy in MASLD is associated with a significant reduction in intrahepatic lipid content, visceral adiposity, GGT and hsCRP without any increased occurrence of dysglycaemia or hypothyroidism.

摘要

多项观察性研究和荟萃分析已将生长激素(GH)缺乏与代谢功能障碍相关脂肪性肝病(MASLD)联系起来。尚无荟萃分析评估GH治疗对MASLD不同方面的疗效和安全性。我们进行这项荟萃分析以填补这一知识空白。通过电子数据库搜索涉及接受GH治疗的MASLD患者的随机对照试验(RCT)。主要结局是评估MASLD的影像学指标(磁共振波谱(MRS)和超声检查)及肝酶的变化。次要结局是评估身体成分参数[双能X线吸收法(DXA)]、血脂、血糖及副作用的改变。从最初检索到的1047篇文章中,分析了3项符合所有标准的RCT(120例患者)的数据。在对MASLD患者进行6个月的GH治疗后,与安慰剂相比,GH治疗组肝内脂质(MRS)降低百分比显著更高[平均差(MD)-5.85%(95%置信区间:-11.41至-0.30);P = 0.04;I² = 63%]。GH治疗组内脏脂肪组织(VAT)面积减少(DXA)显著更多[MD -9.94 cm²(95%置信区间:-19.04至-0.84);P = 0.03;I² = 0%]。与安慰剂相比,接受GH治疗的MASLD患者血清胰岛素样生长因子-1(IGF-1)显著升高[MD +166.86 ng/ml(95%置信区间:79.19至254.53);P < 0.001;I² = 90%]。接受GH治疗的患者高敏C反应蛋白(hsCRP)显著更低[MD -0.89 mg/L(95%置信区间:-1.40至-0.38);P = 0.0006;I² = 0%]。接受GH治疗的患者甘油三酯[MD -1.06 mg/L(95%置信区间:-20.45至18.34);P = 0.91;I² = 15%]和空腹血糖[MD -0.56 mg/L(95%置信区间:-4.67至3.55);P = 0.79;I² = 39%]变化相似。接受GH治疗的患者γ-谷氨酰转肽酶显著更低[MD -7.86 U/L(95%置信区间:-12.46至-3.27);P = 0.0008;I² = 0%]。未发现新发甲状腺功能减退增加[比值比(OR)5.49(95%置信区间:0.25至121.18);P = 0.28]。对MASLD进行为期6个月的短期GH治疗与肝内脂质含量、内脏脂肪、γ-谷氨酰转肽酶和hsCRP显著降低相关,且未增加血糖异常或甲状腺功能减退的发生率。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2a8f/11451958/57e96563bff3/IJEM-28-336-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2a8f/11451958/a03dd232470a/IJEM-28-336-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2a8f/11451958/480a627da2fc/IJEM-28-336-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2a8f/11451958/9ec9077f3a74/IJEM-28-336-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2a8f/11451958/57e96563bff3/IJEM-28-336-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2a8f/11451958/a03dd232470a/IJEM-28-336-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2a8f/11451958/480a627da2fc/IJEM-28-336-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2a8f/11451958/9ec9077f3a74/IJEM-28-336-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2a8f/11451958/57e96563bff3/IJEM-28-336-g004.jpg

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