口腔疾病防治 ›› 2021, Vol. 29 ›› Issue (11): 721-732.DOI: 10.12016/j.issn.2096-1456.2021.11.001
收稿日期:
2021-03-27
修回日期:
2021-04-20
出版日期:
2021-11-20
发布日期:
2021-07-20
通讯作者:
郑家伟
基金资助:
Received:
2021-03-27
Revised:
2021-04-20
Online:
2021-11-20
Published:
2021-07-20
Contact:
Jiawei ZHENG
Supported by:
摘要:
血管瘤及脉管畸形是临床上常见的疾病,根据临床及影像学表现,国际脉管异常研究学会(International Society for the Study of Vascular Anomalies,ISSVA)对其进行了详细分类,得到广泛认可和应用。迄今为止,大多数脉管畸形涉及PI3K/Akt/mTOR和RAS/MAPK/ERK这两条信号通路,这一发现对脉管畸形的诊疗产生了3个重大影响:增强了对脉管畸形生物学的理解;细化了基于基因型的脉管畸形分类;促进了治疗脉管畸形靶向药物的研发。随着基因测序、分子生物学和放射成像技术的发展,脉管畸形分类的相关性和诊断的准确性不断提高,硬化治疗、介入栓塞及靶向疗法取得了不断进步。目前,关于脉管畸形的研究多为回顾性临床研究或者低级别临床试验。本文旨在全面回顾婴幼儿血管瘤、淋巴管畸形、静脉畸形和动静脉畸形治疗的文献资料,对婴幼儿血管瘤与脉管畸形循证治疗研究进展作一述评。
中图分类号:
郑家伟, 赵泽亮. 婴幼儿血管瘤与脉管畸形的循证治疗研究进展[J]. 口腔疾病防治, 2021, 29(11): 721-732.
ZHENG Jiawei, ZHAO Zeliang. Progress in evidence-based research on the clinical treatment of infantile hemangioma and vascular malformations[J]. Journal of Prevention and Treatment for Stomatological Diseases, 2021, 29(11): 721-732.
Grades of recommendations | Levels of evidence | Therapy/Prevention/Etiology |
---|---|---|
A | 1a | Systematic reviews (with homogeneity) of randomized controlled trials |
1b | Individual randomized controlled trials (with narrow confidence interval) | |
1c | All or none randomized controlled trials | |
B | 2a | Systematic reviews (with homogeneity) of cohort studies |
2b | Individual cohort study or low quality randomized controlled trials (< 80% follow up) | |
2c | “Outcomes” research; ecological studies | |
3a | Systematic review (with homogeneity) of case-control studies | |
3b | Individual case-control study | |
C | 4 | Case-series (and poor-quality cohort and case-control studies) |
D | 5 | Expert opinion without explicit critical appraisal, or based on physiology, bench research or “first principles” |
表1 牛津循证医学中心证据分级和推荐强度
Table 1 Oxford center for evidence-based medicine: levels of evidence and grades of recommendation
Grades of recommendations | Levels of evidence | Therapy/Prevention/Etiology |
---|---|---|
A | 1a | Systematic reviews (with homogeneity) of randomized controlled trials |
1b | Individual randomized controlled trials (with narrow confidence interval) | |
1c | All or none randomized controlled trials | |
B | 2a | Systematic reviews (with homogeneity) of cohort studies |
2b | Individual cohort study or low quality randomized controlled trials (< 80% follow up) | |
2c | “Outcomes” research; ecological studies | |
3a | Systematic review (with homogeneity) of case-control studies | |
3b | Individual case-control study | |
C | 4 | Case-series (and poor-quality cohort and case-control studies) |
D | 5 | Expert opinion without explicit critical appraisal, or based on physiology, bench research or “first principles” |
Literature | Research methods | Target/drug | Mechanisms |
---|---|---|---|
Zhang, et al (129) | In vivo, in vitro | Macrophages | Macrophages in IHs promoted the progression of hemangioma by promoting lesion proliferation and endothelial cell differentiation while inhibiting lipogenesis of hemangiomastem cells, thereby promoting the progression of hemangioma |
Wu, et al (130) | In vitro | M1 macrophages | M1 macrophage induced the transformation of endothelial cells in hemangioma into mesenchyme, promoting hemangioma regression |
Li, et al (131) | In vitro, immunohistochemistry, quantitative RT-PCR | PEDF | PEDF expression was increased during the IH regression phase and may have effects on promoting IH regression |
Itinteang, et al (132) | In vitro, immunohistochemistry, enzyme activity assays, mass spectrometry, and Nano String gene expression assay | Cathepsins B, D, G | The expression of cathepsins B, D, and G was detected in various stages of IHs. Cathepsin B promoted the production of renin; cathepsin D induced the production of angiotensinⅠ, and cathepsin G induced the conversion of angiotensin Ⅰ to angiotensin Ⅱ |
Chisholm, et al (133); Dal, et al (134) | In vitro, histochemistry, immunohistochemistry, enzyme-linked immunosorbent assay, and colorimetry | β3-adrenergic receptor | the β3-adrenergic receptor was highly expressed in various stages of IHs and played a role in the pathogenesis of IHs, stimulating the release of VEGF and affecting various intracellular pathways and vascular functions |
Amaya, et al (135) | In vitro, histochemistry, and immunohistochemistry | Programmed cell death protein-1 (PD-1) | Programmed cell death protein 1 was highly expressed in endothelial cells, whereas expression of programmed death-ligand 1 was negative in six IH cases, which provided the possibility for immunotherapy |
Cai, et al (136) | In vivo, in vitro | 15,16-dihydrotanshinone I | Increased expression of apoptosis-associated proteins and significantly inhibited angiogenesis. In vivo experiments showed significant inhibition of hemangiomas |
Wang, et al (137); Liu, et al (138) | In vitro, histochemistry | Linc00152 | Linc00152 was highly expressed in IH tissues. Downregulation of Linc00152 expression inhibited Akt/mTOR and Notch1 pathways, thereby inhibiting the proliferation of endothelial cells and inducing apoptosis in the hemangiomas |
Zhang, et al (139) | In vitro, histochemistry | UCA1 | UCA1 was upregulated during the proliferative phase of hemangiomas. Inhibition of UCA1 expression upregulated miR-200c expression subsequently and further inhibited mTOR, AMPK, and Wnt/β-catenin pathways, thereby inhibiting cell proliferation, migration, and invasion of hemangiomas. |
表2 婴幼儿血管瘤的潜在治疗靶点
Table 2 Potential therapeutic targets for infantile hemangioma
Literature | Research methods | Target/drug | Mechanisms |
---|---|---|---|
Zhang, et al (129) | In vivo, in vitro | Macrophages | Macrophages in IHs promoted the progression of hemangioma by promoting lesion proliferation and endothelial cell differentiation while inhibiting lipogenesis of hemangiomastem cells, thereby promoting the progression of hemangioma |
Wu, et al (130) | In vitro | M1 macrophages | M1 macrophage induced the transformation of endothelial cells in hemangioma into mesenchyme, promoting hemangioma regression |
Li, et al (131) | In vitro, immunohistochemistry, quantitative RT-PCR | PEDF | PEDF expression was increased during the IH regression phase and may have effects on promoting IH regression |
Itinteang, et al (132) | In vitro, immunohistochemistry, enzyme activity assays, mass spectrometry, and Nano String gene expression assay | Cathepsins B, D, G | The expression of cathepsins B, D, and G was detected in various stages of IHs. Cathepsin B promoted the production of renin; cathepsin D induced the production of angiotensinⅠ, and cathepsin G induced the conversion of angiotensin Ⅰ to angiotensin Ⅱ |
Chisholm, et al (133); Dal, et al (134) | In vitro, histochemistry, immunohistochemistry, enzyme-linked immunosorbent assay, and colorimetry | β3-adrenergic receptor | the β3-adrenergic receptor was highly expressed in various stages of IHs and played a role in the pathogenesis of IHs, stimulating the release of VEGF and affecting various intracellular pathways and vascular functions |
Amaya, et al (135) | In vitro, histochemistry, and immunohistochemistry | Programmed cell death protein-1 (PD-1) | Programmed cell death protein 1 was highly expressed in endothelial cells, whereas expression of programmed death-ligand 1 was negative in six IH cases, which provided the possibility for immunotherapy |
Cai, et al (136) | In vivo, in vitro | 15,16-dihydrotanshinone I | Increased expression of apoptosis-associated proteins and significantly inhibited angiogenesis. In vivo experiments showed significant inhibition of hemangiomas |
Wang, et al (137); Liu, et al (138) | In vitro, histochemistry | Linc00152 | Linc00152 was highly expressed in IH tissues. Downregulation of Linc00152 expression inhibited Akt/mTOR and Notch1 pathways, thereby inhibiting the proliferation of endothelial cells and inducing apoptosis in the hemangiomas |
Zhang, et al (139) | In vitro, histochemistry | UCA1 | UCA1 was upregulated during the proliferative phase of hemangiomas. Inhibition of UCA1 expression upregulated miR-200c expression subsequently and further inhibited mTOR, AMPK, and Wnt/β-catenin pathways, thereby inhibiting cell proliferation, migration, and invasion of hemangiomas. |
图1 脉管畸形的突变谱及潜在治疗靶点
Figure 1 Vascular malformation mutation spectrum and medical therapy targets VEGFR: vascular endothelial growth factor receptor; TIE2: transmembrane receptor tyrosine kinase functioning as receptor for angiopoetin family proteins; PDGFRB: platelet-derived growth factor; Ras: small guanosine triphosphatase protein involved in cellular signal transduction resulting in cell growth and division; Raf: protein kinase; MEK (MAP2K1): mitogen-activated protein kinase; PI3K (PIK3CA): phosphoinositide 3-kinase, catalytic subunit; Akt: protein kinase B (serine and threonine protein kinase); mTOR: mammalian target of rapamycin (serine and threonine protein kinase)
图2 根据病灶及邻近静脉的解剖及血流动力学特征对静脉畸形进行分类
Figure 2 Venous malformations were classified according to the anatomical and hemodynamic characteristics of the lesions and adjacent veins
Overall(95% CI) | |
---|---|
Complete cure | 64.7(57.4-72.0) |
Partial cure | 28.0(22.1-34.0) |
No benefit | 4.5(3.0-6.1) |
Improvement in QoL | 78.9(67.0-90.8) |
Patient satisfaction | 91.0(86.1-95.9) |
Pulmonary complication | 0.6(0.2-1.0) |
Skin necrosis/scar | 1.5(0.8-2.1) |
Any permanent morbidity/mortality | 0.8(0.3-1.3) |
Local temporary complication | 41.8(27.0-56.5) |
表3 静脉畸形硬化治疗总体疗效总结
Table 3 Summary of the overall curative effect of sclerotherapy for venous malformations %
Overall(95% CI) | |
---|---|
Complete cure | 64.7(57.4-72.0) |
Partial cure | 28.0(22.1-34.0) |
No benefit | 4.5(3.0-6.1) |
Improvement in QoL | 78.9(67.0-90.8) |
Patient satisfaction | 91.0(86.1-95.9) |
Pulmonary complication | 0.6(0.2-1.0) |
Skin necrosis/scar | 1.5(0.8-2.1) |
Any permanent morbidity/mortality | 0.8(0.3-1.3) |
Local temporary complication | 41.8(27.0-56.5) |
Nidus type | Description | Treatment approach |
---|---|---|
Ⅰa | Direct AVF | Mechanical occluding device |
Ⅱa | Typical AVM nidus | Transcatheter and direct puncture ethanol embolization |
Ⅱb | AVM nidus shunting into aneurysmal vein | Same as type Ⅱa as well as coiling outflow vein |
Ⅲa | Aneurysmal small vein where nidus resides in vein wall with single outflow vein | Coiling single aneurysmal outflow vein |
Ⅲb | Type IIIa with multiple outflow veins | Coiling each outflow vein |
Ⅳ | Tissue infiltrative AVM | Transcatheter or direct puncture embolization |
表4 动静脉畸形的Yakes分类及相应治疗建议
Table 4 Yakes classification of arteriovenous malformations and corresponding treatment recommendations
Nidus type | Description | Treatment approach |
---|---|---|
Ⅰa | Direct AVF | Mechanical occluding device |
Ⅱa | Typical AVM nidus | Transcatheter and direct puncture ethanol embolization |
Ⅱb | AVM nidus shunting into aneurysmal vein | Same as type Ⅱa as well as coiling outflow vein |
Ⅲa | Aneurysmal small vein where nidus resides in vein wall with single outflow vein | Coiling single aneurysmal outflow vein |
Ⅲb | Type IIIa with multiple outflow veins | Coiling each outflow vein |
Ⅳ | Tissue infiltrative AVM | Transcatheter or direct puncture embolization |
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