Journal of Prevention and Treatment for Stomatological Diseases ›› 2021, Vol. 29 ›› Issue (11): 721-732.doi: 10.12016/j.issn.2096-1456.2021.11.001

• Expert Commentary • Previous Articles     Next Articles

Progress in evidence-based research on the clinical treatment of infantile hemangioma and vascular malformations

ZHENG Jiawei(),ZHAO Zeliang   

  1. Shanghai Key Laboratory of Stomatology & Shanghai Research Institute of Stomatology, Shanghai 200011, China
  • Received:2021-03-27 Revised:2021-04-20 Online:2021-11-20 Published:2021-07-20
  • Contact: Jiawei ZHENG E-mail:davidzhengjw@hotmail.com
  • Supported by:
    National Natural Science Foundation of China(81771087)

Abstract:

Hemangiomas and vascular malformations are common clinical diseases. According to their clinical and imaging characterizations, the International Society for the Study of Vascular Anomalies (ISSVA) has systematically classified infantile hemangioma and vascular malformations, and the classification has been widely recognized and applied. To date, most vascular malformations involve the following important signaling pathways: PI3K/Akt/mTOR and RAS/MAPK/ERK. This discovery has major impacts on the diagnosis and treatment of vascular malformations including the following: the understanding of the biology of vascular malformations has been increased; the understanding of vascular malformations based on genotype has been refined; and the development of targeted drugs for the treatment of vascular malformations has been promoted. Despite facing many challenges, with the development of gene sequencing, molecular biology and imaging technology, the relevance of vascular malformation classification and the accuracy of diagnosis are improving, and this is accompanied by innovations in surgical treatment and sclerotherapy, interventional embolization, and continuous progress in targeted therapy. At present, investigations on vascular malformations are mostly retrospective clinical studies or low-level clinical trials. The purpose of this paper is to review the literature on the treatment of infantile hemangioma, lymphatic malformation, venous malformation and arteriovenous malformation and to review the research progress in evidence-based treatment of infantile hemangioma and vascular malformation.

Key words: infantile hemangioma, venous malformation, lymphatic malformations, arteriovenous malformations, gene mutation, signaling pathway inhibitor, treatment, evidence-based research

CLC Number: 

  • R78

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”

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.

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)"

Figure 2

Venous malformations were classified according to the anatomical and hemodynamic characteristics of the lesions and adjacent veins"

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)

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

Tissue infiltrative AVM
Transcatheter or direct puncture embolization

Figure 3

Yakes classification of arteriovenous malformations"

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