Endocan: A Novel Marker of Endothelial Dysfunction in C1-Inhibitor-Deficient Hereditary Angioedema

Demirtürk, Mustafa; Akpınar, Timur Selçuk; Köse, Murat; Gelincik, Aslı; Çolakoğlu, Bahattin; Büyüköztürk, Suna

doi:10.1159/000481256

Cited by 12 publications

(10 citation statements)

References 21 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…As the endothelium is inherently related to microvascular permeability and, in consequence, the swelling phenomenon, it represents another area of interest regarding potential biomarkers in HAE. Studies in this field involved vascular endothelial cadherin (transmembrane adhesive protein) [ 72 , 76 ], von Willebrand factor (marker of endothelial damage), soluble E-selectin (cytokine-induced adhesion molecule), endothelin-1 (vasomotor activity regulator) [ 30 , 77 , 78 ], arginine vasopressin , adrenomedullin [ 78 ], atrial natriuretic peptide [ 79 ], as well as endothelial-derived endocan and vascular cell adhesion molecule-1 (markers of endothelial function) [ 80 ]. The subsequently studied modulators of vascular permeability included vascular endothelial growth factors , angiopoietin-1 (which promotes endothelial stabilization) and angiopoietin-2 (which facilitates vascular permeability) [ 81 , 82 ], secreted phospholipases A2 (particularly the 2A group) [ 83 ], and platelet-activating factor acetylhydrolase [ 81 ].…”

Section: Biochemical Biomarkersmentioning

confidence: 99%

Biomarkers in Hereditary Angioedema

Porębski

Kwitniewski

Reshef

2021

Clinic Rev Allerg Immunol

View full text Add to dashboard Cite

A biomarker is a defined characteristic measured as an indicator of normal, biologic, pathogenic processes, or biological responses to an exposure or intervention. Diagnostic biomarkers are used to detect a disease or a subtype of a disease; monitoring biomarkers are measured serially to assess a medical condition; response biomarkers are used to check biologic response following a medical intervention; predictive biomarkers are used to identify patients who are more likely to respond to a medical intervention; and prognostic biomarkers are used to assess the future likelihood of a clinical event. Although biomarkers have been extensively investigated and validated in many diseases and pathologies, very few are currently useful for the diagnosis, evaluation of disease activity, and treatment of hereditary angioedema (HAE). Pathophysiologic pathways involved in HAE reveal a plethora of molecules from the complement, coagulation, and fibrinolysis systems or from the vascular endothelium, which may serve as biomarkers. The most promising candidates, together with their laboratory readout systems, should be evaluated with regard to their analytical and clinical validity and utility. To be highly specific, such biomarkers should be linked to the pathomechanisms of HAE, particularly the bradykinin-generating cascade. Additionally, major advances in high-throughput omics-based technologies may facilitate the discovery of new candidate biomarkers in the future. This review will cover the existing as well as future potential biomarkers that will support the diagnosis, monitor disease activity, and can be used to assess the efficacy of new avenues of therapy of HAE and other forms of angioedema.

show abstract

Section: Biochemical Biomarkersmentioning

confidence: 99%

Biomarkers in Hereditary Angioedema

Porębski

Kwitniewski

Reshef

2021

Clinic Rev Allerg Immunol

View full text Add to dashboard Cite

show abstract

“…Endocan is evaluated by peripheral blood serum level, and it is easy to obtain the sample. However, endocan is also not a specific marker and is also increased in atopic dermatitis in serum and lesional skin [ 136 ], psoriasis [ 137 ], and angioedema [ 138 ].…”

Section: Clinical Sign and Biomarker For Drug Eruptionmentioning

confidence: 99%

Diagnostic Tools and Biomarkers for Severe Drug Eruptions

Yoshioka

Sawada

Nakamura

2021

IJMS

View full text Add to dashboard Cite

In accordance with the development of human technology, various medications have been speedily developed in the current decade. While they have beneficial impact on various diseases, these medications accidentally cause adverse reactions, especially drug eruption. This delayed hypersensitivity reaction in the skin sometimes causes a life-threatening adverse reaction, namely Stevens-Johnson syndrome and toxic epidermal necrolysis. Therefore, how to identify these clinical courses in early time points is a critical issue. To improve this problem, various biomarkers have been found for these severe cutaneous adverse reactions through recent research. Granulysin, Fas ligands, perforin, and granzyme B are recognized as useful biomarkers to evaluate the early onset of Stevens-Johnson syndrome and toxic epidermal necrolysis, and other biomarkers, such as miRNAs, high mobility group box 1 protein (HMGB1), and S100A2, which are also helpful to identify the severe cutaneous adverse reactions. Because these tools have been currently well developed, updates of the knowledge in this field are necessary for clinicians. In this review, we focused on the detailed biomarkers and diagnostic tools for drug eruption and we also discussed the actual usefulness of these biomarkers in the clinical aspects based on the pathogenesis of drug eruption.

show abstract

“…Pathophysiology studies have identified biomarkers (endocan, VE-cadherin) that can help to better clarify the etiology and/or the severity of the disease. [43,44] Genotype-phenotype correlations in C1-INH-HAE disease are currently being extensively investigated. [38,45,46] Speletas et al [45] conducted research in various European countries (Greece, Germany, Romania, and Hungary) and found that abdominal attacks were less common in Hungarians, and that the onset of the C1-INH-HAE type of the disease was delayed in Romanian patients.…”

Section: Serping1 Genementioning

confidence: 99%

Novelties in Hereditary Angioedema Patho-physiology

Özdemir¹

2019

South Clin Ist Euras

View full text Add to dashboard Cite

Hereditary angioedema (HAE) is a rare, inherited disease mostly associated with mutations in the SERPING1 gene (serpin family G member 1), which encodes the C1 inhibitor (C1-INH) protein. Regulation can lead to plasma deficiency and ensuing repeated attacks of severe angioedema. This disease was first described clinically and genetically in 1888 by William Osler, who named it "hereditary angioneurotic edema (HANE)." It took 75 years until Donaldson and Evans identified the fundamental role of C1-INH in the pathophysiology of so-called HANE by Osler. Significant progress has been made in the research of this genetic disease when the role of neural factors was documented as being too small to lead to edema, the name was changed as HAE. Therefore, the name of more than 490 different mutations have been reported in the region of the C1-INH gene (SERPING1) until mid-2018. It is now known that C1-INH deficiency overstimulates the plasma contact (kallikrein-kinin) system, which eventually results in the overproduction of bradykinin. By binding to the bradykinin B2 receptor, bradykinin increases vascular permeability (vasodilation) and causes contraction of nonvascular smooth muscle, and acts as a main/major mediator in the pathophysiology of HAE. Reports since 2000 have described a new type of HAE with "normal" CI-INH levels, primarily in Caucasians. A number of abnormalities in the genes encoding for factor XII, angiopoietin-1, and plasminogen have been identified in this novel disease entity. The establishment of treatment modalities for HAE with normal C1-INH is also expected.

show abstract

Endocan: A Novel Marker of Endothelial Dysfunction in C1-Inhibitor-Deficient Hereditary Angioedema

Cited by 12 publications

References 21 publications

Biomarkers in Hereditary Angioedema

Biomarkers in Hereditary Angioedema

Diagnostic Tools and Biomarkers for Severe Drug Eruptions

Novelties in Hereditary Angioedema Patho-physiology

Contact Info

Product

Resources

About