Influence of gene polymorphisms in ulcer healing process after superficial venous surgery

Gemmati, Donato; Tognazzo, Silvia; Catozzi, Linda; Federici, Federica; Palma, Massimiliano De; Gianesini, Sergio; Scapoli, G; Mattei, Monica De; Liboni, A; Zamboni, Paolo

doi:10.1016/j.jvs.2006.05.011

Cited by 45 publications

(60 citation statements)

References 37 publications

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“…In addition, chronic skin lesions were negatively associated with FXIII activity and with L34-allele (7). Finally, other FXIII gene variants responsible for increased molecule activity were associated with better prognosis and shorter healing time after surgery (8,47). Considering that VV34-carriers have a basal mean FXIII activity of about 70%-90% (7,33,this paper) and that after acute MI, a reduction of circulating FXIII begins (37,this paper), VV34-patients might be disadvantaged in recovering myocardial functions respective to L34-carriers with significantly higher activity (7,33,this paper).…”

Section: Discussionmentioning

confidence: 97%

“…In addition, carrier patients with chronic vascular insufficiency and venous leg ulcer had a significantly shorter mean healing time of the skin lesion after venous reflux correction. This happened despite the fact that the elective vascular surgery intervention was completely successful in all treated patients (8). Reper-fusion treatment by percutaneous coronary intervention (PCI) is the most efficacious and utilized medical strategy in acute MI (9,10).…”

Section: Introductionmentioning

confidence: 99%

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Factor XIIIA-V34L and Factor XIIIB-H95R Gene Variants: Effects on Survival in Myocardial Infarction Patients

Gemmati

Federici

Campo

et al. 2007

Mol Med

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It has been demonstrated recently that coagulation factor XIII (FXIII) plays an extraordinary role in myocardial healing after infarction, improving survival in a mouse model. Common FXIII gene variants (i.e. FXIIIA-V34L and FXIIIB-H95R) significantly influence the molecular activity. To evaluate whether there is a relationship between the two FXIII gene variants and survival in patients after myocardial infarction (MI), V34L and H95R were PCR-genotyped in a cohort of 560 MI cases and follow-up was monitored. Cases with ST-segment elevation MI (STEMI) were 416 (74.3%) and 374 of these were treated with primary percutaneous coronary intervention (PCI) (89.9%). The remaining 144 patients showed non-ST-segment elevation MI (NSTEMI) at enrollment. The combined endpoint was the occurrence of death, re-infarction, and heart failure. Kaplan-Meier analysis at one year yielded an overall rate for adverse events of 24.5% with a lower incidence in the L34-carriers (28.8% vs 17.1%; log-rank, P = 0.00025), similar to that of the 416 STEMI (23.8%) being (28.0% and 16.9%; VV34-and L34-carriers respectively; log-rank, P = 0.001). Primary PCI-group had a slight lower incidence (22.9%) of adverse events (26.8% and 17.1%; VV34-and L34-carriers respectively; log-rank, P = 0.009). During hospitalization, 506 patients received PCI (374 primary PCI and 132 elective PCI). Significance was conserved also in the overall PCIgroup (28.6% and 17.8%; VV34-and L34-carriers respectively; log-rank, P = 0.001). Similar findings were observed at 30 days follow-up. Cases carrying both FXIII variants had improved survival rate (log-rank, P = 0.019). On the other hand, minor bleeding complications were found increased in L34-carriers (P = 0.0001) whereas major bleeding complications were not. Finally, more direct evidence on the role of FXIII molecule on survival might come from the fact that despite significant FXIII antigen reductions observed in cases after MI, regardless the FXIII genotype considered, L34-carriers kept almost normal FXIII activity (VV34-vs L34-carriers; P < 0.001). We conclude that FXIII L34-allele improves survival after MI in all the groups analyzed, possibly through its higher activity associated with assumable positive effects on myocardial healing and recovered functions. Genetically determined higher FXIII activity might influence post-MI outcome. This paves the way for using FXIII molecules to improve myocardial healing, recovery of functions, and survival after infarction.

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Section: Discussionmentioning

confidence: 97%

Section: Introductionmentioning

confidence: 99%

Factor XIIIA-V34L and Factor XIIIB-H95R Gene Variants: Effects on Survival in Myocardial Infarction Patients

Gemmati

Federici

Campo

et al. 2007

Mol Med

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“…It has been proposed that the FXIII-A 34L variant displays improved crosslinking activity towards extracellular matrix components, thus further augmenting the antifibrinolytic properties of FXIII. Consequently, this modification should result in enhanced fibroblast migration followed by significantly improved ulcer healing (72)(73)(74). Indeed, these suggestions were confirmed by Gemmati et al (72) and Tognazzo et al (73), who found that 34LL homozygous patients displayed a 2-fold higher FXIII activity at the same FXIII blood level compared to wild-type 34VV homozygotous ones.…”

Section: Cvu Healing-promoting Variantsmentioning

confidence: 78%

“…In contrast to the previously described CVU formation-inducing polymorphisms, variants of certain genes also facilitate wound healing. Among these is a polymorphism concerned with a gene encoding for coagulation factor XIII (FXIII) subunit A (72)(73)(74).…”

Section: Cvu Healing-promoting Variantsmentioning

confidence: 99%

Genetic risk factors of chronic venous leg ulceration: Can molecular screening aid in the prevention of chronic venous insufficiency complications?

Grzela¹

2010

Mol Med Rep

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Abstract. Venous leg ulceration is a severe complication of chronic venous insufficiency. Despite numerous studies, understanding of the possible mechanisms involved in venous ulceration development remains incomplete. It is assumed that, in addition to well-documented behavioral and/or environmental conditions, as yet poorly defined genetic risk factors may play important roles in chronic wound progression or healing. It is difficult to overestimate the clinical usefulness of genetic screening in the determination of the risk of wound development and/or its healing course. From a pharmacogenomic perspective, genetic screening may aid in the planning of individualized treatment. In addition, the detection of venous ulcer-promoting gene variants may facilitate the decision to introduce prophylaxis or, if necessary, appropriate treatment for venous insufficiency, long before a leg ulcer develops. In addition to significant economic benefits, this approach would reduce the risk of health-and life-threatening conditions. In this review, we focus on several gene mutations/polymorphisms with previously documented significance in leg ulceration pathophysiology, and briefly speculate about possible candidates for further study.

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“…Specific Factor XIII genotypes have favorable ulcer healing rates, while the HFE gene mutation, despite its importance in venous ulcer risk, has no influence on healing time. 22 …”

Section: Genetic Influencesmentioning

confidence: 99%

Venous leg ulceration pathophysiology and evidence based treatment

Chi

Raffetto

2015

Vasc Med

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Venous leg ulceration (VLU) is one of the most predominate medical disorders worldwide and in the western hemisphere it affects around 1.5% of the general population and up to 5% of the elderly population. Unfortunately, this trend will only increase given the growth of an aging population worldwide. Understanding its pathophysiology that begins with venous hemodynamic abnormalities and leads to inflammatory alterations with microcirculatory changes is critical to delivering effective curative therapy. As such, the main component to treatment is reversing the underlying venous hypertension and pro-inflammatory milieu using compression treatment along with various adjuvant therapies. Given its impact, a comprehensive multi-pronged approach to care, treatment and prevention is required to reverse the increasing trend that is observed worldwide.

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Influence of gene polymorphisms in ulcer healing process after superficial venous surgery

Cited by 45 publications

References 37 publications

Factor XIIIA-V34L and Factor XIIIB-H95R Gene Variants: Effects on Survival in Myocardial Infarction Patients

Factor XIIIA-V34L and Factor XIIIB-H95R Gene Variants: Effects on Survival in Myocardial Infarction Patients

Genetic risk factors of chronic venous leg ulceration: Can molecular screening aid in the prevention of chronic venous insufficiency complications?

Venous leg ulceration pathophysiology and evidence based treatment

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