scholarly journals Theoretical Study on Pressure Damage Based on Clinical Purpura during the Laser Irradiation of Port Wine Stains with Real Complex Vessels

2019 ◽  
Vol 9 (24) ◽  
pp. 5478
Author(s):  
Hao Jia ◽  
Bin Chen ◽  
Dong Li

Port wine stains (PWSs) are congenital dermal vascular lesions composed of a hyperdilated vasculature. Purpura represented by local hemorrhage from water vaporization in blood during laser therapy of PWS is typically considered a clinical feedback, but with a low cure rate. In this study, light propagation and heat deposition in skin and PWSs is simulated by a tetrahedron-based Monte Carlo method fitted to curved bio-tissues. A curvature-corrected pressure damage model was established to accurately evaluate the relationship between purpura-bleeding area (rate) and laser therapy strategy for real complex vessels. Results showed that the standard deviation of Gaussian curvature of the vessel wall has negative relation with the fluence threshold of vessel rupture, but has positive relation with the effective laser fluence of vessel damage. This finding indicated the probable reason for the poor treatment of PWS, that is, considering purpura formation as a treatment end point (TEP) only leads to partial removal of vascular lesions. Instead, appropriate purpura area ratio with marked effects or rehabilitation should be adopted as TEP. The quantitative correlation between the fluence of a pulsed dye laser and the characteristics of vascular lesions can provide personalized and precise guidance for clinical treatments.

2006 ◽  
Vol 10 (3) ◽  
pp. 151-153 ◽  
Author(s):  
F. Sule Afsar ◽  
Ragıp Ortac

Background: Acquired port-wine stains (PWSs) are vascular lesions that are identical to congenital PWSs morphologically and histopathologically. Objective: Because acquired PWSs are rarely seen in adult and pediatric patients, we present a 9-year-old boy with an acquired PWS on his left forearm. Conclusion: None of the proposed etiologies, such as trauma, chronic sun exposure, or hormonal medication, was applicable to our patient, and a literature review showed us that acquired PWSs give a faster and better response to pulsed dye laser therapy than congenital lesions do.


Pharmaceutics ◽  
2020 ◽  
Vol 12 (6) ◽  
pp. 591
Author(s):  
Mingjuan Li ◽  
M. Ingmar van Raath ◽  
Shervin Khakpour ◽  
Ahmet Seçilir ◽  
Bart C. Sliggers ◽  
...  

Antifibrinolytic site-specific pharmaco-laser therapy (SSPLT) is an experimental treatment modality for refractory port wine stains (PWS). Conceptually, antifibrinolytic drugs encapsulated in thermosensitive liposomes are delivered to thrombi that form in semi-photocoagulated PWS blood vessels after conventional laser treatment. Local release of antifibrinolytics is induced by mild hyperthermia, resulting in hyperthrombosis and complete occlusion of the target blood vessel (clinical endpoint). In this study, 20 thermosensitive liposomal formulations containing tranexamic acid (TA) were assayed for physicochemical properties, TA:lipid ratio, encapsulation efficiency, and endovesicular TA concentration. Two candidate formulations (DPPC:DSPE-PEG, DPPC:MPPC:DSPE-PEG) were selected based on optimal properties and analyzed for heat-induced TA release at body temperature (T), phase transition temperature (Tm), and at T > Tm. The effect of plasma on liposomal stability at 37 °C was determined, and the association of liposomes with platelets was examined by flow cytometry. The accumulation of PEGylated phosphocholine liposomes in laser-induced thrombi was investigated in a hamster dorsal skinfold model and intravital fluorescence microscopy. Both formulations did not release TA at 37 °C. Near-complete TA release was achieved at Tm within 2.0–2.5 min of heating, which was accelerated at T > Tm. Plasma exerted a stabilizing effect on both formulations. Liposomes showed mild association with platelets. Despite positive in vitro results, fluorescently labeled liposomes did not sufficiently accumulate in laser-induced thrombi in hamsters to warrant their use in antifibrinolytic SSPLT, which can be solved by coupling thrombus-targeting ligands to the liposomes.


1988 ◽  
Vol 3 (1-4) ◽  
pp. 7-11 ◽  
Author(s):  
S. W. Lanigan ◽  
J. A. Cotterill

2003 ◽  
Vol 29 (1) ◽  
pp. 49-55 ◽  
Author(s):  
Kristen Hansen ◽  
Clarence D Kreiter ◽  
Marcy Rosenbaum ◽  
Duane C Whitaker ◽  
Christopher J Arpey

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