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1.
Int J Surg Case Rep ; 115: 109238, 2024 Feb.
Article in English | MEDLINE | ID: mdl-38232416

ABSTRACT

INTRODUCTION: Reconstructing large defects of the columella and upper lip is an interesting challenge in facial reconstruction due to the high visibility of this aesthetic subunit and the difficulties posed by the unique characteristics of the skin in these areas, which differs from that of the surrounding regions. Among the various techniques proposed, the use of local flaps remains the most commonly used and effective method in this type of reconstruction. PRESENTATION OF THE CASE: A 47-year-old man in good clinical condition presented with a nodular lesion on the columella and upper lip. The lesion was excised (revealing it to be a squamous cell carcinoma) and reconstructed using two opposing nasogenian flaps, resulting in an optimal aesthetic and functional restoration. DISCUSSION: The use of local flaps remains the most effective technique for columella defect reconstruction. However, many described techniques require multiple surgical stages or result in visible scarring. Additionally, they do not guarantee effective reconstruction in cases involving the upper lip. On the other hand, the use of free flaps, while more expensive and requiring expert teams, may not ensure optimal color and skin texture matching. CONCLUSIONS: The use of opposing nasogenian flaps allows for a rapid and effective reconstruction of defects involving the columella and upper lip, leading to a swift return to normal life for the patient.

5.
Photodiagnosis Photodyn Ther ; 27: 276-279, 2019 Sep.
Article in English | MEDLINE | ID: mdl-30965148

ABSTRACT

BACKGROUND: Cutaneous warts are an extremely common problem, whose eradication can be challenging. Topical PDT involves applying a porphyrin precursor, 5-aminolevulinic acid (ALA) or methyl aminolevulinate (MAL) to the affected area. ALA-PDT has been well documented to be successful in the treatment of recalcitrant warts. PDT has a limited role in the treatment of thicker lesions because the photosensitizer does not penetrate keratotic lesions well, though this is vehicle dependent. OBJECTIVE: The aim of this study was to evaluate the efficacy and safety of curettage + microneedling + ALA-PDT for the treatment of resistant acral warts. We hypothesized that microneedling may increase the efficacy of PDT, providing a channel to deliver the ALA to deeper areas of warts. METHODS: Our study was carried out between November 2017 and July 2018. Eligible participants had one or more resistant plantar or palmar warts. Thirteen patients were recruited. They underwent a thorough curettage, followed by the application of 5-ALA 10% cream on the wart, and by microneedling. Later, the pricked skin was covered for three hours by an occlusive polyurethane dressing, and finally irradiated with a red-light source. Patients performed one session every three weeks for a total of three cycles. RESULTS: After 3 treatments of curettage + microneedling + ALA-PDT, 11 patients (84.6%) showed complete remission (defined as complete disappearance of their warts). One patient (7.7%) showed partial remission (defined as greater than 50% decrease in the wart area) after 3 sessions; this patient needed other 2 sessions to achieve complete remission. The mean follow-up period after healing was 4.3 months. Adverse effects were recorded. CONCLUSION: We have demonstrated, for the first time to our knowledge, that the combination of curettage + microneedling + topical ALA-PDT may offer an effective and safe alternative for the treatment of acral resistant warts, even when PDT alone has already been insufficient.


Subject(s)
Aminolevulinic Acid/analogs & derivatives , Curettage/methods , Needles , Photochemotherapy/methods , Photosensitizing Agents/therapeutic use , Warts/therapy , Adolescent , Adult , Aminolevulinic Acid/administration & dosage , Aminolevulinic Acid/adverse effects , Aminolevulinic Acid/therapeutic use , Combined Modality Therapy , Curettage/adverse effects , Female , Humans , Male , Middle Aged , Photochemotherapy/adverse effects , Photosensitizing Agents/administration & dosage , Photosensitizing Agents/adverse effects , Warts/drug therapy , Young Adult
6.
J Lipid Mediat ; 7(3): 253-67, 1993 Jul.
Article in English | MEDLINE | ID: mdl-8219005

ABSTRACT

The coumarin derivative, cloricromene, an antithrombotic drug previously indicated as AD6, is known to inhibit the release of radioactive arachidonic acid from human platelets prelabelled with arachidonic acid and stimulated with thrombin. This effect might be due to the drug itself or to its catabolite, cloricromene acid. When added to platelet lysates neither compound inhibited phospholipase A2 activity assayed either with endogenous or with exogenous substrates. However, some inhibition was instead shown when intact platelets were first exposed to cloricromene and then enzyme activity was assayed in the lysate. Preincubation of platelets with the drug caused a dose-dependent inhibition of arachidonic acid mobilization in fluoroaluminate-stimulated platelets. beta-Thromboglobulin (beta-TG) release, a phenomenon previously shown to share common steps with phospholipase A2 activation, was also dose-dependently inhibited by cloricromene. Cloricromene also reduced the radioactivity associated with phosphatidic acid in fluoroaluminate-stimulated platelets but not in platelets stimulated with thrombin. These results are consistent with the hypothesis that cloricromene, or its catabolite, inhibits the production of arachidonic acid in stimulated platelets by interfering with a G-protein mediated activation of phospholipase A2 that is independent from the receptor-activated phosphoinositide phospholipase C.


Subject(s)
Blood Platelets/enzymology , Chromonar/analogs & derivatives , GTP-Binding Proteins/physiology , Phospholipases A/blood , Aluminum/pharmacology , Arachidonic Acid/blood , Blood Platelets/drug effects , Chromonar/pharmacology , Cytosol/enzymology , Enzyme Activation/drug effects , Fluorine/pharmacology , Humans , Phosphatidylinositols/blood , Phospholipases A2 , Thrombin/pharmacology , beta-Thromboglobulin/metabolism
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