Orejas en asa. Presentación de casos y revisión bibliográfica / Earpining. Presentation of cases and bibliographic review

Las orejas prominentes se deben a una o varias anomalías congénitas que pueden asociarse entre sí en grados diversos. Los pabellones auriculares son considerados demasiado visibles tanto por la falta de plegamiento del antihélix, la abertura del ángulo cefaloconchal y la hipertrofia de la concha, según la clasificación de Davis. Son un problema estético frecuente, observándose en el 5% de la población. El conocimiento de la anatomía del pabellón normal y de los criterios antropométricos es indispensable. El grosor del cartílago condiciona la rigidez y la elasticidad del pabellón, mientras que sus relieves definen la forma y la posición. La finalidad en la otoplastia es corregir estas anomalías, remodelando el cartílago para obtener unas orejas con una plicatura adecuada, situadas y orientadas según parámetros estéticos, simétricas, con un tamaño y aspecto natural. Se pueden combinar distintos procedimientos quirúrgicos los cuales deben ser simples, rápidos, tener un resultado armonioso y duradero. Se realizó una revisión retrospectiva entre los años 2018 a 2020 en el Servicio de Cirugía Plástica del Hospital Tornú, en la que se presentan 4 casos de orejas prominentes a los cuales se les realizaron diferentes técnicas quirúrgicas de otoplastia (Davis, Stentstrom y Furnas). El total de los pacientes (n=4) tratados presentó un resultado satisfactorio tanto para el paciente como para el equipo quirúrgico, sin complicaciones significativas. La resolución quirúrgica de las orejas prominentes puede realizarse mediante numerosas técnicas; estas se dividen entre aquellas que realizan un procedimiento agresivo sobre el cartílago (resectivas) y las que intentan ser más conservadoras, sin resección del mismo para evitar al máximo las complicaciones. La diversidad de enfoques indica que no existe una técnica definitiva para corregir estos problemas. Las orejas prominentes o en asa, si bien no presentan alteraciones funcionales, tienen consecuencias sobre los efectos estéticos y psicológicos en el paciente que pueden ser sustanciales. Es importante conocer su base anatómica y realizar una adecuada evaluación, elegir técnicas para la corrección de la deformidad y conocer las posibles complicaciones del procedimiento para obtener un buen resultado estético y duradero.

Prominent ears are due to one or more congenital anomalies that may be associated with each other to varying degrees. The pinnae are considered too visible due to the lack of folding of the antihelix, the opening of the cephalo-conchal angle and the hypertrophy of the concha, according to the Davis classification. They are a frequent esthetic problem, being observed in 5% of the population. Knowledge of normal pinna anatomy and anthropometric criteria is essential. The thickness of the cartilage determines the rigidity and elasticity of the pinna, while its relief defines its shape and position. The purpose of otoplasty is to correct these anomalies, remodeling the cartilage to obtain ears with an adequate plication, positioned and oriented according to aesthetic parameters, symmetrical, with a natural size and appearance. Different surgical procedures can be combined, which must be simple, fast, have a harmonious and lasting result. A retrospective review was performed from 2018 to 2020 in the Plastic Surgery Department of the Tornú Hospital, presenting 4 cases of prominent ears which underwent different otoplasty surgical techniques (Davis, Stentstrom and Furnas). The total number of patients (n=4) treated presented a satisfactory result for both the patient and the surgical team without significant complications. Surgical resolution of protruding ears can be performed by numerous techniques, divided between those that perform an aggressive procedure on the cartilage (resective) and those that try to be more conservative, without resection of the cartilage to avoid complications as much as possible. The diversity of approaches indicates that there is no definitive technique to correct these problems. Prominent or protruding ears, although they do not present functional alterations, the consequences on the esthetic and psychological effects on the patient can be substantial. It is important to know their anatomical basis and to perform an adequate evaluation, to choose techniques for the correction of the deformity and to know the possible complications of the procedure in order to obtain a good esthetic and lasting result.

Transient receptor potential channels in human platelets: expression and functional role.

Recent studies have demonstrated that mammalian homologues of Drosophila transient receptor potential (TRP) channels are widely expressed in human platelets. Occupation of G protein-coupled receptors by agonists results in activation of these channels, which results in Na+ and Ca2+ entry. Canonical or classic TRP (TRPC) family members have been reported to associate with different Ca2+-handling proteins, including the type II inositol 1,4,5-trisphosphate receptor, the endoplasmic reticulum Ca2+ sensor STIM1 (STromal Interaction Molecule-1) or the Ca2+ permeable channel Orai1. The dynamic interaction of TRPC channels with the above mentioned proteins has been found to be important for both store-operated and capacitative Ca2+ entry, as well as for non-capacitative Ca2+ influx. The former is a major mechanism for Ca2+ entry in human platelets. This mechanism, activated by a reduction in the concentration of free Ca2+ in the intracellular stores, results in the formation of signaling complexes involving STIM proteins, Orai1, Orai2, TRPC1 and TRPC6. There is a growing body of evidence supporting that Ca2+ signaling dysfunction plays an important role in the pathogenesis of several platelet-linked disorders, including those associated to type 2 diabetes mellitus. Abnormal Ca2+ signals in response to physiological agonists have been associated to platelet hyperactivity. The expression of several TRPCs, STIM1 and Orai1, as well as their interaction, has been reported to be altered in platelets from type 2 diabetic patients, which results in attenuated capacitative Ca2+ entry but enhanced non-capacitative Ca2+ influx; thus suggesting a role for Ca2+ handling proteins, including TRPs, in the pathomechanism of diabetic complications.

Functional role of the calmodulin- and inositol 1,4,5-trisphosphate receptor-binding (CIRB) site of TRPC6 in human platelet activation.

BACKGROUND: All identified mammalian TRPC channels show a C-terminal calmodulin (CaM)- and inositol 1,4,5-trisphosphate receptors (IP(3)Rs)-binding (CIRB) site involved in the regulation of TRPC channel function. OBJECTIVES: To assess the basis of CaM/IP(3)Rs binding to the CIRB site of TRPC6 and its role in platelet physiology. METHODS: Protein association was detected by co-immunoprecipitation and Western blotting, Ca(2+) mobilization was measured by fluorimetric techniques and platelet function was analyzed by aggregometry. RESULTS: Co-immunoprecipitation of TRPC6 with CaM or the IP(3)Rs at different cytosolic free Ca(2+) concentrations ([Ca(2+)](c)) indicates that the association between these proteins is finely regulated by cytosolic Ca(2+) via association of CaM and displacement of the IP(3)Rs at high [Ca(2+)](c). Thrombin-stimulated association of TRPC6 with CaM or the IP(3)Rs was sensitive to 2-APB and partially inhibited by dimethyl BAPTA loading, thus suggesting that the association between these proteins occurs through both Ca(2+)-dependent and -independent mechanisms. Incorporation of an anti-TRPC6 C-terminal antibody, whose epitope overlaps the CIRB region, impaired the dynamics of the association of TRPC6 with CaM and the IP(3)Rs, which lead to both inhibition and enhancement of thrombin- and thapsigargin-evoked Ca(2+) entry in the presence of low or high, respectively, extracellular Ca(2+) concentrations, as well as altered thrombin-evoked platelet aggregation. CONCLUSIONS: Our results indicate that the CIRB site of TRPC6 plays an important functional role in platelets both modulating Ca(2+) entry and aggregation through its interaction with CaM and IP(3)Rs.

Homocysteine, intracellular signaling and thrombotic disorders.

Homocysteine, a sulphur-containing amino acid derived from methionine, has been presented as an independent risk factor for cardiovascular disorders, including atherosclerosis and thrombogenesis. The mechanisms underlying homocysteine-induced effects have been intensively investigated over the last two decades. Homocysteine can induce oxidative stress promoting oxidant injury to vascular and blood cells. Hyperhomocysteinemia often results in intracellular Ca2+ mobilization, endoplasmic reticulum (ER) stress, with the subsequent development of apoptotic events, chronic inflammation leading to endothelial dysfunction and remodeling of the extracellular matrix. Homocysteine has also been reported to induce modulation of gene expression through alteration of the methylation status. The effects of elevated concentrations of circulating homocysteine on the vascular wall, platelet function and coagulation factors promote the development of a pro-coagulant state. The pathophysiological significance of homocysteine in the development of vascular disorders through the induction of endothelial dysfunction and abnormal platelet activity and blood coagulation is discussed in this review.