Efficacy of Ear Molding in Infants using the EarWell Infant Correction System and Factors Affecting Outcome.

BACKGROUND: One-third of infants have ear anomalies, and less than one-third self-correct. Correction of ear deformities by molding exploits the plasticity of the auricular cartilage because of circulating maternal estrogen during infancy. In this study, the authors assess the efficacy of the EarWell Infant Correction System in the correction of ear deformities and determine the factors that affect its outcome. METHODS: The authors conducted a single-center prospective study over a 3-year period. Consecutive full-term infants who underwent ear molding with the EarWell system were recruited. Primary outcome was successful correction of ear anomaly. Secondary outcomes included complications and maintenance of ear shape. Factors identified included type of anomaly, age at application, duration of application, and breastfeeding. RESULTS: Sixty-seven patients with a total of 105 ears were recruited. The anomalies were classified into deformations (66.7 percent) and malformations (33.3 percent). The median age group at presentation was 0 to 7 days (67 percent). Average duration of application was 4.1 weeks. Successful correction was achieved in 86 percent of patients. Ear deformations achieved a significantly higher rate of successful outcome (98 percent) compared with malformations (64 percent) (p < 0.001). Skin complications were common (46 percent) and attributed to our tropical climate. Patients with complications were of a higher mean age (22.1 days) compared with patients with no complications (10.6 days) (p = 0.037). CONCLUSIONS: The EarWell system is an effective nonsurgical option for the treatment of ear anomalies. The type of anomaly was the only predictor of successful correction, whereas age at application, duration of molding, and breastfeeding were not. Complications were more common in older infants. CLINICAL QUESTION/LEVEL OF EVIDENCE: Therapeutic, IV.

Thrombospondin-4 reduces binding affinity of [(3)H]-gabapentin to calcium-channel α2δ-1-subunit but does not interact with α2δ-1 on the cell-surface when co-expressed.

The α2δ proteins are auxiliary subunits of voltage-gated calcium channels, and influence their trafficking and biophysical properties. The α2δ ligand gabapentin interacts with α2δ-1, and inhibits calcium channel trafficking. However, α2-1 has also been proposed to play a synaptogenic role, independent of calcium channel function. In this regard, α2δ-1 was identified as a ligand of thrombospondins, with the interaction involving the thrombospondin synaptogenic domain and the α2δ-1 von-Willebrand-factor domain. Co-immunoprecipitation between α2δ-1 and the synaptogenic domain of thrombospondin-2 was prevented by gabapentin. We therefore examined whether interaction of thrombospondin with α2δ-1 might reciprocally influence (3)H-gabapentin binding. We concentrated on thrombospondin-4, because, like α2δ-1, it is upregulated in neuropathic pain models. We found that in membranes from cells co-transfected with α2δ-1 and thrombospondin-4, there was a Mg(2+) -dependent reduction in affinity of (3)H-gabapentin binding to α2δ-1. This effect was lost for α2δ-1 with mutations in the von-Willebrand-factor-A domain. However, the effect on (3)H-gabapentin binding was not reproduced by the synaptogenic EGF-domain of thrombospondin-4. Partial co-immunoprecipitation could be demonstrated between thrombospondin-4 and α2δ-1 when co-transfected, but there was no co-immunoprecipitation with thrombospondin-4-EGF domain. Furthermore, we could not detect any association between these two proteins on the cell-surface, indicating the demonstrated interaction occurs intracellularly.