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生长期脱发作为头皮重建组织扩张器并发症的病例报告。

Telogen Effluvium as a complication of scalp reconstruction with tissue expander: a case report.

机构信息

Plastic Surgery and Burn Unit; Ospedale Maggiore di Parma.

Plastic surgery Unit, Policlinico di Modena.

出版信息

Acta Biomed. 2021 Oct 27;92(S1):e2021431. doi: 10.23750/abm.v92iS1.12066.

DOI:10.23750/abm.v92iS1.12066
PMID:34747392
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC10523059/
Abstract

BACKGROUND AND AIM

The treatment of burn alopecia is still considered a challenging task for plastic surgeons. Tissue expansion has been extensively described as a useful technique used in order allow the reconstruction of large scalp defects with reliable hair-bearing tissue, enhancing the final aesthetic outcome.

CASE REPORT

We present the case of a 43-tear-old woman affected by scarring burn alopecia of left parietal area, treated with staged tissue expansion and local flap reconstruction. Despite the complete flap survival, a reversible acute hair loss 12 days after surgery, ascribable as Telogen Effluvium (TE), was reported.

CONCLUSIONS

TE is a rare and self-limiting condition potentially related with any kind surgery or stressful events. Plastic surgeons should be aware of this condition, particularly when performing scalp reconstruction, as it can be misled with other local complications. Clinical diagnosis is of paramount importance to avoid useless or even harmful treatments: reassuring the patient remains the most effective therapeutic pathway.

摘要

背景与目的

烧伤后脱发的治疗仍然是整形外科医生面临的一项挑战。组织扩张已被广泛描述为一种有用的技术,用于用可靠的带毛发组织来重建大面积头皮缺损,从而提高最终的美学效果。

病例报告

我们报告了一例 43 岁女性的病例,该女性患有左顶区瘢痕性烧伤脱发,采用分期组织扩张和局部皮瓣重建进行治疗。尽管完全皮瓣存活,但术后 12 天报告了一种可逆转的急性脱发,即休止期脱发(TE)。

结论

TE 是一种罕见的自限性疾病,可能与任何类型的手术或应激事件有关。整形外科医生应该意识到这种情况,特别是在进行头皮重建时,因为它可能会与其他局部并发症混淆。临床诊断至关重要,以避免不必要甚至有害的治疗:向患者提供安慰仍然是最有效的治疗途径。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4d28/10523059/679e00445531/ACTA-92-431-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4d28/10523059/11341171582a/ACTA-92-431-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4d28/10523059/73db40b170f8/ACTA-92-431-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4d28/10523059/cc90bd1399b6/ACTA-92-431-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4d28/10523059/679e00445531/ACTA-92-431-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4d28/10523059/11341171582a/ACTA-92-431-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4d28/10523059/73db40b170f8/ACTA-92-431-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4d28/10523059/cc90bd1399b6/ACTA-92-431-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4d28/10523059/679e00445531/ACTA-92-431-g004.jpg

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Regulation of the ER stress response by a mitochondrial microprotein.线粒体微小蛋白对 ER 应激反应的调控。
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