RESUMO
PURPOSE: Lacrimal gland ptosis has a prevalence of 10% to 15% in Caucasian patients, reaching up to 60% in older age. Its involuntary resection during blepharoplasty carries the potential risk of compromising corneal lubrication. The purpose of this systematic review is to check whether there is a consensus in the literature regarding the surgical procedure of choice and which outcomes and complications have been observed. METHODS: A systematic review was carried out following the Preferred Reporting Items for Systematic Reviews and Meta-Analyses guidelines. A search was carried out in the Medline, Scopus, and Cochrane databases in March 2022. RESULTS: A total of 16 studies involving 483 patients with lacrimal gland ptosis have been included. In 90.06% of patients, resuspension or direct refixation of the gland to the lacrimal fossa with suture to the orbital periosteum was performed. Follow up has been inconsistent, with an average of 18 months. Regarding complications, 5 recurrences and only 2 patients with persistent dry eye were observed. CONCLUSIONS: In general, the evidence is sparse. Nevertheless, repair of lacrimal gland ptosis is a relatively simple, reproducible, and safe surgical technique, with a low likelihood of recurrence, severe, or persistent complications. A classification is proposed for both the grading of ptosis and its treatment.
RESUMO
Although the basis of Alzheimer's disease (AD) etiology remains unknown, oxidative stress (OS) has been recognized as a prodromal factor associated to its progression. OS refers to an imbalance between oxidant and antioxidant systems, which usually consist in an overproduction of reactive oxygen species (ROS) and reactive nitrogen species (RNS) which overwhelms the intrinsic antioxidant defenses. Due to this increased production of ROS and RNS, several biological functions such as glucose metabolism or synaptic activity are impaired. In AD, growing evidence links the ROS-mediated damages with molecular targets including mitochondrial dynamics and function, protein quality control system, and autophagic pathways, affecting the proteostasis balance. In this scenario, OS should be considered as not only a major feature in the pathophysiology of AD but also a potential target to combat the progression of the disease. In this review, we will discuss the role of OS in mitochondrial dysfunction, protein quality control systems, and autophagy associated to AD and suggest innovative therapeutic strategies based on a better understanding of the role of OS and proteostasis.
