PURPOSE: We report three patients with large angle exotropia had lost medial rectus muscle (MR) and who attained good alignment postoperatively. METHODS: Patient 1 was a 51-year-old female with a history of strabismus surgery done at 10 years of age. Exotropia of 80 prism diopter (PD) gradually developed with limitation of adduction in the right eye. Patient 2 was a 52-year-old male with fixed exotropia of 95 PD in his left eye, which became blind after a severe contusion injury. The third patient was a 46-year-old male who had MR of the right eye cut during endoscopic sinus surgery. Severe limitation of adduction followed with exotropia of 50 PD. We could not find MR in any of the three patients and noted severe adhesion between eyeball and Tenon's capsule. Ocular movement was severely limited horizontally and even vertically. RESULTS: Postoperatively Patient 1 showed orthophoria in follow-up of 2 years. Patient 2 had 16PD of exotropia in follow-up of 13 months, which was cosmetically acceptable. Patient 3 obtained orthophoria after surgery and developed 10 degrees of left head turning to avoid diplopia. CONCLUSIONS: When a patient shows longstanding large angle exotropia with limitation of adduction, we may consider the MR loss. A reasonable treatment may be to align the eyes cosmetically in primary position by weakening the abducting power and suturing the anterior part of nasal Tenon's capsule to the MR insertion site after adhesiolysis.
Contusions ; Diplopia ; Exotropia* ; Female ; Follow-Up Studies ; Head ; Humans ; Male ; Middle Aged ; Strabismus ; Tenon Capsule

Treatment options for patients with chronic kidney disease (CKD) are currently limited; therefore, there has been significant interest in applying mesenchymal stem/stromal cell (MSC)-based therapy to treat CKD. However, MSCs harvested from CKD patients tend to show diminished viability and proliferation due to sustained exposure to uremic toxins in the CKD environment, which limits their utility for cell therapy. The application of melatonin has been demonstrated to improve the therapeutic efficacy of MSCs derived from and engrafted to tissues in patients suffering from CKD, although the underlying biological mechanism has not been elucidated. In this study, we observed overexpression of hexokinase-2 (HK2) in serum samples of CKD patients and MSCs harvested from an adenine-fed CKD mouse model (CKD-mMSCs). HK2 upregulation led to increased production levels of methylglyoxal (MG), a toxic metabolic intermediate of abnormal glycolytic processes. The overabundance of HK2 and MG was associated with impaired mitochondrial function and low cell proliferation in CKD-mMSCs. Melatonin treatment inhibited the increases in HK2 and MG levels, and further improved mitochondrial function, glycolytic metabolism, and cell proliferation. Our findings suggest that identifying and characterizing metabolic regulators such as HK2 in CKD may improve the efficacy of MSCs for treating CKD and other kidney disorders.