Objective:To investigate the potential of 8-iso-prostaglandin F2α (8-iso-PGF2α) as a biomarker for disease activity and oxidative stress in the CSF of patients with multiple sclerosis (MS).Methods:The isoprostane 8-iso-PGF2α is an established biomarker for in vivo oxidative stress and lipid peroxidation. We measured CSF 8-isoPGF2α levels in 231 patients with MS (74 with relapsing-remitting MS, 67 with primary progressive MS, and 90 with secondary progressive MS [SPMS]) and 40 controls using a competition ELISA.Results:We found increased CSF levels of 8-iso-PGF2α in patients with MS compared to controls, with the most striking values in a subgroup of patients with SPMS. Furthermore, the increase in 8-iso-PGF2α correlated with other parameters of lipid peroxidation as well as with a decrease in the total antioxidant status in the MS CSF samples.Conclusions:Our study demonstrates that CSF levels of 8-iso-PGF2α may serve as a biomarker of oxidative stress in MS. Further investigation will help establish the pathologic and clinical significance of our preliminary findings.

Purpose: This work assesses bilateral ganglion cell layer–inner plexiform layer (GCL-IPL) thickness changes in patients with unilateral neovascular age-related macular degeneration (nAMD) treated with antivascular endothelial growth factor (anti-VEGF). Methods: In this single-center, retrospective, cohort study, the medical records of patients with unilateral nAMD treated with anti-VEGF were reviewed. The treated group included eyes with newly diagnosed nAMD that subsequently underwent treatment with intravitreal anti-VEGF injections. The control group was the fellow eye with dry AMD. Eyes receiving at least 10 intravitreal injections were included. Measurement of GCL-IPL thickness was performed at different time points using spectral domain–optical coherence tomography. Results: A total of 216 eyes of 108 patients met the inclusion criteria. The mean age ± SD was 80.1 ± 10.7 years. Eyes in the treated group underwent a mean ± SD of 20.2 ± 7.2 injections in 21.3 ± 6.8 months. At baseline, average mean ± SD of GCL-IPL thickness was 73.71 ± 8.81 µm and 73.84 ± 8.26 µm in the treated and fellow eye, respectively ( P = .795). After 10 injections the average thickness was 65.41 ± 14.08 µm and 68.77 ± 13.24 µm in the treated and fellow eye, respectively ( P = .007). The absolute decrease in thickness was significantly greater in the treated eye than the fellow eye (mean ± SD, 8.31 ± 11.19 µm vs 5.07 ± 10.83 µm, respectively; P = .002). Conclusions: GCL-IPL thickness decreased significantly in the treated group more than in the control group after 10 anti-VEGF injections. The mechanism and clinical significance of this observation warrants further study.

Case Reports inflammation in the surrounding rim of compressed tissues (the "pseudocapsule"). One of the 4 (Case 4) had marked cystic and hyaline degeneration in a very longstanding tumor, this case also having cholesterol clefts that probably arose from degenerate tissues; Perls' staining did not show any evidence of iron deposits from prior hemorrhage. The characteristic, but nonspecific, histological feature of sarcoid-like inflammation is the formation of noncaseating granulomas, sometimes with asteroid bodies (as case 1) or Schaumann bodies within giant cells, and often a relative lack of intervening lymphocytic infiltrate. 3 However, investigations for systemic sarcoidosis were negative in all our patients at the time of orbital disease, and no organisms were shown in any of the lacrimal gland tissues.Dacryoadenitis alongside pleomorphic adenomas appears to be rare, being reported in <2% of the Moorfields' patients with LGPA, and the cause for such an inflammation is uncertain: it remains highly unlikely to be due to a chance coincidence of 2 rare diseases (LGPA and dacryoadenitis). Conjecturally, the chronic lymphocytic inflammation (especially with granuloma formation) might suggest a giant-cell reaction to leakage from disrupted lacrimal gland ductules-especially given the proximity of the granulomata to the ductules in 1 of our patients (case 2).Two cases of chronic nongranulomatous sialadenitis alongside salivary pleomorphic adenomas have been reported, the authors suggesting that chronic sialadenitis may result in progressive sialectasis (with stasis and acinar destruction), and that this inflammation later leads to development of neoplasia. 4,5 A recent histological study of 40 major and minor salivary glands identified areas of inflammation in the peritumoral area, pseudocapsule, and in the connective tissue stroma in 95% of the examined specimens. 6 Several cases of a focal foreign-body-like reaction around the pseudocapsule of parotid gland adenomas, and 1 case of cholesterol clefting, have also been described although it was unclear whether these occurred as a result of diagnostic procedures (such as fine needle aspiration biopsy) or extravasation of the cellular products. 7,8 Cholesterol clefts have also been described rarely with salivary adenomas that have not undergone prior biopsy. 9,10 There would appear to be only a single case-report of parotid adenoma and sarcoid-like sialadenitis.