Tear osmolarity can now be considered a test suitable to be performed in a clinical setting. It showed a good performance in dry eye diagnosis, higher than the other tests considered, mainly in severe dry eye. Tear osmolarity values should be interpreted as an indicator of DED evolutionary process to severity.

Purpose: To analyze tear protein variations in patients suffering from dry eye symptoms in the presence of tear film instability but without epithelial defects. Methods: Five microlitres of non-stimulated tears from 60 patients, suffering from evaporative dry eye (EDE) with a break-up time (BUT) o10 s, and from 30 healthy subjects as control (no symptoms, BUT 410 s) were collected. Tear proteins were separated by mono and bi-dimensional SDS-PAGE electrophoresis and characterized by immunoblotting and enzymatic digestion. Digested peptides were analyzed by liquid chromatography coupled to electrospray ionization quadrupole-time of flight mass spectrometry followed by comparative data analysis into Swiss-Prot human protein database using Mascot. Statistical analysis were performed by applying a t-test for independent data and a MannWhitney test for unpaired data (Po0.05). Results: In EDE patients vs controls, a significant decrease in levels of lactoferrin (data in % ± SD): 20.15 ± 2.64 vs 24.56 ± 3.46 (P ¼ 0.001), lipocalin-1: 14.98±2.70 vs 17.73±2.96 (P ¼ 0.0001), and lipophilin A-C: 2.89±1.06 vs 3.63±1.37 (P ¼ 0.006) was revealed, while a significant increase was observed for serum albumin: 9.45 ± 1.87 vs 3.46 ± 1.87 (P ¼ 0.0001). No changes for lysozyme and zinc a-2 glycoprotein (P ¼ 0.07 and 0.7, respectively) were shown. Proteomic analysis showed a downregulation of lipophilin A and C and lipocalin-1 in patients, which is suggested to be associated with post-translational modifications. Conclusions: Data show that tear protein changes anticipate the onset of more extensive clinical signs in early stage dry eye disease.

Neurotrophic keratitis (NK) is a degenerative corneal disease caused by damage of trigeminal corneal innervation, which leads to spontaneous epithelial breakdown and corneal ulceration. The impairment of corneal sensory innervation causes the reduction of both protective reflexes and trophic neuromodulators that are essential for the vitality, metabolism, and wound healing of ocular surface tissues. A wide range of ocular and systemic conditions, including herpetic keratitis, ocular chemical burns, corneal surgery, diabetes, multiple sclerosis, and neurosurgical procedures, can cause NK by damaging trigeminal innervation. Diagnosis of NK requires careful investigation of any ocular and systemic condition associated with the disease, complete ocular surface examination, and quantitative measurement of corneal sensitivity. The clinical stages of NK range from corneal epithelial alterations (stage 1) to persistent epithelial defect (stage 2) and ulcer (stage 3), which may progress to corneal perforation. Management of NK is based on clinical severity, and the aim of the therapy is to halt the progression of corneal damage and promote epithelial healing. Although several medical and surgical treatments have been proposed, no therapies are currently available to restore corneal sensitivity, and thus, NK remains difficult and challenging to treat. The purpose of this review is to summarize available evidence on the pathogenesis, diagnosis, and treatment of NK. Novel medical and surgical therapies including the topical administration of nerve growth factor and corneal neurotization are also described.

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These data indicate significant alterations of subfoveal choroidal hemodynamic in RP and suggest a link between the alteration of ChBF and the RP-associated central cone-mediated dysfunction as assessed by the FERG.