Objective To determine the prevalence and risk factors of diabetic retinopathy in the inpatient diabetic population in the USA and to determine the barriers to ophthalmic examinations and treatment among this population. Research design and methods A cross-sectional analysis of 113 inpatients with diabetes mellitus admitted to an inner city community teaching hospital in Pittsburgh. Digital fundus photographs of the posterior pole were taken of each eye after pharmacological dilation. Presence, absence and severity of diabetic retinopathy and macular edema were graded on the basis of internationally accepted criteria. An investigator-administered questionnaire and review of the medical record were used to obtain data about patient demographics, clinical characteristics and barriers to ophthalmic care. The association between these data and the presence of diabetic retinopathy was tested. Results The estimated prevalence of diabetic retinopathy in the inpatient population was 44% (95% CI 34% to 53%). The prevalence of previously undiagnosed diabetic retinopathy and sight-threatening retinopathy was 25% (95% CI 17% to 33%) and 19% (95% CI 11% to 26%), respectively. Renal disease was independently associated with the presence of diabetic retinopathy (OR, 3.86; 95% CI 1.22 to 12.27), as well as a longer duration of diabetes (OR, 1.08 per year; 95% CI 1.014 to 1.147). Diabetic retinopathy was seen in 15 of 17 patients admitted with diabetic foot ulcers or osteomyelitis. Frequently reported barriers to ophthalmic examinations included lack of transportation and physical disability. Conclusions The prevalence of diabetic retinopathy and sight-threatening diabetic retinopathy in the inpatient population is likely significantly higher than in the general diabetic population in the USA. These patients have barriers to care that need to be addressed to make standard of care ophthalmic examinations and treatment possible in this population.

Background: Primordial germ cells (PGCs) are the embryonic precursors of the sperm and eggs. Environmental or genetic defects that alter PGC development can impair fertility or cause formation of germ cell tumors.

Purpose: To present a case of unusual corneal infection early in the course of peripheral ulcerative keratitis in a patient with severe vitamin A deficiency. Method: Single observational case report in urban USA. Case Presentation: An alcoholic patient with pancreatitis, chronic diarrhea, and vitamin A deficiency presented with a marginal corneal ulcer from which two bacteria of the family Micrococcaceae were cultured and identified by genome sequence analysis, namely Kocuria palustris and Rothia mucilaginosa. Soon after, severe bilateral peripheral ulcerative keratitis developed, later accompanied by eyelid cellulitis of one lid. These conditions improved with antibiotics, treatment of the underlying gastrointestinal conditions, and treatment of the vitamin deficiency. Conclusion: Susceptibility to keratitis with unusual bacteria of the Micrococcaceae family can occur in the setting of alcoholism-related gastrointestinal disease with severe vitamin A deficiency. To our knowledge, K. palustris is a species not previously identified in any human disease, and the Kocuria genus has not previously been reported as a participant in eye infection. Documented cases of R. mucilaginosa in ocular disease are rare. These unusual infections heralded the onset of severe marginal corneal melts.

Photoreceptor death and retinal gliosis underlie the majority of vision threatening retinal diseases including retinal detachment (RD). Although the underlying pathobiology of vision limiting processes in RD is not fully understood, inflammation is known to play a critical role. We conducted an iTRAQ proteomic screen of up- and down-regulated proteins in a murine model of RD to identify potential targetable candidates. Macrophage migration inhibitory factor (MIF) was identified and evaluated for neurotoxic and pro-gliotic effects during RD. Systemic administration of the MIF inhibitor ISO-1 significantly blocked photoreceptor apoptosis, outer nuclear layer (ONL) thinning, and retinal gliosis. ISO-1 and MIF knockout (MIFKO) had greater accumulation of Müller glia pERK expression in the detached retina, suggesting that Müller survival pathways might underlie the neuroprotective response. Our data show the feasibility of the MIF-inhibitor ISO-1 to block pathological damage responses in retinal detachment and provide a rationale to explore MIF inhibition as a potential therapeutic option for RD.

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