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Introduction: Diabetic macular edema (DME) is an important cause of vision loss. England has a national systematic photographic retinal screening programme to identify patients with diabetic eye disease. Grading retinal photographs according to this national protocol identifies surrogate markers for DME. We audited a care pathway using a spectraldomain optical coherence tomography (SDOCT) clinic to identify macular pathology in this subset of patients. Methods: A prospective audit was performed of patients referred from screening with mild to moderate non-proliferative diabetic retinopathy (R1) and surrogate markers for diabetic macular edema (M1) attending an SDOCT clinic. The SDOCT images were graded by an ophthalmologist as SDOCT positive, borderline or negative. SDOCT positive patients were referred to the medical retina clinic. SDOCT negative and borderline patients were further reviewed in the SDOCT clinic in 6 months. Results: From a registered screening population of 17 551 patients with diabetes mellitus, 311 patients met the inclusion criteria between (March 2008 and September 2009). We analyzed images from 311 patients' SDOCT clinic episodes. There were 131 SDOCT negative and 12 borderline patients booked for revisit in the OCT clinic. Twenty-four were referred back to photographic screening for a variety of reasons. A total of 144 were referred to ophthalmology with OCT evidence of definite macular pathology requiring review by an ophthalmologist. Discussion: This analysis shows that patients with diabetes, mild to moderate non-proliferative diabetic retinopathy (R1) and evidence of diabetic maculopathy on non-stereoscopic retinal photographs (M1) have a 42.1% chance of having no macular edema on SDOCT imaging as defined by standard OCT definitions of DME when graded by a retinal specialist. SDOCT imaging is a useful adjunct to colour fundus photography in screening for referable diabetic maculopathy in our screening population. [ABSTRACT FROM AUTHOR]

Maternally inherited diabetes with deafness is rare diabetes caused by a mitochondrial DNA defect. 85% of cases are associated with m.3243A > G mutation. It is important to diagnose this form of diabetes because of the unique management issues and associated comorbidities. A very strong family history of diabetes, deafness and presence of retinal dystrophy should prompt an investigation for MIDD. Microvascular complications out of keeping with duration of diabetes are another clue to the diagnosis. Retinal and renal manifestations of mitochondrial disease may be confused for diabetic complications. Glutamic acid decarboxylase (GAD) autoantibody negativity in a nonobese diabetic is another clue. Cardiac conduction defects and GDM may also raise suspicion as to the diagnosis. Recognizing this etiology of DM should promote family screening, genetic counseling, screening of associated comorbidities, avoidance of metformin, and cautious use of statins. We report a 77 years old lady with MIDD who was being followed up as insulin requiring type 2 diabetes. We then identified 5 more patients with MIDD in the same clinic. They all had A3243 mutation with characteristic clinical presentation. The pharmacological approaches discussed in the paper are unlikely to work in these patients as they were diagnosed late. [ABSTRACT FROM AUTHOR]