This issue of the Asia-Pacific Journal of Ophthalmology includes the expert panel consensus guidelines for the management of diabetic macular edema (DME) in Asians.1 The guidelines describe various aspects of the therapy of DME like the need for classification of patients before treatment, the first-line treatment by anti-vascular endothelial growth factor (anti-VEGF) antibodies or steroids, and as an alternative for extrafoveal DME the focal application of a retinal laser coagulation. Pars plana vitrectomy with membrane peeling with or without adjunctive intravitreal steroid treatment is recommended for patients with tractional DME. These purely ophthalmological procedures may be supplemented by general measures, in particular such as alerting the patient of his/her own responsibility to improve his/her condition, according to the saying that a patient with DME can help him/herself more than all doctors together can do. It implies a loss of weight in the case of overweight or obesity, a better metabolic control (ie, a lowering of the HbA1c level), and more physical activity.2–5 Since patients with DME are afraid of getting blind, the ophthalmologist as compared to the long-term diabetologist may have a higher influence on the patients to change their lifestyle.
Another nonophthalmological aspect in the therapy of DME is to lower an elevated arterial blood pressure, since it belongs to the risk factors for the incidence and progression of diabetic retinopathy.2–5 The reason for the association between an increased arterial blood pressure and DME may be that an increased blood pressure leads to an increased cerebrospinal fluid pressure which in turn is associated with an elevated retinal vein pressure and presumably higher retinal capillary pressure.6,7 If the capillary vessel wall is damaged by the diabetic microangiopathic process, a higher capillary blood pressure will lead to a higher volume of fluid leaking into the macular retinal tissue.
In the discussion of anti-VEGF drugs and steroids, some additional aspects may be taken into account. The so-called anti-VEGF drugs are highly specific, whereas steroids suppress a whole panoply of cytokines and growth factors including VEGF. Steroids may therefore be called “nonspecific anti-VEGF drugs.” Interestingly, diabetic retinopathy is characterized by an increase in many cytokines and growth factors, with VEGF being only one of them.8 Although the specific anti-VEGF drugs address only VEGF, the steroids have an effect on many of the cytokines and growth factors involved in diabetic retinopathy including DME.
As also mentioned in the article, DME is characterized by inflammatory components, including an activation of retinal microglial cells.9 These microglial cells are the immune-competent cells of the central nervous system and thus of the retina, and as the “gardener of the system” they are involved in any process of degeneration, apoptosis, and preservation. Intravitreal steroids (triamcinolone) have been shown to reduce the activity of retinal microglial cells.10 With specific anti-VEGF drugs having no direct influence on the microglial cells, the wide-spread effect of steroids on many components of the inflammatory process may be a reason to consider the intravitreal use of steroids in pseudophakic nonglaucomatous eyes of elderly diabetic patients. The probability of a steroid-induced ocular hypertension with the risk of an incident secondary open-angle glaucoma increases with younger age (and the presence of glaucoma). Another aspect to be potentially considered is the relatively long duration of effects (and side-effects) of high-dose steroids applied intravitreally.
In conclusion, the guidelines for the therapy of DME in Asians are highly welcome to describe the up-to-date best therapeutic procedures in dependence of the clinical situation. The guidelines have also taken into account the decrease in the importance of retinal laser coagulation, which as a destructive procedure is associated with an irreversible morphological damage in the retina. From a psychophysical aspect, the retinal laser coagulation can lead to a constriction of the peripheral visual field (if the laser therapy is applied in a panretinal manner), or to paracentral scotomas if the therapy applied in the pericentral region. Paracentral scotomas, in particular if located in the horizontal line passing through the fovea, can, even in the presence of perfect central visual acuity, be associated with marked problems in reading, since the scotomas make it difficult to follow the line or to find the next line. Taking into account that obese and arterially hypertensive patients with type 2 diabetes may have the chance to markedly improve their general diabetic condition, one may consider delaying the decision of an irreversible laser therapy by choosing the intravitreal medical therapy so as to buy some extra time and a chance to improve diabetic retinopathy and DME through simply becoming healthier.
1. Chhablani J, Wong K, Tan GS, et al. Diabetic macular edema management in Asian population: expert panel consensus guidelines. Asia Pac J Ophthalmol (Phila)
2. Cheung N, Mitchell P, Wong TY. Diabetic retinopathy. Lancet
3. Tan GS, Cheung N, Simó R, Cheung GC, Wong TY. Diabetic macular oedema. Lancet Diabetes Endocrinol
4. Chua J, Lim CXY, Wong TY, Sabanayagam C. Diabetic retinopathy in the Asia-Pacific. Asia Pac J Ophthalmol (Phila)
5. Sabanayagam C, Banu R, Chee ML, et al. Incidence and progression of diabetic retinopathy: a systematic review. Lancet Diabetes Endocrinol
6. Jonas JB, Wang N, Xu J, et al. Diabetic retinopathy and estimated cerebrospinal fluid pressure. The Beijing Eye Study 2011. PLoS One
7. Jonas JB, Nangia V, Khare A, et al. Prevalence and associated factors of diabetic retinopathy in rural central India. Diabetes Care
8. Jonas JB, Jonas RA, Neumaier M, Findeisen P. Cytokine concentration in aqueous humour of eyes with diabetic macular edema. Retina
9. Zeng HY, Green WR, Tso MO. Microglial activation in human diabetic retinopathy. Arch Ophthalmol
10. Wang J, Chen S, Zhang X, Huang W, Jonas JB. Intravitreal triamcinolone acetonide, retinal microglia and retinal ganglion cell apoptosis in the optic nerve crush model. Acta Ophthalmol