Data of real-world received from numerous studies show a real difficulty on the part of the patient with diabetes in maintaining tight control over the plasma glucose. Consequently, despite the diagnostic measures and treatments available today, the diabetic retinopathy (DR) remains the leading cause of blindness among adults of working age.
Leukocytes or white blood cells, the immune system's main defence, play an important role in the progression of diabetic retinopathy, and various studies have shown that DR is a disease of a predominantly inflammatory nature. In fact, inflammatory cytokines and chemokines are regulated in a complex manner in the vitreous body of DR patients and interact in a complex manner to influence disease progression.
Diabetic macular oedema (EMD), a condition that can develop at any stage of DR, is distinguished from the latter by an increased thickness or swelling of the macula due to fluid leaking from retinal vessels damaged by diabetic disease. The onset of EMD is determined by various factors including hyperglycaemia, hypoxia, inflammation and vascular permeability.
The inflammatory processes, which take place during the onset of DR in the retina and choroid, are both acute and chronic. I acute phase factors are regulated in response to inflammation, these include C-reactive protein (CRP), ferritin, serum amyloid A, procalcitonin and fibrinogen. Furthermore, acute phase factors are involved in the microvascular dysfunction associated with type 2 diabetes mellitus. Indeed, it is known that ferritin is overexpressed in response to stress such as hypoxia and during activation of the immune response, while serum amyloid A and interleukin-6 concentrations in the vitreous body have, to date, only been found in patients with proliferative diabetic retinopathy.
A recent retrospective study measured the levels of these acute phase factors in the vitreous body taken during the vitreoretinal surgery of EMD patients. In addition, the study examined the relationships between the concentrations of these factors and visual acuity or central retinal thickness (CRT) of the oedema measured by optical coherence tomography (OCT). Levels of serum amyloid P, procalcitonin, ferritin and fibrinogen in the vitreous humour were significantly higher in patients with EMD than in study control subjects. Furthermore, procalcitonin and fibrinogen levels in EMD patients were inversely correlated with visual acuity, both before and 3 months after vitrectomy. In contrast, concentrations of these factors were not significantly correlated with CRT values or vascular endothelial growth factor (VEGF) levels.
These results indicate that the acute phase factors contribute to the pathogenesis and progression of EMDas well as its resolution in response to therapy and suggest that they may influence the inflammatory state or tissue damage associated with EMD. Furthermore, the study suggests that increased procalcitonin and fibrinogen concentrations in the vitreous body may have a detrimental effect on retinal function and their removal during vitrectomy could contribute to the recovery of visual acuity in patients with EMD. Therefore, these factors could act as genuine prognostic markers.
Clearly, further studies are needed to better elucidate the complex nature of diabetes-related retinal disease, but these data point to the fact that optimal therapy for EMD patients should be able to address and resolve the inflammatory process that sets in during the progression of DR, thus emphasising the need for therapies that are anti-inflammatory in nature.
Bibliography
Kimura K et al. Jpn J Ophthalmol. 2017 Jul 28.
Dr. Carmelo Chines
Direttore responsabile
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