How to preserve vision in diabetes
Diabetes mellitus and diabetic retinopathy
Alexey Yerdyakov, Post-science
Diabetes mellitus is currently an urgent disease, since a large number of people suffer from it – about four hundred million, and this is from 1 to 8% of the population. One of the serious complications of diabetes mellitus is diabetic retinopathy – retinal pathology. Visual impairment develops against the background of progressive diabetes mellitus. Such complications develop in a large number of patients. Up to 50% of patients with diabetes mellitus have diabetic retinopathy as a complication.
Classically, there are two types of diabetes mellitus: type I diabetes mellitus, or insulin-dependent diabetes mellitus, and type II diabetes mellitus, or insulin-independent diabetes mellitus. Type I diabetes mellitus is usually congenital and is associated with the fact that our pancreas stops producing insulin due to autoimmune damage. That is, the cells of the pancreas, beta cells of the islets of Langerhans, are destroyed and do not produce insulin. Since there is little or no insulin in the body, the concentration of glucose in the blood increases extremely, and thus diabetes mellitus is realized.
The root cause of type 2 diabetes mellitus is not the pathology of the pancreas, although over time, pathology from the pancreas can also join. The root cause is insulin resistance of body tissues. That is, insulin is present in a normal amount in the systemic bloodstream, but it cannot realize its effect on the cells of our body. And insulin, when it sits on its receptors located on the cells, causes them to absorb glucose from the systemic bloodstream. Since insulin cannot affect cells for some reason, these may be mutations of receptors, for example, some genetically determined ones to insulin, the concentration of glucose in the bloodstream increases.
Therefore, the root causes of the two types of diabetes are different, but lead to the same consequences – an extreme increase in the concentration of glucose in the blood. Diabetes mellitus of the first type can be compensated by using hormone replacement therapy. Such patients receive insulin injections to balance the intake of glucose and its consumption by tissues.
The main traumatic factor in diabetes mellitus is precisely an increase in the concentration of glucose in the blood. Glucose begins to modify everything that comes in its way purely chemically – glycation processes are realized. The same applies to the vessels that supply blood to the eye, and the vessels that supply blood to the retina. Due to the fact that microvessels are glycated (and the retina is a rather delicate organ, the vessels there are small in size and diameter), their glycation occurs, microangiopathy develops. That is, the violation concerns the blood supply to the retina.
As a result of the development of microangiopathy, capillaries that supply blood to the retina become clogged, and oxygen starvation of the retina will develop over time. But nutrients, too, in sufficient quantities will not come to her. Against the background of oxygen starvation, the retina will begin to produce various factors that would stimulate the processes of neoangiogenesis, that is, the growth of new vessels. In principle, this is a normal reaction of any tissue. If there is not enough oxygen, then over time this tissue will want new vessels to germinate there and ensure the delivery of oxygen and nutrients. Therefore, one of the key factors in the pathogenesis of diabetic retinopathy is vascular endothelial growth factor (VEGF). It is produced by the retina and stimulates the processes of neoangiogenesis.
Diabetic retinopathy can be divided into two stages: non-proliferative and proliferative. The non-proliferative stage is realized until the active processes of formation of new vessels, the processes of neoangiogenesis have begun. The proliferative stage begins when new vessels germinate in large quantities into the retina just under the action of vascular endothelial growth factor.
When it comes to the proliferative stage and the effect of vascular endothelial growth factor, which stimulates the growth of these new vessels, it turns out that the new vessels are imperfect. They have weak walls, and as a result, against the background of partial blockage of some vessels, against the background of the constant traumatic effect of glucose due to the high concentration of glucose in the bloodstream, vascular walls rupture, hemorrhages occur. Hemorrhages may first be under the retina, inside it, above it, but the blood does not enter the vitreous body. And then the blood can massively pour into the vitreous body. Then hemophthalmos will develop – the presence of blood in the vitreous body. And if such hemorrhages are massive and abundant enough, then by themselves they will largely interfere with visual perception purely mechanically, because light will not fall on the retina. In such extreme cases, vitreous removal is resorted to – vitrectomy. The vitreous body is completely removed, because there are no other ways to deal with it.
The permeability of the vessel walls is significantly impaired against the background of all kinds of traumatic processes. The permeability of the hematophthalmic barrier, in particular the hematoretinal barrier, is impaired. This means that the retina becomes vulnerable to the body's own immune cells. And you and I remember that there are autoantigens in the retina, for which specific autoantibodies circulate in the systemic bloodstream. They normally do not fall under the retina, because there is a hematophthalmic barrier. And as soon as it is violated, an autoimmune reaction is realized. Therefore, with diabetic retinopathy, an autoimmune component is also possible, when our own body will attack the cells of our retina. And this is an additional traumatic factor.
Ultimately, diabetic retinopathy can be corrected in various ways. I told about vitrectomy – removal of the vitreous body. There are approaches from pharmacotherapy, the use of various drugs. These may be drugs that bind vascular endothelial growth factor, as a result, it will not contribute to the transition to the stage of proliferative diabetic retinopathy from non-proliferative, that is, it is preventive therapy, preventive. Or it will not contribute to the further progression of neoangiogenesis, depending on at what stage this drug was prescribed.
In some cases, it is necessary to resort to cauterization of vessels that are imperfectly formed and from which bleeding is carried out. These are already surgical methods: laser photocoagulation, when retinal vessels are cauterized, and as a result they no longer bleed. But even with this measure, it is impossible to completely cure a person, because diabetic retinopathy is a disease that develops against the background of diabetes mellitus. This is a complex problem.
If we look at the primary factors of pathogenesis, we need to focus the patient's attention on proper and balanced nutrition and adequate insulin therapy. If you keep the glucose concentration in the systemic bloodstream at normal intervals for as long as possible, eat right, follow a diet and use prescribed medications correctly, then it will be possible to delay the appearance of various manifestations of diabetes mellitus, including diabetic retinopathy, for as long as possible.
About the author:
Alexey Yerdyakov – Candidate of Biological Sciences, Lomonosov Moscow State University, Faculty of Fundamental Medicine.
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