notes by dr Claudio Italiano
The prospective controlled studies have shown with certainty that chronic
hyperglycemia is the necessary condition for the development of diabetic
microangiopathy, even if in determining it, genetic factors contribute. The
hyperglycemia toxicity is mainly due to the glycation processes and subsequent
oxidation of various protein molecules (basal membranes, circulating proteins,
etc.) which undergo irreversible denaturation processes.
The glucose itself gives rise to oxidative phenomena with the formation of free
radicals. Activation of the polyol pathway is also oxidative stress. An
important mechanism of glucotoxicity has been recognized in the activation of
protein-kinase C.
So what if I'm diabetic?
Certainly I must implement a good metabolic control, which is the basis for the
prevention of microangiopathy.
The most important clinical forms of diabetic microangiopathy are:
Retinopathy
Nephropathy
Neuropathy
Tissue damage, however, affects all tissues (skin and myocardium in particular)
Diabetic retinopathy is the most prevalent and potentially serious complication
of the diabetic patient, especially if suffering from type 1 diabetes mellitus,
as according to studies by Wisconsin, in 71% of cases it is present in such
patients; vice versa in the subject with diabetes mellitus type 2 is present in
39% of cases, in Italy, fortunately, unlike the US, the percentage is between 46
and 58% for type 1 diabetes and for 14-35 % in type 2 diabetes.
Retinopathy is the consequence of three fundamental alterations of the retinal
capillaries:
- Capillary exclusions
- Wall waterproofing
-Proliferation of newly formed vessels
We distinguish different degrees of retinal damage that are at the base of the
classification:
- basic retinopathy or background
- preproliferant
- proliferative
The background form is characterized by microaneurysms, haemorrhages and hard
exudates and cottony; hard exudates are due to extravasation of plasma proteins
and especially lipoproteins.
Fortunately, they are not stable lesions, in the sense that microaneurysms can
regress. Hemorrhages have a point-like or flame-like appearance. The cottony
exudates are an expression of the accumulation of an axoplasmic material at the
border of a microvascular infarct.
When the lesions compromise the retina, then we talk about the maculopathy that
underlies the serious reductions in the visus. Preproliferative retinopathy is
characterized by ischemic areas caused by multiple capillary occlusions.
Retinal hypoxia underlies local release of endothelial growth factors. The
result is a revascularization process called "proliferating retinopathy". The
haemorrhages are followed by the development of fibrous branches that can also
cause detachment of the retina with permanent loss of the visus.
Still other complications are the rubeosis of the iris when the proliferation of
the vessels reaches the anterior segment of the eye.
Makes use of :
- good diabetes therapy with particular attention to the control of glycated or
HBA1C values which must tend, according to the modern guidelines to be <6.5%;
- control of arterial hypertension
- laser photoglulation that reduces the incidence of blindness from
proliferating retinopathy by 50%
- in cases of repeated vitreous hemorrhage there is cloudiness of the vitreous
and retinal detachment and it is necessary to resort to vitrectomy.
Hence the need for a screening program on the entire population of diabetics;
patients, that is, must be controlled starting from the diagnosis of diabetes
with a direct ophthalmoscopic examination and, if there are evolutionary lesions,
they must undergo retinal fluorangiography, an examination obtained by coloring
the retinal vessels with an injected intravenous dye and studying the end
retinal circulation under the microscope. Controls are scheduled at 6 months in
case of serious complications and at 12 months if there are none, as routine
screening.
Finally we remember that diabetes is responsible for cataracts, glaucoma and
ophthalmoplegia, ie the paralysis of the eyeball due to neuropathic suffering.