الفهرس 
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Abstract
Diabetic retinopathy is one of the leading causes of
blindness worldwide. It has long been considered as a
microvascular disease but recent animal and human studies
have demonstrated that neurodegeneration precedes the
microvascular changes.
Several factors have been reported to contribute to the
neurodegenerative process in diabetic patients. The major
contributor reported in the past few decades was
hyperglycemia. Recent studies implemented to assess the
pathophysiology of diabetic neurodegeneration in the retina
have shown that other factors contribute to this
neurodegenerative process. These include glutamate
excitotoxicity, hyperhomocysteinemia, RAS
overexpression and finally dysregulation of the release of
growth factors including VEGF and insulin.
The two hallmarks of this neurodegenerative process
reported in animal models are glial activation and apoptosis
mainly of the ganglion cells.
Optical coherence tomography has been used to assess the
retinal layers. There is no built in method in the OCT
machines to measure the ganglion cell layer thickness and
all the attempts are manual ones. On the other hand, the
retinal nerve fiber layer, formed of the axons of ganglion
cells, can be measured by the machine in the peripapillary
region where it is most thick.
So peripapillary RNFL thickness assessment by OCT can
be used for in vivo measurement of RGC layer loss and
thus diabetic neurodegeneration. Several studies have been implimented to assess RNFL
thickness in diabetic patients but the results were
controversial. Some reported a reduction in the
peripapillary RNFL thickness while others found no
difference in the RNFL thickness in diabetics versus age
matched controls. On the other extreme some reported an
increase in the peripapillary RNFL thickness.
Another point of controverse in the studies which reported
reduction in the RNFL thickness was the affected
quadrants.
Again the relation between the RNFL thickness and several
parameters including HbA1c level, duration of diabetes
mellitus and severity of diabetes were a matter of
controverse.
No previous study assessed the relation between RNFL
thickness and insulin therapy.
So in this study we included ninety eyes of 60 diabetic
Egyptian patients who met the inclusion criteria. Thirty
eyes of 23 healthy subjects acted as age matched controls.
All patients were recruited from the ophthalmic outpatient
clinic in Ain Shams university hospitals in the period
between March 2011 and January 2013.
Diabetic eyes were further divided as follows:
Group 1: Thirty eyes of 17 diabetic patients with no or
mild non-proliferative diabetic retinopathy.
Group 2: Thirty eyes of 21 diabetic patients with moderate
non-proliferative diabetic retinopathy. Group 3: Thirty eyes of 22 diabetic patients with severe
non-proliferative diabetic retinopathy.
Group 4: Thirty eyes of 23 normal healthy subjects were
included as age matched control eyes.
And as we analyzed the results we found:
A statistically significant reduction in the mean nasal
RNFL thickness in eyes with no diabetic retinopathy
and eyes with mild non-proliferative diabetic
retinopathy in comparison to the age matched
controls.
The mean inferior RNFL was statistically
significantly thinner in eyes with moderate nonproliferative
diabetic retinopathy in comparison to
the age matched controls.
No statistically significantly difference between the
RNFL thickness in eyes with severe nonproliferative
diabetic retinopathy and age matched
controls and that was related to edema in the RNFL
in late stages of diabetic retinopathy.
In the early stages of diabetic retinopathy, the
RNFL thickness is not related to the severity of
diabetic retinopathy.
On the other hand the RNFL thickness in the nasal
quadrant was statistically significantly higher in eyes
with severe non-proliferative diabetic retinopathy in
comparison to eyes with mild non-proliferative
diabetic retinopathy.There was only a weak negative correlation between
Hb A1c and both the average RNFL thickness and
the RNFL thickness in the inferior quadrant.
There was no statistically significant correlation
between the RNFL thickness and sex, the duration of
diabetes mellitus, insulin use and macular edema not
reaching the disc.
So we can conclude from this:
1. That retinal neurodegeneration occurs in the early
stages of diabetic retinopathy even before micovascular
abnormalities are visible.
2. This neurodegeneration can be assessed by
peripapillary RNFL assessment even before diabetic
changes appear.
3. This effect may be masked in the late stages of
diabetic retinopathy due to subclinical edema in the retinal
nerve fiber layer.