الفهرس 
Pathogenesis of NIDOMOnly 14 pages are availabe for public view
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Abstract
Long-term complications of non-insulin-dependent diabetes, including retinopathy, nephropathy and
neuropathy cause major morbidity and mortality. Many mechanisms have been ·suggested to explain the
pathogenesis of diabetic microangiopathies. However, the pathogenesis of diabetic retinopathy is
not known.
Serum viscosity has been found to increased in diabetes especially with clinical evidence of
microangiopathy. This increase in serum viscosity may be caused by many variables, most important
is the change in serum protein composition especially globulin elevation. This elevation was
dominated by increased levels of serum globulins belonging to the ”acute-phase reactant” group
produced by the liver. Increased production of these proteins is so common following injury and in
both acute and chonic medical disorders.
The major proteins of hepatic origin involved in the acute phase reaction are alpha- I
antitrypsin, alpha- I acidglycoprotein, ceruloplasmin, haptoglobin and C-reactive protein.
Individual acute-phase protein levels have been found to be elevated in adult diabetes, but normal
or nearly normal in childhood and adolescent diabetes .suggesting that their increase might be
caused by developing microvascular disease rather than the early metabolic disorder in diabetes or
may suggest that serum
protein pattern become disturbed as the metabolic abnormality develop.
The aim of this study was to :
1- Examine the degree of acute-phase proteins changes in established diabetes with and without
microangiopathy.
2- The relation between acute-phase proteins changes and the degree of hyperglycemia, duration of
diabetes mellitus, age of the patients and the presence of microangiopathy i.e. retinopathy &
microalbuminuria.
This work included 45 male subjects classified into 3 equal
, groups. GI, non-insulin dependent diabetic patients with evidence of retinopathy, group II,
non insulin dependent diabetic patients without evidence of retinopathy and group III, normal
healthy non diabetic subjects as a control group. Exclusion criteria included clinical evidence of
active inflammatory and infectious diseases.
All subjects were submitted to the following:
- History taking and general clinical examination.
- The following laboratory investigations: Fasting and post prandial blood glucose levels,
ESRIWBCS, urine analysis for microalbuminuria, serum albumin and globulin, acute-phase proteins
(a-1 antitrypin, a-1 acidglycoprotein, ceruloplasmin. C reactive protein and haptoglobin), and
serum viscosity.
- Ophthalmoscopic examination was done for the evidence of retinopathy.
The results were summarized as the following:
The three groups were matched for age, ESR,1WBCS, also both diabetic group were comparable as
regards, FBG and PBG levels.
- Serum albumin levels were significantly lower while serum globulin levels were significantly
higher in both diabetic groups than in control group. These changes were more evidenced in
diabetic patients with evidence of retinopathy.
- Microalbuminuria was significantly higher in both diabetic groups than in non-diabetic group,
with more significant higher values in the presence of retinopathy.
- Diabetic patients showed higher values of acute-phase proteins (o:-1 antitrypsin, o:-1
acidglycoprotein, ceruloplasmin, C reactive protein and haptoglobin) than in non-diabetic healthy
subjects. However, diabetic patients with retinopathy showed significantly higher values in
comparison to patients without retinopathy except C-reactive protein.
- Higher serum viscosity values were detected in both diabetic groups than in control group. Higher
serum viscosity values were found In diabetic patients with evidence of retlnopathy than In
diabetic patients without retinopathy.
- A positive correlation was found between fasting blood glucose values and acute-phase
proteins and serum viscosity. While , no correlation was found between duration of DM and
acute-phase proteins.
from our results we can conclude that elevation of acute-phase proteins and depression of albumin
were clearly detectable in diabetes especially with microangiopathy, positive correlation between
viscosity and acute-phase proteins and no correlation between duration of DM and acute-phase
proteins. This gives the magnitude of acute-phase proteins elevation potential importance in
the pathogenesis of diabetic microangiopathies.
Recommendations :
On the basis of our and previous studies, we may recommend :
1- Further studies to determine directly if more aggressive insulin treatment is able to reduce the
plasma protein changes shown to be presen t in non-insulin dependent diabetic microangiopathies.
2- The need to alternative approach to prevent the develeopment of long term diabetic complications
e.g to inhibit the mechanism (s) by which elevated glucose levels cause complications.