الفهرس 
Material and methodsOnly 14 pages are availabe for public view
 |  | from | 265 |  |  |
| | | from | 265 | | |
Abstract
This study was carried out on 70 diabetic men (and 16 normal men as a
control) who were attending the diabetic outpatient clinic ofKasr-AI-Aini University
hospital, Diabetes Institute, and T.V. Medical Center since 1997. On the basis of
history taking .clinical examination, and laboratory investigation, they proved to be
free from hepatorenal disorders, schistosomiasis and infectious diseases. They were
under treatment [diet, oral hypoglycemic agents (gliclazide = diamicron), or insulin).
Diabetes Mellitus was diagnosed on the following criteria:
(1) History: previous history of polyuria, polydepsia, and polyphagia, history ofloss
of weight, family history suggestive of diabetes.
(2) Urine examination: some patients showed glycosuria.
(3) Two hours oral glucose tolerance test using 75 gm glucose orally.
Diabetic patients were divided to two subgroups according to age and onset of the
disease:
A) Type 1: Insulin-Dependent Diabetes Mellitus (ID.D.M.): Juvenile-Type
(25 patients)
B) Type II: Non-Insulin Dependent Diabetes Mellitus (NID.DM): Adult-Type
(45 patients)
NIDDM was further subdivided into patients taking and responding well to oral
hypoglycemic drugs according to their fasting and post-prandial blood glucose (21
patients), and those not responding well to oral hypoglycemic drugs and taking insulin
(24 patients).
_The control group comprised 16 healthy male volunteers.
-_.- ---------------
210
The diabetic patients and control were screened for the following laboratory
investigations:
(I)Fasting and two hours blood glucose.
(2)Glycosylated hemoglobin HbAlc.
(3) Serum C-peptide.
(4) Serum autoantibodies against Islet Cell Antigens (ICA).
(5) Serum autoantibodies against Glutamic Acid Decarboxylase (GAD).
(6) Serum Vascular Cell Adhesion Molecule- J (VCAM-l).
(7) Serum E-Selectin.
Diabetic patients were further classified into:
Diabetic patients free of GAD and ICA autoantibodies (n= 26 patients) and
diabetic patients proved to have GAD and ICA autoantibodies (n= 27 patients).
The Prevalence of Islet Cell autoantibodies (ICA) in Type I & II
Diabetes Mellitus
The prevalence ofIslet Cell autoantibodies (ICA) in 100M group was (60%)
which was higher than that ofNIODM group on insulin treatment (45.8%) and higher
than ofNIDDM group on oral treatment (19%). All controls had no ICA in their
sera. In NIDDM patients with circulating ICA represented an early of a disease
process culminating in 100M. ICA might serve as an early indicator of the disease.
An early detection ofICA is important in order to identify the individuals in general
population who are at a high risk of developing the disease
•
211
The Prevalence of Glutamic Acid Decnrboxylase autoantibodies (GAD)
in Type I & II Diabetes Mellitus
In the present study, the prevalence of Glutamic Acid Decarboxylase autoantibodies
(GAD) in IDDM group was (72 %) which was higher than that ofNIDDM group on
insulin treatment (66.7%) and higher than that ofNIDDM group on oral treatment
•
(38.1 %). GAD could not be detected in the control group. IDDM is an autoimmune
disease in which the immune system mistakenly attacked and destroyed the beta cells
of the pancreas. GAD could be of help in familial screening of type I. It has a better
predictive value thanlCA . GAD could also detect insulin dependency in NIDDM
adult patients.
Correlation Studies:
(I) There was a significant positive correlation between Islet Cell autoantibodies
(lCA) and Glutamic Acid Decarboxylase autoantibodies (GAD) in NIDDM (oral,
insulin) and lODM groups.
(2) There was no significant correlation between Islet Cell autoantibodies (lCA) and
C-peptide levels in NIDDM (on oral therapy) group but there were significant
negative correlations between Islet Cell autoantibodies (lCA) and C-peptide levels in
NIDDM (on insulin therapy) and IDDM groups. The presence of autoantibodies to the
beta cells of the pancreas led to their destruction and loss of beta-reserve capacity and
decrease in C-peptide level. C-peptide level had decreased significantly in ICA (+ve)
patients but not in lCA (-ve) patients.
(3) There was no significant correlation between Islet Cell autoantibodies (lCA) and
soluble Vascular Cell Adhesion Molecule-I (sVCAM-I) in NIDDM (on oral therapy)
group, but there was a significant positive correlation between Islet Cell
--------- ------------ ---
212
autoantibodies (lCA) and soluble Vascular Cell Adhesion Molecule-l (sVCAM-I) in
NIDDM (on insulin therapy) group, as well as in IDDM group. Adhesion molecules
mediated leucocyte adhesion to the endothelium in the atherosclerosis process. The
elevated levels of the soluble adhesion molecules in diabetic patients could be of
pathogenic importance for the developing of atherosclerosis. •
(4) There was no significant correlation between Islet Cell autoantibodies (ICA) and
soluble E-Selectin (sE-Selectin) levels in NIDDM (oral therapy, insulin) and IODM
groups. Elevated levels ofE-Selectin occurred independently ofICA which probably
reflected ongoing immune response in diabetic patients.
(5) There was no significant correlation between Islet CeB autoantibodies (lCA) and
glycosylated hemoglobin (HbAlc) levels in NIDDM (on oral and insulin therapy) and
IDDMgroups
(6)There was no significant correlation between Islet Cell autoantibodies (lCA) and
fasting blood glucose (FBG) levels in NIDDM (on oral and insulin therapy) and
IDDM groups
(7)There was no significant correlation between Islet Cell autoantibodies (lCA) and
postprandial blood glucose (PPBG) levels in NIDDM (on oral and insulin therapy)
and IDDM groups.
(8) There was no significant correlation between Glutamic Acid Decarboxylase
autoantibodies (GAD) and C-peptide levels in NIDDM (on oral therapy) group,
but there was a significant negative correlation between Glutamic Acid
---------------------------------
- ------ -- - - -------
213
Decarboxylase autoantibodies (GAD) and C-peptide levels in NTDDM (on insulin
.therapy) group as well as IDDM group. Differentiation between type I and II diabetes
mellitus in adults was difficult only GADA was signed for insulin dependency in type
II patients with lower C-peptide levels.
(9)There was no significant correlation between Glutamic Acid Decarboxylase
autoantibodies (GAD) and soluble Vascular Cell Adhesion Molecule-I (sVCAM-I)
levels in NIDDM (on oral therapy) group but there was a significant positive
correlation between Glutamic Acid Decarboxylase autoantibodies (GAD) and soluble
Vascular Cell Adhesion Molecule-l sVCAM-I) in NTDDM (on insulin therapy) group
as well as IDDM group. Elevated sVCAM-l levels in TDDM and NTDDM patients
occurred in diabetic patients with vascular complications.
(10) There was no significant correlation between Clutamic Acid Decarboxylase
autoantibodies (GAD) and soluble E-Selectin (sE-Selectin) levels in NTDDM (oral,
insulin therapy) and IDDM groups. Increased levels ofE-Selectin concentration
occurred in patients with IDDM and NIDDM. E-Selectin was related to vascular
complications in diabetic patients and concentration ofE-Selectin might be related to
metabolic control.
(II) There was no significant correlation between Glutamic Acid Decarboxylase
autoantibodies GAD and glycosylated hemoglobin (HbAlc) levels in NIDDM (on
oral and insulin therapy) and IDDM groups.
(12) There was no significant correlation between Glutamic Acid Decarboxylase
autoantibodies (GAD) and fasting blood glucose (FBG) levels in NIDDM (oral,
insulin therapy) and IDDM groups.
•
------
----- - --------
214
(13) There was no significant correlation between Glutamic Acid Decarboxylase
autoantibodies (GAD) and postprandial blood glucose (PPBG) levels in NIDDM
(oral, insulin therapy) and IDDM groups.
(14) Serum C-peptide levels in NIDDM on oral (Gliclazide=diamicron), insulin
treatment and IDDM groups were significantly lower than that of control group. Cpeptide
had a discriminative power between type I and H diabetic patients and could
be recommended as a classification tool.
(15) There was a significant negative correlation between C-peptide and soluble
Vascular Cell Adhesion Molecule-I (sVCAM-) levels in NIDDM (oral and insulin
therapy) and IDDM groups.
(16) There was no significant correlation between C-peptide and soluble E-Selectin in
NIDDM (oral, insulin) and IDDM groups.
(17) There was no significant correlation between C-peptide and glycosylated
hemoglobin (HbAlc) in NIDDM (oral, insulin) and IDDM groups.
(18) There was no significant correlation between C-peptide and fasting blood
glucose (FBG) in NIDDM (oral, insulin) and IDDM groups.
(19) There was no significant correlation between C-peptide and postprandial blood
glucose (PPBG) level in NIDDM (oral, insulin) and IDDM groups.
(20) Soluble Vascular Cell Adhesion Molecule-I (sVCAM-I) in NIDDM (oral
gliclazide, insulin therapy) and IDDM groups were significantly higher than that of
control group. sVCAM- I had been associated with early stages of atherosclerosis and
might reflect early vascular perturbation on diabetic vasulopathy and indicator of
ongoing cellular dysfunction in diabetic patients and a marker of atherosclerotic
lesions in diabetic patients.
•
------------------------ - ---------------------_ .._---- - - -- ----
215
(21) There was no significant correlation between suluble Vascular Cell Adhesion
Molecule-I (sVCAM-I) levels and soluble E-Selectin in NIDDM (oral. insulin) and
IDDMgroups
(22) There was no significant correlation between soluble Vascular Cell Adhesion
Molecule and glycosylated hemoglobin (HbAlc) in NIDDM (oral, insulin) and IDDM
groups.
(23) There was no significant correlation between soluble Vascular Cell Adhesion
Molecule (sVCAM-I) and fasting blood glucose (FBG) in NIDDM (oral, insulin)
and IDDM groups.
(24) There was no significant correlation between soluble Vascular Cell Adhesion
Molecule (sVCAM-I) and postprandial blood glucose levels (PPBG) in NIDDM
(oral, insulin) and IDDM groups.
(25) sE-Selectin levels in NIDDM (oral gliclazide and insulin therapy) and IDDM
groups were significantly higher than that of control group.
(26) There was no significant correlation between soluble E-Selectin and glycosylated
hemoglobin (HbAlc) levels in IDDM, NIDDM (oral and insulin) and control groups.
(27) There was no significant correlation between soluble E-Selectin and fasting
blood glucose levels (FBG) in NIDDM (oral, insulin) and IDDM groups
(28) There was no significant correlation between soluble E-Selectin and postprandial
blood glucose (PPBG) levels in NIDDM (oral, insulin)and IDDM groups.
,
216
Conclusion:
(I) In NIDOM patients with circulating leA represented an early ofa disease process
culminating in IDOM. The frequency of positive antibodies declined with duration of
the disease. ICA might serve as an early indicator of the disease. An early detection of
ICA was important in order to identify the individuals in general population who are
at a high risk of developing the disease.
(2) GAD could be of help in familial screening of type one, better predictive value
than ICA and IAA. GAO could also detect insulin dependency in NIDOM adult
patients.
(3) C-peptide had decreased significantly in leA (+ve) patients but not in ICA (-ve)
patients. C-peptide levels were inversely correlated with ICA level. C-peptide had a
discriminative power between type I and II and could be recommended as a
classification tool.
(4) Adhesion molecules mediated leucocyte adhesion to the endothelium in the
atherosclorosis process. The elevated levels of the soluble adhesion molecules in
diabetic patients could be of pathogenic importance for the developing of
atherosclorosis. Elevated levels of E-Selectin and sVCAM-I in IDOM and NIDOM
might occurred in diabetic patients with vascular complications.