الفهرس 
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Abstract
PCOS is a complex and heterogeneous disorder; it is
likely that different factors can contribute to its pathogenesis and characteristic features in different groups of patients.
Visfatin, which is found primarily in the cell nucleus and cytoplasm, lacks a signal sequence and is released during lipolysis.
Actually, the ability of norepinephrine to stimulate
lipolysis in visceral fat cells has been shown to be 50% higher in women with PCOS.
High visfatin level in normal weight women with PCOS
may suggest an impaired mechanism of visfatin signaling in target tissues in states of insulin resistance. Moreover, these findings could reflect a compensatory response to tissuespecific
insulin resistance and hyperinsulinemia, an intrinsic
dysregulation in visfatin biosynthesis.
Moreover, there is increased serum visfatin concentration
in women with PCOS and its relationships with indices of
insulin resistance and hyperandrogenism. These findings might suggest that visfatin could play a role in the pathogenesis of
PCOS.
The aim of the present study was to asses plasma visfatin
Concentrations in women with polycystic ovary syndrome and correlate serum visfatin with their BMI.
The study was conducted on 24 female patients with
polycystic ovary syndrome and 20 healthy control females; they were selected from endocrine clinic, at Ain shams university hospital, the selected cases were divided into two groups:
٭ Group 1 (patients group) consists of 24 female patients with polycystic ovary syndrome subdivided into(12 lean cases&12obese).
٭ Group 2 (control group) consists of 20 healthy control female cases matching same age and body weight (10 lean females and 10 obese females) with regular menstrual cycles.
All cases were subjected to the following:
• Full medical history taking including history of diabetes,
hypertension,dyslipideamia, menstrual irregularities, thyroid disease, ovulatory dysfunction, with exclusion of other known disorder with special stress on (hyperprolactinemia,
hypercortisolemia, hypothyroidism) and other clinical diseases.
• Thorough clinical examination with special stress on clinical
hyperandrogenism (i.e.hirsutism and or hypergonadism).
• Anthropometric measurements including: Weight and
height, Body mass index (weight in kilograms divided by height in meters squared), Waist circumference.
• Laboratory measurements including: FPG, FPI, HOMA,
Lipid profile, Fasting plasma visfatin, LH\FSH ratio.
• Pelvic ultrasound scans for all the cases.
On comparing the 4 subgroups with each other:
1-On comparing the obese PCO group with the obese control group:
-A highly statistically significant difference (P≤0.001) was recorded as regards the following parameters: FPG
(91.75±6.79 and 78.3±7.78 respectively), cholesterol
(188.33±11.33 and 127.6±47.19 respectively), LDL
(141.08±22.83 and 108.5±19.06).
-An insignificant statistical difference (P>0.05) was recorded as regards the following parameters, LH (12.83±3.64 and 5.97±1.33 respectively), FSH (5.48±1.54 and 5.34±0.69 respectively), LH\FSH ratio (2.36±0.26 and 1.133±0.3 respectively) & TG (183±15.9 and 109.5±32.77 respectively) & HDL (43.67±7.06 and 49.8±4.41 respectively) & waist
circumference (93.58±4.66 and 91.3±4.27 respectively).
- Also a statistically significant difference (P≤ 0.05) was
found regarding visfatin (86.08±6.35 and 58.8±8.22 respectively),
HOMA (3.31±0.69 and 1.592±0.53 respectively), fasting plasma
insulin (14.92±3.55 and 9.1±3.54 respectively), BMI (32.43±3.14 and 31.254±0.71 respectively).
2- On comparing the Lean PCO group with the Lean control group:
-A highly statistically significant difference (P≤0.001) was recorded as regards the following parameters: LH
(12.46±2.33 and 9.24±2.27 respectively).
-An insignificant statistical difference (P>0.05) was
recorded as regards the following parameters: FPG (89.58±4.98 and 85.9±9.45 respectively) & LH\FSH ratio (2.34±0.35 and 1.49±0.38 respectively) & TG (119.33±28.25 and105.6±18.99
respectively) & LDL (115.58±10.15 and 111.4±10.15
respectively) & HDL (47.58±5.05 and 48±17.64 respectively) & BMI (23.19±1.28 and 23.45±0.63 respectively).
-Also a statistically significant difference (P≤ 0.05) was
found regarding the following parameters: visfatin (79.25±6.85 and 59.7±12.42 respectively) & Fasting plasma insulin (13.33±3.47 and 8±1.63 respectively)) &HOMA (3.00±0.72
and 1.662±0.22 respectively) &FSH (5.38±1.03 and 6.22±0.618 respectively), cholesterol (177.92±8.57and 143.9±35.99 respectively), Waist circumference (77.92±6.93 and 72.9±3.84
respectively).
3- On comparing the Lean PCO group with the obese control group:
-A highly statistically significant difference (P≤0.001) was recorded as regards the following parameters: FPG
(89.58±4.98 and 78.3±7.78 respectively), Fasting plasma
insulin (13.33±3.47 and 9.1±3.54 respectively), cholesterol (177.92±8.57 and 127.6±47.19 respectively), LDL (115.58±10.15 and 108.5±19.06 respectively).
-An insignificant statistical difference (P>0.05) was recorded as regards the following parameters: LH(12.46±2.33 and 5.97±1.33
respectively), FSH(5.38±1.03 and 5.34±0.69 respectively),
LH\FSH ratio(2.34±0.35and 1.133±0.3 respectively),
TG(119.33±28.25 and 109.5±32.77 respectively),waist
circumference (77.92±6.93 and 91.3±4.27 respectively).
-Also a statistically significant difference (P≤ 0.05) was
found regarding the following parameters visfatin (79.25±6.85 and
58.8±8.22 respectively) ,HOMA(3.00±0.72 and 1.592±0.53 respectively), HDL (47.58±5.05 and 49.8±4.41 respectively),BMI(23.19±1.28 and 31.254± 0.71 respectively).
4-On comparing the obese PCO group with the lean PCO
group:
-A highly statistically significant difference (P≤0.001) was recorded as regards the following parameters: LDL
(141.08±22.83and 115.58±10.15 respectively).
-An insignificant statistical difference (P>0.05) was
recorded as regards the following parameters: FPG(91.75±6.79 and 89.58±4.98 respectively), LH (12.83±3.64 and 12.46±2.33
respectively), FSH(5.48±1.54 and 5.38±1.03 respectively),
LH\FSH ratio(2.36±0.26 and 2.34±0.35 respectively),
TG(183±15.9 and 119.33±28.25 respectively),
HDL(43.67±7.06 and 47.58±5.05 respectively), waist
circumference (93.58±4.66 and 77.92±6.93 respectively).
- Also a statistically significant difference (P≤ 0.05) was
found regarding the following parameters: visfatin (86.08±6.35 and79.25±6.85 respectively), Fasting plasma insulin (14.92±3.55 and 13.33±3.43 respectively), HOMA (3.31±0.69
and 3.00±0.72 respectively), cholesterol (188.33±11.33 and
177.92±8.57 respectively), BMI(32.43±3.14 and 23.19±1.28 respectively).
As regards the correlation between the serum visfatin and the different parameters in lean PCO patients,
There was a highly statistically significant positive
correlation (P≤0.001) between visfatin and Wt (r=0.020917)
and there was a highly statistically significant negative correlation (P≤0.001) between visfatin and FPG(r=-0.32022).
Also there was a significant statistical positive correlation
(P≤ 0.05) between visfatin and cholesterol (r=0.130610), while
there was a statistical significant negative correlation with Age
(r=-0.20096).
As regards the correlation between the serum visfatin
and the different parameters in obese PCO patients, there
was a highly statistically significant positive correlation
(P≤0.001) between visfatin and LH\FSH ratio (r =0.0125) and
there was a highly statistically significant positive correlation
(P≤0.001) between visfatin and HOMA (r=0.075). Also there
was a significant statistical positive correlation (P≤0.05)
between visfatin and Fasting plasma insulin (r=0.149), LH
(r=0.508), FSH (r=0.47), TG(r=0.141), BMI (r=0.741) and Waist circumference (r=0.16) while there was a statistical significant negative correlation with LDL(r=-0.05),HDL(r=-0.29) and Ht(r=-0.32).
So we concluded that Visfatin and IR are higher in obese
PCO patients compared to lean PCO patients.