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BACKGROUND: Metabolic syndrome occurs more often among people living in poorer social conditions. The health status of the largest minority ethnic group in Hungary lags in many aspects behind that of the general population. METHODS: To estimate the prevalence of metabolic syndrome a screening was initiated in the city of Gyor among subjects aged 20-70 years who declared themselves as Gypsy. Subjects with known diabetes and cardiovascular disease were excluded. The diagnosis of metabolic syndrome was based on the ATP-III criteria. RESULTS: Among the 77 individuals screened (35 men, 42 women, age 46.9 ± 10.6 years, x ± SD) diabetes mellitus was found in 14 cases (18.2 %), and pre-diabetes (impaired fasting blood glucose (IFG) or impaired glucose tolerance (IGT) could be diagnosed in further 14 cases (18.2 %). Individual components of the metabolic syndrome occurred as follows: hypertension in 47 subjects (61.0 %), abnormal waist circumference in 40 individuals (51.9 %), abnormal HDL-cholesterol in 39 cases (50.6 %), abnormal triglycerides in 35 individuals (45.5 %) and abnormal fasting blood glucose in 15 subjects (19.5 %). Within the cohort metabolic syndrome could be diagnosed in 39 individuals (50.6 %) without a significant gender difference (males 20/35 = 57.1 %; women: 19/42 = 45.2 %, p>0.05). CONCLUSION: The occurrence of metabolic syndrome and that of glucose intolerance is high among adult Gypsy people in Hungary. In order to recognise cardio-metabolic risks and to prevent their cardiovascular consequences, continuous health promotion and adequate medical care should be provided for the Gypsy population in Hungary (Tab. 5, Ref. 32).

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The metabolic syndrome is characterised by hyperinsulinaemia (insulin resistance) leading to an increased risk of atherosclerotic cardiovascular diseases. Carotid intima-media thickness (IMT) can be easily measured to detect early atherosclerosis. In order to evaluate the clinical characteristics of the metabolic syndrome a screening procedure was performed and carotid IMT was determined by high-resolution B-mode ultrasonography in a cohort of middle-aged (40-60 years) subjects who proved to be hyperinsulinaemic [fasting plasma insulin >15 microU/ml and/or post-prandial (120 min) insulin > 45 microU/ml; n = 91; men/women: 35/56; homeostasis model assessment (HOMA)-index: 6.42 +/- 3.65; x +/- SD]. Subjects known to have diabetes were not involved. Subjects were divided into subgroups according to the stages of glucose intolerance (normal glucose tolerance, n = 46; impaired glucose tolerance, n = 26; diabetes mellitus, n = 19). As controls, age- and sex-matched non-diabetic and non-hyperinsulinaemic subjects (n = 20; HOMA-index: 2.09 +/- 0.85) were investigated. The values of IMT of the internal carotid arteries were higher in hyperinsulinaemic subjects than in controls (0.93 +/- 0.39 mm vs 0.57 +/- 0.13 mm,p < 0.001), whereas the lumen diameter proved to be smaller than in control subjects (5.04 +/- 0.75 mm vs 5.45 +/- 0.71 mm; p < 0.05). In hyperinsulinaemic subjects only a trend of increasing IMT values and that of decreasing lumen diameter of the internal carotid arteries were observed when subgroups classified according to the stages of glucose intolerance were compared. No significant changes in IMT or lumen diameter of the common carotid arteries were observed. Early and asymptomatic signs of atherosclerosis could be detected in middle-aged subjects who proved to be hyperinsulinaemic in a screening procedure. The prevention of clinically manifest cardiovascular diseases in these subjects could be of great importance.

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In order to evaluate the clinical characteristics of metabolic syndrome, a screening procedure was performed and in a cohort of middle-aged (40-60 years) hyperinsulinaemic (fasting plasma insulin > 15 microU/ml) and/or postprandial [120 min after 75 g glucose load] insulin > 45 microU/ml) subjects (n = 91; men/women: 38/53; age mean +/- SD 47.6 +/- 4.3 years; body mass index: 34.6 +/- 4.9 kg/m2; waist-hip ratio: 0.92 +/- 0.07; actual blood pressure 146 +/- 16/87 +/- 9 mmHg; fasting insulin: 24.2 +/- 11.3 microU/ml; postprandial insulin 125.5 +/- 103.8 microU/ml; serum LDL-cholesterol: 3.73 +/- 1.09 mmol/l; HDL-cholesterol: 1.12 +/- 0.30 mmol/l; triglycerides: 2.97 +/- 2.38 mmol/l; uric acid 279 +/- 79 mumol/l) plasma fasting homocysteine, vitamin B12 and folic acid levels were simultaneously determined. The values were separately evaluated according to the stages of glucose tolerance (normal glucose tolerance [n = 47]; impaired glucose tolerance [n = 24] and diabetes mellitus [n = 20]). Laboratory normal values were determined in 47 healthy subjects (control group, age: 45.0 +/- 7.8 years, men/women: 19/28). There was no significant difference between hyperinsulinaemic and control subjects regarding plasma homocysteine (9.28 +/- 3.81 mumol/l vs. 9.63 +/- 2.70 mumol/l), folic acid (8.5 +/- 5.9 ng/ml vs. 7.5 +/- 2.1 ng/ml) and vitamin B12 levels (423 +/- 141 pg/ml vs. 356 +/- 121 pg/ml). Plasma homocysteine levels were significantly (p < 0.001) higher in hyperinsulinaemic men than women (11.34 +/- 4.72 mumol/l [n = 38] vs. 7.86 +/- 2.13 mumol/l [n = 53]). There was no significant difference between subgroups classified according to the stages of glucose tolerance in hyperinsulinaemic groups. Plasma homocysteine values exceeding the upper limit of normal range (> 12.45 mumol/l) were detected at a similar prevalence rate in control (4/47 = 8.5%) and in hyperinsulinaemic subjects (10/91 = 10.9%). A weak but statistically significant correlation was found between plasma homocysteine values and age of subjects (r = 0.222; p < 0.05) whereas a stronger correlation was documented between plasma homocysteine and serum creatinine values (r = 0.658; p < 0.001) in hyperinsulinaemic groups (n = 91). Plasma homocysteine values independently from the stages of glucose tolerance are not elevated in hyperinsulinaemic subjects. Hyperhomocysteinaemia is not a characteristic feature of hyperinsulinism suggesting that plasma homocysteine levels are of no considerable importance in the complex pathomechanism of atherosclerosis at early stages of metabolic syndrome.

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