International Journal of Clinical Case Reports 2018, Vol.8, No.3, 10-13
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We have also done an evaluation of eating habits and physical activity status and made a comparison between
patients with hyperglycemia and patients with normal blood glucose levels as depicted in Table 3.
Table 1 Comparison of patients with hyperglycemia and patients with normoglycemia
Parameters
Patients with hyperglycemia
Patients with normoglycemia
p
Age (years)
54.4
1.1
45.7
0.8
<0.001
BMI (kg/m
2
)
31.5
0.5
28.8
0.4
<0.001
FT4 (pmol/l)
6.10
0.43
8.40
0.44
<0.01
Triglyceride (g/l)
1.57
0.09
1.41
0.07
<0.05
High blood pressure (%)
54.4%
21.5%
<0.001
Positive family history of
type 2 diabetes (%)
36.3%
29.8%
<0.05
Table 2 Comparison of patients who resumed normoglycemia and patients in whom hyperglycemia persisted
Parameters
Patients who resumed normoglycemia
Patients in whom hyperglycemia persisted
p
Age (years)
53.8
3.9
59.1
2.1
<0.0005
BMI (kg/m
2
)
32.2
1.1
31.8
0.9
0.10
Triglyceride (g/l)
1.23
0.14
1.59
1.33
0.10
High blood pressure (%)
29.4%
70.7%
<0.01
Positive family history of
type 2 diabetes (%)
23.5%
29.3%
0.50
Table 3 Eating habits and physical activity status in patients with hyperglycemia and patients with normal blood glucose
Parameters
Patients with hyperglycemia
Patients with normoglycemia
Bread (grams/day)
150
130
Sodas (frequency/week)
4
2
Fried food (frequency/week)
4
1
Green vegetables (frequency/week)
3
7
Fruits (frequency/week)
4
5
Candies (frequency/week)
3
2
Physical activity (% of patients)
14%
54%
3 Discussion
Thyroid hormones modulate glucose metabolism through effects on insulin action, intracellular insulin signaling,
ß-cell function, hepatic gluconeogenesis, lipolysis and lipid oxidation (Crunkhorn and Patti, 2008).
Hypothyroidism one of the most common endocrine disorders may predispose to hyperglycemia through
development of insulin resistance and metabolic syndrome.
Experiments performed in muscle of hypothyroid rats and adipose tissue fragments isolated from patients with
hypothyroidism showed that rates of glucose transport did not increase when insulin was increased within the
physiological range (Pedersen et al., 1988; Cettour-Rose et al., 2005). Furthermore, observations in hypothyroid
subjects using euglycemic hyperinsulinemic clamps have shown resistance of whole body glucose disposal to
plasma insulin levels (Rochon et al., 2003; Maratou et al., 2009; Mitrou et al., 2010).
In Dimitriadis’ study, forearm and adipose tissue blood flow and glucose disposal rates in hypothyroid patients
were significantly decreased at 60-90 min after the meal when plasma insulin levels reached their peak. Decrease
in blood flow was postulated to be responsible for the defect in insulin-stimulated glucose disposal in the forearm
and adipose tissue. Indeed, calculated fractional glucose extraction was not impaired, suggesting that the
resistance of glucose disposal to insulin in hypothyroidism could be accounted for by the impairment of
vasodilatation as a consequence of endothelial dysfunction and impairment of the sympathetic system action
(Dimitriadis et al., 1997; Lekakis et al., 1997; Haluzik et al., 2002; Dimitriadis et al., 2006).
