GIGTGestational Impared Glucose Tolerance
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Table-I: Clinical characteristics of patients in the GDM GIGT and NGT groups (n/%).
Basic demographic data of the patients: We tested 336 pregnant women in total among which NGT patients accounted for 51.8% (174 cases) GIGT patients accounted for 25.6% (86 cases) and GDM patients for 22.6% (76 cases).
higher in the GDM compared to the GIGT and NGT groups (pless than 0.05) (Table-I).
Pregnancy weight gain and HOMA-IR correlated with OGTT hyperglycemia in the one hour GIGT subgroup: We divided the GIGT patients in subgroups depending whether one blood glucose concentration was higher than 10.3mmol / L 8.6 mmol / L or 6.7 mmol / L at 1 2 and 3 hours after 75 gram oral glucose uptake.
Table-II: Metabolic parameters in the GDM GIGT and NGT groups.
Table-III: Clinical characteristics and metabolic parameters in GIGT subgroups.
The data indicate that HOMA-IR abnormalities in the first hour of the OGTT can be used to determine GIGT.
In this study we diagnosed 86 GIGT (25.6%) and 76 GDM (22.5%) cases in 336 pregnant women and both correlated with age BMI before pregnancy as well as family history of diabetes while blood pressure was highest in GDM patients.
studied 14 women who had a history of GDM and did not have signs of either diabetes or impaired glucose tolerance after birth but in all of them serum glucose levels after oral glucose tolerance tests were significantly enhanced compared to the control group which they attributed to a defect of insulin secretion.20 Also others described that women with normal glucose tolerance and a history of gestational diabetes had significant impairments of beta-cell function at normal insulin sensitivity after birth.21 We also assessed insulin resistance with HOMAIR in this study and found that HOMA-IR values in the GDM group were significantly higher than in GIGT or NGT patients which indicated a significant insulin resistance.
suggested that increased insulin resistance combined with beta cell dysfunction is associated with the severity of glucose intolerance and total insulin dosage required for GDM patients.2425 The deficiencies might become manifest due to the women's' hormonal changes during pregnancy such as corticosteroids human placental lactogen (HPL) estrogen and progesterone placental enzymes adiponectin26 and leptin.27 In our study we found that the weight gain as well as the HOMA-IR were significantly higher in the 1-hour GIGT hyperglycemia than in the 2-hourand 3-hour subgroups showing that a 1-hour glucose abnormality in GIGT patients was associated with higher insulin resistant severity.
Our finding that 1-hour glucose abnormalities in GIGT patients were associated with more severe insulin resistance supports the latest criteria of IADPSG.
Thus changes in lipid metabolism may be a factor which leads to physiological and pathological changes in women with GDM.29 In addition free fatty acids were a key factor affecting islet cell function and insulin resistance in GDM patients.30 Our results also supported that GDM patients have lipid metabolism disorders which may prelude GIGT in pregnant women.31