Hyperglycemia and beta cell function in pregnancy

• Main Author: Chinonso, Ekwueme
• Format: Web Resource
• Language: English
• Published: Morressier 01.01.2017
• DOI: 10.26226/morressier.59d5184cd462b80296ca3f4a

Presenting authorDr C. EkwuemeFederal Medical CentreOwerriNigeria Abstract stream - Diabetes in Women and ChildreTopic: Pregnancy and gestational diabetesAbstract title: Hyperglycemia and beta cell function in pregnancy Co-authorsC. Ekwueme1, A.C. Anyanwu1, R. Oputa1, S. Chinenye2, C. Unachukwu2, T. Njoku3, E. Nzeribe3, O. Enang4, I. Korubo2.1Federal Medical Centre, Internal Medicine, Owerri, Nigeria.2University of Port Harcourt Teaching Hospital, Internal Medicine, Port Harcourt, Nigeria.3Federal Medical Centre, Obstetrics and Gynaecology, Owerri, Nigeria.4University of Calabar Teaching Hospital, Internal Medicine, Calabar, Nigeria. Abstract bodyBackgroundHyperglycemia is the most common metabolic disorder in pregnancy and it complicates one in six of pregnancies. In 2013, WHO introduced a new criteria for diagnosis of hyperglycemia in pregnancy and this has led to increased prevalence. The global prevalence of hyperglycemia in pregnancy was 16.2% in 2015. It affects 20.9 million live births with majority of cases occurring in low- and medium-income countries. In Nigeria the prevalence varies depending on the diagnostic criteria used.Hyperglycemia first detected in pregnancy consist of gestational diabetes mellitus (GDM) and diabetes in pregnancy (DIP). It is associated with poor maternal, perinatal, and neonatal outcomes. In normal pregnancy insulin sensitivity decreases with an increase in insulin resistance which is mediated by hormones produced by the placenta but this is compensated by an increase in insulin secretion. Hyperglycemia in pregnancy occurs when pancreatic beta-cell insulin secretion is inadequate to meet increasing demand during pregnancy. AimTo evaluate the prevalence of hyperglycemia in pregnancy and adverse outcomeTo investigate the beta-cell function in pregnancy MethodIt was a longitudinal observational study of 300 pregnant women with singleton pregnancy attending antenatal clinics at Obstetrics and Gynaecology department, Federal Medical Centre Owerri. Subjects with pre-gestational diabetes mellitus, multiple pregnancy, chronic kidney disease or receiving drugs that affect glucose tolerance were excluded. Ethical approval was obtained from the Ethical Committee of the Federal Medical Centre Owerri. Clinical data were collected using interviewer administered questionnaire. Height, weight, and blood pressure were measured using the appropriate tools. Venous blood samples were collected after 8 hours of overnight fast for fasting plasma glucose (FPG) and fasting plasma c-peptide. 75 g anhydrous glucose dissolved in 250 ml of water was administered to each subject. Blood samples were collected for oral glucose tolerance test (OGTT). Hyperglycemia first detected in pregnancy was diagnosed using WHO 2013 criteria. Homeostasis model assessment 2 calculator was used to calculate beta-cell function (HOMA2%u03b2), insulin resistance (HOMA2 IR), and insulin sensitivity (HOMA2%S). SPSS version 21 was used to analyse the dataResultsA total of 300 pregnant women participated in the study.The prevalence of hyperglycemia in pregnancy was 24.3% (GDM 22.3 and DIP 2%). FPG identified 88.1% of the women with GDM and the mean gestational age of women with normoglycemia and GDM were similar (p = 0.354). Subjects with GDM had higher prepregnancy weight (p = 0.005), prepregnancy BMI (p = 0.000), systolic blood pressure (p = 0.000) and diastolic blood pressure (p = 0.000) compared with normoglycemic subjects. The median HOMA2%u03b2 in normoglycemic women and those with GDM were 137.7 (112.6 -164.5) and 88.2 (67.6-110.4) respectively (p < 0.000). Similarly HOMA2%S was higher in normoglycemic women (p < 0.000). HOMA2 IR in women with GDM was 1.12 (0.90 - 1.56) and it was higher when compared with normoglycemic women (p < 0.000). Glycosuria was not associated with GDM or DIP (p = 0.320). Independent predictors of hyperglycemia in pregnancy were family history of DM (OR 2.40, 95% CI 1.10-5.2, p< 0.028), previous stillbirth (OR 2.93, 95% CI 1.29-6.70, p<0.011) and presence of hirsutism (OR 4.00, CI 1.52-10.49). Nulliparity was protective (OR 0.42, 95% CI 0.210-0.843, p<0.015). Adverse pregnancy outcomes were more in subjects with hyperglycemia (OR 2.78, 95% CI 1.51-5.11)DiscussionThe prevalence of GDM was 22.3% and it is higher than 8.3% reported in Nigeria. The difference in prevalence maybe due to different diagnostic criteria used. Arora et al had reported a prevalence of 35% in India using WHO 2013 criteria, this maybe attributed to predominant ethnic nationality used in the study. Independent predictors of hyperglycemia in pregnancy were family history of DM, previous stillbirth and hirsutism. Hirsutism may suggest underlying hyperandrogenism which causes insulin resistance and hyperglycemia. Beta cell function and insulin sensitivity were significantly lower in women with GDM. Decline in beta-cell function and insulin sensitivity results in glucose intolerance in pregnancy. The prevalence of hyperglycemia in pregnancy is high and it is associated with adverse pregnancy outcome. We recommend universal screening for all pregnant women. It is important to adopt treatment modalities that will address the underlying mechanism of hyperglycemia in pregnancy.