This is the full version of the Australasian Diabetes in Pregnancy Society (ADIPS) 2020 guideline for pre-existing diabetes and pregnancy. The guideline encompasses the management of women with pre-existing type 1 diabetes and type 2 diabetes in relation to pregnancy, including preconception, antepartum, intrapartum and postpartum care. The management of women with monogenic diabetes or cystic fibrosis-related diabetes in relation to pregnancy is also discussed. E19 V. L. Rudland et al. GUIDELINE DEVELOPMENT AND METHODOLOGY This guideline is a consensus-based guideline, designed to provide practical guidance to clinicians. It was developed with a multidisciplinary writing team including obstetricians, endocrinologists, obstetric physicians, credentialled diabetes educators (CDE), midwives, lactation consultants and accredited practising dietitians (APD) with expertise in diabetes in pregnancy. It had input from both Australian and New Zealand clinicians. The writing group members were drawn from a variety of clinical backgrounds, including practitioners from metropolitan, regional and rural/ remote settings. The guideline did not aim to meet the National Health and Medical Research Council standard for guidelines, and rating quality of evidence or strength of each recommendation was out of scope. There was no funding available and this work was completed on a purely voluntary basis. The literature was reviewed, and each member of the writing group was assigned a section of the guideline to write. Sections were then reviewed by all members, and a consensus of expert opinion was achieved. The guideline was reviewed by the Australasian Diabetes in Pregnancy Society (ADIPS) board, and then widely disseminated throughout Australia and New Zealand for stakeholder review, with feedback from 14 professional organisations and 17 ADIPS members (obstetricians, endocrinologists, midwives, dietitians). The guideline writing group would like to acknowledge the valuable and extensive feedback provided. Each item of feedback was reviewed by the writing group and a consensus decision was made in response to each item of feedback. There are key areas that this guideline does not address: 1. Routine pregnancy care: This guideline specifically addresses issues of pre-existing diabetes and pregnancy. It does not include details of routine pregnancy care. Women with pre-existing diabetes and pregnancy require all the usual preconception, antenatal, peripartum and postnatal care that every other woman requires. This guideline is designed to supplement all the usual guidelines for regular pregnancy care for all women. 2. Social determinants of disease are important contributors to the excess burden of type 2 diabetes in Aboriginal and Torres Strait Islander, Maori and Pasifika women. The relationship between social determinants of disease and disease management is critically important. The complexity of these important issues is beyond the scope of this document and cannot be given due consideration in this already lengthy clinical guid...

Glucokinase–maturity-onset diabetes of the young (GCK-MODY) is an autosomal dominant disorder caused by heterozygous inactivating GCK gene mutations. GCK-MODY is one the most common MODY subtypes, affecting 0.1% of the population and 0.4–1% of women with gestational diabetes mellitus. Glucokinase is predominantly expressed in pancreatic beta cells and catalyzes the phosphorylation of glucose to glucose-6-phosphate. The unique kinetics of glucokinase enable it to change the rate of glucose phosphorylation according to the glucose concentration, thereby regulating insulin secretion. Individuals with GCK-MODY have mildly elevated fasting blood glucose levels (5.5–8.0 mmol/L) and regulate glucose perturbations to a higher set-point, resulting in a relatively flat glucose profile on a 75 g oral glucose tolerance test. The hyperglycemia is usually subclinical and may only be detected on incidental glucose testing. It is important to correctly identify GCK-MODY as the clinical course and management differs substantially from other types of diabetes. Diabetes-related complications are relatively uncommon, so glucose-lowering treatment is not usually required. The exception is pregnancy, where fetal growth and therefore glucose-lowering treatment are predominantly determined by whether or not the fetus inherits the GCK mutation. The fetal genotype is not usually known but can be inferred from serial fetal ultrasound measurements. If there is evidence of accelerating fetal abdominal circumference on serial ultrasounds, the fetus is assumed to not have the GCK mutation and treatment of maternal hyperglycemia is indicated to reduce the risk of macrosomia, Caesarean section and neonatal hypoglycemia. If there is no evidence of accelerating fetal growth, the fetus is assumed to have inherited the GCK mutation and will have a similarly elevated glucose set-point as their mother, so maternal hyperglycemia is not treated. With recent advances in genetic technology, such as next-generation sequencing and noninvasive fetal genotyping, the detection and management of GCK-MODY in pregnancy should continue to improve.

OBJECTIVEGlucokinase monogenic diabetes (GCK-maturity-onset diabetes of the young [MODY]) should be differentiated from gestational diabetes mellitus (GDM) because management differs. New pregnancy-specific screening criteria (NSC) have been proposed to identify women who warrant GCK genetic testing. We tested NSC and HbA 1c in a multiethnic GDM cohort and examined projected referrals for GCK testing. RESEARCH DESIGN AND METHODSUsing a GDM database, 63 of 776 women had a postpartum oral glucose tolerance test suggestive of GCK-MODY. Of these 63 women, 31 agreed to undergo GCK testing. NSC accuracy and HbA 1c were examined. Projected referrals were calculated by applying the NSC to a larger GDM database (n = 4,415). RESULTSFour of 31 women were confirmed as having GCK-MODY (prevalence ∼0.5-1/100 with GDM). The NSC identified all Anglo-Celtic women but did not identify one Indian woman. The NSC will refer 6.1% of GDM cases for GCK testing, with more Asian/Indian women referred despite lower disease prevalence. Antepartum HbA 1c was not higher in those with GCK-MODY.