The management of type 1 diabetes in adults. A consensus report by the American Diabetes Association (ADA) and the European Association for the Study of Diabetes (EASD)

Abstract

The American Diabetes Association (ADA) and the European Association for the Study of Diabetes (EASD) convened a writing group to develop a consensus statement on the management of type 1 diabetes in adults. The writing group has considered the rapid development of new treatments and technologies and addressed the following topics: diagnosis, aims of management, schedule of care, diabetes self-management education and support, glucose monitoring, insulin therapy, hypoglycaemia, behavioural considerations, psychosocial care, diabetic ketoacidosis, pancreas and islet transplantation, adjunctive therapies, special populations, inpatient management and future perspectives. Although we discuss the schedule for follow-up examinations and testing, we have not included the evaluation and treatment of the chronic microvascular and macrovascular complications of diabetes as these are well-reviewed and discussed elsewhere. The writing group was aware of both national and international guidance on type 1 diabetes and did not seek to replicate this but rather aimed to highlight the major areas that healthcare professionals should consider when managing adults with type 1 diabetes. Though evidence-based where possible, the recommendations in the report represent the consensus opinion of the authors. Graphical abstract.

Keywords: Adjunctive therapy; Diabetic ketoacidosis; Diagnosis; Exercise; Glucose monitoring; Hypoglycaemia; Insulin; Nutrition; Psychosocial care; Schedule of care; Transplantation; Type 1 diabetes.

Fig. 1

Flow chart for investigation of suspected type 1 diabetes in newly diagnosed adults, based on data from White European populations. ¹No single clinical feature confirms type 1 diabetes in isolation. The most discriminative feature is younger age at diagnosis (<35 years), with lower BMI (<25 kg/m²), unintentional weight loss, ketoacidosis, and glucose >20 mmol/l (>360 mg/dl) at presentation also being informative. Other features classically associated with type 1 diabetes, such as ketosis without acidosis, osmotic symptoms, family history or a history of autoimmune diseases are weak discriminators. ²GAD should be the primary antibody measured and, if negative, should be followed by islet tyrosine phosphatase 2 (IA2) and/or zinc transporter 8 (ZNT8) where these tests are available. In those diagnosed below the age of 35 years who have no clinical features of type 2 diabetes or monogenic diabetes, a negative result does not change the diagnosis of type 1 diabetes since 5–10% of people with type 1 diabetes do not have antibodies. ³Monogenic diabetes is suggested by the presence of one or more of the following features: HbA_1c <58 mmol/mol (7.5%) at diagnosis, one parent with diabetes, features of specific monogenic cause (e.g. renal cysts, partial lipodystrophy, maternally inherited deafness, severe insulin resistance in the absence of obesity), and monogenic diabetes prediction model probability >5% (www.diabetesgenes.org/exeter-diabetes-app/ModyCalculator; accessed 20 August 2021). ⁴A C-peptide test is only indicated in people receiving insulin treatment. A random sample (with concurrent glucose) within 5 h of eating can replace a formal C-peptide stimulation test in the context of classification. If the result is ≥600 pmol/l, the circumstances of testing do not matter. If the result is <600 pmol/l and the concurrent glucose is <4 mmol/l (<72 mg/dl) or the person may have been fasting, consider repeating the test. Results showing very low levels (<80 pmol/l) do not need to be repeated. Where a person is insulin-treated, C-peptide must be measured prior to insulin discontinuation to exclude severe insulin deficiency. Do not test C-peptide within 2 weeks of a hyperglycaemic emergency. ⁵Features of type 2 diabetes include increased BMI (≥25 kg/m²), absence of weight loss, absence of ketoacidosis and less marked hyperglycaemia. Less discriminatory features include non-White ethnicity, family history, longer duration and milder severity of symptoms prior to presentation, features of the metabolic syndrome and absence of a family history of autoimmunity. ⁶If genetic testing does not confirm monogenic diabetes, the classification is unclear and a clinical decision should be made about treatment. ⁷Type 2 diabetes should be strongly considered in older individuals. In some cases, investigation for pancreatic or other types of diabetes may be appropriate. ⁸A person with possible type 1 diabetes who is not treated with insulin will require careful monitoring and education so that insulin can be rapidly initiated in the event of glycaemic deterioration. ⁹C-peptide values 200–600 pmol/l are usually consistent with type 1 diabetes or maturity-onset diabetes of the young (MODY) but may occur in insulin-treated type 2 diabetes, particularly in people with normal or low BMI or after long duration

Fig. 2

CGM visualisation in an ambulatory glucose profile (AGP) report. Figure courtesy of R. M. Bergenstal and the International Diabetes Center, Minneapolis, MN, USA. To convert glucose values to mmol/l, values in mg/dl should be divided by 18. DOB, date of birth

Fig. 4

A framework for the follow-up treatment of an individual with type 1 diabetes. ¹The availability of blood and urine ketone measurement varies across healthcare systems

Fig. 5

The four critical times when DSMES is particularly needed for people with diabetes (and their caregivers, when applicable). ICR, insulin:carbohydrate ratio; incl., including; ISF, insulin sensitivity factor

Fig. 6

Choices of insulin regimens in people with type 1 diabetes. CGM improves outcomes with injected or infused insulin and is superior to BGM. Inhaled insulin may be used in place of injectable prandial insulin in the USA. ¹The number of plus signs (+) is an estimate of relative association of the regimen with increased flexibility, lower risk of hypoglycaemia and higher costs between the considered regimens. LAA, long-acting insulin analogue; RAA, rapid-acting insulin analogue; URAA: ultra-rapid-acting insulin analogue