We conducted a cross-sectional study examining consecutive adults with T1DM who attended the Young Adult Diabetes Clinic (individuals with age between 18 and 25 years) and the General Adult Diabetes Clinic (individuals > 25 years old) between 1st January and 25th November 2019 at Southmead Hospital, North Bristol NHS Trust, Bristol, UK. All investigations were performed as part of routine clinical care.
The Patient Safety, Assurance and Audit (PSAA) committee at North Bristol NHS Trust (the ethics committee at the trust which approves clinical audits) approved this audit (audit number: CA8757).
Consent was not needed as this was a retrospective audit performed as part of a service evaluation, rather than a research study – this was approved by the PSAA committee.
Only clinically available data, as part of routine care, was included in the audit. The reporting of the study was carried out in accordance with STrengthening the Reporting of OBservational studies in Epidemiology (STROBE) guidelines on observational studies.
The T1DM diagnosis was determined based on the age of diagnosis, presence of T1DM-related autoantibodies (GAD, IA-2, and zinc 8 transporter), the measurement of urinary or blood c-peptide, and history of diabetic ketoacidosis in accordance with the Association of British Clinical Diabetologists (ABCD) criteria for diagnosing T1DM11. Participants were included in the study if they fulfilled any of the following criteria: 1) low urine or blood c-peptide, regardless of age of diagnosis; 2) two or more positive T1DM-related autoantibodies, regardless of age of diagnosis; 3) one positive T1DM-related autoantibody, and diagnosed < 30 years of age; 4) history of diabetic ketoacidosis (DKA), and diagnosed < 30 years of age; 5) diagnosed < 20 years of age, regardless of T1DM-related autoantibody status. Participants with T2DM, maturity onset diabetes of the young (MODY), diabetes secondary to underlying medical conditions (e.g. due to pancreatitis or steroid induced diabetes), and individuals where the diabetes diagnosis was not clear or yet confirmed were excluded from this study.
Overweight was defined as a BMI of 25-29.9 kg/m2, and obesity as a BMI ≥ 30 kg/m2. For people of Asian ethnic background, BMI cut-offs of 23-27.4 kg/m2 and ≥ 27.5 kg/m2 were used to identify people with overweight and obesity, respectively12.
Participants’ data including height, weight, blood pressure, medications and past medical history, as well as biochemistry information including lipid profile and haemoglobin A1c (HbA1c – measured by high performance liquid chromatography) were collected from electronic Participants’ records. Hypertension was defined as recorded blood pressure > 140/90mmHg; use of blood pressure lowering medications; or a documented relevant diagnosis in the electronic Participant record13. Estimated glucose disposal rate (eGDR) was calculated as a validated proxy of insulin resistance based on the following formula: eGDR = 19.02 – (0.22 x BMI [kg/m2]) – (3.26 x hypertension status [yes = 1, no = 0]) – (0.61 x HbA1c [converted from IFCC mmol/mol to NGSP %])9. An eGDR value of < 8 was used to identify individuals with DD9. Data were collected, anonymised and stored on a secure NHS computer in line with data protection guidelines.
Statistical analysis
Data are presented as median and interquartile range (IQ) or numbers (percentages), unless stated otherwise. Data were checked for normality using Histogram and Shapiro-Wilk test. Between groups comparisons, normal BMI vs. overweight/obesity, were assessed using the Mann-Whitney U test, or chi-square for frequencies. Correlations were assessed using Spearman rank-order correlation coefficient, as appropriate. A p-value of < 0.05, 2-tailed, was considered statistically significant. Data were analysed using PASW statistics 26 package (SPSS Inc., Chicago, USA)14.