ABSTRACT
INTRODUCTION: There have been many recent advances in the treatment of type 1 diabetes (T1D) including in insulin formulations, continuous glucose monitoring (CGM) technology and automated insulin delivery. However, long-term optimal glycemic control is still only achieved in a minority. AREAS COVERED: Adjunct therapy - the use of therapeutic agents other than insulin - is one strategy aimed at improving outcomes. An ideal adjunct agent would improve glycemic control, reduce weight (or weight gain), reduce insulin requirement and prevent complications (e.g. cardiorenal) without increasing hypoglycemia. The amylin analogue pramlintide has been licensed in the USA, while the sodium glucose co-transporter-2 inhibitor (SGLT2i) dapagliflozin, was briefly (2019 - 2021) licensed for type 1 diabetes in Europe and the UK. However, other agents from the type 2 diabetes (T2D) arena including metformin, other SGLT2is, glucagon-like peptide-1 receptor agonists (GLP-1RA) and dipeptidyl peptidase-IV (DPP-4) inhibitors have been investigated. EXPERT OPINION: As evidence emerges for cardiorenal protection by SGLT2is and GLP-1RAs in T2D, it has become increasingly important to know whether people with T1D can also benefit. Here, we review recent trials of adjunct agents in T1D and discuss the efficacy and safety of these agents (alone and in combination) in an era in which continuous glucose monitoring is becoming standard of care.
Subject(s)
Diabetes Mellitus, Type 1 , Diabetes Mellitus, Type 2 , Sodium-Glucose Transporter 2 Inhibitors , Humans , Diabetes Mellitus, Type 1/drug therapy , Hypoglycemic Agents/adverse effects , Diabetes Mellitus, Type 2/drug therapy , Blood Glucose Self-Monitoring , Blood Glucose , Sodium-Glucose Transporter 2 Inhibitors/pharmacology , Insulin , Combined Modality Therapy , Glucagon-Like Peptide-1 Receptor/agonistsABSTRACT
Breast cancer risk is a common indication for referral to clinical genetics services. UK National Institute of Health and Care Excellence (NICE) guidelines use family history (FH) to stratify by 10-year risk of breast cancer from age 40. Patients are stratified into population risk (PR, 10-year risk <3%), moderate (MR, 3-8%) and high risk (HR, >8%). Women at increased risk are offered screening at or prior to age 40. To assess the clinical effectiveness of current risk stratification, FH data were obtained for all unaffected women with a FH of breast cancer aged <50, referred to cancer genetics from 2000-2010. Patients were risk stratified by NICE criteria, identifying patients who subsequently developed breast cancer. A total of 1409 women had 15,414 patient years of follow-up. Thirty invasive breast cancers developed, 13 in MR and 13 in HR women. Kaplan-Meier analysis demonstrated no significant difference in the rate of breast cancer development between PR and MR women from ages 40 to 49 (Log rank p = 0.431). There was a significant difference between ages 40 and 49 years between PR and HR women (p = 0.036), but not on exclusion of BRCA mutation carriers (p = 0.136). NICE absolute 10-year risk thresholds between ages 40 and 49 were not met in any risk group, when risk was estimated using the guidelines (PR = 0.82%, MR = 1.68%, HR = 3.56%). Our data suggest that improved criteria are required for risk assessment prior to age 50 and screening resources may be best focussed on those with highly penetrant mutations in cancer risk genes.
