Filling the knowledge gap in diabetes management during Ramadan

Saud Al Sifri and Kashif Rizvi. Diabetes Therapy. Doi: 10.1007/s13300-016-0168-9

Clinicians treating Muslim patients often struggle with achieving satisfactory glycaemic control during Ramadan. Reasons for this include the vary length of fasting from year to year as well as significant changes to diet and lifestyle during this period. Although there are some treatment guidelines, it is unclear what the evidence base was for them, especially as most diabetes guidelines are designed around non-fasting patients. This paper reviewed the evidence base for managing glycaemic control in T2DM during Ramadan, including 10 RCTs and 20 observational studies. The over-arching finding was the significant heterogeneity in these studies including targets, definition of hypoglycaemia and treatments, for example the lack of studies which looked at DPP4 inhibitors and GLP1 analogues – medications which would be expected to be suited to periods of fasting. Studies tended to concentrate on HbA1c, (which covers 2-3 months) as a measure of glycaemic control, rather than fructosamine which covers the preceding 2-3 weeks. Clearly more rigorous and well designed studies with defined safety and clinical end points are required to refine treatment during Ramadan for patients with T2DM.

http://link.springer.com/article/10.1007%2Fs13300-016-0168-9

 

Accelerated fetal growth prior to diagnosis of gestational diabetes mellitus in nulliparous women

Ulla Sovio. Diabetes Care. Doi: http://dx.doi.org/10.2337/dc16-0160

The HAPO study showed an association between fetal weight and blood glucose levels below the diagnostic thresholds for gestational diabetes (GDM). Current NICE guidance for GDM advises a screening glucose tolerance test at 24-28 weeks. Too early and the diagnosis may be missed, too late and the fetus may have already developed complications, specifically macrosomia. As a result, timing of the diagnostic test attempts to minimise these potential problems. Using sequential ultrasound measurements of fetal abdominal circumference (AC), this prospective study showed that at 20 weeks, there was no association between AC and a future diagnosis of GDM whilst at 28 weeks there was an increased risk of increased AC. Maternal obesity had a similar 28-week association whilst a combination of obesity and GDM had a 5x increased risk of AC.  Additive with obesity, there is a period of accelerated fetal growth at 20-28 weeks before GDM was diagnosed, possibly associated with rising glucose levels. Perhaps the timing of the GTT should be individualised in order to make the diagnosis as early as possible rather than the current uniform approach.

http://care.diabetesjournals.org/content/early/2016/03/31/dc16-0160.abstract

 

A multicenter observational study of incretin-based drugs and heart failure

Kristian B. Filion et al. NEJM. Doi: 10.1056/NEJMoa1506115

Following the (probably inappropriate) demise of rosiglitazone in 2010, all new pharmacotherapies for diabetes are subjected to cardiovascular (CV) outcome trials to prove safety. Five placebo-controlled studies have reported; three gliptins, one GLP-1 RA (lixisenatide) and one SGLT2-inhibitor (empagliflozin). All studies showed non-inferiority for their primary CV end-point (indeed, empagliflozin demonstrated superiority), however, the SAVOR-TIMI 53 trial of saxagliptin threw up the unexpected finding of a significant increase in hospitalisation due to heart failure (HF). The FDA performed a detailed examination of this trial along with the EXAMINE study of alogliptin (which showed a trend towards increased HF) and in April 2016 issued a drug safety communication of increased risk of HF for both agents. Note that the TECOS study of sitagiptin was not considered and it showed no signal for HF risk. This NEJM publication analysed ‘real-life’ health care data from almost 1.5 million patients. The rate of hospitalization for HF did not increase with the use of incretin-based drugs as compared with other oral antidiabetic-drug combinations. Results were similar for gliptins and GLP-1 RAs. Perhaps the SAVOR-TIMI result was a fluke after all.

http://www.nejm.org/doi/full/10.1056/NEJMoa1506115

 

 

The impact of insulin therapy and attitudes towards insulin intensification among adults with T2D

Elizabeth Holmes-Truscott, Jessica L. Browne, Jane Speight. Diabetes and Its Complications. Doi: DOI: http://dx.doi.org/10.1016/j.jdiacomp.2016.03.027

The NICE guidelines for management of type 2 diabetes (NG28), published in December 2015, recommend intensification of treatment when the HbA1c rises to 58mmol/mol (7.5%) and this includes initiation of insulin. This recommendation is not new; dating back to 2002, NICE has advocated the same upper limit for HbA1c, with insulin as the final therapeutic tool to achieve this. However, despite this long-standing guidance, studies show that HbA1c at insulin initiation in the UK is typically more than 75mmol/mol (9%).  Moreover, once started on insulin, around half of patients remain above the 58mmol/mol target with no optimisation. This phenomenon, labelled ‘clinical inertia’, is the subject of a great deal of research. This study reports twenty face-to-face interviews with adults using insulin for up to 4 years. Positive and negative experiences of insulin therapy were reported but most were receptive to insulin intensification, despite the reported barriers. Perhaps this indicates that clinicians (rather than patients) or the NHS environment is the main barrier to insulin. Or maybe, the majority of patients and clinicians don’t buy into the NICE target.

http://www.jdcjournal.com/article/S1056-8727(16)30064-2/abstract

 

The burden of NAFLD and its characteristics in a nationwide population with type 2 diabetes

Gabriele Forlani et al. Journal of Diabetes Research. Doi: http://dx.doi.org/10.1155/2016/2931985

For clinicians who were trained in the 1980-90’s, the presence of fatty liver identified by ultrasound was a common but benign finding in patients with poorly controlled type 2 diabetes (T2DM). Over the past ten years, this phenomenon has been promoted to disease status, termed nonalcoholic fatty liver disease (NAFLD). This publication examines the prevalence of NAFLD and its clinical correlates in 94,577 patients, using the ‘fatty liver index’ (FLI) as a proxy for NAFLD. FLI is an algorithm based on BMI, waist circumference, triglycerides and GGT. FLI-NAFLD was present in 59.6% of patients and, compared to the ‘normals’, was associated with impaired renal function, higher albumin excretion, HbA1c and blood pressure and lower HDL cholesterol. So, should we be assessing liver function tests as part of the diabetes annual review? Apparently not, since the ALT was within normal limits in 73.6% of the FLI-NAFLD patients. A bigger question though, is does the identification of the ‘burden of NAFLD in T2DM’ make any difference, since treatments and targets probably remain the same? You can tell when I trained.

http://www.hindawi.com/journals/jdr/2016/2931985/