How has your working knowledge and management of diabetes changed in the past six months? For that matter, has it actually even changed? I find that the more I think I know on the subject of diabetes, the more I realise that I still have to learn. I find attendance at diabetes updates and conferences, whether they are half a day or two days, whether they are locally run or nationally, have so much to teach me. I rarely find that I attend a meeting and come away having learnt nothing.
At the beginning of September, I went along to a DESMOND class run in Portsmouth by two of the Diabetes Specialist nurses from Queen Alexandra Hospital. My aim was to find out what was included in this day of structured education for patients with type 2 diabetes, and how useful it might be to them. I had quite a critical eye on all that took place, but found it to be excellent, and the way they explained type 2 diabetes in terms the layperson could understand was superb. I came away, having improved my comprehension of what type 2 diabetes is and why there are specific complications. Already I have been able to apply some of that learning in practice.
Just this past week, through the online diabetes course I have recently started, I had to read an article in Diabetes Care. In the article it was suggested that we might not be treating our patients with type 2 diabetes, in the most effective way. From a large number of research studies the authors demonstrated that by the time someone is diagnosed with type 2 diabetes, they have already lost 80% of their b-cell function. Even when they are still at the higher end of the impaired fasting glycaemia range, ie. when they are at 6.7 -7.0% or 48-53mmol/mol, they have by then lost 50% of their b-cell function.
The article proposed that instead of treating to target, or as was stated there “treating to failure”, where we increase medications as we fail to get the person’s blood glucose under control (with the Hba1c to guide us here) we should instead be targeting the pathophysiological issues underlying the diabetes. This would mean that from diagnosis, the person may need to be on multiple therapies, to combat the obesity, the insulin resistance in the muscles and the liver and associated problems with the renal system, nervous system and glucose metabolism. The thought was that from the start patients would not only take Metformin, but also GLP1 analogues, which can combat a number of the issues just mentioned.
I found this fascinating reading and stimulating to consider what is proposed, and would encourage you to find the article in Diabetes Care Vol 36 supplement 2, August 2013.
Our current treatment algorithm recommends that we initiate metformin therapy to achieve Hba1c <7%, then sequentially adding in Sulphonylurea or now the newer anti diabetes agents. Where is the evidence for this algorithm from the pathophysiology of type 2 diabetes? Even UKPDS demonstrates that failure with these oral medications used in this kind of algorithm means that most patients will end up on Insulin therapy.
This is a real challenge to our current practice, and one that needs further investigation, so that care is really tailored to effectively treating our patients. We might even find ourselves using Glitazones again, well pioglitazone perhaps, as this drug has protective effects on b-cell function, and is also a powerful insulin sensitizer. GLP1 Analogues improve and preserve b-cell function for at least three years, they also enhance weight loss, and delay gastric emptying. The weight loss then has a knock on effect on insulin sensitivity elsewhere in the body.
Why not obtain this article, read it and discuss it with your local experts; let’s check out what this is really all about. If this mean we should look to a change in our practice, let’s make sure we understand the evidence and are ready for the change! After all, our aim is to provide for the wellbeing of our patients.
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