Chapter 5: Management of cystic fibrosis-related diabetes
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1/24/2018 at 3:59:08 PM GMT
Posts: 31
Chapter 5: Management of cystic fibrosis-related diabetes

Dear ISPAD member/friend,

Thank you for your continued interest in the 2018 ISPAD Clinical Practice Consensus Guidelines and in the previous drafts chapters we shared with you.

We are happy to announce that Chapter 5 on the Management of cystic fibrosis-related diabetes is now ready for you to read and comment on. We are looking forward to hearing your thoughts and input on this chapter. 

Kind regards,

David Maahs

ISPAD Secretary-General


 Attached Files: 

Last edited Monday, March 12, 2018
1/26/2018 at 4:42:29 PM GMT
Posts: 5
There is a study comparing insulin Treatment with Repaglinide at the beginning of CFRD (Lancet Diabetes Endocrinol. 2017 Nov 30. Repaglinide versus insulin for newly diagnosed diabetes in patients with cystic fibrosis: a multicentre, open-label, randomised trial.
Ballmann M1, Hubert D2, Assael BM3, Staab D4, Hebestreit A5, Naehrlich L6, Nickolay T7, Prinz N8, Holl RW8; CFRD Study Group.) This study should urgently be added because it shows some evidence for oral antidiabetic treatement especiallay at the beginning of the disease.
There are some limitations in this Trial (high drop Outs in the repaglinide arm) however the Trial should be added to the refernces and be carefully discussed in the Guidelines.


3/5/2018 at 12:06:29 PM GMT
Posts: 31
We want to thank all members who provided feedback on the Manement of cystic fibrosis-related diabetes chapter.

These comments were used to update the chapter.

Specific responses are provided in the attached PDF.

 Attached Files: 

Last edited Monday, March 5, 2018
3/8/2018 at 9:47:59 PM GMT
Posts: -3
My apologies for the lateness of this response, but I remain very concerned that the diagnosis of CFRD (and presumably the indication to start treatment) is still based on the standard ADA criteria. It is eminently clear from the literature, even going back to 2004 paper by Dobson as mentioned in the Guideline, that (as stated in the Guideline):
"Few individuals with CF have truly normal glucose tolerance (NGT). Even when the fasting and 2-hour OGTT glucose levels normal, variable, intermittent post-prandial hyperglycemia can often be detected at home by continuous glucose monitoring (CGM) 2, 3. With time, as glucose tolerance worsens, indeterminate glycemia develops (INDET, mid-OGTT glucose ≥11.1 mmol/L) [Dobson, 2004], followed by impaired glucose tolerance (IGT) and finally diabetes. Early diabetes is characterized by normal fasting glucose levels, but over time fasting hypergly-cemia develops. Isolated impaired fasting glucose (IFG) is sometimes present in persons with CF 4, 5.Few individuals with CF have truly normal glucose tolerance (NGT). Even when the fasting and 2-hour OGTT glucose levels normal, variable, intermittent post-prandial hyperglycemia can often be detected at home by continuous glucose monitoring (CGM) 2, 3. With time, as glucose tolerance worsens, indeterminate glycemia develops (INDET, mid-OGTT glucose ≥11.1 mmol/L) [Dobson, 2004], followed by impaired glucose tolerance (IGT) and finally diabetes. Early diabetes is characterized by normal fasting glucose levels, but over time fasting hypergly-cemia develops. Isolated impaired fasting glucose (IFG) is sometimes present in persons with CF 4, 5."
Given that any hyperglycaemia can result in subtly increased risks of increased susceptibility to infection, increased risk of mild dehydration (and hence increased viscosity of bronchial secretions), and increased nutritional requirements due to glycosuria, surely treatment with insulin is indicated once any persistent hyperglycaemia is identified, or even during episodes of stress-induced hyperglycaemia e.g. during infections, menses, etc.? The use of CGMS is mentioned but not included in the diagnostic criteria (I understand this may be because CGMS is 'not licensed for diagnostic purposes' - an argument I find spurious, as we use CGMS all the time to 'diagnose' hyperglycaemia in children with diabetes) but surely as clinicians we must be a bit bolder in supporting these vulnerable children - as it is in childhood that hyperglycaemia usually develops. I think there is also enough evidence to support the introduction of screening well before the age of ten years. As for the use of HbA1c for diagnosis or on-going monitoring, why can we not use fructosamine levels as these are not affected by increased RBC turnover, as shown in studies in children with conditions such as sickle-cell disease?

Serum fructosamine in the assessment of glycaemic status in patients with sickle cell anaemia.
Yahaya IA, Isah HS, Anaja PO.
Niger Postgrad Med J. 2006 Jun;13(2):95-8.

PMID: 16794643

Glycemic monitoring in diabetics with sickle cell plus beta-thalassemia hemoglobinopathy.
Kosecki SM, Rodgers PT, Adams MB.
Ann Pharmacother. 2005 Sep;39(9):1557-60. Epub 2005 Aug 2.

PMID: 16076916

John Goldsmith FRACP Consultant Paediatrician, Waikato New Zealand


3/12/2018 at 10:11:48 AM GMT
Posts: 1
Dr. Goldsmith makes a good point. “Usual” diabetes criteria based on risk of micro vascular disease may not be appropriate in C F. However, the selection of different numbers upon which to base a diagnosis would at this point be totally arbitrary. Until we have more outcomes data for specific glucose cut-off levels we are stuck with current OGGT criteria.


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