phoenix
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- Type of diabetes
- Type 1
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Maybe it really isn't clearThis seems to back up those who have stated that he is in fact a T2. He seems very coy in most interviews and articles not to mention what type he is
http://docserver.ingentaconnect.com...ser&checksum=73B3D51909F1191D9B32178A3606F2EB
I still think this could be LADA, At the time it hadn't really been described well, it still doesn't get any mention in UK guidelines or on the DUK site.At presentation, he gave a past medical history of intermittent ulcerative colitis diagnosed in 1992,which was then under good control, and of appendicectomy in April 1997. He had required insulin (20–30 units per day) for prednisolone-induced diabetes during treatment for previous exacerbation of colitis. He weighed 105 kg and on examination was a very fit man. He had no diabetic complications(specifically no evidence of peripheral vascular disease) and normal peripheral sensation, power, tone and reflexes. The random blood glucose was 25 mmol/l associated with moderate ketonuria, but no proteinuria. The results of investigation suggested
a diagnosis of type 2 diabetes with a negative islet cell antibody titre and detectable C-peptide.
He wasn't tested for the GAD antibodies that are most common in LADA. http://www.isletsofhope.com/diabetes/sy ... html#chart
Onset was relatively rapid ( onset for LADA tends to be relatively faster at younger ages, he was in his 30s). This man was being tested very frequently with a huge range of metabolic tests, if his glucose levels were gradually rising you would have though it would have been detected. He had detectable C peptide, but unless this was high,it would still accord with T1 (many have some detectable even after 50 years) and certainly LADA.
He appears as an example of someone with LADA on the Swansea uni LADA website : http://www.locallada.swan.ac.uk/exper.html.
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Later in the paper , they describe his problems with a loss of power after 5 minutes and with hypos associated with longer and more intense sessions. They discuss what happens in T1 diabetes to explain the problems (basically loss of counter regulatory hormones which cause the liver to release glucose, also a comparative reduction in the glucagon necessary to activate the production of glucose in the liver). It seemed that he needed 25% of his glucose from the liver but this impaired production of glucose from the liver resulted in insufficient glucose for maximum effort.
( It could be injected insulin causing the problem but it seems to me that people with T2, even on insulin ,more frequently have the opposite problem, their liver is all to willing to give them extra glucose, metformin is thought to work, in part, because it surpress this glucose from the liver)
Maybe though his case demonstrates that little T1, T2 boxes dont really describe the possible variations in diabetes . The previous prednisolone induced diabetes may also have played a part in the development of his particular brand.