I did so because the patient came to my clinic telling me to had been on DIETARY Rx ever since but with a history of limb amputation (left lower limb amputated in 2012!) sometimes recently. His today's glycaemic readings have been FBG of 4.6Mmol/L and 5.8Mmol/L after a 2 hours post glucose load challenge comprising of 100 g of glucose !

This could be glucokinase monogenic diabetes. This is characterised by non-progressive mild fasting hyperglycaemia. This is an autosomal dominant condition caused by loss of function mutations in the GCK gene. A useful test is to look at parent and children to see if they also exhibit the mildly raised glucose, this is often not previously detected.

Find more info here:

www.diabetesgenes.org

Thanks all

@Tim: even though your answer is largely credible, still it is confusing to realise the same person with "mild fasting hyperglycaemia" could end up with amputation following a foot ulcer.

Even though, I do undestand NO glucose value is 100% protective from vascular damages, it is highly improbable for the event to occur to the patient!

Remember: the same person with "mild forms of fasting glycaemia" also has his right leg amputated in 2012!

Makes GCK unlikely, they have no complications!

What hba1c is he running? What's his Bmi and ethnicity.

HbA1c value (last done in December 2013!) was 5.5%. He is black and very much wasted (BMI=17.5kg/M2)

At present busy declaring that he has been cured DIABETES mellitus!

He is also SUPER TALL and hence his BMI might be a relative measure of what so ever underlying pathology I guess...

be careful with its interpretation Tim.

1. Height and peripheral neuropathy : taller the client with diabetes, the higher the likelihood of neuropathic ulceration and greater the rate of amputations.

J Clin Diagn Res. Feb 2013; 7(2): 296–301.

Published online Dec 24, 2012. doi: 10.7860/JCDR/2013/5140.2751

PMCID: PMC3592296. Peripheral Insensate Neuropathy-Is Height a Risk Factor? G S Sharath Kote. et al.

2. IFG- is part of metabolic syndrome. He possibly has insulin resistance. As he not obese (presumably waist circumference is normal) hence he has not gone on to develop T2DM yet!.

3. IGF is common in Blacks/South Asians, alcoholics and obese (waits circumference higher that for given ethnicity)

4. Does any other immediate relatives have IGF?

@Kaz Mawji: thanks for your inputs. I have read the article too. Thanks a million times.

I have no idea about the clinical background surrounding his bloodline as first and foremost in this environment people have no good health care seeking behavior. Its until they get sick for them to get diagnosed of any pathology in their bodies.

At present, I request for more inputs on the following:

1. while I agree the patient might have IFG and possibly be categorised as pre-diabetic, it is still not so clear why his fasting glycaemia initially was in diabetic range (around 12Mmol/L reported back then in one of the incident measurements!) and even reported to have been kept under tabs glibenclamide 5mg od for sometimes before he went to dietary Rx.

2. what proportion of pre-diabetics in your horizon actually tend to develop features that are at present considered to be complications due to diabetes?)

Hi Kelvin,

2. "The prevalence of co-morbidities in the pre-diabetic group are Ischaemic Heart Disease 64 (20.6%), Chronic Kidney Disease 12 (3.9%), cerebrovascular disease 11 (3.5%), PVD 24 (7.7%), eye disease 1 (0.3%), peripheral neuropathy 8

(2.6%) and autonomic neuropathy 17 (5.5%). The prevalence of many of the co-morbidities assessed is statistically the same in pre-diabetes patients with only peripheral vascular disease, eye disease and cerebrovascular disease having a

statistically significant higher prevalence in type 2 diabetes." Ref: Comparison of comorbidities in patients with pre-diabetes to those with diabetes mellitus type 2

Farrell, C; Moran, J Department of General Practice, Brookfield Health Sciences Centre, UCC, Cork.

1. Back in a second!!

thank you a million Kaz.

aren't the findings out of a study sample?

do you have any other evidence that have been a product of a population based survey?

1. That was a long second..lol.

I do not know of any longitudinal study of complications in the IGF group, perhaps this study comes close. Assessment and treatment of cardiovascular risk in prediabetes: impaired glucose tolerance and impaired fasting glucose

RA DeFronzo, M Abdul-Ghani - The American journal of cardiology, 2011 - Elsevier

and this one: Prevalence, diagnosis, and treatment of impaired fasting glucose and impaired glucose tolerance in nondiabetic US adults

A Karve, RA Hayward - Diabetes care, 2010 - Am Diabetes Assoc

2. The effect of glucotoxicity and lipotoxicity on b-cell dysfunction can be somewhat ameliorated when one uses insulin therapy in early stages of treatment of hyperglycaemia. However in your patient is a real possibility that long acting sulphonamide in addition to dietary control has preserved b-cell function and continues to preserve it as his waist circumference presumably has not increased. So his low calorie intake currently suffices to have -ve OGTT. But he certainly not free of day glycemic complications. Perhaps if you could post his current anthropometric readings would than help in further understanding his current metabolic status. Cheers.

Ok...i will work it out about his recorded anthropometric values once back to the office next week.

Cheers!

Hallo, how about measuring c-Peptide? Then you have a solid Information on his endogenic insulin-production.

greetings

Sighart Walter Golf

Have you done the patient's A1C using an HPLC machine?

There are studies on "Reversal of Diabetes". If the patient FPG pr OGTT is not as per the recommendation of ADA or WHO, there are chances that same patient has been entered into remission or reversal of diabetes.