I have an unusual form of diabetes which is the subject of water-cooler conversation in the department at my local hospital, and the source of a continuing existential crisis for myself. I thought I had found closure with my obstetrician’s recent summary of me as ‘late-onset non-autoimmune Type 1’ or Type 1b. My main diabetes doctors still call me a ‘ketosis-prone Type 2’ while treating me as an ‘operational Type 1’. But they always told me, ‘you are not a Type 1 because you don’t have antibodies.’ I have to stress though that since dx, I have received all the proper treatment that I need, so that has never been an issue. A quick timeline:
June 2 2010: Dx in DKA with BG over 540 and A1C over 20%. Initially dx T1, then changed to ‘we’re not sure but you’re going to be on insulin for the rest of your life’.
June 6 2010: Discharged from hospital with labels ‘ketosis-prone Type 2’ and ‘severe insulin resistance’. Otherwise treated as Type 1, given basal-bolus and enrolled on carbs/insulin training course.
March 2011: Enrolled in ‘severe insulin resistance’ research study
April 2011: Results from the study indicated that I am not insulin resistant at all. C-peptide of 0.318 ng/ml (106 mm/ol) indicate I am not producing my own insulin. First paradigm shift: I am insulin-deficient, not insulin resistant! But still called Type 2 (though treated as Type 1) because of lack of antibodies.
July 2011: Finally saw a copy of my antibody test results. Can you believe I never asked to see them until now? IgA was normal and Anti-islet cell antibodies were negative. GAD 65 Antibodies were 415u/ml, reference range 1 to 5.
So why was I told that I had tested negative for antibodies? That GAD number looks convincingly positive to me.
But see, there’s a red herring. So should I say, black. Since the age of five, I have suffered from acanthosis nigricans, a hyperpigmentation of the skin around the neck, groin, armpits and elbows. It is strongly correlated with hyperinsulinemia, insulin resistance and Type 2 diabetes. I also have a strong family history of Type 2. And despite being a normal BMI at dx, I have the sort of fat distribution that means I look fat even at a normal weight.
Acanthosis nigricans indicates that the person is over-producing insulin. But my marks were clear and present, even when I presented in the emergency room in DKA, in a state of absolute insulin deficiency. The marks remain even though my C-peptide shows I hardly make any of my own insulin. The doctors are at a loss to explain this. But the presence of the acanthosis keeps shouting ‘Type 2’ at some of them.
But to me, those antibody test results are shouting something completely different. How can it be possible to slap a Type 2 label on an antibody-positive patient? And then not even tell them they tested positive for antibodies in the first place?
