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Tabea

GAD antibody question

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I'm trying to interpret a Gad 65 Antibody test result of 410 u/ml. Reference range is 1-5. IgA normal, Anti islet cell negative. Presentation in DKA.

 

Does that sound like the patient suffered an autoimmune attack on the pancreas?

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Suffers. The attack is ongoing. That is a very high titre.

 

I presented in DKA but did not get antibody testing till a year after low-carbing.

 

If you are looking for clinical information though it is best to look in a textbook such as Joslin's. In fact, Joslin's has a very good section on LADA Diabetes, (ICA-negative might point to LADA rather than classic Type 1).

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Linda,

 

Thanks for your response. I am now wondering why that patient (me) with 410 GAD was discharged from hospital and told she had Type 2 diabetes.

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Linda,

 

Thanks for your response. I am now wondering why that patient (me) with 410 GAD was discharged from hospital and told she had Type 2 diabetes.

 

Same reason I WAS. You are probably non-insulin dependent at this point. I was ... and they were apprehensive about discharging me without some training in how to use insulin. And after THAT, I had to FIGHT to get GAD testing AND subsequently even to get insulin. The whole experience stank like rotten fish. I am now on the THIRD Endo in that practice, which of course places me at risk of being labeled a malcontent. Well ... I AM.

 

I would still be PO'd though. Were you seen by an Endo?

 

I DID find in a recent handbook (A VA Handbook, no less) the recommendation that ANY patient in DKA should be evaluated for beta cell deficiency. I DO wish the AACE would make that a practice guideline though. Geez.

 

If you look in PubMed at papers on KPD or ketosis prone diabetes, there are statistics on outcomes post-DKA.

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Linda,

 

I was put on basal bolus insulin from the moment I was wheeled out of intensive care. Before leaving hospital I was given training on how to give myself the Novorapid and Lantus. And I was enrolled on a carb-counting course. In other words, they treated me as a Type 1. But they discharged me from hospital with a letter saying I was Type 2. And they told me I was antibody NEGATIVE.

 

That was a year ago. I only saw the results of my antibody tests this week.

 

Since then I have had a C-peptide test done. I produce no insulin of my own.

 

And they still insist on calling me Type 2. I don't understand why!? Surely DKA+zero C-peptide+positive GAD = textbook Type 1 diagnosis?

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Linda,

 

I was put on basal bolus insulin from the moment I was wheeled out of intensive care. Before leaving hospital I was given training on how to give myself the Novorapid and Lantus. And I was enrolled on a carb-counting course. In other words, they treated me as a Type 1. But they discharged me from hospital with a letter saying I was Type 2. And they told me I was antibody NEGATIVE.

 

That was a year ago. I only saw the results of my antibody tests this week.

 

Since then I have had a C-peptide test done. I produce no insulin of my own.

 

And they still insist on calling me Type 2. I don't understand why!? Surely DKA+zero C-peptide+positive GAD = textbook Type 1 diagnosis?

 

Yeah - I get that too ...

 

C-peptide (done on three separate occaisions): no measurable level

GAD - not done

Anti-islet cell: none

 

=> no c-peptide implies that there is no endogenous insulin production

but

no "Anti-islet cell activity" means that when the added some of the blood sample to a culture of artificial pancreatic islet cells, the cells were not destroyed

 

Islet cell destruction = Type 1

No c-peptide = Type 1

 

I tick box 2, but not box 1 (so do you)

 

Positive GAD antibody test = Type 1 (but more closely associated with T1.5)

 

I suspect that you and I are T1.5

 

T2 = Insulin Resistance

 

LADA/T1.5/MODY all fit the bill better than either T2 or T1 for me, for you, and I woud bet many of the other "difficult to diagnose" diabetics on this board.

 

This insistance that there is only 2 types of diabetes is simply wrong. There are at least 40 different underlying causes already identifiedm, and as research continues, the field becomes more complex, not less.

 

Most doctors and insurance companies want a simple binary/black-and-white differentiation between T1 and T2. This tend is exacerbated by the way the general media talk about diabetes, which means that the vast majority of non-diabetics do not understand the issue ... and many people with diabetes also never get properly educated either!!!

 

For legal purposes (driving, piloting, licensing for long distance truck driving or carrying passengers), the most important factor is whether or not the individual is likely to have an unexpected Hypo. If you are on sulpha drugs (T2), or are injecting insulin (T1 or T2), your may suffer a hypo because the insulin in your system is not there as a response to food, but is being generated by an external source (injected or generated under duress). If you are on medication to reduce insulin resistance, to potentiate insulin production in the presence of glucose, or otherwise to affect secondary systems to improve blood glucose levels without directly stimulating insulin generation/release (all the other T2 meds), you will not normally suffer a Hypo, and you will never suffer a severe, untreatable hypo. Thus from the POV of governments and insurance companies, they don't care about the fundamental diagnosis ... they want to know if you are going to have an uncontrollable hypo.

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A LADA or T1.5 with zero insulin production: can someone explain the functional or practical difference between that and T1? This is an example where i think those delineations might hold on some minor level (exact antibody? "Age" (though T1 can strike any time)) but to all intents and purposes: T1, anyway.

 

Guess I'm putting in a vote for a basic T1 diagnosis. Big antibody response. No internal insulin. Go straight to jail, don't collect $200. (if we were playing monopoly that is).

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Yeah, i agree...definately type one in your case...

 

Im the exact opposite...no gad, low normal fasting insulin but hi insulin w glucose challenge, trace elevation of ICA...yeah im just a mystery i guess...just a game of wait and see.

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A LADA or T1.5 with zero insulin production: can someone explain the functional or practical difference between that and T1? This is an example where i think those delineations might hold on some minor level (exact antibody? "Age" (though T1 can strike any time)) but to all intents and purposes: T1, anyway.

 

Guess I'm putting in a vote for a basic T1 diagnosis. Big antibody response. No internal insulin. Go straight to jail, don't collect $200. (if we were playing monopoly that is).

 

Actually in ICD codes, LADA IS simply T1. There MIGHT be a difference in antibody profile, but that is a bout it. And as far as clinical therapy goes, insulin is needed in Late T2, Late LADA, and T1.

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Linda,

 

I was put on basal bolus insulin from the moment I was wheeled out of intensive care. Before leaving hospital I was given training on how to give myself the Novorapid and Lantus. And I was enrolled on a carb-counting course. In other words, they treated me as a Type 1. But they discharged me from hospital with a letter saying I was Type 2. And they told me I was antibody NEGATIVE.

 

That was a year ago. I only saw the results of my antibody tests this week.

 

Since then I have had a C-peptide test done. I produce no insulin of my own.

 

And they still insist on calling me Type 2. I don't understand why!? Surely DKA+zero C-peptide+positive GAD = textbook Type 1 diagnosis?

 

That sounds like a plain old clerical error.

 

Or perhaps they were going by the old definition of adult onset. Clearly not NIDDM v IDDM.

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That sounds like a plain old clerical error.

Or perhaps they were going by the old definition of adult onset. Clearly not NIDDM v IDDM.

 

Nope, it's not a clerical error. I have lots of letters from various doctors in the department and they have me down as an 'atypical Type 2 who must be treated differently from other Type 2s'.

 

Operationally they treat me as a Type 1. I didn't mind the Type 2 label so much when I was under the impression I was antibody negative.

 

But discovering I was actually antibody positive has now made me really angry at being misdiagnosed. I wonder if it's because I *look* fat. Even though I was BMI 23.9 at diagnosis. But BMI means nothing; I have the sort of fat distribution that means I have always looked 10-20 kg heavier than I actually weigh. Certainly if you had me in a room of Type 1s and asked a neutral observer to pick out 'who is the most likely Type 2 in this room', the neutral observer would pick me.

 

I emailed one of the doctors who's been calling me a Type 2 and brought his attention to my antibody tests. He had not seen the antibody results - which makes me think that somewhere down the line, some doctor missed the antibody result and slapped a T2 label on my file and ever since then everybody has just gone by the T2 label without looking at the antibody tests.

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For one thing, on insurance, Type 1 pays for MORE TEST STRIPS. Look up ICD Codes Diabetes, print off the definitions and take them to task on it.

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A LADA or T1.5 with zero insulin production: can someone explain the functional or practical difference between that and T1? This is an example where i think those delineations might hold on some minor level (exact antibody? "Age" (though T1 can strike any time)) but to all intents and purposes: T1, anyway.

 

My sister was just diagnosed this year (February) at the age of 45. She was classified as straight Type 1. She tested for antibodies and had a very low c-peptide. I forget if the results she told me were done while she was in the hospital or immediately after. Either way, I'm glad nobody started talking to her about LADA or Type 1.5 because that would have just been confusing. My sister is also very thin normally and looked skeletal by the time she went to the ER.

 

I was diagnosed in 1987 at age 19 and I was overweight. I was in very bad shape (DKA) when I got to the hospital but other than that I don't know what my numbers/labs were because it meant nothing to me at the time. I also don't know if they were calling it Type 1 then; all I remember is the endo telling me that I no longer make insulin and would have to inject it for the rest of my life. She told me pills would not work and that I couldn't have done anything to prevent it.

 

It sounds to me like Tabea is a typical Type 1. While having a different diagnosis put down in her records may not affect her daily life, it can be a problem later on with insurance as Linda pointed out.

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Liz and Linda,

 

Thanks for your replies. There is no insurance issue because I live in the UK and I am classified as 'diabetes mellitus requiring insulin' which gets me a medical exemption certificate, so all my prescriptions are free.

 

Liz - Good for you that the doctors weren't prejudiced by you being overweight. I used to be clinically obese (BMI 33) but had lost 1/4 of my body weight and kept it off. When I woke up from the DKA the first thing I said to the diabetes doctor was, 'How can this happen? I've lost 1/4 of my body weight over the past 6 years, and kept it off.' She just looked pityingly at me but didn't say anything. Any unprejudiced person looking at my antibody tests would have replied, 'It has nothing to do with your weight. You suffered an autoimmune attack on your pancreas.'

 

Later, I asked another diabetes doctor, 'Could I have done anything to prevent this?' And he said no, I had such a strong genetic predisposition to (T2) diabetes that even the lifestyle of an Olympic athlete couldn't have prevented it. Which was reassuring at the time but again, wrong. Because an autoimmune attack on the pancreas cannot be prevented!

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Clinically it should not make a difference between T1.5 and T1. However recent research articles, for those interested, indicate differing antibody profiles (GAD-65 dominant), and different inflammatory and other metabolic markers, between LADA and Classic Type 1 of juvenile or adult onset. At this point the differences are academic, but in the future they might lead to different genetic markers, and even different therapies.

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Are you sure that you are referring to the same reference ranges? 410 can be high on one scale. I am wondering if you need to convert it to 4.1?

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