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"The only thing that all of the people with APS Type 1 have in common is the will to survive" -- Pablo Ramírez

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My question stems from several late diagnoses as a child of various components of APS type 1. I don't
believe my endocrinologist knew I had APS Type 1 or what to look for. I only heard I had APS type 1 when I was diagnosed with severe aneamia due IF antibodies under the care of a different endocrinologist. so my first question is this: Are autoantibodies for the varying diseases associated with APS type 1 always circulating in the body - say from birth - and remain dormant until they decide to "attack" the organ/gland of its interest? For instance, have I always had the autoantibodies for Hypoparathyroidism, addison's disease, and pernicious anemia? If so, then could testing for them early help to predict the course of APS type 1? Is it possible to have an autoantibody and never develop the disorder? If so, what "triggers" that you know of cause the autoantibodies to start wreaking havoc on
the body? My questions are for one purpose: I've had no new disease diagnoses since 2003 and would like to know what to expect for the future (if possible) - I find it hard to know which common symptoms are common and which may indicate a new disease. Thanks!

Response to your question from Dr MacLaren

Posted by dr at July 17, 2007 08:56 PM
Autoantibodies in APS-1 do an increased risk for component diseases. They are usually present long before the component disease appears. In the case of antibodies to the enzyme 21-hydroxylase, the predictive rate is high. Early disease detection is a goal herein, and can be identified by rising blood levels of renin (a kidney hormone that stimulates the salt retaining steroid hormones) and ACTH (a pituitary hormone that stimulates glucocorticoids such as cortisol). Blood samples are best taken in the mid afternoon after a 20 minute rest for this purpose. However in the case of type-1 diabetes in APS-1, antibodies to islet cells and to there component enzymes such as glutaminic acid decarboxylase or GAD are commonly seen without diabetes following, although this may happen.

In my practice, I do test for such antibodies and follow positive patients for early warnings of the clinical disease. Some years ago, we found APS-1 patients with hypoparathyroidism to have antibodies against the calcium sensing receptor found on the surface of parathyroid cells. Whereas for a while, others could not confirm our finding, other laboratories eventually did. However our test was difficult to perform and so far, has only been used in a research setting. Recently, colleagues at Oxford University in the UK have found antibodies to the immunologically important cytokines named interferons in all patients with APS-1 whatever the stage of their APS-1 or component organs involved. This suggests that such antibodies can be useful diagnostically and their presence may be essential to the development of the wide spread autoimmunities of APS-1. If so, perhaps an intervention to get rid of such antibodies may eventually be developed as a prev! entative treatment.

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