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ERRATA

ERRATA

Pages 343-344 | Published online: 24 Jun 2012
This article refers to:
Approaches to measurement of Vitamin D concentrations - Immunoassays

In the article“Approaches to measurement of Vitamin D concentrations – Immunoassays“, by Dr Beatus Ofenloch-Haehnle, published in Supplement 243 of the current volume of Scandinavian Journal of Clinical and Laboratory Investigation (72(S343): S50-53, DOI 10.3109/00365513.2012.681955), two tables were not published. In addition, one of the tables was misplaced in “Vitamin D – why does it matter? – Defining Vitamin D deficiency and its prevalence“ by Prof Heike A. Bischoff-Ferrari on pages S3-6, DOI 10.3109/00365513.2012.681938, and another omitted from the submitted manuscript.

and in Dr Beatus Ofenloch-Haehnle‘s article are missing and reproduced below:

Table I. Design of Immunoassays.

Table II. Reference Calibration and Traceability of Immunoassays.

Prof Stefan Pilz wants to make the following corrections and clarifications to the “Questions and Answers” following his article “Vitamin D and cardiovascular disease: update and outlook” (72(S343): S83-91, DOI 10.3109/00365513.2012.681972):

S Pilz answering M Kaelin (Switzerland)

I hope that on-going trials will provide definite answers, but these trials have some limitations have severe limitations. These include that study participants are included irrespective of their serum 25(OH)D concentration. Quite a significant vitamin D intake is permitted so that may be a problem.

S Pilz answering M Fukagawa

Yes, but for CKD I agree with what has been said by R Vieth; that we should consider the 25(OH)D concentration. If it is normal, we should think of prescribing active vitamin D. Sometimes there are difficulties in vitamin D deficient patients who are given additional 1,25(OH)2D3. Another issue with CKD patients is that when you give calcitrol or other active vitamin D analogues, they may increase the degradation of 25(OH)D because of a reduction in the by 24 hydroxylases.

S Pilz answering P Rozentryt

You are referring to the paracalcitrol trial which studied renal patients and failed to show an effect on cardiac function. The issue is, was this the right therapy? It may be that the cardiomyocytes need more than then 25(OH)D. If just a small amount of 25(OH)D is intracellularly converted to the active form then a much higher local concentration can be achieved by vitamin D than with systemic therapy with 1,25(OH)2D3 which may be harmful (e.g. due to hypercalcemia) or have and has a very narrow therapeutic window.

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