This debate seems to pop up at regular intervals on this mailbase.
Interpretation of the serum calcium/PTH relationship is complex in a FEW
patients. However to say that "It is meaningless to discuss ANY error in
calcium metabolism unless ionized calcium is measured!!" is wrong.
Normocalcaemic primary hyperparathyroidism certainly does exist but the
diagnosis and (need for) treatment of this entity is controversial. Given a
very liberal definition about 2% of the postmenopausal population can be
defined as having primary hyperparathyroidism (with adenoma). In random
postmorten samples up to 5% or so of the population have findings which an
enthusiastic surgen/pathologist would define as parathyroid adenoma. This
entity probably blurrs into the upper limit of the normal calcium/PTH
relationship. If the aim is to "diagnose" this subgroup, measurement of
ionised calcium is better than albumin corrected calcium.
Measurement of calcitonin is irrelevant in this context. There are many
other hormones which have vastly greater effects on calcium metabolism than
does calcitonin in man. Patients with no calcitonin (athyroid with thyroxine
replacement) or a huge calcitonin excess (MCT) have no proven abnormality of
calcium homeostasis or bone mineral content.
PTH is pretty sensitive as an index of Vitamin D deficiency, and given the
vagaries of Vitamin D assays the finding of "normal" concentrations of
Vitamin D and normal serum alkaline phosphatase is not terribly surprising.
The definition of "normal" Vitamin D concentrations have recently been the
subject of much debate in any event. Normality is increasingly being
described in terms of the relationship with PTH. Some laboratories still
appear to be reporting Vitamin D > 10nmol/L as "normal". If the objective is
to optimize the probability of good health, then it seems reasonable that
serum 25(OH)D should be more than 50nmol/L or so. See Veith, American
Journal of Clinical Nutrition, Vol. 69, No. 5, 842-856, May 1999
and recent issues of Osteoporosis International for a flavour of this
debate.
Aubrey Blumsohn
Senior lecturer in Metabolic Bone Disease
University of Sheffield
----- Original Message -----
From: Sten Öhman <[log in to unmask]>
To: <[log in to unmask]>
Sent: Tuesday, November 21, 2000 7:06 AM
Subject: Re: PTH and normocalcaemia
At 2000-11-21 14:36 +1000, Bruce Campbell wrote:
>In recent times we have been seeing requests for PTH levels in
>normocalcaemic patients, probably as part of an "osteoporosis" or
>"osteoporosis risk" investigation. We have seen a number of patients with
>elevated PTH levels (Immulite intact PTH assay) and normal serum calcium.
I suppose that you mean "serum total calcium". It has been clearly
established since more than 25 years that total calcium is a bad measure of
errors in calcium metabolism. Nevertheless, ionized calcium is not a
standard method in most laboratories.
It is meaningless to discuss ANY error in calcium metabolism unless ionized
calcium is measured!!
Ionized calcium can be highly pathological despite a total calcium well
within its reference range. So, if this is true for a patient, he/she has a
true hyper/hypo-calcaemaia and should be treated accordingly.
On the other side, if ionized calcium is normal, other causes of high/low
levels of PTH etc should be investigated. The ionized calcium level can be
in balance if the primary cause is some calcium-increasing factor e.g. high
levels of calcitonin, vitamin C, high intake of calcium, followed by a
normal compensatory reaction from the parathyroideae.
So: Before speculating in any of all possible causes: Measure ionized
calcium!
Mr Sten Öhman, PhD
Sten Öhman, PhD
Elfin Lab & Milieuconsult
P O Box 133
S-590 70 Ljungsbro
Sweden
Tel Nat: 013-368940 Int: +46 13 368940
Fax Nat: 013-368941 Int: +46 13 368941
[log in to unmask]
%%%%%%%%%%%%%%%%%%%%%%%%%%%%%%%%%%%%%%%%%%%%%%%%%%%%%%%%%%%%
|