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Assays / Trace
Metals/ Zinc
Zinc is an essential trace element, stored mainly in muscle.
Most circulating zinc, some 80%, is present in the red cells. A
similar proportion of plasma zinc is albumin bound. Most of the
remaining plasma zinc is bound to alpha-2 macroglobin, although
a small percentage is present as amino acid complexes.
Zinc is a component of many enzymes and other protein
structures (eg the zinc finger, as in transcription activation factors).
Thus zinc is crucial for normal growth and maturation; in malnourished
children, the rate of recovery of lean body mass is related to dietary
zinc intake. Zinc is regulated through its uptake by intestinal
mucosa in processes depending on intracellular zinc binding proteins,
the mechanisms of which are not fully understood. Significant interactions
with other trace elements, especially iron and copper occur. Zinc
supplementation can result in copper deficiency and vice versa;
the efficiency of absorption of both zinc and iron depend on the
ratio in which they are present.
Deficiency
Frank zinc deficiency was originally identified
as the cause of anaemia, growth retardation and hypogonadism in
deprived populations in the third world. Dramatic loss of zinc may
occur during catabolic processes, following operations, or severe
infections; acute zinc deficiency may then be precipitated as anabolic
processes requiring zinc supervene. This has been well documented
in patients on TPN with inadequate supplementation; the symptoms
include a characteristic rash, abdominal pain and diarrhoea with
depression and lethargy. Acrodermatitis enteropathica is a rare,
autosomal, recessive inherited defect of zinc absorption, which
presents with similar symptoms shortly after weaning. Lifelong therapy
with large doses of zinc is effective. Zinc deficiency (and/or copper
deficiency) may occur in premature infants prior to weaning, precipitated
by interrupted feeding or increased requirements (such as an infection),
when maternal milk concentrations of these elements are low. Premature
infants are at risk because they have smaller accumulated stores
at birth. The reversal of symptoms on treatment is dramatic. Many
situations have been described in which plasma zinc is low and marginal
deficiency has been postulated. The exact significance of the findings
is not always clear, as plasma zinc is affected by many factors
such as diet, diurnal variation, binding properties of albumin,
acute phase response, steroid therapy, and pregnancy. Nevertheless,
marginal zinc deficiency has been demonstrated in some situations
and may be more widespread than is generally thought.
Laboratory Indices of Zinc Status
Serum zinc assay is the simplest means of
assessing zinc status, but concentrations vary for many reasons
unconnected with zinc nutriture. There is a diurnal variation with
peak values about 10.00 h. Large fluctuations occur after meals
and fasting leads to an increase. Low values are found in pregnancy,
in certain malignancies (e.g. leukaemia), in patients with renal
failure, and when the serum albumin concentration is low. In situations
of stress or infection, the actions of interleukin and steroids
stimulate entry of zinc into cells and increased production of caeruloplasmin
by the liver. The degree of any acute phase response expected should
be borne in mind when interpreting low serum zinc concentrations;
marginally low values are hard to interpret, but a concentration
below 7 µmol/L indicates marked deficiency.
Urinary zinc excretion is also difficult to interpret;
low excretion may indicate zinc deficiency, but raised or normal
values do not exclude the possibility. Zinc is excreted when substances
to which it can bind are excreted in the urine, such as organic
acids, amino acids, low molecular weight proteins or certain drugs.
In catabolic states, large amounts of zinc released from tissues
may be excreted in the urine, giving rise to marked depletion at
the recovery stage.
When zinc deficiency is present, a relatively low serum
alkaline phosphatase activity is indicative, since the enzyme contains
zinc; blood ammonia may also be slightly increased. Erythrocyte
zinc responds only slowly to changes in zinc status, which are often
rapid. This investigation may, however, be useful to differntiate
between pre-existing thyrotoxicosis and transient hyperthyroidism
during pregnancy. Leucocyte zinc content may offer an improved indication
of zinc status as it correlates well with muscle zinc content. The
test however, requires a large sample of blood, needing particularly
careful handling soon after collection.
Zinc is a common element and precautions against contamination
must always be maintained; collection tubes should be checked and
kept covered; containers with metal or rubber closures or separating
beads must be avoided, as should powder in gloves.
Assessment of altered taste perception by zinc 'taste
tests' is unfortunately very subjective and is of no value in studies
of zinc status.
References:
Lao TTH, Chin RKH, Swaminathan R, Panesar
NS, Cockram CS. Erythrocyte zinc in differential diagnosis of hyperthyroidism
in pregnancy: a preliminary report. BMJ 1987; 294: 1064-5
Vallee BL, Falchuk KH. The biochemical basis of zinc
physiology. Physiol Revs 1993; 73: 79-118
Rhodes D, Kluh A. Zinc fingers. Scientific American
February 1993: 56-65
Taylor A. Detection and monitoring for disorders of
essential trace elements. Annals of Clinical Biochemistry 1996;
33: 486-510
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