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Zinc Deficiency: a Contributing Factor of Short Stature in Growth Hormone Deficient Children

Authors:
Zeynep Siklar at Ankara University
Zeynep Siklar
Ceyda Tuna Kirsaçlioğlu at Ankara University
Ceyda Tuna Kirsaçlioğlu
Yildiz Dallar at T.C. Sağlık Bakanlığı Ankara Eğitim ve Araştırma Hastanesi
Yildiz Dallar
Gülten Tanyer
Gülten Tanyer
Gülten Tanyer
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Abstract

Zinc is an essential trace element which affects growth by promoting DNA and RNA synthesis and cell division. Zinc deficiency causes growth retardation and its frequency is high in developing countries. It could contribute to the effect of growth hormone (GH) treatment in GH deficient children. In this study, we investigated zinc deficiency in GH children. Twenty-four GH deficient children (treated with GH for 2.2 +/- 1.6 years) were recruited for the study. Intracellular erythrocyte zinc levels were measured. Eleven (45.9 per cent) were found to be zinc deficient (Group 1), while 13 patients (54.1 per cent) had normal zinc levels (Group 2). The mean growth velocity was 5.98 +/- 0.8 cm/year in Group 1 and 6.9 +/- 1.4 cm/year in Group 2. Group 2 was given oral zinc supplementation with a resultant growth velocity of 7.51 +/- 0.5 cm/year. During GH treatment in GH deficient children, zinc status should be evaluated as severe zinc deficiency could affect the response to GH treatment.
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Introduction
Zinc is an essential trace element and a cofactor of
many metalloenzymes that are involved in numerous
biochemical processes such as skin integrity,
immunity, bone formation and tissue growth and
development. Zinc deficiency results in depressed
immunity, impaired taste, poor wound healing,
delayed sexual maturation, growth retardation,
weight loss, and abnormal dark adaptation.
1
Rapidly
growing infants and children who have a diet of low
bioavailability of zinc, are more prone to zinc
deficiency.
2
Furthermore, zinc deficiency can be an
important factor on the growth of growth hormone
(GH) deficient children.
3
We, therefore, aimed to evaluate zinc levels of GH
deficient children.
Materials and Methods
Twenty-four GH deficient children (13 boys and 11
girls) who were treated with recombinant GH for at
least 1 year, were recruited for the study. It is thought
that the catch-up growth period during the first year
of the GH treatment could effect the growth rate.
Children with chronic systemic disorders, malab-
sorbtion, malnutrition, Turner syndromes and
multiple hypophysal hormone deficiency were not
included in the study.
We studied intraerythrocyter zinc levels by atomic
absorption spectrophotometry. Normal intraerythro-
cyter zinc levels are 8.2–8.7 ng/ml. Eleven patients
were found to be zinc deficient (Group 1) and 13
patients were found to have normal zinc levels
(Group 2). Zinc supplementation was given in a
dosage of 1 mg/kg/day for 6 months. The growth
velocity of the study groups was evaluated for at least
6 months before and after the zinc treatment. Unfor-
tunately we were unable to measure the insulin like
growth factor-1 (IGF-1) levels in our study.
Statistical analysis was done between groups with
respect to growth velocity by using the
Mann–Whitney U-test.
Results
All patients were prepubertal and diagnosed as
isolated GH deficient. The body mass index of the
patients was normal and there was no statistically
significant difference between the two groups.
Patients’ mean age was 9.3 ± 2.2 years (range 5.6 –
13.5 years). They had been treated with rhGH for 2.2
± 1.6 years (range 1.1 – 4.3 years).
Group 1 (n = 11, 45.9 per cent) were both zinc-
deficient and GH deficient children. Their mean age
was 11.4 ± 2.1 years. Their GH treatment period was
2.6 ± 1.9 years. Before zinc supplementation, the
growth velocity of group 1 was 5.98 ± 0.8 cm/year. At
the beginning of the study, the mean zinc level of
group 1 was 6.9 ± 1.1 ng/ml.
Group 2 was comprised of 13 GH deficient only
children (54.1 per cent); mean age 10.7 ± 1.2 years.
The rhGH treatment period was 2.0 ± 1.7 years. The
initial growth velocity of Group 2 was 6.9 ± 1.4
BRIEF REPORTS
Journal of Tropical Pediatrics Vol. 49 June 2003 187
Zinc Deficiency: a Contributing Factor of Short Stature in
Growth Hormone Deficient Children
by Zeynep Șıklar, Ceyda Tuna, Yıldız Dallar and Gülten Tanyer
Ministry of Health Ankara Hospital, Department of Pediatrics, Turkey
Summary
Zinc is an essential trace element which affects growth by promoting DNA and RNA synthesis and
cell division. Zinc deficiency causes growth retardation and its frequency is high in developing coun-
tries. It could contribute to the effect of growth hormone (GH) treatment in GH deficient children.
In this study, we investigated zinc deficiency in GH children. Twenty-four GH deficient children
(treated with GH for 2.2 ± 1.6 years) were recruited for the study. Intracellular erythrocyte zinc
levels were measured. Eleven (45.9 per cent) were found to be zinc deficient (Group 1), while 13
patients (54.1 per cent) had normal zinc levels (Group 2). The mean growth velocity was 5.98 ± 0.8
cm/year in Group 1 and 6.9 ± 1.4 cm/year in Group 2. Group 2 was given oral zinc supplementation
with a resultant growth velocity of 7.51 ± 0.5 cm/year. During GH treatment in GH deficient
children, zinc status should be evaluated as severe zinc deficiency could affect the response to GH
treatment.
Correspondence: Dr Zeynep Șıklar, Orman Fidanlık Iojmanları
23/4, 06560 Sög˘ütözü, Ankara, Turkey. Tel. 0 312 2158254. E-mail
<zeynepsklr@hotmail.com>.
13 ones (971)(ds) 5/6/03 10:38 AM Page 187
cm/year, and the intraerythrocyter zinc level was 8.8
± 0.4 ng/ml.
After a 6-month period, in Group 1 the growth
velocity was 7.51 ± 0.5 cm/year (p < 0.05); in Group 2
it was 6.8 ± 0.6 cm/year. Hence, the growth velocity
increased in Group 1, but did not change in Group 2
after a 6-month follow-up period.
Only four patients complained of gastric irritation
due to zinc. No other complications were seen.
Discussion
Zinc deficiency can be caused by an inadequate
dietary intake, impaired absorbtion, excessive excre-
tion or inherited defects in zinc metabolism.
2
In Turkey, Aras
4
reported that except for upper-
middle income families, the daily zinc intake was
much lower than the recommended value of 15
mg/day.
Zinc has an important role in protein synthesis and
IGF-1 synthesis can be impaired by zinc deficiency. A
reduction in circulating IGF-1 concentrations has
been proposed as a potential mechanism for growth
retardation induced by zinc deficiency.
5
An import-
ant observation was the significant elevation in the
IGF-1 level after zinc supplementation.
6
Unfortu-
nately we were unable to measure the IGF-1 levels of
our patients.
Lifshitz and Nishi
7
reported that zinc supplemen-
tation improved the growth in patients who had
abnormal growth patterns without any other abnor-
mality except hypozincemia.
During the rGH treatment, an increase in body
growth could cause relative deficiency of essential
elements such as zinc.
2
Cheruvanky, et al.
8
reported
that 22 GH deficient children who were receiving
hGH, were given 50 mg of oral zinc supplementation
daily for a year and had an increased growth rate from
5.1 to 7.3 cm/year. In our study, the incidence of zinc
deficiency among the hormone deficient children was
45.8 per cent while receiving GH treatment, and
growth velocity increased with zinc supplementation.
Six months is a very short time to follow-up, and an
increased case number and follow-up time is desir-
able. Furthermore, controlling the IGF-1 serum level
will also help to emphasize the effect of zinc supple-
mentation.
Zinc deficiency could be a contributory factor to
the decrease in growth in children with growth
disorders. Especially in zinc-deficient countries such
as Turkey, zinc deficiency should be kept in mind for
its effect on growth, while treating GH deficiency
with rhGH.
References
1. Polysangam A, Falciglia GA, Brehm BJ. Effect of marginal zinc
deficiency on human growth and development. J Trop Med 1997;
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2. Ince E, Kemahlı S, Uysal Z, Akar N, Cin Ș, Arcasoy A. Mild zinc
deficiency in preschool children. J Trace Elem Exp Med 1995; 7:
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3. Collip PJ, Castro Magana M, Petrovic M. Zinc deficiency;
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4. Aras NK. Dietary intake of zinc in Turkey. In Abdulla M, et al.
(eds), New Aspects of Trace Element Research. Smith-Gordon,
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5. Prasad A. Zinc and growth. J Am Coll Nutr 1996; 15: 341–42.
6. Nakamura T, Nishiyama S, Suginohara YF, Matsuda I, Higashi
A. Mild to moderate zinc deficiency in short children. J Pediatr
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Effect of growth hormone on hair, serum and urine zinc in
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668–70.
BRIEF REPORTS
188 Journal of Tropical Pediatrics Vol. 49 June 2003
13 ones (971)(ds) 5/6/03 10:38 AM Page 188
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Article
  • May 1996
Zinc deficiency in humans is widespread and is more prevalent in areas where the population subsists on cereal proteins. Conditioned deficiency of zinc is seen in many diseased states. A mild deficiency of zinc in pregnancy is associated with increased maternal morbidity, abnormal taste sensation, prolonged gestation, inefficient labor, atonic bleeding, and increased risks to the fetus. Among the urban poor in the US, a marginal zinc intake during pregnancy was associated with increased risk of preterm and very preterm delivery. Factors responsible for zinc deficiency in premature infants include high fecal losses of zinc, low body stores of zinc at birth, and increased zinc requirement during rapid growth. Zinc supplemented infants demonstrated improved linear growth velocity and maximum motor development scores. Marginal and moderate growth impairment in children as a consequence of inadequate zinc intake has been reported from many developed and developing countries. In one study from Japan, 21 prepubertal children were diagnosed to have zinc deficiency. The caloric intake, growth velocity, serum zinc, and plasma insulin-like growth factor-1 increased significantly in the zinc supplemented group. The clinical manifestations of zinc deficiency include growth retardation, hypogonadism in males, neurosensory disorders, cell-mediated immunological dysfunctions, and skin changes. Approximately 300 enzymes are known to require zinc for their activities. Zinc is required for DNA synthesis, cell division and protein synthesis. Several hundreds of zinc containing nucleoproteins are probably involved in gene expression of various proteins. A deficiency of zinc also affects proliferation and maturity of lymphocytes adversely.
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Effect of Marginal Zinc Deficiency on Human Growth and Development
Article
  • Sep 1997
Growth and development disorders in humans caused by zinc (Zn) deficiency have been investigated for a long time. Although marginal Zn deficiency is a common nutritional problem around the world, especially in the children of developing countries where diets have less Zn available, it is difficult to identify. This review provides the progression of studies in the effect of Zn deficiency on human growth and development, and also explains the possible mechanisms of how Zn promotes these phenomena. These mechanisms involve the effects of Zn on DNA synthesis, RNA synthesis, and cell division. The concept of zn-finger proteins explains the role of Zn in gene expression and endocrine function. Findings indicate that Zn deficiency can result in delayed growth and development which can be corrected in part by Zn supplementation.
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Mild to moderate zinc deficiency in short children
  • Jan 1993
  • 65-9
  • T Nakamura
  • S Nishiyama
  • Yf Suginohara
  • I Matsuda
  • Higashi
Nakamura T, Nishiyama S, Suginohara YF, Matsuda I, Higashi A. Mild to moderate zinc deficiency in short children. J Pediatr 1993; 123: 65–9.
Mineral deficiency during growth Pediatric Disease Related to Calcium
  • Jan 1980
  • 305-326
  • F Lifshitz
  • Y Nishi
Lifshitz F, Nishi Y. Mineral deficiency during growth. In DeLuca HF, Anast CS (eds), Pediatric Disease Related to Calcium. Elsevier, New York, 1980: 305–21.