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Download this complete Project material titled; Analysis Of Serum Calcium And Phosphorus In Rickets And Non Rickets Children Of Gonin-Gora, Kaso And Jankasa Communities In Kaduna State with abstract, chapters 1-5, references, and questionnaire. Preview Abstract or chapter one below

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The beginning of the 20th century witnessed the epidemic of nutritional rickets
among children in many countries of Asia, North America, Northern Europe and Africa.
Nutritional rickets remain a problem in developing countries despite a decline in the
prevalence of the condition in developed countries. Prevalence of rickets among infants
and young children is high in Nigeria and in Gonin-Gora, Jankasa and Kaso in particular.
It was therefore imperative to evaluate some biochemical parameters in rickets disease
prevalence areas of Kaduna state namely: Gonin Gora, Jankasa and Kaso. This study
aimed at determining the serum levels of calcium and phosphorus together with the levels
of associated biochemical parameters for the affected family member in these
communities; as an investigation into the scourge of rickets. Randox Diagnostic test kit
was used to determine the serum levels of calcium and urea while creatinine and
phosphorus serum levels were measured using Agappe Diagnostic kit, serum sodium and
potassium levels were determined using flame photometric method. The results obtained
showed that serum calcium levels were low with mean values of 2.29± 0.01 S.E.M., 2.34+
0.01 S.E.M and 2.24 ± 0.01 S.E.M in Gonin Gora, Jankasa and Kaso respectively
compared with the 2.25-2.75 mmol/l normal limit. Phosphorous levels were toward the
upper limit with mean values of 1.48 ± 0.02 S.E.M and 1.68 ± 0.02 S.E.M in Gonin gora
and Jankasa respectively; compared with the normal limit of 0.8-1.9 mmol/l. However the
mean serum calcium for rickets children from Kaso community (2.19 ± 0.03S.E.M) was
below the normal range value of (2.25-2.75mmol/dL). None of the differences in
measured levels was statistically significant. Rickets among rural children has been
reported to be attributed to low serum calcium levels. The low serum levels of calcium and
high serum phosphorus levels could be the major causes of the disease in these settlements
especially during the period of the children growth. Also when the mean biochemical
parameters for Gonin-Gora, Jankasa and Kaso were compared, the results showed that
calcium levels was much more significantly reduced in Kaso compared with the other two
communities, and this could be the reason why more rickets children were found in Kaso
compared to Gonin-Gora and Jankasa. The results of influence of sex among the rickets
and non rickets males and females children showed that, sex had no significant influence
in the parameters of rickets male and females children living in Gonin-Gora, Jankasa and
Kaso communities.
In conclusion, the concentrations of serum calcium for rickets children were at the
lower limit of normal range while the concentration of serum phosphorus were at the
higher limit of the normal range which can be attributed to rickets disorder among




Title page – – – – – – – – – i
Declaration – – – – – – – – – ii
Certification – – – – – – – – – iii
Dedication – – – – – – – – – iv
Acknowledgement – – – – – – – – v
Abstract – – – – – – – – – vi
Table of Content – – – – – – – – viii
List of Table – – – – – – – – – xi
1.1 Rickets – – – – – – – – 1
1.2 Types of rickets – – – – – – – – 2
1.3 Vitamin D deficiency – – – – – – – 4
1.4 Calcium deficiency- – – – – – – – 7
1.5 Statement of research problem – – – – – – 9
1.6 Aim and objectives of the study – – – – – – 9
2.1 The communities – – – – – – – 11
2.2 Religion and culture – – – – – – – 12
2.3 Review on analysis of calcium, sodium, potassium and phosphorus- – 13
2.4 Review on analysis of creatinine and urea – – – – 15
2.5 Colorimetric methods of analysis – – – – – 16
3.1 Materials – – – – – – – – 18
3.1.1 Chemicals- – – – – – – – – 18
3.1.2 Equipment and glasswares- – – – – – – 18
3.2 Methods – – – – – – – – 19
3.2.1 Study protocol- – – – – – – – – 19
3.2.2 Analysis of serum sodium, potassium, calcium, phosphorus, urea and
creatinine – – – – – – – – – 20 Analysis of calcium – – – – – – – 20 Analysis of phosphorus – – – – – – 20 Analysis of creatinine – – – – – – – 21 Analysis of urea – – – – – – – 21 Analysis of sodium and potassium – – – – – 21
4.1 Determination of Mean serum biochemical indices in rickets and non rachitic children
of Goni-Gora community – – – – – – – – -23
4.2 Mean serum biochemical indices for rickets and non rickets children of Kaso
Community – – – – – – – – – 25
4.3 Mean serum biochemical indices for rickets and non rickets children in Jankasa
Community – – – – – – – – 27
4.4 Comparison of mean serum biochemical parameters for rickets and non rachitic
children in Gonin-Gora, Jankasa and Kaso communities – – 29
4.5 Comparison of the effect of mean serum biochemical parameters in rickets and non
rachitic male and female children in Gonin-Gora, Jankasa and Kaso communities -31
5.1 Mean serum biochemical indices for rickets and non rickets children in Gonin-
Gora community – – – – – – – 35
5.2 Mean serum biochemical indices for rickets and non rickets children in Kaso
Communities – – – – – – – – 35
5.3 Mean serum biochemical indices for rickets and non rickets children in Jankasa
Communities – – – – – – – – 36
5.4 Comparism of mean serum biochemical values for rickets and non rickets children for
the group analysis in Gonin-Gora, Jankasa and Kaso communities – – 36
5.5 The influence of sex on the serum biochemical parameters in rickets and non rickets
children of Gonin-Gora, Jankasa and Kaso communities – – – 37
6.1 Summary – – – – – – – – 38
6.2 Conclusion – – – – – – – – 38
6.3 Recommendations – – – – – – – 39
REFERENCES – – – – – – – – 40
Appendix – – – – – – – – – 46




Rickets causes bone deformities through the impaired mineralization of actively
growing bone. Rickets is ranked among the 5 most prevalent diseases of young children
in developing countries (Guesry et al., 1991), and is frequently found in Africa and
Asia (Pettifor et al., 1978, Thacher et al., 1997; Thacher, 2003; Fischer et al., 1999 and
Bhattacharyya et al., 1992). Up to 9% of children in central Nigeria have physical
findings consistent with rickets (Pfitzner et al., 1998), including bowing of the legs,
impaired mobility, pain, and pathologic fractures. Besides the long-term sequel
associated with the bone deformities, rickets is also associated with an increase in acute
morbidity. In Ethiopia, a case-control study described a 13-fold greater prevalence of
rickets among children with pneumonia than in control children (Muhe et al., 1997).
Although nutritional rickets is often attributable to vitamin D deficiency (Holick
et al., 1999). Recent reports suggest that an insufficient calcium intake is also an
important cause of rickets (Oginni et al., 2003 , DeLucia et al., 2003). Children with
calcium-deficiency rickets have higher serum concentrations of 1,25-dihydroxyvitamin
D [1,25(OH)2D] and parathyroid hormone and lower serum concentrations of calcium
and 25-hydroxyvitamin D [25(OH)D] than do children without rickets. Calcium
supplementation, with or without vitamin D, heals rickets more rapidly in children than
does vitamin D alone (Thacher et al., 1999). However, despite uniformly low calcium
intakes, calcium intakes are not lower in Nigerian children with rickets than in those
without rickets ( Thacher et al., 2000). Reduced calcium absorption or relative
resistance to 1,25(OH)2D could account for rickets in these children.(Thacher et al.,
a) Vitamin D- deficiency rickets or nutritional rickets.
The causes are vitamin D deficiency, phosphorus or calcium deficiency (rare),
inadequate sunlight exposure, secondary to malabsorption syndrome (IBD),
celic disease, cystic fibrosis (rarely). The clinical features include skeletal
findings, abnormal gait, hypocalcemic tetany / seizures developmental delay
and failure to strive.
b) Vitamin D –dependent rickets.
Type 1 is also known as pseudovitamin D deficiency rickets and it is caused by
deficiency of renal 25 (OH) D3-1-alpha-hydroxylase. Inheritance pattern is
autosomal recessive and the clinical features for younger than two years are
hypocalcemic tetany, severe bony changes and seizures.
c) Type 11 or hereditary 1-alpha,25-dihydroxyvitamin D-resistant rickets.
It is caused by defective interaction between calcitriol and receptor. Inheritance
pattern is autosomal recessive and clinical features for younger than one year,
severe bony changes and alopecia.
d) Vitamin D-resistant rickets.
There are two types of vitamin D resistant rickets which are;
di) Familial hypophosphatemic rickets or X-linked hypophosphatemic
rickets caused by impaired proximal renal tubular reabsorption of
phosphorus and inappropriate normal calcitriol levels. Inheritance
pattern is X-linked dorminant and clinical features include short status,
leg bowing and dental abnormalities.
dii) Hereditary hypophosphatemic rickets with hypercalciurea.
It is caused by impaired proximal renal tubular reabsorption of
phosphorus and increased calcitriol. Inheritance pattern are autosomal
recessive and autosomal dorminant. The clinical features are bone pain
and muscular weakness.
e) Miscellaneous
These include renal rickets or renal osteodystrophy which is caused by loss of
functional renal parenchyma caused by chronic renal failure leads to mineral
derangements and decreased calcitriol production. The clinical features include
bone pain, arthralgias, fractures, muscle weakness and failure to thrive.
f) Rickets of prematurity
The cause is multifactorial with osteopenia and fractures as clinical features.
g) Tumor-induced or oncogenic rickets caused by tumor-induced inhibition of
renal 25 (OH)D3 -1-alpha-hydroxylase. The clinical features include fractures,
bone pain and muscle weakness.(American family physician,2006).
The peak age at which rickets is most prevalent is 3-18 months (Salimpour,
1975). Factors that have been shown to be important in the pathogenesis of rickets at
this age include exclusive breast-feeding, maternal vitamin D deficiency, living in
temperate climates, lack of sunlight exposure, and darkly pigmented skin. In the Middle
East and other more-tropical climates, social and religious customs that prevent sunlight
exposure appear to be important (Molla et al., 2000 Bassir et al., 2001 Atiq et al.,
It is well recognized that breast milk normally contains insufficient
concentrations of vitamin D or its metabolites (estimated as 20–60 IU/L) (Specker et
al., 1985; Hillman et al., 1986). To ensure the normal vitamin D status of the nursing
infant relatively high-dose maternal vitamin D supplements (2000 IU/d) are needed to
increase maternal breast milk concentrations to levels that maintain the vitamin D status
of the breast-fed infant (Ala-Houhala et al., 1986).
Breast-fed infants are generally protected from vitamin D deficiency rickets
during the first few months of life, because vitamin D metabolites, especially 25-
hydroxyvitamin D [25(OH)D], do cross the placenta, such that neonatal 25(OH)D
concentrations are approximately two-thirds of maternal values (Hillman et al., 1995).
It is estimated that the half-life of serum 25(OH)D is about 3 weeks; therefore, even if
neonates do not receive an exogenous supply of vitamin D during the first weeks of life,
25(OH)D concentrations should decrease to values associated with vitamin D
deficiency only towards the second month, provided that the maternal vitamin D status
is adequate during pregnancy.
Several studies from the Middle East, North America, and northern Europe have
highlighted the prevalence of low circulating concentrations of 25(OH)D during
pregnancy (Henriksen et al., 1995; Daaboul et al., 1997; Datta et al., 2002). Factors
found to be important include increased skin pigmentation, immigration from non-
European countries to countries of high latitude, limited skin exposure as a result of
religious and social customs, and vegetarian diets. Congenital rickets has been observed
in such situations, although its occurrence is rare (Mohapatra et al., 2003; Anatoliotaki
et al., 2003; Zeghoud et al., 1997), and neonatal hypocalcemia is more frequent among
neonates born to mothers with low 25(OH)D concentrations than among those born to
mothers with normal vitamin D status (Zeghoud et al., 1997).
The development of clinical vitamin D deficiency rickets is dependent not only
on the severity of the vitamin D deficiency [circulating concentrations of 25(OH)D] but
also on the duration of the deficiency, on the rate of the child’s growth (which
influences calcium demands), and on the dietary calcium content. Studies from northern
Europe and North and South America have highlighted the marked seasonal
fluctuations in serum 25(OH)D concentrations, with values being lowest in late winter
and highest in late summer or early autumn (McLaughlin et al., 1974, Olivieri et al.,
1993; Harris et al., 1998). Several studies have documented spontaneous healing of
radiologically evident rickets during the summer months (Gupta et al., 1974) and
seasonal fluctuations in serum parathyroid hormone (PTH) ( Guillemant et al., 1995)
and 1,25-dihydroxyvitamin D [1,25(OH)2D] (Woitge et al., 2000) concentrations in
association with changes in serum 25(OH)D concentrations. Clinical vitamin D
deficiency rickets is also well recognized to have seasonal fluctuations in prevalence,
with the highest prevalence being in spring and early summer (Salimpour.,1975).
The seasonal changes in 25(OH)D concentrations, the lag period between the
decrease in 25(OH)D concentrations and the development of biochemical, radiologic,
or clinical rickets, and the influence of diet on the development of rickets have made it
difficult to define a clear division between vitamin D deficiency and sufficiency on the
basis of serum 25(OH)D concentrations. Nevertheless, there is widespread agreement in
the pediatric literature that vitamin D deficiency should be defined as 25(OH)D
concentrations of <10–12 ng/mL (Greer et al., 2003 and Shaw et al., 2002). The value
varies, however, depending on the assay method used to determine 25(OH)D
concentrations (Lip et al., 1999). In the past decade, considerable discussion has taken
place regarding the definition of vitamin D sufficiency and what should be considered
the normal range for serum 25(OH)D concentrations (Viet, 1999). In population
studies, the term vitamin D insufficiency has been used to indicate serum 25(OH)D
concentrations between those associated with vitamin D deficiency and those
considered to be optimal. Vitamin D insufficiency is associated with mildly elevated
PTH concentrations, although values remain within the normal reference range
(Jesudason, 2002). Few studies have been conducted among infants and children to
determine whether the concept of vitamin D insufficiency is valid. Among young
infants, it appears that PTH concentrations increase only when 25(OH)D concentrations
are in the vitamin D3-deficient range (Zeghoud et al, 1997). Studies with adolescents
reported increased PTH concentrations when 25(OH)D concentrations decreased below
12–16 ng/mL (Guillemant et al., 2001 and Outila et al, 2001), whereas Docio et al
(1998) suggested that perturbations in calcium homeostasis occur among prepubertal
children when 25(OH)D concentrations are between 12 and 20 ng/mL. Therefore, it
appears that, if the concept of vitamin D insufficiency is valid for children, values are
very close to the upper limit of what is defined as vitamin D deficiency, a pattern that is
very different from that reported for adults.
The role of low dietary calcium intakes in exacerbating the development of
vitamin D deficiency rickets has been known for many years. More than 80 years ago,
Mellanby (1919) showed the deleterious effects of low dietary calcium intakes on the
development of rickets among vitamin D-deficient animals. Sly et al (1984)
demonstrated a similar effect with the addition of unrefined maize to a vitamin Ddeficient
diet for baboons. However, the mechanisms were not known.
Among humans, one of the most well-studied communities with a high
prevalence of rickets has been the Asian community in the United Kingdom. Since the
early 1960s, numerous studies have highlighted the predisposition of this community to
rickets and osteomalacia (Dunnigam et al., 1962; Ford et al., 1976; Hodgkin et al.,
1973). Several pathogenetic mechanisms have been proposed, including lack of
sunlight exposure, increased skin pigmentation, lack of dietary vitamin D intake,
genetic predisposition, low-calcium diets, and high phytate contents in the diet. Clement
et al (1987) using a rat model, demonstrated that the elevation of 1,25(OH)2D
concentrations through feeding of the rats with low-calcium or high-phytate diets
resulted in increased catabolism of 25(OH)D to inactive metabolites and increased
excretion of these products in the stool, with resultant reduction of 25(OH)D
concentrations. Similarly, infusion of 1,25(OH)2D led to a reduction in the serum
25(OH)D half-life and a 7-fold increase in 24,25-dihydroxyvitamin D production by the
kidney (Halloran et al., 1986). In human studies, the half-life of 25(OH)D was reduced
by nearly 40% among patients with partial gene, secondary hyperparathyroidism, and
elevated 1,25(OH)2D concentrations (Davies et al., 1997), and similar findings were
noted among patients with intestinal malabsorption (Batchelor et al.,1982) and subjects
consuming high-fiber diets (Batchelor et al., 1983). The administration of 1,25(OH)2D
to normal subjects was shown to reduce the circulating 25(OH)D half-life and to induce
vitamin D deficiency among those with relatively low 25(OH)D concentrations
(Clement et al., 1992).
Therefore, it was proposed by Clement (1989) that the pathogenesis of rickets in
the Asian community in the United Kingdom is attributable to the high-cereal, lowcalcium
diet, which induces mild hyperparathyroidism and elevation of 1,25(OH)2D
concentrations, with a resultant reduction in vitamin D status. In situations in which the
vitamin D status is marginal, because of reduced sun exposure, increased skin
pigmentation, and/or limited dietary vitamin D intake, the reduction in 25(OH)D halflife
is sufficient to produce vitamin D deficiency and rickets. It follows that rickets in
the Asian community can be treated either by increasing the vitamin D intake or by
reducing the phytate content of the diet. Both of these treatments have been found to be
effective (Ford et al., 1972; Pietrek et al., 1976).
The role of low dietary calcium intakes in the pathogenesis of vitamin D
deficiency is probably greater than originally recognized. This has been proposed as a
mechanism for rickets among young children in India (Balasubramanian et al., 2003)
and among toddlers in the United States (DeLucia et al., 2003) and probably accounts
for the lower 25(OH)D concentrations among rachitic subjects, compared with control
subjects, in Nigeria (Thacher et al., 1999).
Visitors to Gonin-Gora, Jankasa and Kaso communities with a population of
about four thousand people can not fail to notice the prevalence of rickets disorder.
Most of the children in these communities appear to be suffering from a disease
condition called Rickets. Medical experts attribute the causes of rickets to nutritional
disorder characterized by softening and weakening of bones in children resulting in
skeletal deformities. Giving birth in these villages is normal, but the feelings that run
through parents can better be imagined. However, to a discerning mind or visitor to the
area the reason is not far fetched as children born here end up with deformities. The
prevalence rate of the disease in these villages is high as there is hardly a family
without a child afflicted with the disease. Children in these villages with the disease
were not born with these deformities; it began when they started walking. Driven by
some kind of superstition, men here see their wives and mothers of the children as
being possessed by some evil spirit. This belief as an explanation for the medical
condition of the children is strongly rooted amongst the Gbaygi people, such that when
new babies are born, parents are seldom happy. What hits them is the thought of what
will become of their children. According to Kitz (1997), when the case was first
reported in 1997 only about twelve (12) cases were known. Today, over two hundred
and fifty (250) cases are known and the fear is that in a few years time it may be
This present work aims at investigating the probable causes of rickets in Gonin-
Gora, Jankasa and Kaso communities by estimating the serum levels of calcium,
phosphorus and associated biochemical parameters.
The above aim will be achieved by the following objectives;
• Collecting blood samples from the rickets and non rickets children from
families with a rickets child or children in Gonin-Gora, Jankasa and
Kaso communities of Kaduna state with their informed consent.
• Estimating the sodium, potassium, calcium, phosphorus, urea and
creatinine levels in the sera samples collected from rickets and non
rickets children. Randox diagnostic kit, Agappe diagnostic kit and flame
photometric method will be for these analyses.
• Comparing the serum levels of the estimated parameters for the rickets
children with those of the non rickets children.

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