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| | | Year : 2009 | Volume : 20 | Issue : 2 | Page : 260-265 | | | Epidemiology of nutritional rickets in children | | | MS Al-Atawi1, IA Al-Alwan2, AN Al-Mutair1, HM Tamim3, NA Al-Jurayyan4
1 Department of Pediatric, National Guard Health Affairs, King Abdulaziz Medical City, Riyadh, Saudi Arabia
2 Department of Pediatric, National Guard Health Affairs, King Abdulaziz Medical City, Riyadh; College of Medicine, King Saud bin Abdulaziz University for Health Sciences, Riyadh, Saudi Arabia
3 College of Medicine, King Saud bin Abdulaziz University for Health Sciences, Riyadh, Saudi Arabia
4 Department of Pediatrics, College of Medicine and King Khalid University Hospital, King Saud University, Riyadh, Saudi Arabia
Click here for correspondence address and email | |      | |  Abstract | | | In most developing countries, nutritional rickets is a major health problem. The aim of this study was to explore the magnitude of nutritional rickets among Saudi infants, and the various clinical presentations, as well as to address the possible operating risk factors behind the disease. We carried out a retrospective study at King Abdulaziz Medical City-King Fahad National Guard Hospital in Riyadh, Saudi Arabia. The records of Saudi infants under the age of 14 months over a 10-year period (between January 1990 and January 2000) were reviewed. Information collected included age, sex, clinical presentations, biochemical, radiological findings, infant nutrition, presence of other nutritional deficiencies and exposure to sunlight. There were 283 infants diagnosed with nutritional rickets due to Vitamin D deficiency (67% males) who were between 6 and 14 months of age. Among the total, 70% were exclusively breast-fed, and 23% were breast-fed until the age of 1 year. The most frequent clinical presentation was hypo-calcemic convulsions (34%) followed by chest infections (33%) and gastroenteritis (25%). In conclusion, nutritional rickets is still prevalent in Saudi Arabia with the primary etiology being vitamin D deficiency. Therefore we recommend that every infant, who is exclusively on breast-feeding, has routine supplement of vitamin D in the range of 200 IU/day (alone or as apart of multivitamin), started soon after birth until the time of weaning. Keywords: Nutritional rickets, Epidemiology, Saudi Arabia How to cite this article:
Al-Atawi M S, Al-Alwan I A, Al-Mutair A N, Tamim H M, Al-Jurayyan N A. Epidemiology of nutritional rickets in children. Saudi J Kidney Dis Transpl 2009;20:260-5 |
How to cite this URL:
Al-Atawi M S, Al-Alwan I A, Al-Mutair A N, Tamim H M, Al-Jurayyan N A. Epidemiology of nutritional rickets in children. Saudi J Kidney Dis Transpl [serial online] 2009 [cited 2014 Mar 3];20:260-5. Available from: http://www.sjkdt.org/text.asp?2009/20/2/260/45575 |
| Introduction | |  |
Vitamin D plays an essential role in calcium homeostasis, normal development and maintenance of human bones, and enhancement of the immune system.
In most developing regions worldwide, nutritional rickets is a prominent health problem probably because the risk factors still operate. In the industrialized regions of the world in which infant formulas are obligatorily supplemented with vitamin D, rickets recurred as outbreaks or "waves". [1],[2],[3],[4],[5] In the Kingdom of Saudi Arabia, despite having economic affluence and adequate sunlight all year round, vitamin D deficiency is fairly common in infants, children, adolescents, as well as pregnant and lactating Saudi women. [6],[7],[8],[9] It is common cultural practice to keep infants and young children indoors with minimal or total avoidance of direct sunlight. For growing infants, there are two recognized sources for obtaining the daily requirement of vitamin D. The first is oral intake, and the second is the cutaneous source activated by sunshine.
The aim of this study was to explore the magnitude of nutritional rickets among Saudi infants, and the various clinical presentations, as well as to address the possible operating risk factors behind the disease and identify recommendations to prevent its occurrence.
| Materials and Methods | | |
This is retrospective study conducted at King Abdulaziz Medical City-King Fahad National Guard Hospital in Riyadh. The records of Saudi infants and children under the age of 14 months over a 10-year period (between January 1990 and January 2000) were reviewed. Patients with liver disease, renal disease, hypoparathyroidism, infants on anti-convulsions medications, and those with non-nutritional forms of rickets were excluded. Only those with nutritional rickets were included.
A total of 283 infants were studied. Each patient's record was reviewed, as well as radiological findings, infant nutrition, the presence of other nutritional deficiencies, and exposure to sunlight (average number of hours per week). The diagnosis of vitamin D deficiency rickets was based on clinical, biochemical, and radiological findings and normalization of alkaline phosphatase level after 6 weeks course of daily Vitamin D therapy. Total and ionized calcium, serum phosphate, serum alkaline phosphatase, serum proteins, 25-vitamin D level, parathyroid hormone levels, hemoglobin levels, renal function tests, complete urine analysis, and X-ray of the ends of long bones at the wrist, and ankle joints. Hypocalcemia is defined as total calcium less than 2 mmol/L and severe if less than 1.75 mmol/L (2.2-2.75 mmol/L). Hypophosphatemia is defined as serum phosphate less than 1.45 mmol/L (1.45-2.16 mmol/L). Alkaline phosphatase is considered abnormal if more than 500 IU/L, and significantly elevated if the level exceeds 1000 IU/L. [10] Severe hypovitaminosis D is defined by serum 25-OHD concentrations below 20 nmol/L (22-94 nmol/L). [11],[12]
Data were entered and analyzed using SPSS statistical program (version 11.5). Data were summarized by calculating the number and the percentage, as all the variables were recorded on a categorical scale. No p-value was presented as the objective of the study was just to provide a description of the patients rather than identifying risk factors.
| Results | | |
The age and sex distribution of infants, as well as their nutritional source are summarized in [Table 1]. Overall, 196 infants (70%) were exclusively on breast-feeding (127 males, 69 females) with no supplementation. In 79 infants (23%) the breast-feeding extended until the end of their first year. All patients had no significant history of direct sun exposure.
The most frequent clinical presentation was hypocalcemic convulsions reported in 98 infants (34%), followed by chest infections in 89 infants (33%), gastroenteritis in 71 patients (25%), hypotonia in seven infants (2%) and fractures in four patients (1%) [Table 2].
The most frequent clinical signs were wide wrist (29%) and rachitic rosary (28%), wide anterior fontanelle (15%), frontal bossing (16%), bow legs (10%), craniotapes (2%) and hypotonia (2%) [Table 2].
One hundred infants (36%) had total calcium below 1.75 mmol/L [Table 3], among whom 84 infants developed hypocalcemic seizures. In 198 infants (70%) the serum phosphate levels were reduced while normal in eighty- five infants (30%) [Table 3]. In 73 infants 25-vitamin D levels were measured and all were below 12 nmol/L, indicating severe vitamin D deficiency. Parathyroid hormone (PTH) levels were measured in 101 infants and were elevated in 94 infants. About 65 infants (22%) were diagnosed to have iron deficiency anemia (IDA) in addition to active rickets, while 41 infants (15%) had past history of IDA.
| Discussion | | |
Nutritional rickets is still prevalent in Saudi Arabia with the primary etiology being vitamin D deficiency. All of our patients were below the age of 14 months and none was younger than six months of age. Male infants outnumbered the females 2:1. There is no apparent explanation for this finding but this has been also observed in several reports. [13],[14],[15],[16]
The prolongation of exclusive breast-feeding until the age of one year without vitamin D supplement is an important factor leading to the development of rickets in the rapid growth period of infancy; in addition, none of our infants where exposed to direct sunlight. None of the lactating mothers received any form of vitamin D supplementation during their lactation. Hypocalcemic seizures were the most common clinical presentation of nutritional rickets in our patients. In fact 84% of the hypocalcemic infants developed hypocalcemic seizures significantly higher than 50% reported in the western literature. [17],[18]
Chest infections were the second commonest clinical presentation in our patients, 33% of cases; which could be due to the fact that phagocytosis is impaired in this condition. [19]
The third most common clinical presentation was gastroenteritis seen in 71 infants (25%). Among the 196 exclusively breast-fed infants, 33 (14%) infants presented with gastroenteritis compared to 22 (24%) of 63 formula-fed infants indicating the value of breast milk in reducing the incidence of infectious diarrhea. [20] Seven infants (2%) presented with hypotonia as the main clinical presentation. Four infants (1%) presented with fractures and diagnosed to have nutritional rickets; femur was the commonly involved bone.
The most common physical signs of rickets where wide wrist (29%), rachitic rosary (28%), frontal bossing (16%), and wide anterior fontanel (15%). Craniotapes were reported in only 13 patients (2%) and it was the least documented and demonstrated physical sign.
Serum alkaline phosphatase was abnormal in all of our infants (100%) none had a level below 500 IU/L. This finding has an important clinical implication and it suggests that serum alkaline phosphatase remains a reliable and less expensive biochemical marker for screening, and diagnosing vitamin D deficiency rickets, and monitoring the effectiveness of treatment. Although we did not measure bone specific alkaline phosphatase isoenzyme, total alkaline phosphatase is widely used to detect and follow the course of infants and children with vitamin D deficiency rickets. Indeed, in healthy infants most of the alkaline phosphatase present in serum is derived from bone. [21] It is the normalization of previously elevated serum alkaline phosphatase that signals the onset of skeletal recovery and rachitic healing. [22] 25-OH vitamin D levels were below 12 nmol/L in all infants who had 25-OH vitamin D levels done, indicating severe vitamin D deficiency, in contrast to other studies where they have calcium deficiency as the primary cause. [23] It is of interest that nine infants (aged 6-7 months) had normal serum phosphate despite elevated serum alkaline phosphatase and marked elevation of PTH level. They had very low vitamin D level but all of these infants normalized their alkaline phosphatase and PTH levels after the vitamin D treatment.
This biochemical finding may be explained by the fact that the young infant renal tubules are not very sensitive to the phoshaturic action of PTH or because the growing infant has the tendency to favor phosphate retention. 65 infants in this study (22%) were diagnosed to have iron deficiency anemia (IDA) in addition to active rickets, while 41 infants (15%) had past history of IDA. Therefore the pediatrician needs to screen the infant with active nutritional rickets for the possibility of co-existence IDA.
Human milk must be endorsed as the "perfect food" for the human infants. However, it contains an average 20-40 IU/L vitamin D in contrast to cow's milk (400 IU/L). [23],[24] Therefore, human milk is a relatively small source of dietary vitamin D for most infants and its level correlates with maternal vitamin D status. [25]
In its position statement, the American Academy of Pediatrics (2003) continued to endorse breast-feeding of infants for at least the first 12 months. The statement indicates that vitamin D may need to be given before the age of six months in those infants whose mothers are vitamin D deficient or in those infants not exposed to adequate sunlight. [26] However, recently (2003) the American Academy of Pediatrics indicated that vitamin D supplementation should begin within the first 2 months of life. [26] Sunshine remains an efficient and safe source.
In humans, exposing as little as 5% of a white adolescent's body (which is equivalent to infant head) to direct sunlight for 20 minutes a day supplies an average of 435 IU vitamin D per day in contrast to total body exposure which results in as much as 10,000 IU/day. [27] It was shown that exposing the infants to direct sunshine, wearing only a diaper, for half an hour per week or three hours per week with full clothing with an uncovered head was adequate to prevent rickets. [28] In real life, this natural exposure may not be practical because of the many barriers that come between infants and sunshine, including climate, latitude, smog, housing, economic factors and the mothers' belief. The lack of a "formal policy" from health professionals recommending "routine" vitamin D supplementation for all breastfed infants is also a concern.
All these factors sustain the vicious circle of nutritional rickets or enhance its emergence. The need for vitamin D supplementation should not imply that human milk is nutritionally inadequate. How much Vitamin D growing infants need is not fully known. [29] The current Dietary Reference Intake (DRI) for vitamin D is 200 IU for all infants and children. [29] Fortified formulas provide an average of 400 IU per day and are therefore sufficient. Routine supplementary vitamin D 400 IU/day in breast-fed infants has been proven adequate to prevent rickets caused by vitamin D deficiency. [30] Glorieux recommended 500 IU of vitamin D each day during the rapid growth of the first year of life. [31]
In conclusion, nutritional rickets is still prevalent in Saudi Arabia with the primary etiology in our cases being vitamin D deficiency. It is therefore recommend that every infant who is exclusively breastfed has a routine supplement of vitamin D in the range of 200 IU/day (alone or as apart of multivitamin), started soon after birth until the time of weaning. This dose is very safe, yet sufficient to prevent rickets. We hope that our recommendation will be supported by formal policy with sunshine exposure for infants and young children encouraged.
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Correspondence Address:
I A Al-Alwan
Department of Pediatric, King AbdulAziz Medical City, P.O. Box 22490, Riyadh 11426
Saudi Arabia
PMID: 19237815
[Table 1], [Table 2], [Table 3] | |
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