Vitamin D Deficiency Rickets in Riyadh

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1 Ahmed Abanamy, MD; Hussein Salman, MD; Mamen Cheriyan, MRCP(UK); Mohammed Shuja, MD; Saleh Siddrani, PhD From the Suleimania Children's Hospital (Drs. Abanamy, Salman, Cheriyan, and Shuja) and College of Science (Dr. Siddrani), King Saud University, Riyadh. Address reprint requests and correspondence to Dr. Salman: Suleimania Children's Hospital, P.O. Box 59046, Riyadh 11525, Saudi Arabia. Accepted for publication 15 February Despite the fact that much of Saudi Arabia is sunny throughout most of the year, vitamin D deficiency rickets is not rare. Different factors are responsible for this phenomenon, especially nutritional, social, and maternal vitamin D deficiency. We identified 500 cases of rickets out of a total of 27,236 hospital admissions, and followed at Suleimania Children's Hospital in Riyadh over three years (1986 to 1988). Eighty-one percent of the patients were Saudi (mean age, 8.2 months), which is significantly lower than that usually observed. Most of the patients had nonspecific findings at onset, indirectly related to the vitamin D deficiency, particularly recurrent chest infections (66%) and hypocalcemic convulsions (17.2%). The young age at onset, which was 39.2% in patients younger than six months at onset and 14.2% in those younger than three months, is unusual compared with ages cited in the literature, and this most probably relates to maternal vitamin D deficiency. Subclinical forms of rickets, detected by the screening, also seem to be common. We conclude that rickets is a major health problem in Saudi Arabia and more attention needs to be paid to its detection, treatment, and prevention. A Abanamy, H Salman, M cheriyan, M Shuja, S Siddrani, Vitamin D Deficiency Rickets in Riyadh. 1991; 11(1): Vitamin D deficiency rickets is due to dietary factors and poor sunlight exposure. The incidence of vitamin D rickets is therefore usually low in sunny countries, but in Riyadh it is not rare. We evaluated the factors associated with the development of rickets in our community, and discuss the preventive measures that should be adopted. Patients and Methods Rickets was diagnosed in 500 patients (out of a total of 27,236 admissions) and patients were followed at Suleimania Children's Hospital in Riyadh over a period of three years (1986 to 1988). Diagnosis was based on clinical (widened wrists and rosary rickets), radiological (rosary rickets, widening, cupping, fraying of distal ends of the ulna and radius), and biological (high alkaline phosphatase activity) findings. Furthermore, 1213 breastfed Saudi children below two years of age, seen in the outpatient clinic for nonspecific

2 symptoms, were screened for rickets using x-ray studies of the wrist and measurement of alkaline phosphatase activity. Nationality, sex, and age of the children were recorded, as were the nutritional status (breastfeeding, food diversification), sociofamilial status (residential location, type of housing, maternal age, educational level of parents, clothing styles), and history of exposure to sunlight. Laboratory investigations included complete blood count, red blood cell morphology, calcium and phosphorus levels, and alkaline phosphatase activity. Chest and wrist x-ray studies were done in all patients. X-ray wrist studies and determinations of alkaline phosphatase activity were also done in 76 sex- and agematched control children, for whom nutritional status and history of exposure to sunlight were also recorded. The dosage of hydroxylated vitamin D metabolites (25 hydroxy D 3 [250HD] and 1.25 dihydroxy D 3 [1.25 DiOHD]) using a competitive protein-binding assay was determined in 188 Saudi children of both sexes; 103 were rachitic and 85 were control subjects, matched by age, who had had adequate nutritional and sunlight exposure and came from a sociofamilial background that would encourage these conditions. Results In our series, vitamin D deficiency rickets was seen in 1.83% of the total number of patients admitted during the three years. Of this group of rachitic patients, 81% were Saudi and 19% were non-saudi (of these, 6.8% were Sudanese and 4.8% were Yemenite), 64.4% were male and 35.6% were female. Table 1 shows the age distribution in our patients, with a high prevalence seen in very young children. The age of onset ranged from 25 days to 2 years, 6 months (mean, 8.2 months). Among the 1213 breastfed children of both sexes screened, 85 (7%) were found to have subclinical rickets, based on an alkaline phosphatase value of at least 400 IU/L along with early metaphyseal changes (early cupping and irregular fraying). Alkaline phosphatase activity in our control children was 4.78 ± 1.12 μkat/l and local pediatric values ranged from 0.67 to 6.67 μkat/l [1,2]. X-ray studies of the wrists in control children were normal. Table 1. Age distribution. Age Number Percentage 0 1 mo > 1 3 mo > 3 6 mo > 6 mo 1 yr >l 2yr >2yr Total Sixty-seven percent of the patients were exclusively breastfed, compared with 42% of the control children; 31.8% had mixed alimentation (i.e., breastfed and adequate diversification), and six children (1.2%) who were not breastfed had rickets due to factors other than nutritional causes. About 50% of the patients lived in overcrowded areas and were affected by major sociocultural and educational problems. More than 50% of the patients lived in apartments or houses without a yard or garden and with high small windows, which did not allow for much exposure to sunlight. No patients lived in tents and 19.2% lived in traditional mud or brick houses. Finally, 72% of our patients (compared to 37% of the control children) were not exposed to sunlight. The majority of mothers (51.1%) considered sunlight harmful for the children; only 11.2% thought it beneficial. The maternal age in our series varied from 17 to 40 years (mean, 25.3 ± 5.9 years); 7.2% were 40 years or older. Illiteracy was found in 75.2% of the mothers. No comparable statistics were obtained for the control children. Most of the small infants were wrapped until they were six months old (Figure 1).

3 Figure 1. Wrapping of infant up to 6 months of age. Figure 2. (A) Widened wrist. (B) Rosary rickets. More than 75% of the patients presented at onset with symptoms indirectly related to rickets, especially recurrent chest infection (66%) and hypocalcemic convulsions (17.2%) in younger infants. Other findings were variable and not characteristic(e.g., delayed walking, delayed teething, gastrointestinal symptoms), occurring in 16.6%.

4 Table 2. Classic signs and symptoms. Classic signs Percentage Widened wrists 82.5 Rosary rickets 44.2 Frontal bossing 27.7 Craniotabes 4.2 Fracture 0.2 Others 16.8 Table 3. Vitamin D metabolites. 25 OHD 3 (nmol/l) 1.25DiOHD 3 (pmol/l) Patients No. Mean Range Mean Range Male Rachitic Control Female Rachitic Control OHD 3 = 25 hydroxy D 3; 1.25 DiOHD 3 = 1.25 dihydroxy D 3 Classic signs and symptoms were found in a variable percentage of the patients (Figure 2, Table 2). X-ray studies of the wrist and chest showed the classic bone changes (Figures 3 to 5) [3]. These bone changes were seen in the first months of life in some patients. This, in association with the high alkaline phosphatase activity in breastfed infants, is important, although rickets in its earliest stage is not usually detected radiologically [3]. Cupping of the distal end of the ulna in young infants is not necessarily abnormal, and has been observed in some nonrachitic children during the first months of life [3]. The x-ray studies of the wrists in pur control children were normal, however. There were low calcium and phosphorus levels in 17.2% and 14.8% of the patients, respectively, and a high alkaline phosphatase activity in all patients (range, μkat/l). Microcytic hypochromic anemia was seen in 57 patients (8.79%), most of them aged one year or less. The levels of vitamin D metabolites 25 OHD and 1.25 DiOHD were significantly lower in the patients of both sexes than those in the controls (Table 3), but our results for 25 OHD seem higher than those reported in previous studies (9.23 ± 5.74 nmol/l) [4,5,10]. However, they are still significantly different from the values observed in control groups. Other authors have reported lower levels of 25 OHD for both Saudi adult patients (7.98 ± 5.74 nmol/l) and for normal controls (8.98 ± 5.74 nmol/l), compared with control values obtained from Western subjects (42.68 ± nmol/l) [10], and higher values seen in the rural population (10.43 ± 7.03 nmol/l) than in the urban one (7.83 ± 5.29 nmol/l) [10]. No study of 1.25 DiOHD levels in Saudi rachitic and nonrachitic children has been conducted.

5 Figure 3. Bone changes seen in the first months of life. Most of our patients (98.6%) had vitamin D deficiency rickets that was due to nutritional factors. Other causes (liver disease [0.4%], anticonvulsant therapy using agents such as phenytoin [0.2%], and vitamin D resistant rickets [0.8%]) were rare. Discussion Rickets is a relatively common disorder in Riyadh and has been attributed to several factors. Saudi children are breastfed for usually the first two years of life, without adequate nutritionaldiversification [4,5] as shown in our series. It is well known that maternal milk, as a unique source of vitamin D, does not supply enough of the daily requirements for the children [6,7]. This is even more true when the mothers are already deficient in vitamin D. Vitamin D deficiency in Saudi mothers has been proved in several studies [4,5,8 10]. The 25 OHD levels were found to be low in pregnant women and in lactating mothers and were significantly lower than those measured in Western women or women from other Arabian countries who were living in the Kingdom [5,8]. These results have a greater consequence when considering the almost continuous cycle of pregnancies and lactation of Saudi mothers. All these elements explain the presence of obvious clinicaland radiological signs of rickets in Saudi children during the first months of life. The mean age at onset of symptoms and signs in our series was 8.2 months, compared with 11 months quoted in other similar local studies [4,5] and with those reported elsewhere in the literature. Figure 4. Rosary rickets.

6 Figure 5. Wrist fracture. Saudi children do not get much exposure to sunlight, and this is due to such local factors as housing design and clothing styles, as well as the strong tendency to avoid sunshine and heat. It has been proved that, despite frequent haze and sandstorm, there is no significant seasonal variation in the ultraviolet light reaching the earth's surface in the Kingdom [11 13]. No genetic factor (invoked initially) seems to be involved in the pathogenesis of the disease. Subclinical forms of rickets also seem to be common, as shown by the results of outpatient screening in breastfed children. Because of the relative frequency of vitamin D deficiency rickets in Riyadh, a concerted effort must be made to screen breastfed children to detect subclinical forms of rickets and to educate the public about the importance of sunlight exposure and diversified nutrition. We consider vitamin D supplementation the most appropriate measure to prevent rickets, both for children during the entire time of breastfeeding and for pregnant and lactating mothers. References 1. Pathology Handbook. Riyadh Al-Kharj Hospital Program Al-Hazmi MAF, Manser WT. A manual of biochemistry services, ed 1. Riyadh: Laboratory of King Saud University Hospital, Caffey JP. Pediatrics X-ray Diagnosis, Vol. 1, ed. 8. Chicago: Year Book, Elidrissy ATH, Taha SA. Rickets in Riyadh. In: Proceedings of the 5th Saudi Medical Meeting, pp Sedrani SH, Elidrissy ATH, El Arabi KM, et al. Are Saudis at risk of developing vitamin D deficiency? Saudi Med J 1986;7(5): Lakdawala DR, Widdowson EM. Vitamin D in human milk. Lancet 1977;1(8004): Finberg L. Human milk feeding and vitamin D supplementation (editorial). J Pediatr 1981;99(2): Elidrissy ATH, Sedrani SH, Lawson DE. Vitamin D deficiency in mothers of rachitic infants. Calcif Tissue Int 1984;36(3): Belton NR, Elidrissy ATH, Aldress A, et al. Maternal vitamin D deficiency as a factor in the pathogenesis of rickets in Saudi Arabia. In: Norman AW, Schefer K, Herrath DV, Grigoleil HG, eds. Vitamin D, chemical, biochemical endocrinology of calcium metabolism. New York: Walter De Gryter, 1982; Woodhouse NJY, Norton WL. Low vitamin D levels in Saudi Arabians. King Faisal Specialist Hosp Med J 1982:2(3): Saudi Arabian Meteorological Department. Annual report. Riyadh: Ministry of Aviation Sedrani SH, Elidrissy ATH, Al Arabi KM. Sunlight and vitamin D status in normal Saudi subjects. Am J Clin Nutr 1983:39: Mohammed A, El-Yazigi A, Al Watban FAH, Feteih N. Measurement of solar ultraviolet-b in Riyadh: its significance in studies on vitamin D deficiency in Saudi Arabia. King Faisal Specialist Hosp Med J 1984;4(4):