Low Vitamin D Levels in Saudi Arabians
1982; King Faisal Specialist Hospital and Research Centre; Volume: 2; Issue: 3 Linguagem: Inglês
10.5144/0256-4947.1982.127
ISSN0975-4466
AutoresNicholas Woodhouse, Walter L. Norton,
Tópico(s)Bone health and osteoporosis research
ResumoOriginal ArticlesLow Vitamin D Levels in Saudi Arabians Nicholas J. Y. Woodhouse and MB BS MRCP Walter L. NortonMD FACP Nicholas J. Y. Woodhouse * Endocrinologist, Department of Medicine; King Faisal Specialist Hospital and Research Centre Search for more papers by this author and Walter L. Norton * Endocrinologist, Department of Medicine; King Faisal Specialist Hospital and Research Centre Search for more papers by this author Published Online:1 Jul 1982https://doi.org/10.5144/0256-4947.1982.127SectionsPDF ToolsAdd to favoritesDownload citationTrack citations ShareShare onFacebookTwitterLinked InRedditEmail AboutABSTRACTABSTRACTCirculating 25-hydroxycholecalciferol (25-OHD) levels were measured in 134 adults; 82 Saudi Arabian patients, 43 normal Saudi Arabians, and nine Western employees of the King Faisal Specialist Hospital. The mean circulating 25-OHD level was much lower in the normal Saudis (3.6 ng/ml) and Saudi patients (3.2 ng/ml) than in Westerners (17.1 ng/ml) (p < 0.01). There was no significant difference between the mean, normal Saudi male (3.9 ng/ml) and female (3.2 ng/ml) values, but rural Saudi (4.18 ng/ml) were higher than urban Saudi (3.14 ng/ml) values (p < 0.05). The 25-OHD levels were undetectable (< 2.0 ng/ml) in three patients with florid osteomalacia as well as in eight normal subjects and 26 patients without clinical or biochemical evidence of vitamin D deficiency. The 25-OHD levels increased from a mean of 2.8 ng/ml to 10.2 ng/ml during oral administration of vitamin D, 800 to 1200 IU daily (p < 0.01).We conclude that the circulating level of 25-OHD is low in the Saudi Arabian population. This results from a poor dietary intake and reduced synthesis of vitamin D by the skin. Both men and women avoid sunlight exposure and completely cover the skin with clothing.Individuals at risk, such as patients confined to the house for any reason, women during pregnancy and lactation, growing children, and patients on certain anticonvulsant medications should receive dietary supplements of vitamin D. Fortification of grain and milk products could help eliminate nutritional rickets and osteomalacia in Saudi Arabia.INTRODUCTIONIn the past two years we have seen at least ten adults and 16 children with florid clinical, biochemical, and often severe radiological manifestations of vitamin D deficiency. Eight of the adult patients were female, two of whom related the onset of their symptoms to pregnancy. Two adult males were taking anticonvulsant drugs which are known to predispose to vitamin D deficiency.1,2 Of the children, boys were affected as often as girls.Vitamin D deficiency is recognized as occurring in Bedouin females and has been attributed to minimal exposure to sunlight.3 However, the status of vitamin D levels in Saudi Arabians is unknown. We therefore measured 25-OHD levels in normal Saudi subjects and Saudi patients and compared them with values obtained from Westerners living in Saudi Arabia.SUBJECTS AND METHODSBlood samples for SMAC-20™ analyses and measurement of 25-OHD levels were obtained from 82 Saudi patients, 43 normal Saudis who were relatives or attendants of the patients, and nine Western employees at the King Faisal Specialist Hospital. The Saudi patients were seen in the endocrine or rheumatology clinics between June 1980 and June 1981. Informed consent was obtained from each of the normal individuals. Samples were not obtained from individuals suspected of taking vitamin D preparations during the preceding three months. Features of the subjects included in the study are shown in Table 1. Urban dwellers came from the major cities of Saudi Arabia, approximately one-half from Riyadh.Table 1. Subjects included in studyTable 1. Subjects included in studyRural dwellers came from small villages or the desert. Saudi patients were divided into four groups: (A) miscellaneous; 44 patients with diagnoses mainly of diabetes, thyroid disorders, Sheehan’s syndrome, or nonspecific joint pains; (B) rheumatoid arthritis, 20 patients; (C) fibrositis, ten patients; and (D) metabolic bone disease, eight patients: Cushing’s disease (1), primary hyperparathyroidism (3), osteomalacia (3), and epilepsy on anticonvulsants (1).Serum calcium, phosphorus and alkaline phosphatase were measured using SMAC-20™ blood analyzer. Serum 25-OHD levels were measured commercially by Bio-Science Laboratories, California, using a competitive protein-binding assay (normal quoted range for the United States ten to 55 ng/ml).4 Student’s “t” test was used for the comparison of two independent means and calculation of the probability (p) values.5 Individuals with undetectable 25-OHD levels (< 2.0 ng/ml) were considered to have values of one ng/ml for the purpose of statistical calculations.RESULTS25-OHD LevelsThe comparison between normal Western and Saudi individuals is shown in Table 2. Levels were significantly higher in Westerners than in Saudis, and in rural Saudis compared with urban Saudis.Table 2. 25-OHD levels in normal subjectsTable 2. 25-OHD levels in normal subjectsThe difference between the mean values for Saudi males and Saudi females was not significant.The comparison between normal Western and Saudi subjects and Saudi patients is shown in Figure 1. Western values are significantly higher than all other groups. The mean normal Saudi value (3.6 ng/ml) is significantly higher than in Saudi patients with rheumatoid arthritis (2.7 ng/ml) (p < 0.02).Figure 1.: 25-OHD levels in normal Saudis, Saudi patients, and Westerners.Download FigureThe mean values for patients with fibrositis (2.7 ng/ml) was not significantly different from those of normal Saudi individuals. Of the eight patients with metabolic bone disease, five had undetectable 25-OHD levels.Levels Before and After Vitamin D (19 Patients)The 25-OHD levels increased from a mean of 2.8 ng/ml to 10.2 ng/ml (p < 0.01) after one to two months' treatment with 800 to 1200 IU/day. Figure 2. After treatment, 25-OHD levels remained undetectable in two patients. One had severe osteomalacia; during treatment, clinical improvement was marked and the serum calcium rose from 6.5 to 9.0 mg per 100 ml. The other patient had rheumatoid arthritis and it was not certain that she was taking the medication.Figure 2.: 25-OHD levels in 19 Saudi patients before and after oral vitamin D supplementation (800 to 1200 IU/day for four to eight weeks).Download FigureExposure to SunlightOf 84 patients questioned, 40 reported some degree of sunlight exposure of the face and arms. The mean 25-OHD level in this group, although higher (3.8 ng/ml), was not significantly different from the other 44 patients who denied exposure (3.1 ng/ml). The amount of ultraviolet light exposure in urban dwellers acknowledging sun exposure is probably relatively slight, because the subjects remain clothed and do not sit in the sun for long periods.On the other hand, outdoor activities are greater in rural than in urban areas, and women are generally not veiled around family members. Hence, there is probably a greater degree of “basal” sun exposure in rural than in urban dwellers in addition to the higher rate of reporting sun exposure in rural compared to urban dwellers (84 percent versus 45 percent).Dietary Intake of Vitamin DThe Dietetic Department of the King Faisal Specialist Hospital estimates an average dietary vitamin D intake in rural Saudis of approximately 40 IU/day and 70 IU/day in urban Saudis. Average United States intake is approximately 400 IU/day.Serum ChemistryThere was no significant difference between the mean serum calcium level of normal Saudi subjects (9.6 mg/dl), the miscellaneous patients (9.5 mg/dl), patients with rheumatoid arthritis (9.3 mg/dl) and the Westerners (9.6 mg/dl). Calcium, phosphorus and alkaline phosphatase levels in the 20 miscellaneous patients with the highest 25-OHD levels were compared with 20 miscellaneous patients who had undetectable 25-OHD levels (< 2 ng/ml). Although the mean serum phosphate level is lower (3.1 ng/ml versus 3.5 ng/ml) and the mean alkaline phosphatase level higher (140 U/L versus 110 U/L) in those patients with undetectable 25-OHD, the differences are not statistically significant.DISCUSSIONWe have shown that the circulating levels of 25-OHD are much lower in Saudi Arabians than in Westerners living in Saudi Arabia. They are also lower than quoted, mean, normal values in the United States (19.0 ng/ml) and the United Kingdom (15.4 ng/ml) but almost identical to those of Asian imigrants to the U.K. (3.5 ng/ml) in whom there is a high incidence of rickets and osteomalacia.6–9 The frequent occurrence of vitamin D deficiency rickets and osteomalacia in Saudi Arabia suggests that many Saudis have low body stores of vitamin D.10 This idea is supported by the fact that 25-OHD levels were undetectable in 19 percent of the normal Saudi subjects and 32 percent of the patients in this study.Dietary deficiency of vitamin D is probably an important contributing factor. Malabsorption is an unlikely explanation as a substantial rise in 25-OHD levels occurred in the patients receiving physiological supplements of vitamin D. In spite of the low dietary intake it seems paradoxical to find low 25-OHD levels in Saudi Arabia as vitamin D deficiency is readily overcome by exposure to sunlight.11Presumably, the avoidance of sunlight and extensive covering of the skin by clothing provides an effective barrier to ultraviolet light in the two sexes as the 25-OHD levels are low in both men and women. Sunlight exposure, however, must be of value in protecting against vitamin D deficiency, particularly in rural Saudi subjects whose 25-OHD levels are higher but whose vitamin D intake is probably less than their urban counterparts. Furthermore, rural Saudis have a higher reported frequency of sun exposure than urban Saudis (84 percent versus 45 percent). As more people migrate from the country to work in the cities there is likely to be an increasing risk of osteomalacia.Westerners living in the middle region of Saudi Arabia have frequently commented on the absence of skin erythema even after long periods of sunbathing. This has also been the authors’ experience. We postulate therefore that significant shielding from ultraviolet light may occur, perhaps due to atmospheric dust particles. The striking rise of serum 25-OHD levels with moderate doses of vitamin D3 indicates the potential importance of dietary supplementation in repleting low body stores. Patients with rheumatoid arthritis had significantly lower 25-OHD levels than normal Saudi subjects. Similarly, four of nine patients with painful fibrositis had undetectable circulating 25-OHD. These observations suggest that chronically ill patients, likely to be inactive or confined to the house, are at risk of developing osteomalacia as are patients taking long-term, anticonvulsant medication. These high-risk individuals should receive supplementary vitamin D.In conclusion, the Saudi population has low body stores of vitamin D. This could result from a relatively low vitamin D intake and low ultraviolet exposure. Therefore, individuals with further reduced dietary intake or ultraviolet exposure or increased vitamin D demand as in nursing, pregnancy, rapid growth, or those on certain anticonvulsant therapy are at greater risk of developing clinical osteomalacia. The low level of body stores in the population as a whole may account for the high frequency of symptomatic osteomalacia seen in Saudi Arabia.Because we have shown that moderate amounts of supplementary vitamin D administered orally is readily absorbed, we suggest that supplementation of milk and milk products, particularly laban (yogurt) and Arabic style bread would help eliminate nutritional vitamin D deficiency in Saudi Arabia.ARTICLE REFERENCES:1. Kruse R: "Osteopathien bei antiepileptischer Langzeittherapie" . MSCHR Kinderheilk 116:3781968. Google Scholar2. Richens A, Rowe DJ: "Disturbances in calcium metabolism by anticonvulsant drugs" . Br Med J 4:731970. Google Scholar3. Groen JJ, Eschar J, Ben-Ishay D, et al.: "Osteomalacia among the Bedouin of the Negev desert" . Arch Intern Med 116:1951965. Google Scholar4. Haddad JG, Chyu KJ: "Competitive protein-binding radio-assay for 25-hydroxy-cholciferol" . J Clin Endocrinol Metab 33:9921971 p 128. Google Scholar5. Cotton T: Statistics in Medicine. Little, Brown & Co., Boston, 1974. Google Scholar6. Haddad JG, Hahn TJ: "Natural and synthetic sources of circulating 25-hydroxy-vitamin D in man" . Nature 244:5151973. Google Scholar7. Stamp TC, Round JM, Rowe DJ, et al.: "Plasma levels and therapeutic effect of 25-hydroxchole calciferol in epileptic patients taking anticonvulsant drugs" . Br Med J 4:91972. Google Scholar8. Stamp TCB, Walker PG, Perry W, et al.: "Nutritional osteomalacia and late rickets in greater London 1974–1979: Clinical and metabolic studies in 45 patients" . Clinics in Endocrinology and Metabolism 9(1): 811980. Google Scholar9. Holmes AM, Enoch BA, Taylor JL, et al.: "Occult rickets and osteomalacia among the Asian immigrant population" . Quar J Med 42: 1251973. Google Scholar10. Elidrissy ATH, Taha SA: Rickets in Riyadh. 5th Saudi Medical Meeting Riyadh, Saudi Arabia. 1980. Google Scholar11. Stanbury SW, Mawer EB, de Silva P, et al.: "The skin, vitamin D and the control of its 25-hydroxylation" . Mineral and Electrolyte Metabolism 3: 511979. Google Scholar Next article FiguresReferencesRelatedDetails Volume 2, Issue 3July 1982 Metrics History Published online1 July 1982 KeywordsVitamin D deficiency Hydroxycholecalciferols Saudi ArabiaACKNOWLEDGEMENTSThe authors would like to thank Dr John T. Godwin and his colleagues in the Division of Biochemistry, Mrs Lou McNece and the other members of the Dietetic Department, and Mrs Yvonne Lock and Mrs Jean Weirich for their kind assistance in making this paper possible.InformationCopyright © 1982, Annals of Saudi Medicine
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