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Convulsions as a Possible Manifestation of Vitamin D Deficiency Rickets in Infants One to Six Months of Age

1992; King Faisal Specialist Hospital and Research Centre; Volume: 12; Issue: 1 Linguagem: Inglês

10.5144/0256-4947.1992.34

0975-4466

Puthenpurackal M. Mathew, George W. Imseeh,

Electrolyte and hormonal disorders

Original ArticlesConvulsions as a Possible Manifestation of Vitamin D Deficiency Rickets in Infants One to Six Months of Age Puthenpurackal M. Mathew and MD, MRCP George W. ImseehMD Puthenpurackal M. Mathew Address reprint requests and correspondence to Dr. Mathew: Pediatric Services Division, Saudi Aramco Dhahran Health Center, P.O. Box 76, Room A-406, Dhahran 31311, Saudi Arabia. From the Pediatric Services Division, Saudi Aramco Dhahran Health Center, Dhahran, Saudi Arabia. Search for more papers by this author and George W. Imseeh From the Pediatric Services Division, Saudi Aramco Dhahran Health Center, Dhahran, Saudi Arabia. Search for more papers by this author Published Online:1 Jan 1992https://doi.org/10.5144/0256-4947.1992.34SectionsPDF ToolsAdd to favoritesDownload citationTrack citations ShareShare onFacebookTwitterLinked InRedditEmail AboutABSTRACTABSTRACTDuring the 42 months from January 1985 through June 1988, five infants between the ages of one and six months had hypocalcemic convulsions associated with vitamin D deficiency rickets. Despite abundant sunlight, convulsions as a manifestation of vitamin D deficiency in young infants are not uncommon in Saudi Arabia and should be considered as a probable cause for hypocalcemic seizure in breast fed infants.IntroductionRickets is a disorder of growing children. In older children, clinical manifestations of rickets occur only after a long period of Vitamin D insufficiency [1]. Rickets associated with hypocalcemic convulsions in breast fed infants without vitamin D supplementation has been described [2–5], but is not usually recognized as a cause before the age of four months [1]. Convulsions in young babies are a symptom with potentially serious implications [6] and a cause should always be sought. The presence of hypocalcemia in a young infant with convulsions may suggest vitamin D deficiency rickets [5]. Vitamin D deficiency is common in Saudi Arabia especially in pregnant women, lactating mothers and their infants because of minimal exposure to the sun [7,8]. Young children are kept indoors until they are independent, approximately two years of age, as their mothers are of the opinion that the sun is harmful to the child [9]. The purpose of this paper is to highlight the occurrence of convulsions as a manifestation of vitamin D deficiency rickets in early infancy, despite abundant sunlight in Saudi Arabia.MATERIAL AND METHODSSaudi Aramco, an oil company in the Eastern Province of Saudi Arabia, has a defined population of employees and their dependents are provided inpatient and outpatient care at Saudi Aramco medical facilities. We reviewed all infants between one and six months of age admitted for evaluation of convulsions during the three and a half years from January 1985 through June 1988. Among the total group, those with convulsions associated with hypocalcemia were identified and the etiology for hypocalcemia was ascertained from the history and clinical and biochemical and radiological findings. Hypocalcemia was initially treated with intravenous (IV) calcium gluconate 100 to 200 mg/kg/day as a slow continuous infusion and later orally when able to take solid food, until the serum calcium level was normal. During admission, one dose of vitamin D, 300,000 units was administered intramuscularly to all infants with rickets.Serum for 25 hydroxycholecalciferol (25 OH D), 1,25 dihydroxycholecalciferol (1,25 (OH)2D) and parathormone C terminal (PTH C term) were drawn at the time of admission before initiating treatment and analyzed at Bioscience Laboratories, Houston, Texas, USA.RESULTSDuring the study period of 42 months, 1554 infants between one and six months of age were admitted to our hospital. Of these, 53 were admitted with their first episode of convulsion. Six of these infants had hypocalcemia, five were diagnosed as having vitamin D deficiency and one as having vitamin D resistant rickets. Each of the six infants had two to five episodes of short (< 10 seconds) generalized convulsions during the first 24-hours of presentation and admission to the hospital. None of the infants had a history suggestive of convulsions related to breath-holding spells, and no family history of epilepsy or febrile convulsions. All six infants were born at term and were entirely breast fed. The clinical presentation and biochemical findings on admission of the five infants with vitamin D deficiency are summarized in Table 1. All were boys and of Saudi nationality. All infants were growing satisfactorily and had normal developmental milestones but had wide wrist margins and prominent costochondral junctions. On x-ray examination of the wrists all had changes of rickets. All infants had normal serum albumin, magnesium and glucose. Maternal calcium, phosphorus and alkaline phosphatase were checked in the mothers of three infants and all had normal serum calcium and phosphorus. Only one mother had an elevated alkaline phosphatase level (646 U/L). Follow-up over the next 12 months following diagnosis demonstrated complete normalization of biochemical and x-ray findings in all five patients. There was no recurrence of convulsion in any of the five infants and all had normal developmental milestones during the period of follow-up. The biochemical abnormality was corrected on follow-up with good healing of the rickets and satisfactory growth. Electroencephalogram (EEG) was not done on any of the infants because of the lack of recurrence of convulsion following diagnosis and treatment of hypocalcemia as well as normal development on follow-up.Table 1. Features at presentation o f infants with vitamin D deficiency rickets and convulsions.Table 1. Features at presentation o f infants with vitamin D deficiency rickets and convulsions.DISCUSSIONConvulsion with or without infection as a manifestation of infantile rickets is well known [3,4,10]. The period between the newborn and toddler stages is a period of relative freedom from seizures, but when convulsions do occur, the prognosis is often gloomy [6, 11]. Population based data from the American National Collaborative Perinatal Project confirmed a high incidence of epilepsy and mental retardation after only minor motor seizures in the first year [12]. The proper identification and treatment of a biochemical cause of the seizures, like hypocalcemia, will improve the ultimate prognosis of the affected infants. Unlike the West, hypocalcemia has been an important cause for seizures (11%) in our patient population. Rickets have been reported in as many as 18% of infants in parts of China with the highest incidence in infants two to four months of age [13]. Lubani et al [14] reported that the incidence of vitamin D deficiency rickets in a certain area of Kuwait was just over 1% in children aged two years or younger. The incidence of convulsions was 1.6% in this group of 250 children with rickets. Between the ages of four months and three years convulsions in vitamin D deficiency are said to occur frequently. In our population hypocalcemic convulsion with vitamin D deficiency was also present in later infancy. A seven-month-old male had hypocalcemic convulsion secondary to vitamin D deficiency rickets. Following appropriate treatment his rickets healed completely and he was symptom-free. Nutritional rickets is a disease caused by inadequate exposure to sunlight [4]. Dietary vitamin D is essential when there is poor exposure of the skin to ultraviolet irradiation [9]. Infants receiving breast milk alone may have low circulating levels of vitamin D and an increased incidence of rickets when not exposed to the sun [15, 16]. Despite the abundance of sunlight, vitamin D deficiency is common in Saudi Arabia, especially among Saudi women and young children because of minimal exposure to the sun [7–9]. This probably compounded by poor compliance with vitamin D supplementation to exclusively breast fed infants, makes hypocalcemia related to vitamin D deficiency more common in our very young infants. Breast feeding is a nutritious, natural and inexpensive source of milk and provides the infant and mother with a unique physical and emotional closeness. All the same, the nutritional status of these breast fed infants including clinical evidence of vitamin D deficiency needs to be looked into on routine admissions, outpatient consultations and well-baby clinic visits for immunization, to prevent the development of a potentially serious disorder like convulsions. It has been suggested [17] that vitamin D supplementation is not necessary in breast fed infants when the mother has adequate vitamin D synthesis and/or intake, but is appropriate when the mother is herself deficient in vitamin D [18]. Long-term follow-up is needed to ensure that the diagnosis is correct and treatment adequate to resolve the clinical, biochemical and radiological changes and that proper dietary practices are established in infants with a history of seizures associated with hypocalcemia.It may be advantageous to administer a single dose 7,500 to 15,000 mcg of vitamin D (300,000 to 600,000 I/U) [1,14,19]. Single dose parenteral therapy may result in more rapid healing, possibly with earlier differentiation from genetic vitamin D resistant rickets and less dependence on parents for daily administration of the vitamin. All five infants had clinical and radiological evidence of rickets. This, along with the high serum alkaline phosphatase and low serum 25 OH D levels and good clinical and radiological response without recurrence to a single dose parenteral vitamin D, confirms the diagnosis of vitamin D deficiency as the cause of rickets in these infants. As in the literature [2–5], hypocalcemic convulsions in our five infants < 6 months of age were most likely related to vitamin D deficiency rickets.All the infants tested had 1,25 (OH)2D levels in the normal range or above as previously reported [20]. Hypocalcemia, hypophosphatemia and elevated levels of parathyroid hormone increases the production of 1,25 (OH)2D [21]. Nutritional vitamin D deficiency is known to occur in the presence of normal or elevated plasma concentrations of 1,25 (OH)2D in both children and adults [20,22]. The values of 1, 25 (OH)2D found in vitamin D deficiency are inappropriately low for the panoply of factors that stimulate its synthesis [22,23]. The role of other vitamin D metabolites (like 24, 25 (OH)2D) cannot be commented on as they were not measured in any of our infants [2].ARTICLE REFERENCES:1. Barnes LA. Rickets and vitamin D deficiency. In: Behrman RE, Vaughan VC, eds. Nelson Textbook of Pediatrics, 13 ed. Philadelphia: WB Saunders, 1989;149–53. 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Eastwood JB, de Wardener HE. "Normal plasma 1, 25-(OH): vitamin D concentrations in nutritional osteomalacia" . Lancet. 1979; 1:1377–8. Google Scholar23. Chessney RW, Rosen JF, De Luca HF. Disorders of calcium metabolism in children. In: Chiumella G, Sperling M, eds. Recent progress in pediatric endocrinology. New York: Raven Press; 1983;5–24. Google Scholar Previous article Next article FiguresReferencesRelatedDetails Volume 12, Issue 1January 1992 Metrics History Accepted23 January 1991Published online1 January 1992 ACKNOWLEDGMENTSWe thank Dr. Mark Young for critical review of the manuscript and Miss Susan Rankapole for secretarial help.InformationCopyright © 1992, Annals of Saudi MedicinePDF download