Study below my comments: If a dentist saw this 18-month old patient, he/she would have prescribed fluoride for the obvious dental caries; but the correct prescription for this baby, who his worried parents brought to a physician because he didn't walk yet, is calcium and vitamin D for the diagnosis of rickets. In recent years, there has been a resurgence of rickets, particularly in darkskinned, breastfed babies.2-5
In the 1940s, the fortification of milk with vitamin D was a critical step in rickets control. This coincides with when water fluoridation began. The reduction in tooth decay could have been from vitamin D fortification. Doubt this was ever studied by fluoride-obsessed dental establishment.
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An 18-month-old who could not walk: A case report / Commentary Source: Clinical Pediatrics Publication date: 2002-11-01 Arrival time: 2002-12-13
The following Brief Report was written by a resident. A discussion by a member of the resident's faculty follows. We invite any resident to submit such articles, together with commentary by a faculty member. Patient Report
An 18-month-old AfricanAmerican male was brought into clinic because he had not yet begun to walk. Past medical history revealed an uneventful pregnancy and labor with no problems at birth. He had been breastfed almost exclusively until 1 year of age when he began to eat some foods; he was a very picky eater, and the majority of his calories continued to come primarily from breast milk. He had not been ill; family history was negative for any diseases. His mother worked days and slept at night and his father worked nights and slept during the day, so he very seldom went out of the house.
His mother stated that he had sat up at 6 months, had pulled to standing about 9 months along with minimal crawling, but at 1 year of age had stopped trying to stand and now acted like he was in pain when she tried to encourage him to stand. He was a happy baby who had good control of his hands and good fine motor control of the upper extremities.
On physical examination his growth chart showed that he followed the 75th percentile until about 9 months, when he began to drop off the chart. Currently he was less than 5th percentile for height and weight. During the physical examination he sat on the bed smiling and playing with some toys appropriate for his age. He appeared thin but was not distressed or anxious. His vital signs were all within normal limits for his age. His head was symmetric, although there was a prominence of his forehead. He had several obvious dental caries. Ears, eyes, nose, and mouth were unremarkable. His chest was thin and had a slightly increased anteroposterior diameter with palpable nodules on his ribs. His precordium was hyperdynamic with a 2/6 systolic ejection murmur. His lungs were clear to auscultation. His abdomen was soft with no masses or organomegaly. His extremities were warm and well perfused although very little muscle was present. He had some tenderness on manipulation with decreased range of motion in his lower extremities. When he was lifted to stand, he refused to bear weight and cried when any weight was placed on his feet.
Laboratory studies showed calcium of 7.2 mg/dL (8-10.5 mg/dL), ionized calcium of 3.0 mg/dL (normal: 4.52-5.28 mg/dL), alkaline phosphatase of 3,866 U/L (normal: 100-320 U/L), parathyroid hormone 324.6 (normal 10-65), sedimentation rate 18 mm/hr (normal: <20), creative kinase 117 U/L (normal: 10-80 U/L), hydroxycholecalciferol or 25(OH)D <5 pg/mL (normal 25-45 pg/mL), dihydroxycholecalciferol or 1,25(OH)^sub 2^ D 59 pg/mL (normal: 25-45 pg/mL).
Radiographic studies of wrists and legs showed marked osteopenia, cupping and fraying at the metaphysis of the long bones, and bilateral greenstick fractures of both lower extremities. The diagnosis of nutritional rickets was made, and he was prescribed 1,25 dihydroxycholecalciferol, calcium, and phosphorus. Within 3 weeks healing could be demonstrated in follow-up radiographs. In follow-up 6 months after presentation, he was walking with no problems.
Commentary
Diagnosis: Vitamin D Deficiency Rickets
Between 1910 and 1961, more than 13,000 deaths in the United States resulted from Vitamin D deficiency rickets.' In the 1940s, vitamin D was added to milk, and as a result, the disease was virtually eradicated in industrialized nations. However, in recent years, there has been a resurgence of rickets, particularly in darkskinned, breastfed babies.2-5 Breast milk is widely acknowledged to be the most nearly complete form of nutrition for infants, benefiting infants' health, growth, immunity, and development. In fact, the American Academy of Pediatrics considers breastfeeding to be "the ideal method of feeding and nurturing infants."6 It is ironic, therefore, that most of the cases of vitamin D deficiency rickets in the United States that have recently been reported have been in exclusively breastfed infants during the first year of life.2-4 Almost all of the children reported, like our case, have been dark-skinned and have not been exposed to much sunlight. It is speculated that more sunlight is needed in darkskinned babies because of poorer penetration of the dark skin by UVB radiation?
Vitamin D is generated initially either by ingestion in the diet or by endogenous production in the skin following ultraviolet irradiation. It is transported to the liver where it is hydroxylated to 25(OH)D or hydroxycholecalciferol, which in turn circulates to the kidneys and undergoes further hydroxylation to 1,25(OH)2 D (dihydroxycholecalciferol). This final metabolite is the most active form of the vitamin and acts on the intestinal lumen to enhance calcium and phosphorus absorption as well as on the renal tubules to increase phosphorus reabsorption.
In vitamin D deficiency there is inadequate substrate for renal hydroxylase resulting in a deficiency of 1,25 dihydroxycholecalciferol and deficient absorption of calcium and phosphorus from the gut; serum concentrations of both are low. The hypocalcemia activates the parathyroid glands, causing mobilization of calcium and phosphorus from the bone. Simultaneously, in vitamin D deficiency, the parathyroid hormone (PTH) induces wasting of phosphate in the urine and calcium retention. Consequently, the serum concentrations of calcium are normal or nearly normal early on and phosphate is low; hence mineralization is impaired. Mobilization of calcium and bone matrix breakdown are associated with an increase in alkaline phosphatase.10
Over the years, there has been considerable disagreement over the use of supplemental vitamins in breastfed, term infants in the United States. Deficiencies of the fat-soluble vitamins D and K have been well described in breastfed infants, and these are the only 2 vitamins of which supplementation for breastfed infants is recognized in the current edition of the American Academy of Pediatrics Pediatric Nutrition Handbook. When supplementation is used, most pediatricians use 1 of 2 types of multivitamins: 1 combination of vitamins A, C, and D; the other a combination of vitamins A, B, C, D. Both types of preparations contain 400 Units of vitamin D.
The most recent statement from the AAP Work Group on Breastfeeding states that "Vitamin D may need to be given before 6 months of age in selected groups of infants such as infants whose mothers are vitamin D-deficient or infants not exposed to adequate sunlight."10
The most recent Dietary Reference Intakes from the Institute of Medicine recommends "assuming infants are not obtaining any vitamin D from sunlight, an intake of 200 IU/day is recommended" for infants through the first 12 months of life. They also state that "with habitual small doses of sunlight, breastfed infants do not require supplemental vitamin D."11,12 Pediatricians will need to determine individually if their patients require supplementation.
In addition to inadequate sunlight or faulty nutrition, a number of other conditions have been associated with the development of rickets.11,12 Examples include conditions associated with inadequate synthesis of vitamin D, decreased absorption of vitamin D, derangements in metabolism of vitamin D, end organ resistance to 1,25(OH)2 D, and conditions associated with phosphate depletion. All are considered risk factors for developing rickets (Table 1).
Clinical Manifestations and Laboratory Diagnosis of Rickets
Rickets can have varied symptoms including the following: bone pain and tenderness; skeletal deformities, such as bowlegs, pigeon chest, bumps in the rib cage ("rachitic rosary"); asymmetrical or odd-shaped skull; spine deformities such as scoliosis or kyphosis; pelvic deformities; and dental deformities with delayed teeth formation. 11,12 Our patient had most of these abnormalities.
Table 1
Patients with rickets can also present with less specific symptoms such as fever, restlessness, weakness, muscle cramps, and failure to thrive. In many cases, physical findings may not be obvious or appreciated by even the most astute clinician during the early stages of vitamin D deficiency rickets. In advanced stages vitamin D deficiency frequently is associated with short stature and poor weight gain. Despite different presentations, most patients have common historical findings.
The differential diagnosis of rickets is extensive and includes other metabolic bone disease (vitamin D-resistant rickets, vitamin D- dependant rickets, congenital rickets, and osteogenis imperfecta); renal disease (renal tubular acidosis and renal osteodystrophy); and other general diagnoses such as trauma, child abuse, hyperphosphatasia, prematurity, or primary chondrodystrophy). 11, 12
While the diagnosis of rickets is based primarily on an accurate history and physical examination, it must be confirmed by laboratory data. Initial work-up should include measurement of calcium, phosphorus, alkaline phosphatase, and parathyroid hormone (PTH) concentrations. Renal function tests and hydroxyvitamin D and dihydroxyvitamin D concentrations should also be obtained. The most important laboratory abnormality is hypocalcemia, for critically low concentrations of calcium may cause tetany and seizures.
The different types of rickets have sev\eral distinguishing laboratory features. Vitamin D-deficiency rickets is characterized by low calcium, phosphorus, and hydroxyvitamin D concentrations, and increased PTH. Vitamin D-resistant rickets, on the other hand, is characterized by a defect in reabsorption of phosphate with resultant low serum phosphorus. In this condition, the other electrolytes are normal, as is PTH. Reduced activity of 25(OH) 1- alpha-- hydroxylase is the dominant feature of vitamin D-dependent rickets and serum values of phosphorus and 1,25(OH)2 vitamin D are decreased. In all types of rickets alkaline phosphatase is elevated and has been found to be the best marker in determining and following treatment of rickets.
Radiologic abnormalities are often helpful in making the diagnosis of vitamin D-deficiency rickets. Osteopenia, widening of the metaphysis, cupping and fraying of the long bones, flaring of the ribs, and sometimes fractures in various stages of healing can be seen on plain films.
Treatment of Vitamin D-Deficiency Rickets
The good news about vitamin D-deficiency rickets is that radiologic changes can be seen after as few as 2-4 weeks of treatment with vitamin D.13-15 Early treatment is essential to minimize the skeletal abnormalities and growth delay caused by vitamin D deficiency. Dosage starts out high for 6-12
weeks: 0.05 to 0.125 mg (2,000-5,000 IU) of vitamin D daily, followed by a maintenance dose of 0.01 mg (400 IU) a day. Oral phosphate is given every 4 hours in a dose of 0.5 to 4 g per day depending on the age of the child. Treatment for tetany or critical levels of calcium can be done orally or intravenously if the oral route is contraindicated. Our patient fortunately responded well to the medication.
Of course the best approach is to try and prevent vitamin D deficiency. It is essential for parents to be educated about proper sunlight and dietary sources of vitamin D. They need to be made aware of the nutritional content of foods and encouraged to select the foods that will meet their nutritional requirements.
REFERENCES
1. Weick MT. A history of rickets in the United States. Am J Clin Nutr 1967;20: 1234-1241.
2. Kreiter SR. Nutritional rickets in African-American breast- fed infants. J Pediatr. 2000;137:153-157.
3. Tomashek KM. Nutritional rickets in Georgia. Pediatrics. 2001;107:e45.
4. Bhowmick SK. Rickets caused by vitamin D deficiency in breast- fed infants in the southern United States. Amj Dis Child. 145:127- 130.
5. Young YR. Achievements in public health, 1900-1999: safer and healthier foods. MMWR 1999;48:905-913.
6. Data from Committee on Nutrition, American Academy of Pediatrics. In: Kleinman RE. Pediatric Nutrition
Handbook, ed 4. Elk Grove Village, IL: American Academy of Pediatrics; 1998:631-632.
7. Kovar MG. Review of the epidemiological evidence for an association between infant feeding and infant health. Pediatrics. 1984;74:5615-5638.
8. Howie PW. Protective effect of breast feeding against infection. Br Med J. 1990;300:11-16.
9. Webb AR. The role of sunlight in the cutaneous production of vitamin Ds. Annu Rev Nutr 1988;8:375-399.
10. American Academy of Pediatrics, Work Group on Breastfeeding. Breastfeeding and the use of human milk. Pediatrics. 1997;100:1035- 1039.
11. Standing Committee on the Scientific Evaluation of Dietary Reference Intakes. Dietary Reference Intakes for Calcium, Phosphorus, Magnesium, Vitamin D and Fluoride. Washington, DC: National Academy Press; 1997:264-266.
12. Blecker U. Fat soluble vitamin deficiencies. Pediatr Rev. 1999;20:394-395.
13. Joiner TA. The many faces of vitamin D deficiency rickets. Pediatr Rev. 2000; 21:296-301.
14. Adam H. Planning the treatment of a patient who has rickets. Pediatr Rev. 2000;21:286.
15. Baroncelli G. Bone turnover in children with vitamin D deficiency rickets before and during treatment. Acta Pediatrics. 2000;89:513-518.
April L. Hartman, MD
Commentary
John T. Benjamin, MD
Department of Pediatrics, Medical College of Georgia, Augusta, Georgia.
Reprint requests and correspondence to: John I Benjamin, MD, Professor of Pediatrics, Children's Medical Center, 1446 Harper Street, Medical College of Georgia, Augusta, GA 30912.
John T Benjamin, MD
Department of Pediatrics, Children's Medical Center, Medical College of Georgia, Augusta, GA
Copyright Westminster Publications, Inc. Nov/Dec 2002
Publication date: 2002-11-01
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