Letters to the Editor
Determining the Nutritional Cause of Rickets in Children
TO THE EDITOR: The article in the August 15, 2006, issue of American Family Physician1 draws attention to the global resurgence of rickets, which has been reported in at least 59 countries in the past 20 years.2 However, the article did not emphasize the role of inadequate calcium intake in nutritional rickets. Vitamin D deficiency often is assumed to be the cause of rickets, but calcium deficiency also may be a cause. Calcium deficiency is increasingly recognized as a cause of rickets in the United States, and is prevalent in parts of Africa and Asia where the intake of dairy products by children is negligible.
Whereas children with rickets related to vitamin D deficiency typically present in the first 18 months of life, children with rickets related to calcium deficiency usually present after 18 months of age. In the illustrative case described in the article, no value is provided for the child's calcidiol (25[OH]D3) level to assess the vitamin D status, although it is described as being decreased. Children with calcium-deficiency rickets have reduced or normal calcidiol values, but they do not have the extremely low calcidiol values (less than 10 ng per mL) characteristic of vitamin D-deficiency rickets. Without measurement of serum calcidiol, it is difficult to distinguish rickets caused by calcium deficiency from rickets caused by vitamin D deficiency on clinical grounds alone. As many as 50 percent of American children with rickets have calcidiol values greater than 20 ng per mL, consistent with calcium deficiency.3 In children with calcium deficiency, the 1,25-hydroxyvitamin D concentration is markedly elevated. Children with rickets from calcium deficiency respond better to treatment with calcium than vitamin D.4 Nutritional rickets may more often result from combined calcium and vitamin D deficiencies interacting than from either cause alone. Inadequate calcium intake induces degradation of calcidiol,5 and inadequate vitamin D results in poor intestinal calcium absorption. Thus, each deficiency exacerbates the other. High intake of dietary inhibitors of calcium absorption (e.g., phytates in grains), limited sun exposure, and genetic variation of vitamin D enzymes and receptors also contribute to individual susceptibility to nutritional rickets.
Supplementation of vitamin D and calcium is prudent for children with nutritional rickets. Generally, 1,000 mg of elemental calcium daily in divided doses is safe and effective; chewable, flavored tablets of calcium carbonate are accepted by children. Children with calcium deficiency avidly absorb calcium because their 1,25-hydroxyvitamin D concentrations are elevated.6
Prolonged breastfeeding has been implicated as a predisposing cause of rickets. Although the calcium in breast milk is more bioavailable than that in cow's milk, the concentration of calcium in breast milk (260 to 330 mg per L) declines with increasing duration of lactation and is only about one fourth the concentration of calcium in cow's milk (1,200 mg per L). Introduction of vitamin D-fortified dairy products after one year of age can help prevent calcium deficiency by contributing toward the adequate intake of 500 mg of calcium in this age group.
Author disclosure: Nothing to disclose.
REFERENCES
1. Nield LS, Mahajan P, Joshi A, Kamat D. Rickets: not a disease of the past. Am Fam Physician 2006;74:619-26.
2. Thacher TD, Fischer PR, Strand MA, Pettifor JM. Nutritional rickets around the world: causes and future directions. Ann Trop Paediatr 2006;26:1-16.
3. DeLucia MC, Mitnick ME, Carpenter TO. Nutritional rickets with normal circulating 25-hydroxyvitamin D: a call for reexamining the role of dietary calcium intake in North American infants. J Clin Endocrinol Metab 2003;88:3539-45.
4. Thacher TD, Fischer PR, Pettifor JM, Lawson JO, Isichei CO, Reading JC, et al. A comparison of calcium, vitamin D, or both for nutritional rickets in Nigerian children. N Engl J Med 1999;341:563-8.
5. Clements MR, Johnson L, Fraser DR. A new mechanism for induced vitamin D deficiency in calcium deprivation. Nature 1987;325:62-5.
6. Graff M, Thacher TD, Fischer PR, Stadler D, Pam SD, Pettifor JM, et al. Calcium absorption in Nigerian children with rickets. Am J Clin Nutr 2004;80:1415-21.
Hip Protectors Ineffective at Preventing Hip Fractures
TO THE EDITOR: The article "Management of Hip Fracture: The Family Physician's Role,"1 in American Family Physician, referenced a meta-analysis2 that purportedly showed "that hip protectors may help prevent hip fractures."1 I stopped recommending these devices several years ago after reading a number of studies that did not support their use; I was hopeful that new data showed efficacy for what appears to be a nifty idea. When I looked up the supporting information, I was crestfallen to see a Cochrane publication2 concluding that there is no benefit from using the protectors-or so it seemed from my review of that publication.
Author disclosure: Nothing to disclose.
REFERENCES
1. Rao SS, Cherukuri M. Management of hip fracture: the family physician's role. Am Fam Physician 2006;73:2195-200.
2. Parker MJ, Gillespie WJ, Gillespie LD. Hip protectors for preventing hip fractures in older people. Cochrane Database Syst Rev 2005;(3):CD001255.
editor's note: This letter was sent to the authors of "Management of Hip Fracture: the Family Physician's Role," who stated that they agreed with Dr. Ippel about the lack of clinically significant benefit from using hip protectors in nursing home residents.
Editor's Note: Importance of Revealing Any Author Conflicts of Interest
The November 1, 2006, issue of American Family Physician contained a letter titled "Medication Options for the Treatment of CAP."1 Each of the authors of this letter was instructed at the time of submission and asked again at the time of acceptance to disclose any potential conflicts of interest, including financial relationships with the manufacturers of the medications that they discussed. At the time of publication, none of the authors had disclosed any potential conflicts of interest. When numerous financial relationships were later discovered to exist, the authors responded that they had not realized that it was necessary to disclose these relationships. The editors of American Family Physician feel that it is important for our readers to be aware that the following relationships existed at the time of the letter's1 publication:
Lionel A. Mandell, M.D., has received research funding from Bayer Corp., Chiron Corp., Ortho-McNeil Pharmaceutical Corp., Oscient Pharmaceuticals, and Pfizer Pharmaceuticals, Inc.; has served as a paid consultant to Bayer, Cempra Pharmaceuticals, Novexel, Oscient, Ortho-McNeil, Pfizer, Sanofi-Aventis, Targanta Therapeutics, and Wyeth Laboratories; and is on the speaker's bureaus for Bayer, Ortho-McNeil, Oscient, Pfizer, and Sanofi-Aventis.
Thomas M. File, Jr., M.D., has received research funding from Binax, Ortho-McNeil, Oscient, Pfizer, and Sanofi-Aventis; has served as a paid consultant to Bayer, GlaxoSmithKline, Merck & Co., Ortho-McNeil, Oscient, Pfizer, Sanofi-Aventis, Schering-Plough Pharmaceuticals, and Wyeth; and is on the speaker's bureaus for Abbott, GlaxoSmithKline, Merck, Ortho-McNeil, Oscient, Pfizer, Sanofi-Aventis, Schering Plough, and Wyeth.
Paul B. Iannini, M.D., has served as a paid consultant, received honoraria from, and is on the speaker's bureaus for Oscient, Sanofi-Aventis, and Schering-Plough.
REFERENCES
1. Mandell LA, File TM Jr, Iannini PB. Medication options for the treatment of CAP [letter]. Am Fam Physician 2006;74:1479.
Send letters to Kenny Lin, M.D., Assistant Editor, American Family Physician, e-mail: afplet@aafp.org. Letters submitted via regular mail should be sent to: 11400 Tomahawk Creek Pkwy., Leawood, KS 66211-6272.
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