Am Fam Physician. 2005;71(1):46-49
to the editor: I read with interest the article on hyperparathyroidism in the January 15, 2004, issue of American Family Physician.1 However, I noticed that hypovitaminosis D (vitamin D insufficiency) was not mentioned in much detail. Although the concept is not new, I would like to point out that this is an under-recognized but increasingly important cause of secondary hyperparathyroidism, which is a condition that may be of significant relevance to family physicians and their patients.
Hypovitaminosis D increases the risk for fractures, bone pain, and the development of either osteomalacia or rickets. Risk factors include lack of sun exposure, inadequate dietary intake, and advanced age (caused by the skin’s decreasing ability to synthesize vitamin D). Studies have shown a prevalence of 30 to 50 percent in elderly persons in community settings.2 Even in the nonelderly, 57 percent of hospitalized patients in Boston had evidence of vitamin D deficiency.3 In a recent study conducted in Minnesota,4 an alarming 93 percent of children and adults with chronic musculoskeletal pain were vitamin D deficient. Surprisingly, the most severely deficient persons were patients aged 10 to 29 years.
Diagnosis of vitamin D deficiency is based on a low 25-hydroxyvitamin D3 level. Traditionally, levels less than 12 ng per mL (31 nmol per L) have been considered the lower limits of normal. However, levels of 25-hydroxyvitamin D3 less than 20 ng per mL (52 nmol per L) triggers a compensatory increase in parathyroid hormone (PTH) and, hence, accelerates bone resorption. This suggests that vitamin D deficiency occurs before the lower limits of traditional population-based values for PTH.5 Unlike primary hyperparathyroidism, PTH levels are usually less than 100 pg per mL (850 pmol per L) in secondary hyperparathyroidism caused by hypovitaminosis D. Overall, optimal bone health may occur with 25-hydroxyvitamin D3 levels greater than 30 to 50 ng per mL (78 to 130 nmol per L).
Treatment for hypovitaminosis D is supplementation with vitamin D and calcium. Two methods are suggested here. Replacement with 50,000 IU vitamin D once a week for eight weeks given with supplemental calcium will restore tissue stores quickly and may be more useful for patients with levels of 25-hydroxyvitamin D3 less than 20 ng per mL. Daily supplementation with 800 IU of vitamin D and calcium for those patients with levels between 20 and 30 ng per mL also is safe and effective.6 Repeating levels of 25-hydroxyvitamin D3 and PTH after two to three months ensures adequate treatment and compliance.
Family physicians should consider screening for hypovitaminosis D in all patients who may be at risk, regardless of age. Elderly persons, and even children with dietary lack and limited sun exposure, are vulnerable to vitamin D deficiency. The American Academy of Pediatrics recently recognized the continuing reports of rickets and recommends 200 to 400 IU of daily vitamin D supplementation to all children. Older adults also may warrant vitamin D and calcium supplementation without screening. Understanding the risk factors, and recognizing subnormal 25-hydroxyvitamin D3 levels and mild hyperparathyroidism will allow the family physician to detect hypovitaminosis D. Early diagnosis and treatment is critical to prevent the more serious complications of rickets in children and osteomalacia in adults.