JOURNAL OF BONE AND MINERAL RESEARCH Volume 5, Number 5,1990 Mary Ann Liebert, h e . , Publishers
Letter to the Editor To the Editor:
The report of the NOF Task Force on bone mass measurement") is a valuable first step that delineated four clinical indications, concerning which there is widespread agreement. The report also noted that additional indications may prove to be of clinical value; I believe that assessment of the skeletal impact of secondary hyperparathyroidism is clearly such an indication. Significant osteopenia is common in chronic renal in intestinal malabsorption, regardless of etiology,('-*) and in nutritional vitamin D d e f i c i e n ~ y . ' ~The ' pattern of bone loss, with the preferential involvement of appendicular cortical bone, is identical t o that in primary hyperparathyroidism, although often more severe.(lo,ll'Cancellous bone mass tends to be increased in chronic renal failure("' and decreased in intestinal disease,(S.8.11) but cortical bone mass is reduced in both. Such bone loss has been found with every cause of secondary hyperparathyroidism that has been studied, a group of disorders in which increased P T H secretion is the only common factor.'10' As in primary hyperparathyroidism, two strategies of therapeutic intervention can be proposed for asymptomatic patients: t o treat all patients with high PTH levels, or t o restrict treatment t o those with objective evidence that PTH hypersecretion is causing harm. Since treatment will usually require the lifelong administration of some form of vitamin D, with its well-known dangers, a selective strategy based on bone mass measurement appears t o have the same logical and scientific justification as in primary hyperparathyroidism." Evidence that appropriate treatment will arrest cortical bone loss is as strong in secondary hyperparathyr~idism",~~) as it is in primary: In neither case is the evidence based on controlled trials, and in neither case is fracture prevention a realistic end point for assessing efficacy. The selective strategy has the further advantage that some patients with intestinal disease will be found t o have non-PTH-mediated osteopenia,'8) and t o be candidates for other forms of treatment.
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A. Michaef Parfitt, M.D.
Bone and Mineral Research Laboratory Education & Research Building 2799 West Grand Boulevard 1 1 . Detroit, MI 48202-2689
REFERENCES
12.
1 . Johnston CC Jr, Melton LJ, Lindsay R, Eddy DM 1989
533
Clinical indications for bone mass measurements: A report from the Scientific Advisory Board of the National Osteoporosis Foundation. J Bone Min Res 4(Suppl 2):l-28. Parfitt AM, Oliver I, Walczak N, Levin N, Santiago G , Cruz C 1976 Effect of chronic renal failure and maintenance hemodialysis on bone mineral content of radius. Am J Roentgenol 126:1292-1293. Parfitt AM 1977 Metacarpal cortical dimensions in hypoparathyroidism, primary hyperparathyroidism and chronic renal failure. Calcif Tissue Res 22(Suppl):329-331. Parfitt AM, Rao DS, Kleerekoper M, Walczak N, Levin N, Oliver 1, Frame B 1980 Midshaft and distal radius bone mineral in primary and secondary hyperparathyroidism: Diagnostic value and response to treatment. In: Proceedings of the Fourth International Conference on Bone Measurement, 1980. US Dept. H.H.S. NIH 80-1938, Bethesda, pp 183-190. Kleerekoper M, Villanueva AR, Mathews CHE, Rao DS, Pumo B, Parfitt AM 1983 PTH mediated bone loss in primary and secondary hyperparathyroidism. In: Frame B, Potts JT Jr (eds) Clinical Disorders of Bone and Mineral Metabolism. Excerpta Medica, Amsterdam, pp 328-332. Rao DS, Mare1 G , Wong K, Zonca M, Kleerekoper M, Frame B, Parfitt AM 1984 Reversible and irreversible skeletal disease in adult coeliac disease. In: Cohn DV, Potts JT Jr, Fujita T (eds) Endocrine Control of Bone and Calcium Metabolism. Elsevier Science Publishers, Amsterdam, pp 279-280. Rao DS, Kleerekoper M, Rogers M, Frame B, Parfitt AM 1984 Is gastrectomy a risk factor for osteoporosis? In: Christiansen C, Arnuad CD, Nordin BEC, Parfitt AM, Peck WA, Riggs BL (eds) Osteoporosis. Proceedings of Copenhagen International Symposium on Osteoporosis, June 3-8, 1984. Aalborg Stiftsbortrykkeri, pp 775-777. Parfitt AM, Podenphant J, Villanueva AR, Frame B 1985 Metabolic bone disease with and without osteomalacia after intestinal bypass surgery: A bone histomorphometric study. Bone 6:211-220. Fonseca V, Agnew JE, Nag D, Dandona P 1988 Bone density and cortical thickness in nutritional vitamin D deficiency: Effect of secondary hyperparathyroidism. Ann Clin Biochem 2527 1-274. Parfitt AM 1986 Accelerated cortical bone loss: Primary and secondary hyperparathyroidism. In: Uhthoff H, Jaworski ZFG (eds) Current Concepts of Bone Fragility. Springer-Verlag, Berlin, pp 279-285. Parfitt AM, Rao DS, Stanch J, Villanueva AR, Kleerekoper M, Frame B 1985 Irreversible bone loss in osteomalacia: Comparison of radial photon absorptiometry with iliac bone histomorphometry during treatment. J Clin Invest 76:24032412. Frame B, Honasoge M, Kottamasu S 1987 Osteosclerosis, Hyperostosis and Related Disorders. Elsevier Science Publishers, New York.
Letter to the Editor To the Editor:
The report of the NOF Task Force on bone mass measurement") is a valuable first step that delineated four clinical indications, concerning which there is widespread agreement. The report also noted that additional indications may prove to be of clinical value; I believe that assessment of the skeletal impact of secondary hyperparathyroidism is clearly such an indication. Significant osteopenia is common in chronic renal in intestinal malabsorption, regardless of etiology,('-*) and in nutritional vitamin D d e f i c i e n ~ y . ' ~The ' pattern of bone loss, with the preferential involvement of appendicular cortical bone, is identical t o that in primary hyperparathyroidism, although often more severe.(lo,ll'Cancellous bone mass tends to be increased in chronic renal failure("' and decreased in intestinal disease,(S.8.11) but cortical bone mass is reduced in both. Such bone loss has been found with every cause of secondary hyperparathyroidism that has been studied, a group of disorders in which increased P T H secretion is the only common factor.'10' As in primary hyperparathyroidism, two strategies of therapeutic intervention can be proposed for asymptomatic patients: t o treat all patients with high PTH levels, or t o restrict treatment t o those with objective evidence that PTH hypersecretion is causing harm. Since treatment will usually require the lifelong administration of some form of vitamin D, with its well-known dangers, a selective strategy based on bone mass measurement appears t o have the same logical and scientific justification as in primary hyperparathyroidism." Evidence that appropriate treatment will arrest cortical bone loss is as strong in secondary hyperparathyr~idism",~~) as it is in primary: In neither case is the evidence based on controlled trials, and in neither case is fracture prevention a realistic end point for assessing efficacy. The selective strategy has the further advantage that some patients with intestinal disease will be found t o have non-PTH-mediated osteopenia,'8) and t o be candidates for other forms of treatment.
2.
3. 4.
5.
6.
7.
8.
9.
10.
A. Michaef Parfitt, M.D.
Bone and Mineral Research Laboratory Education & Research Building 2799 West Grand Boulevard 1 1 . Detroit, MI 48202-2689
REFERENCES
12.
1 . Johnston CC Jr, Melton LJ, Lindsay R, Eddy DM 1989
533
Clinical indications for bone mass measurements: A report from the Scientific Advisory Board of the National Osteoporosis Foundation. J Bone Min Res 4(Suppl 2):l-28. Parfitt AM, Oliver I, Walczak N, Levin N, Santiago G , Cruz C 1976 Effect of chronic renal failure and maintenance hemodialysis on bone mineral content of radius. Am J Roentgenol 126:1292-1293. Parfitt AM 1977 Metacarpal cortical dimensions in hypoparathyroidism, primary hyperparathyroidism and chronic renal failure. Calcif Tissue Res 22(Suppl):329-331. Parfitt AM, Rao DS, Kleerekoper M, Walczak N, Levin N, Oliver 1, Frame B 1980 Midshaft and distal radius bone mineral in primary and secondary hyperparathyroidism: Diagnostic value and response to treatment. In: Proceedings of the Fourth International Conference on Bone Measurement, 1980. US Dept. H.H.S. NIH 80-1938, Bethesda, pp 183-190. Kleerekoper M, Villanueva AR, Mathews CHE, Rao DS, Pumo B, Parfitt AM 1983 PTH mediated bone loss in primary and secondary hyperparathyroidism. In: Frame B, Potts JT Jr (eds) Clinical Disorders of Bone and Mineral Metabolism. Excerpta Medica, Amsterdam, pp 328-332. Rao DS, Mare1 G , Wong K, Zonca M, Kleerekoper M, Frame B, Parfitt AM 1984 Reversible and irreversible skeletal disease in adult coeliac disease. In: Cohn DV, Potts JT Jr, Fujita T (eds) Endocrine Control of Bone and Calcium Metabolism. Elsevier Science Publishers, Amsterdam, pp 279-280. Rao DS, Kleerekoper M, Rogers M, Frame B, Parfitt AM 1984 Is gastrectomy a risk factor for osteoporosis? In: Christiansen C, Arnuad CD, Nordin BEC, Parfitt AM, Peck WA, Riggs BL (eds) Osteoporosis. Proceedings of Copenhagen International Symposium on Osteoporosis, June 3-8, 1984. Aalborg Stiftsbortrykkeri, pp 775-777. Parfitt AM, Podenphant J, Villanueva AR, Frame B 1985 Metabolic bone disease with and without osteomalacia after intestinal bypass surgery: A bone histomorphometric study. Bone 6:211-220. Fonseca V, Agnew JE, Nag D, Dandona P 1988 Bone density and cortical thickness in nutritional vitamin D deficiency: Effect of secondary hyperparathyroidism. Ann Clin Biochem 2527 1-274. Parfitt AM 1986 Accelerated cortical bone loss: Primary and secondary hyperparathyroidism. In: Uhthoff H, Jaworski ZFG (eds) Current Concepts of Bone Fragility. Springer-Verlag, Berlin, pp 279-285. Parfitt AM, Rao DS, Stanch J, Villanueva AR, Kleerekoper M, Frame B 1985 Irreversible bone loss in osteomalacia: Comparison of radial photon absorptiometry with iliac bone histomorphometry during treatment. J Clin Invest 76:24032412. Frame B, Honasoge M, Kottamasu S 1987 Osteosclerosis, Hyperostosis and Related Disorders. Elsevier Science Publishers, New York.
