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1. Predetermination of PTH and Vitamin D levels before Therapy of Osteoporosis with PTH (1-84)

   • Francisco R. Lafita, MD, PhD, FACP
   • Belinda Garcia MD (CMAP. Mora 'Ebre. Spain)

   Gabinet Mèdic. 43850 Cambrils.Baix Camp. Spain

   In their interesting study Greenspan and colleagues (1) found that PTH (1-84) effectively prevented the appearing of new or worsened vertebral fractures. However, an important rate of adverse events was observed, which in the PTH group were mainly nausea (22.6%), vomiting (7.7%), dizziness and headache, symptoms that strongly suggest the presence of hypercalcemia (actually found in 27.8% of PTH group).

   An important issue missed in this study was the determination of PTH and vitamin D levels (even phosphate levels) before starting PTH therapy. The most common cause of secondary osteoporosis is vitamin D deficiency being secondary hyperparathyroidism a frequent finding in patients with hypovitaminosis D (2, 3). It is not unlike to find increases in serum and urinary calcium levels when patients with raised levels of endogenous PTH are treated with PTH (1-84). Moreover, changes in levels of 1,25 dihydroxyvitamin D (from its baseline value) during treatment with PTH (1- 84) have been found to correlate with larger increases in BMD (4).

   Because of the high rate of hypercalcemia / hypercalciuria showed in this study we must be cautious when administering PTH (1-84). Serum PTH and vitamin D levels must be measured before initiating the therapy.

   1. Greenspan SL, Bone HG, Ettinger MP, et al, for the Treatment of Osteoporosis with Parathyroid Hormone Study Group. Effect of recombinant human parathyroid hormone (1-84) on vertebral fracture and bone mineral density in postmenopausal women with osteoporosis: a randomized trial. Ann Intern Med 2007; 146: 326-39.

   2. Giusti A, Barone A, Razzano M, et al. High prevalence of secondary hyperparathyroidism due to hypovitaminosis D in hospitalized elderly with and without hip fracture. J Endocrinol Invest. 2006 Oct;29(9):809-13.

   3. Dobnig H, Piswanger-Solkner JC, Obermayer-Pietsch B, et al. Hip and Non-Vertebral Fracture Prediction in Nursing Home Patients: Role of Bone. Ultrasound and Bone Marker Measurement. J Clin Endocrinol Metab. 2007 Feb 20; [Epub ahead of print]

   4. Sellmeyer DE, Black DM, Palermo L, et al. Hetereogeneity in skeletal response to full-length parathyroid hormone in the treatment of osteoporosis. Osteoporos Int. 2007 Feb 28; [Epub ahead of print]

   Conflict of Interest:

   None declared

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   Published March 12, 2007
2. Thiazolidinediones, parathyroid hormone and fractures.

   • Luca Mascitelli, MD
   • Francesca Pezzetta, MD

   Comando Brigata alpina Julia, Udine 33100 Italy

   TO THE EDITOR – Greenspan and colleagues (1) found that recombinant human parathyroid hormone reduced the risk for new or worsened vertebral fractures in postmenopausal women with or without previous vertebral fracture. Women who were taking medications known to affect bone mineral metabolism were excluded from the study (1). However, only recently (2) it has been suggested that the antidiabetic drugs thiazolidinediones (TZD) may have a detrimental action on bone. In fact, a recent observational study (3) found that treatment of diabetic women with TZD was associated with a significant 50% increase in the annualized rate of whole-body bone loss. Furthermore, even short-term therapy with rosiglitazone, a commonly prescribed TZD, has been shown to inhibit bone formation and accelerate bone loss in healthy postmenopausal women (4). Indeed, it has been recently reported (5) a higher incidence of fractures, detected as adverse events, in female diabetic subjects randomized to receive rosiglitazone compared to those randomized to receive either metformin or glyburide, during a 4 years study of glycemic durability of oral monotherapies. Therefore, given its detrimental effects on bone, TZD assumption might have been a confounder in the study by Greenspan and colleagues (1).

   Luca Mascitelli, MD Sanitary Service Comando Brigata alpina “Julia” Udine, Italy 33100

   Francesca Pezzetta, MD Cardiology Service Ospedale di San Vito al Tagliamento San Vito al Tagliamento, Italy 33078

   REFERENCES

   1. Greenspan SL, Bone HG, Ettinger MP, et al, for the Treatment of Osteoporosis with Parathyroid Hormone Study Group. Effect of recombinant human parathyroid hormone (1-84) on vertebral fracture and bone mineral density in postmenopausal women with osteoporosis: a randomized trial. Ann Intern Med 2007; 146: 326-39.

   2. Mascitelli L, Pezzetta F. Thiazolidinediones. N Engl J Med 2005; 352: 206.

   3. Schwartz AV, Sellmeyer DE, Vittinghoff E, Palermo L, Lecka-Czernik B, Feingold KR, et al. Thiazolidinedione use and bone loss in older diabetic adults. J Clin Endocrinol Metab 2006; 91: 3349-54.

   4. Grey A, Bolland M, Gamble G, Wattie D, Horne A, Davidson J, Reid IR. The peroxisome-proliferator-activated receptor-gamma agonist rosiglitazone decreases bone formation and bone mineral density in healthy postmenopausal women: a randomized, controlled trial. J Clin Endocrinol Metab 2007 Jan 30; [Epub ahead of print].

   5. Kahn SE, Haffner SM, Heise MA, et al, for the ADOPT Study Group. Glycemic durability of rosiglitazone, metformin, or glyburide monotherapy. N Engl J Med 2006; 355: 2427-43.

   Conflict of Interest:

   None declared

   Submit response
   Published March 9, 2007