Effects of bisphosphonate administration on the bone mass in immune thrombocytopenic purpura patients under treatment with steroids.
Immune thrombocytopenic purpura (ITP) is an acquired hemorrhage condition involving accelerated platelet consumption caused by antiplatelet autoantibodies. Although various therapeutic strategies are used to treat patients with ITP, the standard treatment method is steroid therapy. The most important problem with steroid administration may be a prolonged use tendency in many cases, because there are many refractory chronic patients. To elucidate the effects of glucocorticoid on bone mineral density (BMD) in patients with ITP, we retrospectively evaluated the relationship between BMD and the total dose of glucocorticoid or the mean daily dose given. We observed decreased BMD in 66.7% of the patients with ITP to whom glucocorticoid was given, although normal bone BMD was observed in 28.6% of patients with ITP treated without steroids. The mean level of BMD was markedly decreased in steroid-treated patients compared with nonsteroid-treated patients (P < .01). The relationship between BMD and the total dose of glucocorticoid (P = .023) or the mean daily dose revealed a negative correlation (P = .022). Administration of bisphosphonate revealed a significant increase in bone mass in patients at 6 and 12 months after the start of bisphosphonate treatment, despite the aggravation of thrombocytopenia. In conclusion, glucocorticoid-induced osteoporosis was observed in patients with ITP, similar to situation seen in patients with other diseases. Bisphosphonate may be an effective agent for the prevention and treatment of glucocorticoid-induced osteoporosis in patients with ITP scheduled to receive long-term steroid treatment.
Nomura
Shosaku
S
Kishiwada City Hospital, Osaka, Japan. shosaku-n@mbp.ocn.ne.jp
Kurata
Yoshiyuki
Y
Tomiyama
Yoshiaki
Y
Takubo
Takayuki
T
Hasegawa
Minoru
M
Saigo
Katsuyasu
K
Nishikawa
Masakatsu
M
Higasa
Satoshi
S
Maeda
Yasuhiro
Y
Hayashi
Kunio
K
D000328:Adult; D000368:Aged; D019386:Alendronate / Q000627:therapeutic use; D015519:Bone Density / Q000187:drug effects*; D050071:Bone Density Conservation Agents / Q000627:therapeutic use*; D004164:Diphosphonates / Q000627:therapeutic use*; D005260:Female; D005938:Glucocorticoids / Q000009:adverse effects* / Q000627:therapeutic use; D006801:Humans; D008297:Male; D008875:Middle Aged; D010024:Osteoporosis / Q000139:chemically induced* / Q000188:drug therapy*; D016553:Purpura, Thrombocytopenic, Idiopathic / Q000188:drug therapy* / Q000378:metabolism / Q000473:pathology; D011788:Quality of Life; D012189:Retrospective Studies; D055815:Young Adult
D050071:Bone Density Conservation Agents; D004164:Diphosphonates; D005938:Glucocorticoids; D019386:Alendronate