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Assessment of Optimum Duration of Therapy With Oral Dichloromethylene Diphosphonate (Clodronate) in the Treatment of Paget’s Disease By S. Khan, E.V. McCloskey, K.S. Eyres, E.D. Fern, and J.A. Kanis A RETROSPECTIVE study of 51 patients with Paget’s disease treated with oral clodronate (1,600 mg) was performed to assess the optimum duration of treatment to achieve the greatest degree and duration of disease suppression. Patients were treated for three different periods: group A, 1 month (n = 23); group B, 3 months (n = 13); group C, 6 months (n = 15). Alkaline phosphatase (AP) activity was mea- sured before treatment and at regular intervals thereafter until biochemical relapse. Statistical analysis was performed on log-transformed data. Serum ALP activity at initial diagnosis and immediately before oral clodronate therapy showed no significant difference (P = .26 and .95, respectively; one-factor analysis of vari- ance). Clodronate induced a response in all patients except for one in group A. The number of patients with normalized disease activity was significantly higher in group C (73%, 11 patients; P < .Ol) than in groups A and B (21%, 5 patients, and 39%, 5 patients, respectively). There was no significant difference in the time to response between groups (median time, 2 months for all groups). Maximum suppression of disease activity (as judged by nadir values of AP activity) occurred significantly earlier in groupA(P < .05). There was significantly greater suppression of disease activity from the pretreatment value in groups B and C (decreased by 56% ? 5% and 62% + 6%, respectively) than in group A (45% + 4%). The time to biochemical relapse (defined as a 25% increase from the nadir value) was significantly shorter in group A than in groups B and C (median time, 11, 18, and 23 months, respectively) . The proportion of patients remaining relapse- free among the three treatment groups at 12 months was greater in groups B and C (69% and 67%, respectively) than in group A (32%). At 24 months, all patients in group A had relapsed, whereas 31% and 40% were still relapse-free in groups B and C, respectively. We conclude that in Paget’s disease, clodronate (1,600 mg orally) induces suppression of disease activity in 98% of patients. Suppression of disease activity and duration of response was significantly less with 1 month of therapy than with 3 or 6 months. In this study, there was no significant difference between 3- and 6-month treatments in duration of suppression of disease activity. Therefore, we recommend a minimum of 3 months’ treatment with oral clodronate (1,600 mg) in Paget’s disease. From the Department of Human Metabolism and Clinical Biochemistry, WHO Collaborating Centre for Metabolic Bone Disease, University of Shefield Medical School, Sheffield, England. Address reprint requests to S. Khan, Department of Human Metabolism and Clinical Biochemistty, WHO Collaborating Centre for Metabolic Bone Disease, University of Sheffield Medical School, Sheffield SIO ZRX, England. Copyright 8 1994 by W.B. Saunders Company 0049-0172/94/2304-OO27$5.OOlO Seminars in Arthritis and Rheumafism, Vol23, No 4 (February), 1994: p 271 271

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Assessment of Optimum Duration of Therapy With Oral Dichloromethylene Diphosphonate (Clodronate) in the

Treatment of Paget’s Disease

By S. Khan, E.V. McCloskey, K.S. Eyres, E.D. Fern, and J.A. Kanis

A RETROSPECTIVE study of 51 patients with Paget’s disease treated with oral clo-

dronate (1,600 mg) was performed to assess the optimum duration of treatment to achieve the greatest degree and duration of disease suppression. Patients were treated for three different periods: group A, 1 month (n = 23); group B, 3 months (n = 13); group C, 6 months (n = 15).

Alkaline phosphatase (AP) activity was mea- sured before treatment and at regular intervals thereafter until biochemical relapse. Statistical analysis was performed on log-transformed data. Serum ALP activity at initial diagnosis and immediately before oral clodronate therapy showed no significant difference (P = .26 and .95, respectively; one-factor analysis of vari- ance).

Clodronate induced a response in all patients except for one in group A. The number of patients with normalized disease activity was significantly higher in group C (73%, 11 patients; P < .Ol) than in groups A and B (21%, 5 patients, and 39%, 5 patients, respectively). There was no significant difference in the time to response between groups (median time, 2 months for all groups). Maximum suppression of disease activity (as judged by nadir values of AP activity) occurred significantly earlier in groupA(P < .05).

There was significantly greater suppression of disease activity from the pretreatment value in groups B and C (decreased by 56% ? 5% and 62% + 6%, respectively) than in group A (45% + 4%).

The time to biochemical relapse (defined as a 25% increase from the nadir value) was significantly shorter in group A than in groups B and C (median time, 11, 18, and 23 months, respectively) .

The proportion of patients remaining relapse- free among the three treatment groups at 12 months was greater in groups B and C (69% and 67%, respectively) than in group A (32%). At 24 months, all patients in group A had relapsed, whereas 31% and 40% were still relapse-free in groups B and C, respectively.

We conclude that in Paget’s disease, clodronate (1,600 mg orally) induces suppression of disease activity in 98% of patients. Suppression of disease activity and duration of response was significantly less with 1 month of therapy than with 3 or 6 months. In this study, there was no significant difference between 3- and 6-month treatments in duration of suppression of disease activity. Therefore, we recommend a minimum of 3 months’ treatment with oral clodronate (1,600 mg) in Paget’s disease.

From the Department of Human Metabolism and Clinical Biochemistry, WHO Collaborating Centre for Metabolic Bone Disease, University of Shefield Medical School, Sheffield, England.

Address reprint requests to S. Khan, Department of Human Metabolism and Clinical Biochemistty, WHO Collaborating Centre for Metabolic Bone Disease, University of Sheffield Medical School, Sheffield SIO ZRX, England.

Seminars in Arthritis and Rheumafism, Vol23, No 4 (February), 1994: p 271 271

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