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Serum Levels of Type I and III Procollagen Fragments in Paget's Disease of Bone^*

Department of Medicine, Harvard Medical School, Medical Service (Arthritis Unit), Massachusetts General Hospital, and the New England Deaconess Hospital Boston, Massachusetts 02215

Address requests for reprints to: Dr. Lee S. Simon, Deaconess Medicine, Section on Internal Medicine, Rheumatology, and Metabolic Bone Disease, New England Deaconess Hospital, 110 FrancisStreet, Boston, Massachusetts 02215.

Patients with Paget's disease of bone were found to have elevated serum levels of type I procollagen carboxy-terminal peptide (pColl-I-C) which correlated with other measurements of disease activity. The elevated levels of pColl-I-C decreased within hours after the injection of salmon calcitonin and within weeks after oral dichloromethylene diphosphonate treatment. The decrease in serum pColl-I-C after a single injection of salmon calcitonin was associated with a decrease in urinary hydroxyproline excretion, both of which rose toward pretreatment values within 7 h. The pColl-I-C levels remained normal for months after dichloromethylene diphosphonate therapy was discontinued.

Using a RIA for the type III procollagen amino-terminal peptide (pColl-III-N), it was found that serum levels were also elevated in patients with Paget's disease. The levels of pColl-III-N alsodecreased after the injection of salmon calcitonin, but not to the same extent as those of pColl-I-C. After chronic therapy with dichloromethylene diphosphonate, serum levels of pColl-III-N decreased, but not into the normal range. We postulate that whereas pColl-I-C is derived from synthesis of mineralized bone collagen, pColl-III-N is derived from the loose fibrous stroma replacing marrow in areas closely associated with active Pagetic bone disease.

^* This work was supported by USPHS Grants AM-03564, S07-RR-05486-18, and AM-07258. This is publication 934 of the Robert W. Lovett Memorial Group for the Studyof Diseases Causing Deformities.

Received October 18, 1982.

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