High risk of osteopenia and bone derangement in postsurgical patients with craniopharyngiomas, pituitary adenomas and other parasellar lesions.
Hypopituitarism is a well-known cause of secondary osteoporosis. However, patients receiving surgery for pituitary tumors or parasellar lesions have not been well studied for their bone sequel in Japan. We measured bone mineral density (BMD) and urinary type I collagen N-telopeptide (uNTX) in 35 postoperative patients including 25 with pituitary tumor (PT), 6 with craniopharyngioma (CP), and 4 others who had not been on sex hormone replacement, raloxifene, or bisphosphonate therapy. Compared with patients with PT, patients with CP had lower BMD and higher uNTX. Five out of 6 patients with CP had BMD lower than 80% of young adult mean (YAM), whereas 11 out of 22 patients with PT had BMD less than 80% of YAM. Patients with CP had significantly lower serum levels of gonadotropins, and they also tended to have lower serum levels of sex steroids, although statistically not significantly. Two postoperative patients with CP on sex steroid replacement, who were not included in the current analysis, had normal BMD. Of all the subjects, the prominent difference between patients with normal BMD and normal value of uNTX and patients with low BMD and elevated uNTX value was that the latter received higher dose of hydrocortisone replacement. The present study confirms postsurgical patients with pituitary or parasellar lesions, especially those with CP, are at high risk for osteopenia. In designing replacement therapy for those patients, it is important to consider bone by minimizing the dose of glucocorticoid, including sex steroids, and using other drugs that protect bone.
Okinaga
Hiroko
H
Department of Nephrology and Endocrinology, Faculty of Medicine, University of Tokyo, Tokyo.
Matsuno
Akira
A
Okazaki
Ryo
R
D000293:Adolescent; D000328:Adult; D000368:Aged; D015519:Bone Density / Q000187:drug effects; D001851:Bone Diseases, Metabolic / Q000209:etiology* / Q000378:metabolism / Q000517:prevention & control; D001862:Bone Resorption / Q000209:etiology* / Q000378:metabolism / Q000517:prevention & control; D002648:Child; D003094:Collagen / Q000652:urine; D024042:Collagen Type I; D003397:Craniopharyngioma / Q000378:metabolism / Q000601:surgery*; D004164:Diphosphonates / Q000494:pharmacology / Q000627:therapeutic use; D004967:Estrogens / Q000097:blood; D005260:Female; D005640:Follicle Stimulating Hormone / Q000097:blood; D006062:Gonadotropins / Q000097:blood; D006801:Humans; D006854:Hydrocortisone / Q000494:pharmacology / Q000627:therapeutic use; D007018:Hypopituitarism / Q000150:complications* / Q000188:drug therapy / Q000209:etiology / Q000378:metabolism; D007986:Luteinizing Hormone / Q000097:blood; D008297:Male; D008875:Middle Aged; D010455:Peptides / Q000652:urine; D010911:Pituitary Neoplasms / Q000378:metabolism / Q000601:surgery*; D020849:Raloxifene Hydrochloride / Q000494:pharmacology / Q000627:therapeutic use; D012307:Risk Factors; D013739:Testosterone / Q000097:blood; D013974:Thyroxine / Q000494:pharmacology / Q000627:therapeutic use
D024042:Collagen Type I; D004164:Diphosphonates; D004967:Estrogens; D006062:Gonadotropins; D010455:Peptides; C052929:collagen type I trimeric cross-linked peptide; D013739:Testosterone; D020849:Raloxifene Hydrochloride; D007986:Luteinizing Hormone; D005640:Follicle Stimulating Hormone; D003094:Collagen; D013974:Thyroxine; D006854:Hydrocortisone