title: Presence of sonographically detectable parathyroid glands can predict resistance to oral pulsed-dose calcitriol treatment of secondary hyperparathyroidism.
abstract: Oral pulsed-dose calcitriol administration has been shown to be effective therapy for patients with secondary hyperparathyroidism. However, this effect is not consistently observed in the clinical setting. This study was undertaken to examine whether enlarged parathyroid glands can serve as a clinical marker that predicts the suppressive effect of calcitriol. Thirty-five patients undergoing chronic hemodialysis (HD) were examined (age, 51.9 +/- 14.9 years; duration of HD, 72.0 +/- 56.0 months). Based on the volume of parathyroid glands measured using an ultrasonographic scanner, patients were divided into two groups: 15 patients with undetectable parathyroid glands (ND group) and 20 patients with detectable parathyroid glands (D group; mean volume of parathyroid glands, 261. 9 +/- 347.5 mm(3)). No significant differences were found in serum ionized calcium (Ca(++)) or parathyroid hormone (PTH) levels before calcitriol administration between the two groups. For each patient, 8 microg of calcitriol was administered orally at the end of the HD session, and the changes in serum PTH levels were determined 44 hours after dosing. No significant differences were found between the two groups in serum Ca(++) levels. However, a significant decrease in serum PTH levels was observed in the ND group, whereas no significant changes were found in the D group. The results of the study show that the suppressive effect on PTH through calcitriol therapy was reduced in patients with detectable enlarged parathyroid glands. This may indicate that the size of parathyroid glands is one factor determining the therapeutic potential of pulsed-dose calcitriol administration for secondary hyperparathyroidism.
authors.affiliation: Department of Internal Medicine II, Tokyo Jikei University School of Medicine, Tokyo, Japan. naohiko@nn.iij4u.or.jp
authors.forename: N
authors.initials: N
authors.lastname: Katoh
authors.forename: M
authors.initials: M
authors.lastname: Nakayama
authors.forename: T
authors.initials: T
authors.lastname: Shigematsu
authors.forename: H
authors.initials: H
authors.lastname: Yamamoto
authors.forename: K
authors.initials: K
authors.lastname: Sano
authors.forename: I
authors.initials: I
authors.lastname: Saito
authors.forename: H
authors.initials: H
authors.lastname: Nakano
authors.forename: K
authors.initials: K
authors.lastname: Kasai
authors.forename: H
authors.initials: H
authors.lastname: Kubo
authors.forename: S
authors.initials: S
authors.lastname: Sakai
authors.forename: Y
authors.initials: Y
authors.lastname: Kawaguchi
authors.forename: T
authors.initials: T
authors.lastname: Hosoya
mesh_terms: D000284:Administration, Oral; D000328:Adult; D000368:Aged; D002117:Calcitriol / Q000008:administration & dosage*; D002120:Calcium Channel Agonists / Q000008:administration & dosage*; D005260:Female; D006801:Humans; D006962:Hyperparathyroidism, Secondary / Q000150:complications / Q000188:drug therapy*; D008297:Male; D008875:Middle Aged; D010280:Parathyroid Glands / Q000000981:diagnostic imaging* / Q000473:pathology; D011237:Predictive Value of Tests; D011379:Prognosis; D020551:Pulse Therapy, Drug; D014463:Ultrasonography
chemical_list: D002120:Calcium Channel Agonists; D002117:Calcitriol