title: Suppression of parathyroid hormone secretion in CAPD patients by intraperitoneal administration of Maxacalcitol.
abstract: BACKGROUND
  Maxacalcitol (22-oxacalcitriol; OCT) is a novel vitamin D analogue. In previous clinical studies, OCT was administered three times a week to hemodialysis patients with refractory secondary hyperparathyroidism (2HPT), in whom it acted by inhibiting parathyroid hormone secretion, as well as causing mildly elevated serum calcium. However, intravenous injection of OCT, which requires frequent visits to the outpatient clinic, degrades the quality of life of patients with continuous ambulatory peritoneal dialysis (CAPD) who otherwise visit the clinic only once or twice per month. In the present study, we investigated whether transperitoneal absorption of OCT inhibited intact parathyroid hormone (i-PTH) in CAPD patients when the OCT was added to the peritoneal dialysis fluid.
  
  
  METHODS
  Peritoneal dialysis fluid containing 20 micro g of OCT was injected into the peritoneal cavity of five CAPD patients. The serum and peritoneal fluid levels of OCT, i-PTH, calcium, and phosphate were measured before and after treatment.
  
  
  RESULTS
  The mean concentration of OCT in peritoneal dialysis fluid rapidly decreased, from 25268.0 pg/ml at 0 h to 1694.0 pg/ml at 2 h and 44.9 pg/ml at 4 h. In contrast, the mean serum OCT level increased from the pretreatment level, which was below the detection limit of the assay, to 656.0 pg/ml at 0.5 h and a peak of 759.0 pg/ml at 1 h, and thereafter gradually decreased, to 713.8 pg/ml at 2 h and 555.8 pg/ml at 4 h. Mean i-PTH significantly decreased, to 83.9% of the baseline level, at 1 h (P < 0.05) and thereafter stayed at around 90%. No consistent trends in calcium and phosphate levels were observed in the five patients.
  
  
  CONCLUSIONS
  By injecting OCT into the peritoneal cavity, i-PTH levels could be significantly decreased. These findings indicate the therapeutic efficacy of intraperitoneal administration of OCT for CAPD patients.
authors.affiliation: Department of Nephrology, Fujita Health University School of Medicine, 1-98 Dengakugakubo Kutsukake-cho, Toyoake 470-1192, Japan. jinzou@fujita-hu.ac.jp
authors.forename: Kazutaka
authors.initials: K
authors.lastname: Murakami
authors.forename: Hiromi
authors.initials: H
authors.lastname: Miyachi
authors.forename: Asako
authors.initials: A
authors.lastname: Watanabe
authors.forename: Nahoko
authors.initials: N
authors.lastname: Kawamura
authors.forename: Mikiko
authors.initials: M
authors.lastname: Fujii
authors.forename: Shigehisa
authors.initials: S
authors.lastname: Koide
authors.forename: Masamitsu
authors.initials: M
authors.lastname: Murase
authors.forename: Hiroko
authors.initials: H
authors.lastname: Kushimoto
authors.forename: Midori
authors.initials: M
authors.lastname: Hasegawa
authors.forename: Makoto
authors.initials: M
authors.lastname: Tomita
authors.forename: Yoshiyuki
authors.initials: Y
authors.lastname: Hiki
authors.forename: Satoshi
authors.initials: S
authors.lastname: Sugiyama
mesh_terms: D000328:Adult; D000368:Aged; D000970:Antineoplastic Agents / Q000008:administration & dosage* / Q000097:blood / Q000493:pharmacokinetics; D002117:Calcitriol / Q000008:administration & dosage* / Q000031:analogs & derivatives* / Q000097:blood / Q000493:pharmacokinetics; D015314:Dialysis Solutions / Q000378:metabolism; D005260:Female; D006801:Humans; D006962:Hyperparathyroidism, Secondary / Q000188:drug therapy* / Q000209:etiology / Q000378:metabolism; D007274:Injections, Intraperitoneal; D007676:Kidney Failure, Chronic / Q000150:complications* / Q000628:therapy; D008297:Male; D008875:Middle Aged; D010281:Parathyroid Hormone / Q000378:metabolism*; D010531:Peritoneal Dialysis, Continuous Ambulatory
chemical_list: D000970:Antineoplastic Agents; D015314:Dialysis Solutions; D010281:Parathyroid Hormone; D002117:Calcitriol; C051883:maxacalcitol