|Values are valid only on day of printing.|
Human bone is continuously remodeled through a process of bone formation and resorption. Approximately 90% of the organic matrix of bone is type I collagen, a helical protein that is crosslinked at the N- and C-terminal ends of the molecule. During bone resorption, osteoclasts secrete a mixture of acid and neutral proteases that degrade the collagen fibrils into molecular fragments including C-terminal telopeptide (CTx). As bone ages, the alpha form of aspartic acid present in CTx converts to the beta form (beta-CTx). Beta-CTx is released into the bloodstream during bone resorption and serves as a specific marker for the degradation of mature type I collagen. Elevated serum concentrations of beta-CTx have been reported in patients with increased bone resorption.
Bone turnover markers are physiologically elevated during childhood, growth, and fracture healing. The elevations in bone resorption markers and bone formation markers are typically balanced in these circumstances and are of no diagnostic value. By contrast, bone turnover markers may be useful when the bone remodeling process is unbalanced. Abnormalities in the process of bone remodeling can result in changes in skeletal mass and shape. Many diseases, in particular hyperthyroidism, all forms of hyperparathyroidism, most forms of osteomalacia and rickets (even if not associated with hyperparathyroidism), hypercalcemia of malignancy, Pagets disease, multiple myeloma, and bone metastases, as well as various congenital diseases of bone formation and remodeling, can result in accelerated and unbalanced bone turnover. Unbalanced bone turnover is also found in age-related and postmenopausal osteopenia and osteoporosis.
Disease-associated bone turnover abnormalities should normalize in response to effective therapeutic interventions, which can be monitored by measurement of serum and urine bone resorption markers.
An aid in monitoring antiresorptive therapies (eg, bisphosphonates and hormone replacement therapy) in postmenopausal women treated for osteoporosis and individuals diagnosed with osteopenia
An adjunct in the diagnosis of medical conditions associated with increased bone turnover
Elevated levels of beta-CTx indicate increased bone resorption. Increased levels are associated with osteoporosis, osteopenia, Paget disease, hyperthyroidism, and hyperparathyroidism.
In patients taking antiresorptive agents (bisphosphonates or hormone replacement therapy), a decrease of > or =25% from baseline beta-CTx levels (ie, prior to the start of therapy) 3 to 6 months after initiation of therapy indicates an adequate therapeutic response.
Reduced renal function may lead to reduced urinary excretion of beta-CTx and a consequent increase in the apparent serum beta-CTx concentration.
In patients receiving therapy with high doses of biotin (ie, >5 mg/day), wait at least 8 hours after the last biotin administration before drawing a specimen, to avoid assay interference from the biotin.
As with all tests containing monoclonal mouse antibodies, erroneous findings may be obtained from specimens taken from patients who have been treated with monoclonal mouse antibodies or have received them for diagnostic purposes.
In rare cases, interference due to extremely high titers of antibodies to ruthenium or streptavidin can occur.
<18 years: not established
18-30 years: 155-873 pg/mL
31-50 years: 93-630 pg/mL
51-70 years: 35-836 pg/mL
>70 years: not established
<18 years: not established
Premenopausal: 25-573 pg/mL
Postmenopausal: 104-1,008 pg/mL
1. Christgau S, Bitsch-Jensen O, Hanover Bjarnason N, et al: Serum CrossLaps for monitoring the response in individuals undergoing antiresorptive therapy. Bone 2000 May;26(5):505-511
2. Garnero P, Borel O, Delmas PD: Evaluation of a fully automated serum assay for C-terminal cross-linking telopeptide of type I collagen in osteoporosis. Clin Chem. 2001 Apr;47(4):694-702
3. Delmas PD, Eastell R, Garnero P, et al: The use of biochemical markers of bone turnover in osteoporosis. Committee of Scientific Advisors of the International Osteoporosis Foundation. Osteoporo Int 2000;11:S2-S17