deoxypyridinoline


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deoxypyridinoline

Bone disease A crosslink of type I collagen present in bone which is excreted unmetabolized in urine and is a specific marker of bone resorption, and ↑ in Pts with osteoporosis. See Osteoporosis, Pyrilinks-D®.

deoxypyridinoline

(dē-ŏk″sē-pĭ-rĭ-dĭn′ō-lēn, -lĭn),

Dpd

A component of the structural matrix of bone, principally found in type 1 collagen as a structural cross link. It provides tensile strength to bone.

When bone resorption exceeds bone rebuilding (for example, in osteoporosis), Dpd is released into the circulation and excreted unchanged in the urine. The detection of elevated levels of Dpd in a concentrated urine specimen is used as a marker of ongoing bone loss in osteoporosis. Reduced levels of Dpd are an indicator of the effectiveness of therapies that reduce bone resorption (e.g., bisphosphonates).

The Dpd urine test is performed by obtaining the first urine voided by a patient on awakening—this ensures that the specimen will be maximally concentrated. The level of Dpd obtained is expressed in nmol of Dpd/mmol of urinary creatinine.

References in periodicals archive ?
Increasing urinary cadmium, but not serum retinol, was associated with increases in deoxypyridinoline and decreases in parathyroid hormone concentrations, which indicates the effect of cadmium on bone turnover and increased bone resorption.
Two bone markers were measured: bone-specific alkaline phosphatase (BSAP) and deoxypyridinoline (DPD).
Assessment and recommendations of factors contributing to preanalytical variability of urinary pyridinoline and deoxypyridinoline.
How it works: It tests for the presence of a bone breakdown product in the urine called Deoxypyridinoline (Dpd).
Patent Office has allowed two of its 1987 patent applications for deoxypyridinoline (D-Pyr) bone resorption assays.
However these markers, which were widely used at the outset of this study, have now been superseded by more sensitive and specific assays such as urinary deoxypyridinoline and N-telopeptide.
Daily oral doses of alendronate (5, 20, and 40 mg for six weeks) in postmenopausal women produced biochemical changes indicative of dose-dependent inhibition of bone resorption, including decreases in urinary calcium and urinary markers of bone collagen degradation (such as deoxypyridinoline and cross-linked N-telopeptides of type I collagen).
As a result, PE significantly inhibited the increased urinary Ca excretion and activity of bone resorption markers including tartrate-resistant acid phosphatase (TRAP), deoxypyridinoline crosslinks and cathepsin K in OVX rats, whereas exhibited little effects on the body, uterus and vagina weight.
Commercially available kits were used (Biosource, LINCO Research) to measure TNF-[alpha], IL10, IL6, adiponectine, osteocalcin and urine deoxypyridinoline as it has been known that all kits have already completed inter- and intra-assay CV values.
Serum B2-microglubulin concentration correlates with urinary concentrations of type | collagen cross-linked N-telopeptides and deoxypyridinoline in rheumatoid arthritis.
Serum osteocalcin level was low (68%) and urinary deoxypyridinoline to creatinine ratio was high (79%), which demonstrated low bone formation with high resorption.