Bone Alkaline Phosphatase, Serum
Clinical Information Discusses physiology, pathophysiology, and general clinical aspects, as they relate to a laboratory test
Bone alkaline phosphatase (BAP) is the bone-specific isoform of alkaline phosphatase. A glycoprotein that is found on the surface of osteoblasts, BAP reflects the biosynthetic activity of these bone-forming cells. BAP has been shown to be a sensitive and reliable indicator of bone metabolism.(1)
Normal bone is constantly undergoing remodeling in which bone degradation or resorption is balanced by bone formation. This process is necessary for maintaining bone health. If the process becomes uncoupled and the rate of resorption exceeds the rate of formation, the resulting bone loss can lead to osteoporosis and, consequently, a higher susceptibility to fractures.
Osteoporosis is a metabolic bone disease characterized by low bone mass and abnormal bone microarchitecture. It can result from a number of clinical conditions including states of high bone turnover, endocrine disorders (primary and secondary hyperparathyroidism and thyrotoxicosis), osteomalacia, renal failure, gastrointestinal diseases, long-term corticosteroid therapy, multiple myeloma, and cancer metastatic to the bones.
Paget disease is another common metabolic bone disease caused by excessive rates of bone remodeling resulting in local lesions of abnormal bone matrix. These lesions can result in fractures or neurological involvement. Antiresorptive therapies are used to restore the normal bone structure.
Diagnosis and assessment of severity of metabolic bone disease including Paget disease, osteomalacia, and other states of high bone turnover
Monitoring efficacy of antiresorptive therapies including postmenopausal osteoporosis treatment
Bone alkaline phosphatase (BAP) concentration is high in Paget disease and osteomalacia.
Antiresorptive therapies lower BAP from baseline measurements in Paget disease, osteomalacia, and osteoporosis. Several studies have shown that antiresorptive therapies for management of osteoporosis patients should result in at least a 25% decrease in BAP within 3 to 6 months of initiating therapy.(2,3) BAP also decreases following antiresorptive therapy in Paget disease.(4)
When used as a marker for monitoring purposes, it is important to determine the critical difference (or least significant change). The critical difference is defined as the difference between 2 determinations that may be considered to have clinical significance. The critical difference for this method was calculated to be 25% with a 95% confidence level.(1)
Cautions Discusses conditions that may cause diagnostic confusion, including improper specimen collection and handling, inappropriate test selection, and interfering substances
The assay is not intended as a screening test for osteoporosis. Assay results should be used only in conjunction with information available from the clinical evaluation of the patient and other diagnostic procedures.
Measurements of bone turnover markers are not useful for the diagnosis of osteoporosis; diagnosis of osteoporosis should be made on the basis of bone density.
Human antimouse or other heterophile antibodies may be present in patient specimens. Although the assay has been specifically formulated to minimize their effects on the assay, results from patients known to have these antibodies should be carefully evaluated.
Liver-derived alkaline phosphatase (ALP) has some cross-reactivity in this assay: 100 U/L of liver ALP activity gives a result of 2.5 mcg/L to 5.8 mcg/L. Accordingly, serum specimens with significant elevations of liver ALP activity may yield elevated results.
Reference Values Describes reference intervals and additional information for interpretation of test results. May include intervals based on age and sex when appropriate. Intervals are Mayo-derived, unless otherwise designated. If an interpretive report is provided, the reference value field will state this.
<2 years: 25-221 mcg/L
2-9 years: 27-148 mcg/L
10-13 years: 35-169 mcg/L
14-17 years: 13-111 mcg/L
Adults: < or =20 mcg/L
<2 years: 28-187 mcg/L
2-9 years: 31-152 mcg/L
10-13 years: 29-177 mcg/L
14-17 years: 7-41 mcg/L
Premenopausal: < or =14 mcg/L
Postmenopausal: < or =22 mcg/L
Clinical References Provides recommendations for further in-depth reading of a clinical nature
1. Kress BC: bone alkaline phosphatase: methods of quantitation and clinical utility. J Clin Ligand Assay 1998;21(2):139-148
2. Kress BC, Mizrahi IA, Armour KW, et al: Use of bone alkaline phosphatase to monitor alendronate therapy in individual postmenopausal osteoporotic women. Clin Chem 1999;45(7):1009-1017
3. Garnero P, Darte C, Delmas PD: A model to monitor the efficacy of alendronate treatment in women with osteoporosis using a biochemical marker of bone turnover. Bone 1999;24(6):603-609
4. Raisz L, Smith JA, Trahiotism M, et al: Short-term risedronate treatment in postmenopausal women: Effects on biochemical markers of bone turnover. Osteoporos Int 2000;11:615-620