Bone alkaline phosphatase in rheumatoid arthritis: a longitudinal study

Area of Science:

• Biochemistry
• Rheumatology
• Clinical Chemistry

Background:

• Elevated total alkaline phosphatase (TAP) is observed in patients with active rheumatoid arthritis (RA).
• The primary source of this elevation (bone isoenzyme vs. liver isoenzyme) in RA patients is not well-defined.

Purpose of the Study:

• To ascertain if raised TAP in active RA originates predominantly from bone alkaline phosphatase (BAP) or liver isoenzymes.
• To assess the impact of steroid and disease-modifying antirheumatic drug (DMARD) treatments on BAP levels over time.

Main Methods:

• Studied 58 RA patients treated with gold sodium thiomalate, D-penicillamine, or sulfasalazine for 24 weeks.
• Assessed disease activity and measured BAP using a specific radioimmunometric assay.
• Monitored BAP and TAP levels serially throughout the treatment period.

Main Results:

• BAP correlated with TAP in the overall RA group, but not with intraindividual changes from weeks 4 to 24.
• TAP and gamma-glutamyltranspeptidase correlated with disease activity.
• BAP did not correlate with disease activity, and steroids/DMARDs did not significantly affect BAP levels.

Conclusions:

• Increased TAP in active RA is largely due to liver isoenzymes, not BAP.
• BAP is not a reliable marker for monitoring disease activity or treatment response in RA.
• Inflammatory processes in RA may increase hepatobiliary enzymes, contributing to elevated TAP.