המידע באדיבות מדיקונטקסט
Last Updated: 2001-07-10 18:01:05 EDT (Reuters Health)
By David Douglas
WESTPORT, CT (Reuters Health) – Levels of serum amyloid A (SAA) protein appear valuable in evaluating the prognosis of patients with AA amyloidosis, UK researchers report in the July 7th issue of The Lancet.
Dr. Julian D. Gillmore and colleagues, of Royal Free and University Medical School, London, note that although rare, this reactive systemic amyloidosis is associated with a range of conditions including diabetes and Alzheimer's disease.
The pathogenesis involves "conversion of normally soluble proteins into insoluble fibrillar aggregates." In AA amyloidosis, fibrils are derived from processes involving circulating SAA.
To investigate the relationship of this protein with factors including clinical outcome, the researchers studied 80 AA amyloidosis patients in whom "underlying inflammatory diseases were treated as vigorously as possible."
After follow-up ranging from 1 to almost 10 years, the investigators found that amyloidotic organ function stabilized or improved in 39 of the 42 patients in whom median levels of SAA remained below 10 mg/L. In 25 of these patients amyloid deposits regressed.
Patients in whom median SAA levels persistently remained above 50 mg/mL showed varied outcome "but amyloid load increased and organ function deteriorated in most." Overall, estimated survival at 10 years was 90% in patients in whom median SAA level stayed below 10 mg/L and 40% in those who whose SAA went beyond this level.
Commenting on the findings, Dr. Gillmore told Reuters Health that "we have systematically demonstrated for the first time that AA amyloid deposits do regress when the supply of SAA, the amyloid-forming protein, is significantly reduced. Furthermore, near-normalization of SAA levels was associated with a marked survival benefit."
The researchers conclude that measurement of SAA levels "can provide invaluable prognostic information," and they suggest that "therapeutic strategies to reduce the supply of amyloid fibril precursor proteins," may be useful in such patients.
In an accompanying editorial, Dr. Gaye Cunnane of the University of California, San Francisco, agrees that "SAA is a valuable tool for monitoring inflammatory activity" and is encouraged by the finding that "intensive treatment suppressed inflammatory activity rapidly and completely in many patients."
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