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Randomized Controlled Trial Comparative Study Clinical Trial
Role of A-SAA in monitoring subclinical inflammation and in colchicine dosage in familial Mediterranean fever.
- A Duzova, A Bakkaloglu, N Besbas, R Topaloglu, S Ozen, F Ozaltin, Y Bassoy, and E Yilmaz.
- Department of Pediatrics, Pediatric Nephrology and Rheumatology Unit, Hacettepe University Faculty of Medicine, Ankara, Turkey. aduzova@hacettepe.edu.tr
- Clin Exp Rheumatol. 2003 Jul 1; 21 (4): 509-14.
Objectives1) To compare the sensitivity of serum amyloid A protein (A-SAA) and other acute phase proteins (APPs) in determining subclinical inflammation in patients with familial Mediterranean fever (FMF) during an attack-free period; 2) to define those clinical, laboratory features that may modify the A-SAA level; and 3) to evaluate the effect of an increase in the colchicine dose on the A-SAA level.MethodsA-SAA, CRP, ESR, fibrinogen and ferritin levels were measured in 183 patients [88 F, 95 M; median age 11.0 years (1.0-20.0)] with FMF during an attack-free period. Mutational analysis was available in 157 patients. The colchicine dose was increased in 26 randomly chosen patients with no attacks within the last year; laboratory studies were repeated at the end of the second month.ResultsDuring an attack-free period, the median A-SAA level was 74 (6-1,500) mg/L; other APPs were within normal ranges in 49-93% of the patients. Age, gender, age at onset, age at diagnosis, the duration of treatment and the frequency of attacks had no significant effect on the A-SAA level. Homozygous and compound heterozygous patients had higher A-SAA levels than heterozygous patients [129 mg/L (8-1,500) versus 29 mg/L (6-216); p < 0.005]. There was a dramatic decrease in the A-SAA level [from 244 mg/L (16-1,400) to 35.5 mg/L (8-1,120); p < 0.001] and an increase in the hemoglobin (1.89 +/- 0.10 mmol/L to 1.98 +/- 0.19 mmol/L; p < 0.005) after the increase in colchicine dose in 26 patients.ConclusionSubclinical inflammation continues during an attack-free period in FMF patients. A-SAA was the best marker of subclinical inflammation. Patients who are homozygous or compound heterozygotes of MEFV mutations had higher A-SAA levels. An increase in the colchicine dose resulted in a dramatic decrease in A-SAA and an increase in hemoglobin level. These findings favor the use of A-SAA in drug monitoring.
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