A Single Testing of Serum Amyloid A Levels as a Tool for Diagnosis and Treatment Dilemmas in Familial Mediterranean Fever

“…FMF is caused by mutations in the MEditerranean FeVer (MEFV) gene, located on chromosome 16, and encoding pyrin, an inflammationassociated protein. Amyloidosis is a major complication of FMF that may culminate in renal failure [3,4]. Colchicine treatment relieves or prevents the attacks and the development of AA-amyloidosis and its consequences [3].…”

Section: Introductionmentioning

confidence: 99%

QT interval variability in familial Mediterranean fever: a study in colchicine-responsive and colchicine-resistant patients

et al. 2012

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The association between familial Mediterranean fever (FMF), early atherosclerosis, and electrocardiographic markers for arrhythmias remains controversial. There are conflicting results as to the occurrence of high QT dispersion in FMF. The aim of the present study was to further investigate repolarization dynamics and other repolarization-associated pro-arrhythmogenic markers in FMF patients. To explore repolarization in FMF, patients who responded well to colchicine and patients who had not responded to colchicine, yet were amyloidosis-free, were included. We aimed to evaluate whether increased inflammatory burden, a characteristic of non-responsive patients, was specifically associated with abnormal repolarization. Included in the study were 53 FMF patients (27 colchicine non-responders) and 53 age- and sex-matched control subjects. Electrocardiograms were performed under strict standards. QT variability parameters were computed with custom-made computer software. No significant difference in any of the QT dynamic parameters was found in either FMF group compared with the healthy controls. Mean values of QT variability index, regardless of colchicine response, were similar to previously published results for healthy persons. In conclusion, patients with FMF who are continuously treated with colchicine and have not developed amyloidosis, regardless of their clinical response, have normal QT variability parameters, indicating normal repolarization dynamics and suggesting no increased risk of repolarization-associated cardiac arrhythmias.

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“…39 In about 30% of patients with FMF, the laboratory markers of inflammation, including SAA, do not return to normal levels. 43 The control of subclinical inflammation is a major goal in FMF treatment. 40 Inflammation has several effects on hematopoiesis.…”

Section: Discussionmentioning

confidence: 99%

A variant allele of the Mediterranean‐fever gene increases the severity of gout

et al. 2016

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Background: Gout is a clinical syndrome that occurs as an inflammatory response to increased concentration of uric acid and monosodium urate crystals. Familial Mediterranean fever (FMF) is a hereditary autoinflammatory disease with autosomal recessive inheritance. The Mediterranean fever (MEFV) gene is responsible for FMF and encodes pyrin that suppresses the inflammatory response. Most of the FMF-related mutations have been identified in exon 2 (e.g., E148Q and R202Q) and exon 10 (M680I, M694V, M694I and V726A) of the MEFV gene, and each missense mutation is known to increase production of interleukin-1, a proinflammatory cytokine. Our aim was to investigate effects of MEFV variant alleles on the manifestations of gout.

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A Single Testing of Serum Amyloid A Levels as a Tool for Diagnosis and Treatment Dilemmas in Familial Mediterranean Fever

Cited by 65 publications

References 18 publications

Familial Mediterranean Fever in the World

Familial Mediterranean Fever in the World

QT interval variability in familial Mediterranean fever: a study in colchicine-responsive and colchicine-resistant patients

A variant allele of the Mediterranean‐fever gene increases the severity of gout

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