Mean Platelet Volume in Children with Familial Mediterranean Fever and the Relationship with Attack Status, Colchicine Treatment and Gene Mutation
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Mustafa Kemal University, Faculty of Medicine, Hatay, Turkey
Afyon Kocatepe University, Faculty of Medicine, Afyonkarahisar, Turkey
Publication date: 2014-07-15
Corresponding author
Nilgun Üstün   

Mustafa Kemal Ü Tıp Fak. FTR AD, Hatay, Türkiye
Eur J Gen Med 2014;11(3):169-173
Increased mean platelet volume (MPV) is a manifestation of platelet functions and activation, and accepted as a prognostic biomarker in patients with cardiovascular disease. We aimed to investigate MPV levels in pediatric Famillial Mediterranean Fever (FMF) patients during the attack and attack-free periods, and the effect of colchicine treatment and presence of M694V mutation. Thirty-five pediatric patients with FMF and 38 age-sex-matched healty controls were enrolled retrospectively into the study. Of the patients 11 (31%) had an ongoing attack, and 24 (69%) were in attack-free period. 26 (74%) patients were receiving colchicine and 16 (45.7%) had M694V gene mutation. There was no significant difference in platelet (PLT) and MPV between patients and healthy controls (p=0.196 and p=0.167 respectively). Mean PLT and MPV values of the patients during attack and attack-free period were also not significantly different (p=0.355 and p=0.118 respectively). However, MPV levels during an FMF attack were non-significantly lower than healthy control group (p=0.08). PLT and MPV levels were higher in patients receiving colchicine but the differences were not significant (p=0.097 and p=0.446 respectively). Mean MPV value of the FMF patients with M694V mutation was not significantly different than controls (p=0.773). In conclusion, this study reveals that pediatric FMF patients have similar MPV levels with healthy individuals even in the presence of M694V mutation. MPV as an early atherosclerosis marker, is not significantly elevated in this patient cohort. Regular treatment with colchicine and younger age may have a role in non-impaired platelet activation in FMF patients.
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