Increased platelet reactivity in Klinefelter men: something new to consider. (27th July 2015)

• Record Type: Journal Article
• Authors: Di Minno, M. N. D.; Esposito, D.; Di Minno, A.; Accardo, G.; Lupoli, G.; Cittadini, A.; Giugliano, D.; Pasquali, D.
• Is Part Of: Andrology. Volume 3:Number 5(2015)
• Page Start: 876
• Page End: 881
• Publication Date: 2015-07-27
• Subjects: Andrology -- Periodicals; 616.65
• DOI: 10.1111/andr.12080
• Languages: English
• ISSNs: 2047-2919

Abstract

<abstract abstract-type="main" id="andr12080-abs-0001"> <title>Summary</title> <p>Patients with Klinefelter syndrome (KS) exhibit an increased cardiovascular risk, but underlying mechanisms are largely unknown. The present cross‐sectional study has been conducted to evaluate platelet reactivity and the expression of platelet activation markers (8‐iso‐prostaglandin F2α[8‐iso‐PGF2α] and 11‐dehydro‐thromboxane‐B₂[11‐dehydro‐TXB2]) in KS patients and healthy controls. Twenty‐three consecutive KS patients under testosterone replacement therapy have been included as case group and 46 age‐matched healthy males recruited among hospital staff served as controls. Light transmission aggregometry was performed in both cases and controls and maximal platelet aggregation (max‐A%) was defined as maximal light transmittance reached within 5 min after the addition of 0.2 or 0.4 m<sc>m</sc> arachidonic acid (AA). A ≥ 50% irreversible light transmittance (LT‐50%) following platelet stimulation defined an adequate platelet aggregation and AC‐50% was defined as the minimal agonist concentration needed to achieve LT‐50%. The AC‐50% was 0.26 m<sc>m </sc>AA for KS and 0.36 m<sc>m</sc> for controls (<italic>p</italic> < 0.001). Whereas AA (0.2 m<sc>m</sc>) induced LT‐50% in 69.6% of KS and in 15.2% of controls (<italic>p</italic> < 0.001), the stimulation with AA (0.4 m<sc>m</sc>) determined LT‐50% in all cases and controls. However, max‐A% was higher in KS than in controls both after AA (0.2 m<sc>m</sc>) (65.61% vs. 46.30%, <italic>p</italic> = 0.002, ) and after AA (0.4 m<sc>m</sc>) (96.43% vs. 81.04%, <italic>p</italic> < 0.001). 8‐iso‐PGF2α and 11‐dehydro‐TXB2 were higher in KS than in controls (446.54 pg/mg creatinine vs. 230.00 pg/mg creatinine, <italic>p</italic> < 0.001 and 1278.36 pg/mg creatinine vs. 595.08 pg/mg creatinine, <italic>p</italic> = 0.001, respectively) and AC‐50% inversely correlated with 8‐iso‐PGF2α (ρ = −0.548, <italic>p</italic> < 0.001) and with 11‐dehydro‐TXB2 (ρ = −0.523, <italic>p</italic> < 0.001). In a linear regression model, KS independently predicted a lower AC‐50% (β = −0.597, <italic>p</italic> < 0.001) and higher levels of 8‐iso‐PGF2α (β = 0.709, <italic>p</italic> < 0.001) and 11‐dehydro‐TXB2 (β = 0.605, <italic>p</italic> < 0.001). In contrast, no correlation has been found between max‐A%, testosterone and estradiol levels in KS. We observed increased platelet reactivity in KS. This might, at least in part, explain the increased thrombotic risk associated with this disease.</p> </abstract>