Tumor necrosis factor alpha (TNFα) and its soluble receptor p75 (sTNF-R p75) in familial combined hyperlipidemia (FCHL)

Tumor necrosis factor-α is a marker of familial combined hyperlipidemia, independently of metabolic syndrome

“…However, the difference was significant only with nonaffected relatives but not with normolipidemic control subjects. A possible explanation for the more pronounced differences observed in our study compared with the one by Cavallo et al [27] could be the larger patient population in the present study and the lower sensitivity of previously available methods for the measurement of TNF-α (lowest sensitivity limit of 7 pg/mL in the study by Cavallo et al, 0.5 pg/mL in ours).…”

“…In 2 articles relevant to this issue [26,27], a linkage was suggested between FCHL and the locus 1q21-23 including the TNF superfamily member-1B. Reduced plasma levels of soluble-TNF-receptor p75, 1 of the 2 binding domains of the TNF-α receptor, were found in patients with FCHL [26], thus suggesting an increased number of TNF-α receptors bound to target cells.…”

“…Reduced plasma levels of soluble-TNF-receptor p75, 1 of the 2 binding domains of the TNF-α receptor, were found in patients with FCHL [26], thus suggesting an increased number of TNF-α receptors bound to target cells. The proposed link with the disease was an increased cellular sensitivity to the proinflammatory activity of TNF-α caused by an increased number of cell-bound, active TNF-α receptors [27]. Only in 1 of these 2 articles were TNF-α concentrations elevated in patients with FCHL compared to control subjects [27].…”

“…The proposed link with the disease was an increased cellular sensitivity to the proinflammatory activity of TNF-α caused by an increased number of cell-bound, active TNF-α receptors [27]. Only in 1 of these 2 articles were TNF-α concentrations elevated in patients with FCHL compared to control subjects [27]. However, the difference was significant only with nonaffected relatives but not with normolipidemic control subjects.…”