The aim of this study is to investigate prospectively specific immune system factors in preterm neonates with late-onset sepsis and infection-free controls. Matched preterm neonates (n = 82) were divided into three groups: suspected infection (n = 25), sepsis (n = 17), and infection-free controls (n = 40). Serial measurements were made of interleukin-6 (IL-6), IL-1β, tumor necrosis factor-α (TNF-α), lymphocyte subsets [CD3+, CD4+, CD8+, natural killer (NK) cells, and B cells], the immunoglobulins (IgG, IgM, and IgA), C-reactive protein (CRP), and the total blood count, before, 2 days after initiation of treatment, and after stopping treatment. The percentages of NK and B cells were higher in the sepsis group, but those of CD3+, CD4+, and CD8+ showed no differences. IgG was lower in the sepsis group. IL-6 >30 pg/ml and TNF-α >30 pg/ml were sensitive sepsis predictors with sensitivity 1 (0.78-1) and 1 (0.79-1), respectively, but their specificity was poor. CRP was a specific [0.90 (0.80-0.96)] but not sensitive index [0.68 (0.48-0.85)], and its combination with IL-6 or TNF-α could enhance their diagnostic accuracy. It is concluded that NK and B cells may be elevated in late neonatal sepsis. IL-6 or TNF-α combined with CRP is a good diagnostic marker for late-onset sepsis in preterm neonates.

This article is available online at http://www.jlr.org herpes simplex virus, helicobacter pylori, as well as periodontitis have been studied ( 2-4 ). On the contrary, other studies have disputed the causal role of infectious agents in atherogenesis ( 5-7 ).Current evidence suggests that atherosclerosis develops as a response to infl ammatory stimulus. Therefore, common or uncommon infections could represent a risk factor. Mechanisms that may be implicated in the atherogenesis caused by infectious agents include local increase of proinfl ammatory cells, local effusion of endotoxins, autoimmune reaction, systemic cytokine release, and changes in lipid metabolism ( 8 ).Infection and infl ammation cause similar cytokineinduced changes in lipid and lipoprotein metabolism ( 9 ). These include reductions in serum levels of total cholesterol (TC), HDL-cholesterol (HDL-C), LDL-cholesterol (LDL-C), apolipoproteins (Apo) AI and B, and lipoprotein (a) [Lp(a)] and increases in triglyceride (TG) and ApoE concentrations ( 9-14 ).Current evidence suggests that the host response to infection and infl ammation increases oxidized lipids in serum and induces LDL oxidation in vivo. Oxidative modifi cation of LDL is an important event in the development of atherosclerosis ( 15 ). In addition, the cholesterol ester transfer protein (CETP) plays a central role in HDL metabolism and the regulation of HDL-C levels in serum. High levels of CETP activity lead to a reduction in HDL-C levels and an atherogenic lipoprotein profi le ( 16 ).Platelet-activating factor (PAF) is a potent pro-infl ammatory phospholipid produced by activated platelets, -C), ApoB, ApoAI, and ApoCIII and higher LDL-C/HDL-C and ApoB/ApoAI ratios; 2 ) higher levels of IL-1b, IL-6, and TNFa; 3 ) similar ApoCII and oxLDL levels and Lp-PLA 2 activity, lower PON1, and higher CETP activity; and 4 ) higher small dense LDL-C concentration. Four months later, increases in TC, HDL-C, LDL-C, ApoB, ApoAI, and ApoCIII levels, ApoB/ApoAI ratio, and PON1 activity were noticed compared with baseline, whereas CETP activity decreased. LDL-C/HDL-C ratio, ApoCII, and oxLDL levels, Lp-PLA 2 activity, and small dense LDL-C concentration were not altered. Brucella infection is associated with an atherogenic lipid profi le that is not fully restored 4 months following treatment. There is increasing evidence that a link exists between infection/infl ammation and atherosclerosis ( 1 ). Infections with chlamydia pneumoniae, cytomegalovirus,

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Nebivolol, a selective beta1-lipophilic blocker, achieves blood pressure control by modulating nitric oxide release in addition to b-blockade. This dual mechanism of action could result in minimum interference with lipid metabolism compared to atenolol, a classic beta1-selective blocker. Hypertensive patients commonly exhibit lipid abnormalities and frequently require statins in combination with the anti-hypertensive therapy. We conducted this trial in order to clarify the effect on the metabolic profile of beta-blocker therapy with atenolol or nebivolol alone, or in conjunction with pravastatin. Thirty hypertensive hyperlipidemic men and women (total cholesterol >240 mg/dL [6.2 mmol/L], low-density lipoprotein cholesterol >190 mg/dL [4.9 mmol/L], triglycerides <500 mg/dL [5.6 mmol/L]) were separated in two groups. One group consisted of 15 subjects on atenolol therapy (50 mg daily), and the other group included 15 subjects on nebivolol therapy (5 mg daily). After 12 weeks of beta-blocker therapy, pravastatin (40 mg daily) was added in both groups for another 12 weeks. Atenolol significantly increased triglyceride levels by 19% (P=.05), while nebivolol showed a trend to increase high-density lipoprotein cholesterol by 8% (NS) and to decrease triglyceride levels by 5% (NS). Atenolol significantly increased lipoprotein(a) by 30% (P=.028). Fibrinogen levels were equally and not significantly decreased in both groups by 9% and 7%, respectively. Furthermore, atenolol and nebivolol decreased serum high-sensitivity C-reactive protein levels by 14% (P=.05) and 15% (P=.05), respectively. On the other hand, both atenolol and nebivolol showed a trend to increase homocysteine levels (NS) by 13% and 11%, respectively. Although uric acid levels remained the same, atenolol significantly increased the fractional excretion of uric acid by 33% (P=.03). Following nebivolol administration, glucose levels remained the same, while insulin levels were reduced by 10% and the HOMA index (fasting glucose levels multiplied by fasting insulin levels and divided by 22.5) was reduced by 20% (P=.05). There were no significant differences between the two patient groups in the measured parameters after the administration of beta-blockers, except for triglycerides (P<.05) and the HOMA index (P=.05). The addition of pravastatin to all patients (n=30) decreased total cholesterol by 21% (P<.001), low-density lipoprotein cholesterol by 28% (P<.001), apolipoprotein-B by 22% (P<.001), apolipoprotein-E by 15% (P=.014) and lipoprotein(a) levels by 12% (P=.023). Moreover, homocysteine levels and C-reactive protein were reduced by 17% (P=.05) and 43% (P=.05), respectively. We conclude that nebivolol seems to be a more appropriate therapy in hypertensive patients with hyperlipidemia and carbohydrate intolerance. Finally, the addition of pravastatin could further correct the well-established predictors of cardiovascular events.

In addition to its well-known hypolipidemic effects, fenofibrate may also possess significant anti-inflammatory properties that can contribute its antiatherogenic effect.