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Serum low density lipoprotein subclasses in asthma.

Respir Med. 2013 Sep 14;

Authors: Scichilone N, Rizzo M, Benfante A, Catania R, Giglio RV, Nikolic D, Montalto G, Bellia V

Abstract
BACKGROUND: The levels of serum low-density lipoproteins (LDL) have been implicated in the inflammatory cascade in a murine model of asthma. Recent findings suggest that LDL may modulate the inflammatory state of the asthmatic airways in humans.
OBJECTIVE: We explored whether LDL subclasses are associated with the occurrence and severity of asthma.
METHODS: 24 asthmatics (M/F: 11/13) and 24 healthy individuals, with normal BMI and absence of metabolic syndrome, matched for age and gender. Serum concentrations of LDL subclasses were distributed as seven bands (LDL-1 and -2 defined as large, least pro-inflammatory LDL, and LDL-3 to -7 defined as small, most pro-inflammatory LDL), using the LipoPrint(©) System (Quantimetrix Corporation, Redondo Beach, CA, USA).
RESULTS: LDL-1 was similar in the two groups (56 ± 16% vs. 53 ± 11, p = NS), while LDL-2 was significantly lower in asthmatics as compared to controls (35 ± 8% vs. 43 ± 10%, p = 0.0074). LDL-3 levels were two-fold higher in the asthmatics, but the difference did not reach the statistical significance (8 ± 7.3% vs. 4 ± 3%, p = NS). Smaller subclasses LDL-4 to LDL-7 were undetectable in controls. In asthmatics, LDL-1 was positively associated with VC% predicted (r = +0.572, p = 0.0035) and FEV1% predicted (r = +0.492, p = 0.0146). LDL-3 was inversely correlated with both VC% predicted (r = -0.535, p = 0.0071) and FEV1% predicted (r = -0.465, p = 0.0222).
CONCLUSIONS: The findings of this pilot study suggest a role of LDL in asthma, and advocate for larger studies to confirm the association between asthma and dyslipidemia.

PMID: 24075885 [PubMed - as supplied by publisher]

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HPA axis Effects of Mometasone Furoate/Formoterol Fumarate Versus Fluticasone Propionate/Salmeterol Administered via Metered-Dose Inhaler.

Chest. 2013 Sep 26;

Authors: Kosoglou T, Hubbell J, Cutler DL, Johnson-Levonas AO, Xu D, Kantesaria BS, Kim K, Miller SD

Abstract
ABSTRACT BACKGROUND: The effects of mometasone furoate and fluticasone propionate on the hypothalamic-pituitary-adrenal axis were compared when administered from combination metered-dose inhaler (MDI) products.
METHODS: In a randomized, open-label, placebo-controlled, parallel-group study, 66 patients with mild-to-moderate asthma received one of the following 4 treatments twice daily (BID) via MDI for 42 days: mometasone furoate/formoterol (MF/F) 200 μg/10 μg; MF/F 400 μg/10 μg; fluticasone propionate/salmeterol (FP/S) 460 μg/42 μg; or placebo. Plasma cortisol concentrations were measured over 24 hours on Days -1 (baseline) and 42. Geometric mean ratio (GMR) and 90% confidence interval (90% CI) for mean change from baseline to Day 42 in 24-hr plasma cortisol AUC were calculated for each treatment. If 90% CI for the GMRs fell within 70%-143%, treatments were deemed comparable.
RESULTS: Mean baseline cortisol AUCs were similar across groups. Mean cortisol effects (change from baseline) were similar for MF/F 400 μg/10 μg and FP/S 460 μg/42 μg (GMR 119%; 90% CI 101%-140%). Effects of MF/F 200 μg/10 μg on cortisol AUC were similar to placebo (GMR 92%; 90% CI 78%-110%), whereas MF/F 400 μg/10 μg and FP/S 460 μg/42 μg lowered cortisol AUC versus placebo (GMR 78%; 90% CI 66%-92% and GMR 66%; 90% CI 56%-78%, respectively). All treatments were generally well tolerated.
CONCLUSIONS: MF/F 400 μg/10 μg or FP/S 460 μg/42 μg administered BID via MDI led to similar reductions from baseline in mean cortisol AUC (22% and 34% lower than placebo, respectively), whereas the effect of MF/F 200 μg/10 μg was similar to placebo.

PMID: 24077095 [PubMed - as supplied by publisher]

If there is such a thing as a clinician who has not encountered patients whose lives have been blighted or ended prematurely by addiction to tobacco smoking, he or she is unlikely to be a respiratory physician. Respiratory medicine is dominated by the health consequences of smoking, and the poverty that smoking exacerbates. Preventing smoking is fundamental to improving respiratory health. That is why all in respiratory medicine should welcome the advent of electronic cigarettes.

The principal addictive component of tobacco smoke is nicotine. The mechanisms of nicotine addiction are highly complex but include at least two important reward pathways: one mediated directly and immediately by stimulation of dopamine release in the shell of the nucleus accumbens, and one indirectly and after more sustained use through release of dopamine in the nucleus accumbens core in response to stimuli associated with nicotine administration.1 In animal models the latter...