Early supplementation with Lactobacillus rhamnosus HN001 reduces eczema prevalence to 6 years: does it also reduce atopic sensitization?

BACKGROUND: The role of probiotics in prevention of allergic disease is still not clear; efficacy may depend on the timing, dose, duration, and specific probiotic used. Using a double-blind randomized placebo-controlled trial (Australian New Zealand Clinical Trials Registry: ACTRN12607000518460), we have shown that in a high-risk birth cohort, maternal supplementation from 35 weeks gestation until 6 months if breastfeeding and infant supplementation from birth until 2 years with Lactobacillus rhamnosus HN001 (HN001) (6 × 10(9) cfu/day) halved the cumulative prevalence of eczema at 2 and 4 years. Bifidobacterium animalis subsp lactis HN019 (HN019) (9 × 10(9) cfu/day) had no significant effect. OBJECTIVE: To determine whether differences in effects of HN001 and HN019 on eczema persist to age 6 years, and to investigate effects on sensitization. METHODS: Standard procedures were used to assess eczema (The UK Working Party's Criteria), eczema severity (SCORAD), atopic sensitization [skin prick tests (SPT), total and specific IgE] and standard questions used for asthma, wheeze, and rhinoconjunctivitis. RESULTS: HN001 was associated with significantly lower cumulative prevalence of eczema (HR = 0.56, 95% CI 0.39-0.80), SCORAD ≥ 10 (HR = 0.69, 0.49-0.98) and SPT sensitization (HR = 0.69, 95% CI 0.48-0.99). The point prevalence of eczema (RR = 0.66, 95% CI 0.44-1.00), SCORAD ≥ 10 (RR = 0.62, 95% CI 0.38-1.01) and SPT sensitization (RR = 0.72, 95% CI 0.53-1.00) were also reduced among children taking HN001. HN019 had no significant effect on any outcome. CONCLUSION AND CLINICAL RELEVANCE: This study provides evidence for the efficacy of the probiotic L. rhamnosus HN001 in preventing the development of eczema and possibly also atopic sensitization in high risk infants to age 6 years. The absence of a similar effect for HN019 indicates that benefits may be species specific.

Nebulized beta 2-adrenoceptor agonists do not affect plasma selenium or glutathione peroxidase activity in patients with asthma.

We investigated whether the beta 2-agonists fenoterol and salbutamol decreased plasma selenium and glutathione peroxidase activity in patients with asthma as this may partially explain the findings of reduced selenium status in asthmatic patients. Nine patients with asthma were studied on 3 occasions and inhaled either fenoterol (5 mg), salbutamol (5 mg) or ipratropium bromide (0.5 mg) administered by nebulization using a randomized, double blind, crossover design. Plasma selenium, glutathione peroxidase activity and potassium were measured prior to drug administration and at 15, 30 and 60 minutes after drug. None of the drugs had any effect on plasma selenium or glutathione peroxidase activity. Ipratropium bromide did not affect plasma potassium. Both beta 2-agonists significantly decreased plasma potassium. The mean (SD) maximum decrease was -0.79 (0-18) mmol/l for fenoterol and -0.26 (0-03) mmol/l for salbutamol (both p < or = 0.01) confirming systemic absorption of the drugs. beta 2-agonists are unlikely to be responsible for the reduced selenium status found in some patients with asthma.

The k-complex vasoconstrictor response: evidence for central vasomotor downregulation in borderline hypertension.

Central sympathetic outflow and the baroreflex were measured as an integrated cardiopressor response to a noise stimulus during normal sleep, in 13 normotensives and 14 borderline hypertensives. The pressor response latency was prolonged in the borderline hypertensives, and the stimulus-induced increase in systolic and diastolic intra-arterial pressure was greater in the borderline hypertensives (23.0 +/- 7.3-16.2 +/- 5.6 mmHg) compared with the normotensives (16.7 +/- 5.9-13.6 +/- 4.6 mmHg; P less than 0.001), but the heart rate was not increased. Despite the increased pressor response, the baroreflex-mediated fall in the heart rate following the pressor response was reduced in the borderline hypertensives, indicating secondary adaptation to hypertension and a resetting, or downregulation, of central vasomotor control mechanisms in the borderline hypertensives relative to normotensives.