What's new in atopic eczema? An analysis of systematic reviews published in 2010-11.

This review provides a summary of key findings from 24 systematic reviews of atopic eczema (AE) published or indexed between 1 August 2010 and 31 December 2011, updating published summaries from previous years. Epidemiological evidence points to the protective effects of early daycare, endotoxin exposure, consumption of unpasteurized milk, and early exposure to dogs, but antibiotic use in early life may increase the risk for AE. With regard to prevention of AE, there is currently no strong evidence of benefit for exclusive breastfeeding, hydrolysed protein formulas, soy formulas, maternal antigen avoidance, omega-3 or omega-6 fatty-acid supplementation, or use of prebiotics or probiotics. With respect to AE treatments, the most compelling new systematic review evidence was for proactive treatment with topical anti-inflammatory agents (topical corticosteroids and topical calcineurin inhibitors) for the prevention of AE flares in patients with moderate to severe AE. A meta-analysis of 4 trials confirmed the superiority of tacrolimus 0.1% over pimecrolimus for the treatment of AE, and a review of 17 trials found that tacrolimus (0.1% or 0.03%) was broadly similar in efficacy to mild/moderate topical corticosteroids. Evidence for the role of education in the management of AE was less conclusive, with evidence from randomized controlled trials showing mixed results. Further work is needed in this area to conduct high-quality trials of educational interventions that are clearly described and reproducible. There is no clear evidence for the efficacy of homeopathy, botanical extracts or Chinese herbal medicine in the treatment of AE, as large well-designed trials are lacking in these areas.

Genes, growth factors and acanthosis nigricans.

Acanthosis nigricans (AN) occurs most commonly in association with hyperinsulinaemia and more rarely as a paraneoplastic syndrome. It is also a feature of several genetic disorders. Indirect evidence suggests a role for tyrosine kinase growth factor receptor signalling in the pathogenesis of AN. Defects in the insulin receptor gene causing insulin resistance and AN are well recognized, but recent data in several other syndromes of this association, including lipodystrophic disorders, have identified causative defects in other pathways. The mechanism of AN due to insulin resistance is most probably direct or indirect activation of the insulin-like growth factor 1 receptor by high levels of circulating insulin. However, more direct evidence for abnormal tyrosine kinase receptor signalling in AN has been provided by studies of craniosynostosis and skeletal dysplasia syndromes with AN, which have identified activating mutations in fibroblast growth factor receptors.

Disulfiram treatment of alcoholism.

To assess the efficacy of supervised disulfiram as an adjunct to out-patient treatment of alcoholics, a randomised, partially blind, six-month follow-up study was conducted in which 126 patients received 200 mg disulfiram or 100 mg vitamin C under the supervision of a nominated informant. In the opinion of the (blinded) independent assessor, patients on disulfiram increased average total abstinent days by 100 and patients on vitamin C by 69, thus enhancing by one-third this measure of treatment outcome. Mean weekly alcohol consumption was reduced by 162 units with disulfiram, compared with 105 units with vitamin C, and the disulfiram patients reduced their total six-month alcohol consumption by 2572 units compared with an average reduction of 1448 units in the vitamin C group. Serum gamma-GT showed a mean fall of 21 IU/I in patients on disulfiram but rose by a mean of 13 IU/I with vitamin C. Unwanted effects in the disulfiram group led to a dose reduction in seven patients and to treatment withdrawal in four (and in one vitamin C patient). Two-thirds of the disulfiram group asked to continue the treatment at the end of the study. There were no medically serious adverse reactions.