Evaluation of Interventions to Prevent Disability in Leprosy

What is leprosy? Leprosy is an infecti ous disease dati ng back to ancient ti mes before Christ. Most likely, the infecti on spread slowly from Asia to Europe and from there to the Americas, Australia and New Zealand. In Europe, the number of infected people reached its peak in the 13th century. Aft er the 16th century, leprosy was on the decline over most of Europe and the number of people aff ected by leprosy fell rapidly. Nowadays, many people only know leprosy from stories, pictures or books since the disease has become less and less prevalent. Cause. Leprosy is caused by the bacillus Mycobacterium leprae. Leprosy bacilli are most probably spread through ti ny droplets from the nose or mouth from infected and untreated individuals. Most people will never know that they have been infected because their immune system functi ons well. But when the immune system fails to respond eff ecti vely to the anti gens of the bacilli, the disease will develop. The ti me between infecti on and the fi rst visible signs of leprosy varies greatly and is usually between two and twelve years, but someti mes more than 20 years. Signs, symptoms and classification. To confi rm whether a person has leprosy, at least one of three signs should be found during a clinical examinati on: loss of feeling in typical skin patches, enlargement of peripheral nerves and the presence of leprosy bacilli in a skin smear. In the early stage of leprosy, called indeterminate, one or few unusual spots or patches on the skin may occur. Oft en the disease heals spontaneously, but someti mes the disease progresses to an advanced form. This depends mainly on how the immune system of an individual responds

Left atrial diverticula: Innocent bystanders or wolves in sheep's clothing?

Introduction: The finding of left atria diverticula (LAD) on cardiac computed tomography images obtained from patients with atrial fibrillation (AF) referred for pulmonary vein isolation is not uncommon. Prior studies reporting on LAD do not always provide definitions of LAD resulting in confusion with other anatomical structures such as left atrial accessory appendages (LAAA) and atrial aneurysms. The aim of this review is to identify an accurate definition of LAD and to describe distinctive properties between LAD and other left atrial structures, such as LAAA and aneurysms. Also, the relation between LAD and development of atrial tachyarrhythmias is discussed. Methods: PubMed was searched for studies reporting on atrial aneurysms, left atrial diverticula, left atrial accessory appendages and atrial congenital aneurysms, resulting in 36 papers. Results: LAD can be distinguished from LAAA by taking into account embryologic origins of the left atrium and their locations, resulting in the following definitions: (a) LAAA are contractile, trabeculated structures with circumscriptive ostia and narrow necks, originating from the primitive atria, (b) LAD are contractile, sac like structures with either smooth or trabeculated inner surfaces, circumscriptive ostia, narrow necks, and variable morphologies, originating from the embryologic common pulmonary vein, that incorporates into the LA, and (c) atrial aneurysms are non-contractile structures with wide necks and sac like bodies. There are no differences in prevalences of LAD between patients with sinus rhythm and AF. Conclusion: The pathophysiology of LAD is not yet fully understood. It is unlikely, that LAD are related to the development of atrial tachycardia's and AF by either being a source of ectopic activity or being part of an arrhythmogenic substrate. No differences in LAD prevalences between patients with sinus rhythm and AF have been found. Thus, it is unlikely that LAD could potentially be wolves in sheep's clothing

Corticosteroids for treating nerve damage in leprosy. A Cochrane review.

OBJECTIVE: Corticosteroids are commonly used for treating nerve damage in leprosy. We assessed the effectiveness of corticosteroids for treating nerve damage due to leprosy. METHODS: A systematic search was undertaken to identify randomised controlled trials (RCTs) comparing corticosteroids with placebo or with no treatment. Two authors independently assessed quality and extracted data. Where it was not possible to perform a meta-analysis, the data for each trial was summarised. RESULTS: Three RCTs involving 513 people were found. Two trials compared prednisolone with placebo. One trial treated mild sensory impairment of less than 6 months duration and the other trial treated nerve function impairment of 6 to 24 months duration. Both trials examined nerve function improvement 12 months from the start of treatment, but found no significant difference between the two groups. The third trial compared three corticosteroid regimens for severe type 1 reactions. After 12 months, a significantly higher proportion of individuals on a 3 month course required extra corticosteroids compared to the groups with a high-dose and low-dose regimen of 5 months duration. Diabetes and peptic or infected ulcers were not significantly more often reported in the corticosteroid compared to the placebo group. CONCLUSIONS: Evidence from RCTs does not show a significant long-term effect for either long-standing nerve function impairment or mild sensory impairment. A 5 month corticosteroid regimen was significantly more beneficial than a 3 month corticosteroid regimen. Further RCTs are needed to establish the effectiveness and optimal regimens of corticosteroids and to examine new therapies

Decompression surgery for treating nerve damage in leprosy

This is a protocol for a Cochrane Review (Intervention). The objectives are as follows:To assess the effects of decompression surgery for treating nerve damage in leprosy.<br/