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

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

Future prevalence of WHO grade 2 impairment in relation to incidence trends in leprosy: An exploration

Objectives: To explore the relationship between leprosy incidence trends and the future prevalence of World Health Organization (WHO) grade 2 impairment caused by leprosy. Methods: Three scenarios were defined to estimate incidences and prevalences of leprosy impairment beyond 2000, assuming 6%, 12% and 18% annual declines in case detection rate respectively, and 6% impairment among new patients. Case detection data from 1985 to 2000 were used for projecting leprosy incidences up to 2020. To estimate future prevalences of WHO grade 2 impairment, the survival of existing and new impaired individuals was calculated. Results: In the 6% scenario, 410 000 new patients will be detected in 2010 and 250 000 in 2020. The number of people living with WHO grade 2 impairment in these years will be 1.3 and 1.1 million, respectively. The 12% scenario predicts that 210 000 new patients will be detected in 2010 and 70 000 in 2020. The grade 2 prevalences will be 1.2 and 0.9 million, respectively. In the 18% scenario, the incidence will be 110 000 in 2010 and 20 000 in 2020, and the grade 2 prevalences will be 1.1 and 0.8 million, respectively. Conclusions: Declines in numbers of people living with grade 2 impairment lag behind trends in leprosy incidence. The prevalence of people with grade 2 decreases much slower than leprosy incidence and case detection in all three scenarios. This implies that a substantial number of people will live with impairment and will need support, training in self-care and other prevention of disability interventions in the next decades

Corticosteroids for treating nerve damage in leprosy

Background: Leprosy causes nerve damage which can result in nerve function impairment and disability. Corticosteroids are commonly used for treating nerve damage, although the long-term effect is uncertain. Objectives: To assess the effects of corticosteroids on nerve damage in leprosy. Search strategy: We searched the Cochrane Neuromuscular Disease Group Register, the Cochrane Central Register of Controlled Trials (Issue 4), MEDLINE (from 1966), EMBASE (from 1980), CINAHL (from 1980), LILACS (from 1982) in January 2006. We checked reference lists of the studies identified, the Current Controlled Trials Register (www.controlled-trials.com), conference proceedings and contacted trial authors. Selection criteria: Randomised and quasi-randomised controlled trials of corticosteroids for nerve damage in leprosy. Data collection and analysis: The primary outcome was improvement in sensory and motor nerve function after one year. Secondary outcomes were improvement in nerve function after two years, change in nerve pain and tenderness, and adverse events. Two authors independently extracted data and assessed trial quality. We contacted trial authors for additional information. We collected adverse effects and cost effectiveness information from the trials and non-randomised studies. Main results: We included three randomised controlled trials involving 513 people. Two trials compared prednisolone with placebo. One trial treated mild sensory impairment of less than six months duration and the other trial treated nerve function impairment of 6 to 24 months duration. Both trials examined an effect twelvemonths from the start of treatment. There was no significant difference in nerve function improvement between people treated with prednisolone or with placebo. The third trial compared three corticosteroid regimens for severe type 1 reactions. This trial did not report the prespecified outcomes. However, after 12 months, a significantly higher proportion of individuals on a 3-month course of prednisolone required extra corticosteroids compared to the groups with a high-dose and low-dose regimen of five months duration. Diabetes and peptic or infected ulcer were sometimes reported as serious adverse events in the placebo-controlled trials, but not significantly more often in the corticosteroid than placebo groups. Authors' conclusions: Corticosteroids are used for treating acute nerve damage in leprosy, but evidence from randomised controlled trials does not show a significant long-term effect. Randomised controlled trials are needed to establish their effectiveness, the optimal regimens and to examine new therapies. Copyrigh