Are corticosteroids an effective treatment for nerve damage in leprosy?
Leprosy is a long-term infectious disease. Leprosy bacteria cause damage to the skin and peripheral nerves (nerves outside the brain and spinal cord). This damage can stop nerves from working normally and cause disability. Corticosteroids, especially prednisolone, are often used to treat nerve damage in leprosy, but their long-term effect is uncertain.
We conducted a wide search for reports of clinical trials of treatments for nerve damage in leprosy. We found five clinical trials that met our criteria, involving 576 people with leprosy. Two of the included trials compared prednisolone with placebo. One of these trials, with 84 participants, recruited people who had mild abnormality of feeling of less than six months' duration and the other, with 95 participants, assessed treatment effects in people with abnormal nerve function of 6 to 24 months' duration. A third trial, with 334 participants, compared three 12-month corticosteroid regimens for severe type 1 reactions. Type 1 reactions are episodes in which nerves become inflamed. The fourth trial (21 participants) compared a low dose of prednisone with a high dose of prednisone for people with damage to the ulnar nerve (a nerve in the arm). The fifth trial (42 participants) compared intravenous methylprednisolone and oral prednisolone with intravenous normal saline and oral prednisolone in people with a type 1 leprosy reaction or abnormal nerve function of no more than six months' duration.
Key results and quality of the evidence
There was no important difference in improvement in nerve function between people treated with prednisolone or with placebo after one year, according to two trials. More people on a three-month course of prednisolone failed to respond to treatment and required extra corticosteroids compared to people on either a high-dose or a low-dose regimen of five months' duration. The trials comparing corticosteroids with placebo and a trial comparing intravenous methylprednisolone and oral prednisolone with intravenous normal saline and oral prednisolone found no differences in the occurrence of adverse events between groups. We considered the quality of the evidence to be moderate to low. Although trials were well conducted and designed, they were largely small and did not always use proven measures to capture the effects of corticosteroids.
The evidence in this review is up to date to June 2015.
Corticosteroids are used for treating acute nerve damage in leprosy, but moderate-quality evidence from two RCTs treating either longstanding or mild nerve function impairment did not show corticosteroids to have a superior effect to placebo on nerve function improvement. A third trial showed significant benefit from a five-month steroid regimen over a three-month regimen in terms of response to treatment (need for additional corticosteroids). Further RCTs are needed to establish optimal corticosteroid regimens and to examine the efficacy and safety of adjuvant or new therapies for treating nerve damage in leprosy. Future trials should address non-clinical aspects, such as costs and impact on quality of life, which are highly relevant indicators for both policymakers and participants.
Leprosy causes nerve damage that can result in nerve function impairment and disability. Corticosteroids are commonly used for treating nerve damage, although their long-term effect is uncertain. This is an update of a review first published in 2007, and previously updated in 2009 and 2011.
To assess the effects of corticosteroids on nerve damage in leprosy.
On 16 June 2015, we searched the Cochrane Neuromuscular Specialised Register, the Cochrane Central Register of Controlled Trials (CENTRAL), MEDLINE, EMBASE, CINAHL Plus, and LILACS. We also checked clinical trials registers and contacted trial authors.
Randomised controlled trials (RCTs) and quasi-RCTs of corticosteroids for nerve damage in leprosy. The comparators were no treatment, placebo treatment, or a different corticosteroid regimen.
The primary outcome was improvement in nerve function after one year. Secondary outcomes were change in nerve pain, limitations in activities of daily living, limitations in participation, and adverse events. Two review authors independently extracted data and assessed trial quality. When data were lacking, we contacted trial authors for additional information.
We included five RCTs involving 576 people. The trials were largely at low risk of bias, but we considered the quality of the evidence from these trials as moderate to low, largely due to imprecision from small sample sizes. Two out of the five trials reported on improvement in nerve function at one year. These two trials compared prednisolone with placebo. One trial, with 84 participants, treated mild sensory impairment of less than six months' duration, and the other, with 95 participants, treated nerve function impairment of 6 to 24 months' duration. There was no significant difference in nerve function improvement after 12 months between people treated with prednisolone and those treated with placebo. Adverse events were not reported significantly more often with corticosteroids than with placebo. The other three trials did not report on the primary outcome measure. One (334 participants) compared three corticosteroid regimens for severe type 1 reactions. No serious side effects of steroids were reported in any participant during the follow-up period. Another trial (21 participants) compared low-dose prednisone with high-dose prednisone for ulnar neuropathy. Two participants on the higher dose of prednisone reported adverse effects. The last (42 participants) compared intravenous methylprednisolone and oral prednisolone with intravenous normal saline and oral prednisolone. The trial found no significant differences between the groups in the occurrence of adverse events.