I53. Recognizing Leprosy: Pointers for the Busy Rheumatologist

Abstract

The key messages for rheumatologists vis-à-vis leprosy are (i) remember leprosy causes granulomatous skin lesions and neuropathy; (ii) leprosy may present in patients from leprosy endemic countries years after leaving; (iii) consider leprosy when rheumatological tests are negative; (iv) look for skin lesions in people with peripheral neuropathy; (v) refer to a tropical specialist to have leprosy excluded; (vi) over 50% leprosy patients have inflammation in skin and nerve. It is important to diagnose leprosy early because then anti-bacterial treatment can be initiated and peripheral nerve damage minimized. Leprosy is often a late or missed diagnosis in the UK leprosy patients present with a range of lesions, depending on their underlying immunity to Mycobacterium leprae. Skin lesions include granulomatous lesion, papules, nodules and infiltration. The peripheral neuropathy is associated with nerve trunk damage. Leprosy may also present with acute inflammatory episodes called reactions which mimic vasculitis. We have a cohort of 145 patients in London, UK who have been diagnosed with leprosy in the last 16 years and have found significant delays in diagnosis. The geographical and ethnic profile of patients reflects migration patterns to the UK, 54% of our patients come from the Indian sub-continent, followed by Brazil and Nigeria. Misdiagnoses were made dermatologists, neurologists and rheumatologists. Granulomatous lesions were often diagnosed as sarcoid or cutaneous TB. Leprosy is essentially a clinical diagnosis, made by recognizing skin lesions and peripheral neuropathy. Skin biopsy can help support a diagnosis of leprosy and the typical findings will be shown. I shall also review leprosy patients who were initially seen in rheumatology clinics and misdiagnosed with vasculitis and GPA. Current treatments with the WHO multi-drug combinations (rifampicin, dapsone and clofazimine) are highly effective with relapse rates <1 % year. There is no clinical evidence of significant rifampicin resistance. All patients need to be tested for nerve damage and 60% will have evidence of nerve damage. About 50% of leprosy patients need a course of steroid treatment for their immune mediated skin and nerve damage. The outcomes with steroid treatment are disappointing. We have done trials using methylprednisolone as an early treatment for leprosy reactions but did not find any benefit. 50% of patients needed a further course of steroids. We have also done a study using AZA to treat leprosy reactions. We also found no benefit from adding in this immune-suppressant. Other treatments are needed to stop inflammation. Neuropathic pain is also a newly recognized complication of leprosy and a risk factor is having had immune mediated reactions.