Leprosy is diagnosed by certain cardinal clinical features, including pain and/or thickening of peripheral nerves at sites of predilection and around skin lesions and diminution or loss of either sensory (hypoesthesia) or autonomic functions (sweating and axon reflex) in suspicious skin lesions or the skin areas supplied by the peripheral nerves1. Exceptions to this are the absence of nerve involvement in indeterminate form and skin lesions that can precede any evident sign of peripheral nerve damage in lepromatous leprosy (LL). Also, pure neuritic leprosy does not have skin lesions2. The reason for the exclusion of slit skin smear for diagnosis in this definition is due to its low sensitivity except for highly bacillated types.
While the treatment of leprosy has been simplified by adopting uniform multidrug therapy (MDT), the overriding concern is the high incidence of new cases and disabilities3. This could partly be attributed to possible misdiagnosis by non-dermatologists. We have noticed that this trend extends to tertiary hospitals with misdiagnosis by specialists across the spectrum, including physicians, neurologists, and even infertility specialists4. The multisystem involvement of leprosy and reactions can have myriad manifestations, and we aim to highlight these clinical differentials, including neural involvement, so that early diagnosis of leprosy patients is ensured, as dermatologists are rarely the first point of contact for them.
a0971-5916