Chronic inflammatory demyelinating polyneuropathy and Type 1 lepra reaction: a rare association

Archana Suresh,James Jose,Sarita Sasidharanpillai,Abhay Mani Martin,Joe James

doi:10.47276/lr.92.3.298

Abstract

Lepra reactions are important causes of the disability and deformity associated with leprosy. Normal body tissues suffer during these periods of hypersensitivity response mounted by the body against the antigens of Mycobacterium leprae. Chronic demyelinating polyneuropathy manifesting several years after reversal reaction is reported in the literature. It is attributed to the autoimmune reaction precipitated by the exposure of neural antigens (following the injury caused by the Type 1 lepra reaction) to the body’s immune system. Here we report a patient who presented with chronic inflammatory demyelinating polyneuropathy during a Type 1 lepra reaction.

Highlights

Introduction and case reportLepra reactions play a major role in the disability associated with leprosy.[1]
We report the case of a 71 year old man who manifested chronic inflammatory demyelinating polyneuropathy (CIDP) along with Type 1 lepra reaction (T1R)
Histopathology (Figure 2) of lesional skin confirmed the diagnosis of borderline tuberculoid leprosy with Type 1 lepra reaction

Summary

Introduction and case report

Lepra reactions play a major role in the disability associated with leprosy.[1]. Here we report the case of a 71 year old man who manifested chronic inflammatory demyelinating polyneuropathy (CIDP) along with Type 1 lepra reaction (T1R). The skin lesions showed impaired perception of touch, pain and temperature. The right ulnar nerve was enlarged and tender with sudden onset of ulnar clawing of one week duration Histopathology (Figure 2) of lesional skin confirmed the diagnosis of borderline tuberculoid leprosy with Type 1 lepra reaction. He received rifampicin 600 mg once a month, clofazimine 50 mg once a day and 300 mg once a month and dapsone 100 mg once a day for leprosy. Fourteen weeks after the diagnosis of leprosy and initiation of multidrug therapy, the patient presented with a nasal twang to the voice, nasal regurgitation of fluids, reduced sensory perception on the legs and weakness of limbs, which increased progressively over a period of nine weeks. Owing to a lack of response after two pulses, he was referred to a higher centre, where he received a cyclophosphamide pulse

Distal latency in ms Amplitude in mV

Discussion