02431nas a2200325 4500000000100000008004100001653001000042653002900052653001100081653002300092653001100115653002300126653001200149653000900161653001600170653002200186653003900208653001500247100001500262700001700277700001400294700001500308700001700323245009700340856005100437300001100488490000700499520158500506022001402091 2013 d10aAdult10aAnti-Inflammatory Agents10aFemale10aHistocytochemistry10aHumans10aLeprostatic Agents10aleprosy10aMale10aMiddle Aged10aPeripheral nerves10aPeripheral Nervous System Diseases10aPrednisone1 aCardoso FM1 aFreitas MR G1 aEscada TM1 aNevares MT1 aNascimento O00aLate onset neuropathy in leprosy patients released from treatment: not all due to reactions? uhttps://leprosyreview.org/article/84/2/12-8135 a128-350 v843 a

OBJECTIVES: To evaluate the clinical, neurophysiological and histological features of cases of neuropathy developing after completion of anti-leprosy treatment, where biopsy showed inflammatory changes.

PATIENTS AND METHODS: Seven patients were evaluated by a single neurologist. Electro-neuro-myography and peripheral nerve biopsy were performed in all patients.

RESULTS: Median age was 50-6 years. Time from release from treatment and onset of symptoms ranged from 1 to 12 years (median of 6.6 years). Sensory symptoms were the most common complaint, including pain (71%) and paresthesiae (71%). Muscle weakness was found in 51% and muscle atrophy in 43% of the subjects. Peripheral nerve thickening was present in all patients. Neurophysiological studies suggested sensory-motor polyneuropathy and multiple mono-neuropathy. Nerve biopsy showed inflammatory processes with fibrosis of endoneurium, perineurium and epineurium and total or partial loss of fibres. No bacilli were detected with Wade staining. Patients treated with corticosteroids had some relief of symptoms.

CONCLUSION: After release from treatment, leprosy patients may insidiously develop progressive peripheral nerve symptoms not fulfilling criteria for relapse or leprosy reactions. Sensory symptoms predominate and peripheral nerve thickening is an important finding. We speculate that these late onset symptoms are secondary to chronic immune-mediated processes in response to antigens of M. leprae.

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