Persistent Neuropathy in Lepromatous Leprosy Patients

Abstract Lepromatous leprosy (LL) patients have evidence of extensive peripheral nerve damage as soon as a diagnosis is made, but most of them have few or no symptoms related to peripheral neuropathy. Usually, they do not have the cardinal signal of leprosy neuritis. However, disability caused by peripheral nerve injuries has consequences throughout the entire life of these patients and the pathophysiological mechanisms of nerve damage are still poorly understood. The objective of this study was to evaluate the outcome of peripheral neuropathy in a group of LL patients in an attempt to understand the mechanisms of nerve damage. We evaluated medical records of 14 LL patients that had undergone a neurological evaluation at the beginning of Leprosy treatment then worsened at least 4 years after the end of treatment and underwent nerve biopsy. The symptoms at the beginning of treatment were compared with those at the time of the biopsy. Pain was a symptom in only one patient at the beginning and was a complaint in 9 patients by the time of biopsy. Neurological examination showed that the majority of patients already had alterations in medium and large caliber fibers at the beginning of the treatment, and pain increased by the time of biopsy, while neurological symptoms and signs deteriorated independently of the use of prednisone or thalidomide. Nerve Conduction Studies demonstrated that sensory nerves were the most affected. LL patients can develop a silent progressive degenerative peripheral neuropathy, which continues to develop despite high dose long term corticoid therapy.