Abstract
BackgroundLeprosy neuropathy is considered the most common peripheral neuropathy of infectious etiology worldwide, representing a public health problem. Clinical diagnosis of primary neural leprosy (PNL) is challenging, since no skin lesions are found and the slit skin smear bacilloscopy is negative. However, there are still controversial concepts regarding the primary-neural versus pure-neural leprosy definition, which will be explored by using multiple clinical-laboratory analyses in this study.Methodology/Principal findingsSeventy patients diagnosed with primary neural leprosy from 2014 to 2016 underwent clinical, laboratorial and neurophysiological evaluation. All patients presented an asymmetric neural impairment, with nerve thickening in 58.6%. Electroneuromyography showed a pattern of mononeuropathy in 51.4%. Positivity for ELISA anti-PGL1 was 52.9%, while the qPCR of slit skin smear was 78.6%. The qPCR of nerve biopsies was positive in 60.8%. Patients with multiple mononeuropathy patterns showed lower levels of anti-PGL-1 (p = 0.0006), and higher frequency of neural thickening (p = 0.0008) and sensory symptoms (p = 0.01) than those with mononeuropathy.Conclusions/SignificancePNL is not a synonym of pure neural leprosy, as this condition may include a generalized immune response and also a skin involvement, documented by molecular findings. Immunological, molecular, and neurophysiological tools must be implemented for diagnosing primary neural leprosy to achieve effective treatment and reduction of its resultant disabilities that still represent a public health problem in several developing nations. Finally, we propose a algorithm and recommendations for the diagnosis of primary neural leprosy based on the combination of the three clinical-laboratorial tools.
Highlights
Leprosy is a chronic infectious disease caused by the Mycobacterium leprae, an alcohol- and acid-resistant obligatory intracellular bacillus with predilection to infect peripheral nerves and skin
The long incubation period, insidious symptoms and signs of leprosy produce difficulties in its diagnosis and correct clinical classification, especially in its primary neural form characterized by negative bacilloscopy and lack of cutaneous lesions
The failure of current therapeutic schemes on the incidence of leprosy shows that elimination of this disease, a public health problem, depends on incisive action to interrupt its transmission chain
Summary
Leprosy is a chronic infectious disease caused by the Mycobacterium leprae, an alcohol- and acid-resistant obligatory intracellular bacillus with predilection to infect peripheral nerves and skin. Leprosy is classified into five clinical forms according to the Ridley-Jopling, proposed in 1966, which is based on skin lesion histopathology and bacterial load. According to this classification, cases with cellular immune response mediated by T lymphocytes are classified as tuberculoid (TT), while anergic patients with humoral response are considered to be suffering from lepromatous leprosy (LL). Cases with cellular immune response mediated by T lymphocytes are classified as tuberculoid (TT), while anergic patients with humoral response are considered to be suffering from lepromatous leprosy (LL) Patients between these two extremes are defined as borderline, presenting intermediate immune responses. There are still controversial concepts regarding the primaryneural versus pure-neural leprosy definition, which will be explored by using multiple clinical-laboratory analyses in this study.
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