Abstract
BackgroundMucosal leishmaniasis (ML), the most inflammatory form of tegumentary leishmaniasis, is predominantly caused by Leishmania braziliensis. The disease is characterized by the development of lesions, mainly in the nasal mucosa. An exacerbated inflammatory response has been associated with the presence of destructive and disfiguring lesions, with stages of severity ranging from small nodulations to the complete destruction of the nasal pyramid architecture. As Leishmania is an intracellular parasite, most immunological studies have emphasized the cell-mediated immune response, while relatively few studies aimed to investigate the role antibodies in protection against, or the pathology of ML.MethodsPatients with a confirmed diagnosis of ML were classified according to clinical staging criteria. Serum levels of Leishmania-specific IgG, IgG1 and IgG2 antibodies were determined by ELISA before and after treatment with antimony or antimony plus pentoxifylline.ResultsPatients in stages IV and V produced higher concentrations of IgG and IgG1 antibodies when compared to those in stage I and II. Significant reductions were seen in the concentrations of IgG and IgG2 antibodies in most patients who responded well to treatment.ConclusionsOur data demonstrate an association between IgG antibody titers and the severity of mucosal disease. The observed reduction in antibody production after successful treatment in most patients preliminarily indicates that these tests can be used to aid in the assessment of therapeutic response.
Highlights
American tegumentary leishmaniasis (ATL) is widely distributed around the world, and often presents high morbidity due to the possibility of developing destructive lesions that can disfigure and disable individuals, significantly impacting their quality of life (World Health Organization - Control of Leishmaniasis, 2010)
In endemic areas of Leishmania braziliensis transmission, mucosal leishmaniasis (ML), a disease known as mucocutaneous leishmaniasis, occurs in 3% of patients concomitantly or following the cure of cutaneous leishmaniasis (CL)
Due to the small number of patients classified as stage I or V, patients were divided into three groups: Stages I and II (40.7%), stage III (25.9%) and stages IV and V (33.4%)
Summary
American tegumentary leishmaniasis (ATL) is widely distributed around the world, and often presents high morbidity due to the possibility of developing destructive lesions that can disfigure and disable individuals, significantly impacting their quality of life (World Health Organization - Control of Leishmaniasis, 2010). In endemic areas of Leishmania braziliensis transmission, mucosal leishmaniasis (ML), a disease known as mucocutaneous leishmaniasis, occurs in 3% of patients concomitantly or following the cure of cutaneous leishmaniasis (CL). While ML primarily affects the nasal mucosa (90% of cases), the second most affected site is the pharyngeal mucosa, followed by the laryngeal mucosal and oral cavity (Marsden, 1994; Miranda Lessa et al, 2007). The involvement of these latter areas is an indicator of disease severity (Marsden, 1994; Miranda Lessa et al, 2007). Mucosal leishmaniasis (ML), the most inflammatory form of tegumentary leishmaniasis, is predominantly caused by Leishmania braziliensis. An exacerbated inflammatory response has been associated with the presence of destructive and disfiguring lesions, with stages of severity ranging from small nodulations to the complete destruction of the nasal pyramid architecture. As Leishmania is an intracellular parasite, most immunological studies have emphasized the cell-mediated immune response, while relatively few studies aimed to investigate the role antibodies in protection against, or the pathology of ML
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