Dramatic secukinumab-mediated improvements in refractory leprosy-related neuritis via the modulation of T helper 1 (Th1) and T helper 17 (Th17) immune pathways

Abstract A 39-year-old woman was diagnosed with relapsed multibacillary leprosy and refractory neuritis. Here, we describe an evident loss of therapeutic effectiveness after the third pulse of corticosteroids, which may be attributed to tachyphylaxis and the posterior modulation of interferon- γ (IFN-γ), tumor necrosis factor- α (TNF-α,) interleukin-17A (IL-17A), and IL-12/23p40 after the induction phase of secukinumab. In this case, plasma cytokine analysis showed that secukinumab induced a reduction in IL-17 concomitant with impressive clinical improvements in the patient's neural function. Interestingly, secukinumab induced reductions in cytokines related to Th1 responses and earlier stages of the Th17 response, including IL-23/12.

Effectiveness of the retreatment of patients with multibacillary leprosy and episodes of erythema nodosum leprosum and/or persistent neuritis: a single-center experience

Abstract: Background: Erythema nodosum leprosum may appear before, during or after treatment of leprosy and is one of the main factors for nerve damage in patients. When it occurs or continues to occur after treatment, it may indicate disease recurrence and a new treatment may be instituted again. Objective: To evaluate the retreatment of patients with multibacillary leprosy who underwent standard treatment with multidrug therapy, but developed or continued to present reactions of erythema nodosum leprosum and/or neuritis 3-5 years after its end. Method: For this objective, a new treatment was performed in 29 patients with multibacillary leprosy who maintained episodes of erythema nodosum and/or neuritis 3-5 years after conventional treatment. Results: In general, we observed that 27 (93.10%) had no more new episodes after a follow up period of eight months to five years. In five of these patients the reason for the retreatment was the occurrence of difficult-to-control neuritis, and that has ceased to occur in all of them. Study limitations: Small number of patients.. Conclusion: In the cases observed, retreatment was an effective measure to prevent the occurrence of erythema nodosum leprosum and/or persistent neuritis.

Shall we continue with nerve trunk decompression in leprosy?

There is a tendency to compare the results of surgery with that of oral corticosteroid therapy in leprous neuritis as if the two are competing methods. Surgery helps by removing the external compressive force and improves circulation so that steroids can reach and effectively act at the site of inflammation, minimizing the ischaemic and compression damage to nerve fibres. Often nerve decompression in leprosy is requested rather late so that the desired results are not always achieved. With emphasis on "elimination of leprosy", the disease is being managed in endemic states by field programmes where individual patient is not the priority unlike in the general hospitals and among practitioners where the welfare of the patient is the priority. It is therefore important to create awareness about compression neuropathy in leprosy and the need for combination therapy so as to bring down the morbidity and disability.

Síndrome de POEMS: presentación de un caso y revisión de la literatura / POEMS syndrome: report of a case and review of the literature

Comunicamos un síndrome de Poems con 6 años de evolución, diagnosticado y tratado desde hace un año y medio y caracterizado por: síndrome de Reynaud, polineuropatía, anasarca, edema de papila, osteoesclerosis, poliadenopatias con hiperplasia angiofolicular (enfermedad de Gatleman), hipotiroidismo, hipogonadismo, esclerodermia, hiperpigmentación, hirsutismo, alopecia axilar y trazas de cadenas ivianas lambda en la orina. La normalidade de las biopsias óseas excluye la presencia de un mieloma múltiple y no se encontraron evidencias de un pasmocitoma extramedular. Con metilprednisoma se observó una mejoría clínica consistente en desaparición de la anasarca y de la adenopatías, recuperación de la fuerza muscular y de la marcha. El edema de papila persistió. La fisiopatogenia se desconoce, si bien alguno de los síntomas han sido atribuidos al depósito de paraproteina en los nervios periféricos, a cambios en la permeabilidad vascular por "vasculopatía" y al aumento en la producción de estrógenos o a una mayor conversión de andrógenos. Se discute el tratamiento; en los casos asociados a mieloma se han utilizado la quimioterapia y/o la radioterapia con resultados variables. En algunos pacientes con corticosteroides, se ha logrado una mejoria transitoria. La causa de la muerte de estos enfermos está relacionada con las complicaciones de la polineuropatía. Por el momento es difícil clasificar a este síndrome, pero su original polimorfismo lo hace fácilmente reconocible