TY - JOUR
KW - Leprosy
KW - Hansen disease
KW - Leprosy reactions
KW - Reversal Reactions
KW - Erythema Nodosum Leprosum
KW - Type 1 reaction
KW - Type 2 reaction
AU - Mehta H
AU - Jain S
AU - Narang T
AU - Chhabra S
AU - Dogra S
AB - <jats:p>Leprosy, or Hansen’s disease, caused by <jats:italic>Mycobacterium leprae</jats:italic> and <jats:italic>Mycobacterium lepromatosis</jats:italic>, is a chronic granulomatous infectious disease. Leprosy reactions, characterised by neurocutaneous inflammation, complicate the disease’s indolent course, leading to significant morbidity. However, limited knowledge of reaction pathophysiology stems from a lack of experimental models and the abrupt onset of reactional episodes, posing challenges in delineating initial pathogenic steps. In type 1 reactions, ongoing studies explore the roles of interferon-gamma which results in increased interleukin (IL)-15 and autophagy. Leprosy reactions also exhibit an increase in T helper 17 (Th17) and a decrease in T-regulatory cell (Treg) populations, resulting in diminished tumour growth factor-beta and heightened IL-6 and IL-21 production. Exploring the pathogenesis of erythema nodosum leprosum (ENL) reveals insights into neutrophils, Toll-like receptor 9, B-cells, myeloid-derived suppressor cells, IL-10 pathway and neurotrophins. Noteworthy therapeutic targets include increased expression of cyclooxygenase 2 and vascular endothelial growth factor. Early reaction diagnosis is crucial to limit neural damage, with high-resolution ultrasonography showing promise in detecting minimal nerve involvement. Therapies for ENL management, such as thalidomide, methotrexate, apremilast, minocycline and tumour necrosis factor-alpha inhibitors, hold potential. This review addresses recent advances in leprosy reaction pathogenesis and diagnostics, offering therapeutic insights and preventive strategies to mitigate their onset.</jats:p>
BT - Indian Journal of Dermatology, Venereology and Leprology
DO - 10.25259/ijdvl_915_2024
LA - ENG
M3 - Article
N2 - <jats:p>Leprosy, or Hansen’s disease, caused by <jats:italic>Mycobacterium leprae</jats:italic> and <jats:italic>Mycobacterium lepromatosis</jats:italic>, is a chronic granulomatous infectious disease. Leprosy reactions, characterised by neurocutaneous inflammation, complicate the disease’s indolent course, leading to significant morbidity. However, limited knowledge of reaction pathophysiology stems from a lack of experimental models and the abrupt onset of reactional episodes, posing challenges in delineating initial pathogenic steps. In type 1 reactions, ongoing studies explore the roles of interferon-gamma which results in increased interleukin (IL)-15 and autophagy. Leprosy reactions also exhibit an increase in T helper 17 (Th17) and a decrease in T-regulatory cell (Treg) populations, resulting in diminished tumour growth factor-beta and heightened IL-6 and IL-21 production. Exploring the pathogenesis of erythema nodosum leprosum (ENL) reveals insights into neutrophils, Toll-like receptor 9, B-cells, myeloid-derived suppressor cells, IL-10 pathway and neurotrophins. Noteworthy therapeutic targets include increased expression of cyclooxygenase 2 and vascular endothelial growth factor. Early reaction diagnosis is crucial to limit neural damage, with high-resolution ultrasonography showing promise in detecting minimal nerve involvement. Therapies for ENL management, such as thalidomide, methotrexate, apremilast, minocycline and tumour necrosis factor-alpha inhibitors, hold potential. This review addresses recent advances in leprosy reaction pathogenesis and diagnostics, offering therapeutic insights and preventive strategies to mitigate their onset.</jats:p>
PB - Scientific Scholar
PY - 2024
SP - 1
EP - 12
T2 - Indian Journal of Dermatology, Venereology and Leprology
TI - Leprosy reactions: New knowledge on pathophysiology, diagnosis, treatment and prevention
UR - https://ijdvl.com/view-pdf/?article=108d4925f2ee43c25ace9b78f9606f9fuJ7bT/U8mykABw==
VL - 0
SN - 0973-3922, 0378-6323
ER -