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Abstract
Type 1 reaction (T1R) or reversal reaction is the leading cause of physical disabilities and deformities in leprosy. Leprosy patients, even after being considered cured and released from treatment, may suffer from reactional episodes for long periods of time. Early diagnosis is a great challenge for effectively treating and managing T1R. There is an urgent need to identify the most significant biomarkers to prevent recurrent T1R and to differentiate late T1R from relapse. T1R continues to be treated with corticosteroids and complications due to iatrogenic treatment remain frequent. This review aims to provide a framework from which to approach the great challenges that still persist in T1R management and debate key issues in order to reduce the distance between basic research and the clinic.
Financial & competing interests disclosure
The authors have no relevant affiliations or financial involvement with any organization or entity with a financial interest in or financial conflict with the subject matter or materials discussed in the manuscript. This includes employment, consultancies, honoraria, stock ownership or options, expert testimony, grants or patents received or pending or royalties.
No writing assistance was utilized in the production of this manuscript.
Type 1 reaction is the leading cause of physical disabilities and deformities in leprosy.
Type 1 reaction may occur before, during or after multidrug therapy. Recurrent T1R, which is defined as the reappearance of reactional signs or symptoms after completion of corticosteroid anti-inflammatory treatment, is a frequent problem for clinicians and new drugs are required.
Few drugs are available to treat reactional leprosy. T1R has continued to be treated with corticosteroids since the 1950s. However, there are a number of drugs used in inflammatory and neurodegenerative diseases that might be potentially administered in T1R since there are convergent mechanisms in these clinical conditions.
Both innate and adaptive immune responses are associated with the immunopathogenesis of neural injuries that involve an increase in the excessive production of proinflammatory mediators and drastic morphological changes in skin lesions and the appearance of heterogeneous epithelioid cell CD123+ populations.
There is an urgent need to identify T1R biomarkers to help in early diagnosis. In addition, cytokines that were differentially regulated during T1R may function as predictive markers. Further investigations are required.