Leprosy type 1 reaction (formerly reversal reaction)

Naafs, Bernard; Hees, C.L.M. van

doi:10.1016/j.clindermatol.2015.10.006

Cited by 44 publications

(45 citation statements)

References 57 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

Section: Discussionmentioning

confidence: 99%

“…T1R results from flare-ups of the Th-1 cell-mediated immune response of the host against M. leprae antigens in patients with immunologically instable, borderline forms of leprosy [11]. This diagnosis is observed during MDT but it is also diagnosed either before or after MDT [11]. Paradoxical inflammatory exacerbation in leprosy patients has been described following BCG vaccination, probably as a result of increased M. leprae -reactive cell mediated immunity due to the boosting of the cell-mediated immunity by homologues M. leprae antigens present in BCG [12].…”

Section: Discussionmentioning

confidence: 99%

See 1 more Smart Citation

Severe type 1 upgrading leprosy reaction in a renal transplant recipient: a paradoxical manifestation associated with deficiency of antigen-specific regulatory T-cells?

Vieira

Trindade²,

Paula

et al. 2017

BMC Infect Dis

View full text Add to dashboard Cite

BackgroundDue to its chronic subclinical course and large spectrum of manifestations, leprosy often represents a diagnostic challenge. Even with proper anti-mycobacteria treatment, leprosy follow up remains challenging: almost half of leprosy patients may develop reaction episodes. Leprosy is an infrequent complication of solid organ transplant recipients. This case report illustrates the challenges in diagnosing and managing leprosy and its reactional states in a transplant recipient.Case presentationA 53-year-old man presented 34 months after a successful renal transplantation a borderline-tuberculoid leprosy with signs of mild type 1 upgrading reaction (T1R). Cutaneous manifestations were atypical, and diagnosis was only made when granulomatous neuritis was found in a cutaneous biopsy. He was successfully treated with the WHO recommended multidrug therapy (MDT: rifampicin, dapsone and clofazimine). However he developed a severe T1R immediately after completion of the MDT but no signs of allograft rejection. T1R results from flare-ups of the host T-helper-1 cell-mediated immune response against Mycobacterium leprae antigens in patients with immunologically unstable, borderline forms of leprosy and has been considered an inflammatory syndrome in many aspects similar to the immune reconstitution inflammatory syndromes (IRS). The T1R was successfully treated by increasing the prednisone dose without modifying the other immunosuppressive drugs used for preventing allograft rejection. Immunological study revealed that the patient had a profound depletion of both in situ and circulating regulatory T-cells and lack of expansion of the Tregs upon M. leprae stimulation compared to T1R leprosy patients without iatrogenic immunosuppression.ConclusionsOur case report highlights that leprosy, especially in the transplant setting, requires a high degree of clinical suspicion and the contribution of histopathology. It also suggests that the development of upgrading inflammatory syndromes such as T1R can occur despite the sustained immunosuppressors regimen for preventing graft rejection. Our hypothesis is that the well-known deleterious effects of these immunosuppressors on pathogen-induced regulatory T-cells contributed to the immunedysregulation and development T1R.Electronic supplementary materialThe online version of this article (doi:10.1186/s12879-017-2406-9) contains supplementary material, which is available to authorized users.

show abstract

Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Severe type 1 upgrading leprosy reaction in a renal transplant recipient: a paradoxical manifestation associated with deficiency of antigen-specific regulatory T-cells?

Vieira

Trindade²,

Paula

et al. 2017

BMC Infect Dis

View full text Add to dashboard Cite

show abstract

“…Additional studies have supported the association of LRRK2 variants with Leprosy outcomes, however results are not always consistent across populations or Leprosy subtypes (Wong et al, 2010;Grant et al, 2012;Marcinek et al, 2013;Wang et al, 2015), with analysis presumably complicated by the lower sample sizes available for study of this rarer disease. In ∼30% of patients, Leprosy is associated with acute inflammatory reactions that can lead to debilitating outcomes, in particular pro-inflammatory type-1 reactions (T1R) (Naafs and Van Hees, 2016). Fava and colleagues compared LRRK2 polymorphisms between Leprosy patient families affected and free from type-1 reactions, and concluded that the majority of GWAS reported LRRK2 polymorphisms were actually associated with T1R susceptibility within Leprosy, rather than Leprosy susceptibility per se (Fava et al, 2016).…”

Section: Lrrk2 Is Genetically Implicated In Diseasementioning

confidence: 99%

Leucine Rich Repeat Kinase 2 and Innate Immunity

Rastegar

Dzamko

2020

Front. Neurosci.

View full text Add to dashboard Cite

For more than a decade, researchers have sought to uncover the biological function of the enigmatic leucine rich repeat kinase 2 (LRRK2) enzyme, a large multi-domain protein with dual GTPase and kinase activities. Originally identified as a familial Parkinson's disease (PD) risk gene, variations in LRRK2 are also associated with risk of idiopathic PD, inflammatory bowel disease and susceptibility to bacterial infections. LRRK2 is highly expressed in peripheral immune cells and the potential of LRRK2 to regulate immune and inflammatory pathways has emerged as common link across LRRK2implicated diseases. This review outlines the current genetic and biochemical evidence linking LRRK2 to the regulation of innate immune inflammatory pathways, including the toll-like receptor and inflammasome pathways. Evidence suggests a complex interplay between genetic risk and protective alleles acts to modulate immune outcomes in a manner dependent on the particular pathogen and cell type invaded.

show abstract

“…When the reaction is relieved, the dose is slowly reduced so that it remains above the dose of 0.25 mg/kg/day for at least 3-6 months. In ongoing process, dose reduction is continued with careful follow-up of nerve functions [89]. Cyclosporin is another option when steroids are not usable [90,91].…”

Section: Type 1 Reactionmentioning

confidence: 99%

An Update on the Epidemiology, Diagnosis and Treatment of Leprosy

Akpolat¹,

Akkus²,

Kaynak³

2019

Hansen's Disease - The Forgotten and Neglected Disease

View full text Add to dashboard Cite

Leprosy is a granulomatous, chronic infection caused by Mycobacterium leprae that has been reported for than 2000 years. The infection primarily affects the skin and peripheral nerves.M. leprae is bacterium that cannot be cultured in vitro and transmission and pathophysiological data is still uncertain and limited. Today the prevalence of this ancient disease is declining in most around the world. This decline is a direct effect of widespread administration by public health workers of multidrug therapy. However, emerging despite the use of multidrug therapy, identifying and monitoring resistance are still necessary.

show abstract

Leprosy type 1 reaction (formerly reversal reaction)

Cited by 44 publications

References 57 publications

Severe type 1 upgrading leprosy reaction in a renal transplant recipient: a paradoxical manifestation associated with deficiency of antigen-specific regulatory T-cells?

Severe type 1 upgrading leprosy reaction in a renal transplant recipient: a paradoxical manifestation associated with deficiency of antigen-specific regulatory T-cells?

Leucine Rich Repeat Kinase 2 and Innate Immunity

An Update on the Epidemiology, Diagnosis and Treatment of Leprosy

Contact Info

Product

Resources

About