What's new in the pathogeneses and triggering factors of bullous pemphigoid

Ujiie, Hideyuki

doi:10.1111/1346-8138.16654

Cited by 20 publications

(16 citation statements)

References 88 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…However, the impact of these confounding factors on bullous pemphigoid development was adjusted in multivariate analysis. The association of bullous pemphigoid with aging, 26,27 hypertension, 9,11 diabetes mellitus, 9–11,27 neurological diseases, 10,26–28 psychiatric diseases, 10,28 and DPP4i users 13,26,29 has been documented in many previous studies. DPP4i increased the risk of bullous pemphigoid by 1.6–3.2 fold.…”

Section: Discussionmentioning

confidence: 98%

“…The degree of oxidative modification might be higher in bullous pemphigoid antigens than in pemphigus antigens in chronic dialysis patients. The other possibility is the difference in the pathophysiology of the two immunobullous diseases: pemphigus lesions are directly mediated by autoantibodies, while bullous pemphigoid lesions are mediated by autoantibodies, complement, and inflammatory cells 25,26 . Complement activation and dysregulatory chronic inflammation in dialysis patients might facilitate bullous pemphigoid development.…”

Section: Discussionmentioning

confidence: 99%

See 1 more Smart Citation

Risk of bullous pemphigoid and pemphigus in patients on chronic dialysis: A nationwide population‐based cohort study

Tang,

Sue,

Chang

et al. 2023

The Journal of Dermatology

View full text Add to dashboard Cite

Bullous pemphigoid has a high incidence among dialysis patients. However, whether or not chronic dialysis is an independent risk factor of bullous pemphigoid remains unclear. We aimed to investigate the effect of chronic dialysis on the development of bullous pemphigoid and pemphigus. We performed a retrospective cohort study using records from Taiwan's National Health Insurance Research Database between 2008 and 2019. We identified a dialysis cohort that included patients on chronic hemodialysis and peritoneal dialysis, and the hazard ratios (HRs) for bullous pemphigoid and pemphigus were compared with those of a sex‐, age‐, and index‐matched cohort, then the results were adjusted for various confounding factors. Among 93 538 patients on chronic dialysis and 93 538 patients in the control group, 287 and 139 developed incident bullous pemphigoid, and 45 and 35 developed incident pemphigus after a median follow‐up of 3.7 and 5.6 years, respectively. The incidence rates of bullous pemphigoid in the dialysis patients and the control group were 74.2 and 25.2 per 100 000 person‐years, respectively (difference between groups, P < 0.0001). The incidence rates of pemphigus in the dialysis patients and the control group were 11.6 and 6.3 per 100 000 person‐years, respectively (difference between groups, P < 0.01). Cox proportional hazard adjustment showed the HR for bullous pemphigoid in dialysis patients was 2.12 (95% confidence interval [CI] 1.64–2.74, P < 0.0001) compared with the control group. Dialysis patients aged <75 years had an even higher risk of bullous pemphigoid development (5‐ to 8‐fold) than the control group. The adjusted HR for pemphigus was not elevated in dialysis patients (adjusted HR 1.52, 95% CI 0.87–2.67, P = 0.14). Chronic dialysis is an independent risk factor for developing bullous pemphigoid, but not a risk factor for pemphigus. Physicians should be aware of the predisposition of chronic dialysis patients to bullous pemphigoid.

show abstract

Section: Discussionmentioning

confidence: 98%

Section: Discussionmentioning

confidence: 99%

Risk of bullous pemphigoid and pemphigus in patients on chronic dialysis: A nationwide population‐based cohort study

Tang,

Sue,

Chang

et al. 2023

The Journal of Dermatology

View full text Add to dashboard Cite

show abstract

“…Whether autoantibodies or inflammatory cells are more important in the pathogenesis of BP is unclear. The pathogenesis of BP may involve several immune pathways and infiltrating cell types; clinical presentations and the response to different treatment regimens vary ( 131 – 133 ).…”

Section: Interactions Among Immune Cellsmentioning

confidence: 99%

Adaptive and innate immune pathogenesis of bullous pemphigoid: A review

Yan

Zhang

2023

Front. Immunol.

View full text Add to dashboard Cite

Bullous pemphigoid (BP) is an autoimmune blistering disease that primarily affects elderly individuals. The presentation of BP is heterogeneous, typically manifesting as microscopic subepidermal separation with a mixed inflammatory infiltrate. The mechanism of pemphigoid development is unclear. B cells play a major role in pathogenic autoantibody production, and T cells, type II inflammatory cytokines, eosinophils, mast cells, neutrophils, and keratinocytes are also implicated in the pathogenesis of BP. Here, we review the roles of and crosstalk between innate and adaptive immune cells in BP.

show abstract

“…Pathogenically, IgG binding to either BP180 or BP230 activates a cascade of inflammatory mediators resulting in the loss of dermal-epidermal adhesion ( 18 ). The increasing knowledge of this complex inflammatory cascade is pivotal for developing new therapeutic strategies for the disease, as its therapeutic management is still largely based on long-term immunosuppressive treatments ( 10 ).…”

Section: Introductionmentioning

confidence: 99%

The cytokine milieu of bullous pemphigoid: Current and novel therapeutic targets

et al. 2023

View full text Add to dashboard Cite

Bullous pemphigoid (BP) is the most common autoimmune bullous disease, characterized by severe pruritus and skin blistering. The loss of tolerance against Collagen XVII, also referred to as BP180, is the main pathogenic event of BP, leading to production of IgG autoantibodies which mainly target the juxtamembranous extracellular non-collagenous 16th A (NC16A) domain of BP180. A complex inflammatory network is activated upon autoantibody binding to the basement membrane zone; this inflammatory loop involves the complement cascade and the release of several inflammatory cytokines, chemokines and proteases from keratinocytes, lymphocytes, mast cells and granulocytes. Collectively, these events disrupt the integrity of the dermal-epidermal junction, leading to subepidermal blistering. Recent advances have led to identify novel therapeutic targets for BP, whose management is mainly based on the long-term use of topical and systemic corticosteroids. As an example, targeting type-2 T-helper cell-associated cytokines, such as Interleukin-4 and interleukin-13 has shown meaningful clinical efficacy in case series and studies; targeting IL-17 and IL-23 has also been tried, owing to an important role of these cytokines in the chronic maintenance phase of BP. In this review article, we discuss the complex cytokine milieu that characterized BP inflammation, highlighting molecules, which are currently investigated as present and future therapeutic targets for this life-threatening disease.

show abstract

What's new in the pathogeneses and triggering factors of bullous pemphigoid

Cited by 20 publications

References 88 publications

Risk of bullous pemphigoid and pemphigus in patients on chronic dialysis: A nationwide population‐based cohort study

Risk of bullous pemphigoid and pemphigus in patients on chronic dialysis: A nationwide population‐based cohort study

Adaptive and innate immune pathogenesis of bullous pemphigoid: A review

The cytokine milieu of bullous pemphigoid: Current and novel therapeutic targets

Contact Info

Product

Resources

About