Unique clinical and serological features of bullous pemphigoid associated with dipeptidyl peptidase-4 inhibitors

Horikawa, Hitomi; Kurihara, Yuki; Funakoshi, Takeru; Umegaki‐Arao, Noriko; Takahashi, Hayato; Kubo, Akiharu; Tanikawa, Akiko; Kodani, Noriko; Minami, Yoshimasa; Meguro, Shu; Itoh, Hiroshi; Izumi, Kiyotaka; Nishie, Wataru; Shimizu, Hiroshi; Amagai, Masayuki; Yamagami, Jun

doi:10.1111/bjd.16479

Cited by 55 publications

(64 citation statements)

References 6 publications

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“…In an animal model, DPP‐4 inhibition promotes eosinophil activation in the skin by enhancing the activity of pro‐inflammatory chemokines . In contrast, several studies revealed that there were frequently non‐inflammatory or pauci‐inflammatory clinical presentations in DPP‐4 inhibitor‐related BP . Chijiwa et al.…”

Section: Discussionmentioning

confidence: 99%

“…24 In contrast, several studies revealed that there were frequently non-inflammatory or pauci-inflammatory clinical presentations in DPP-4 inhibitor-related BP. [25][26][27] Chijiwa et al 28 reported that there were significantly lower eosinophils infiltrating into the skin of DPP-4 inhibitor-related BP than non-DPP-4 inhibitor-related BP. Besides, there was a lower positive rate of anti-BP180 NC16a antibody, an autoantibody against the NC16a region of BP180, in BP patients with DPP-4 inhibitors than without DPP-4 inhibitors.…”

Section: Discussionmentioning

confidence: 99%

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Increased risk of bullous pemphigoid in dipeptidyl peptidase 4 inhibitors: A nationwide, population‐based, cohort study in Taiwan

Hung

Liu

Cheng

et al. 2019

The Journal of Dermatology

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Recent studies revealed the risk of bullous pemphigoid (BP) in patients with diabetes mellitus (DM) taking dipeptidyl peptidase 4 (DPP‐4) inhibitors. To clarify the relationship between taking DPP‐4 inhibitors and the risk of BP among patients with DM, we conducted a cohort study by using the National Health Insurance Research Database of Taiwan from 1 January 2009 to 31 December 2015. We identified 6340 patients with DM taking DPP‐4 inhibitors and 25 360 DM patients who had not taken DPP‐4 inhibitors during the 7‐year follow‐up period. Compared with the non‐DPP‐4 inhibitor group, patients taking DDP‐4 inhibitors had a higher risk of BP (adjusted hazard ratio [aHR], 2.382; 95% confidence interval (CI), 1.163–4.883; P = 0.017]. Among the DPP‐4 inhibitors available in Taiwan, vildagliptin showed the highest risk of BP (aHR, 2.849; 95% CI, 1.893–4.215; P < 0.001), followed by saxagliptin (aHR, 2.657; 95% CI, 1.770–3.934; P < 0.001). Subgroup analysis revealed that the higher risk of BP was observed in patients older than 65 years (aHR, 2.403; 95% CI, 1.590–3.627; P < 0.001). This study revealed that treatment with DPP‐4 inhibitors, especially vildagliptin, was significantly associated with an increased risk of BP among DM patients.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Increased risk of bullous pemphigoid in dipeptidyl peptidase 4 inhibitors: A nationwide, population‐based, cohort study in Taiwan

Hung

Liu

Cheng

et al. 2019

The Journal of Dermatology

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“…Though the entire class increases the risk of BP by two‐fold, vildagliptin is implicated more than the others with an increased risk of developing BP by up to 10 fold . Gliptin induced BP generally does not affect the NC16A domain of BP180 resulting in a non‐ inflammatory presentation . BP has been reported to be induced by immune checkpoint inhibitors such as cytotoxic T‐lymphocyte associated protein 4 (CTLA4) inhibitors (eg.…”

Section: Bullous Pemphigoidmentioning

confidence: 99%

“…12 Gliptin induced BP generally does not affect the NC16A domain of BP180 resulting in a non-inflammatory presentation. 21 BP has been reported to be induced by immune checkpoint inhibitors such as cytotoxic T-lymphocyte associated protein 4 (CTLA4) inhibitors (eg. Ipilimumab) and anti-PD-1/PD-L1 agents (eg.…”

Section: Bullous Pemphigoidmentioning

confidence: 99%

Review of autoimmune blistering diseases: the Pemphigoid diseases

Daniel

Murrell

2019

Acad Dermatol Venereol

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Autoimmune Blistering Diseases of the Pemphigoid type is characterised by sub‐epidermal blisters (SEB) with circulating autoantibodies against components of the basement membrane zone (BMZ). The main disorders to date include bullous pemphigoid (BP), pemphigoid gestationis, mucous membrane pemphigoid (MMP), epidermolysis bullosa acquisita (EBA), linear IgA disease (LABD), dermatitis herpetiformis (DH), lichen planus pemphigoides and bullous lupus. This is in contrast to pemphigus and related disorders, which demonstrate intraepidermal acantholysis and a positive Nikolsky sign. The classification and management is based on clinical, histological and direct and indirect immunofluorescence findings. There are, however, overlapping clinical and histological features between the conditions and clinical heterogeneity within each disease.

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“…Recently, a strong association between the use of DPP-4 inhibitors and the risk of BP was reported 46 . Although the mechanism is still unclear, several reports revealed that patients with BP associated with the use of DPP-4 inhibitors tended to exhibit a non-inflammatory clinical phenotype and possessed IgG autoantibodies against full-length COL17, albeit outside of the non-collagenous 16A domain (NC16A) (the major IgG epitope in typical BP) 47, 48 .…”

Section: Pemphigoidmentioning

confidence: 99%

Recent advances in the understanding and treatment of pemphigus and pemphigoid

Yamagami¹

2018

F1000Res

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Pemphigus and pemphigoid are characterized as autoimmune blistering diseases in which immunoglobulin G autoantibodies cause blisters and erosions of the skin or mucosa or both. Recently, understanding of the pathophysiology of pemphigus and pemphigoid has been furthered by genetic analyses, characterization of autoantibodies and autoreactive B cells, and elucidation of cell–cell adhesion between keratinocytes. For the management of pemphigus and pemphigoid, the administration of systemic corticosteroids still represents the standard treatment strategy; however, evidence of the efficacy of therapies not involving corticosteroids, such as those employing anti-CD20 antibodies, is increasing. The goal should be to develop antigen-specific immune suppression-based treatments.

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Unique clinical and serological features of bullous pemphigoid associated with dipeptidyl peptidase-4 inhibitors

Cited by 55 publications

References 6 publications

Increased risk of bullous pemphigoid in dipeptidyl peptidase 4 inhibitors: A nationwide, population‐based, cohort study in Taiwan

Increased risk of bullous pemphigoid in dipeptidyl peptidase 4 inhibitors: A nationwide, population‐based, cohort study in Taiwan

Review of autoimmune blistering diseases: the Pemphigoid diseases

Recent advances in the understanding and treatment of pemphigus and pemphigoid

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