Possible correlations between annular pustular psoriasis and Noonan syndrome

Catharino, Antônio Marcos da Silva; Daiha, E.; Carvalho, Carlos; Martinez, Daniela de Abreu e Silva; Lima, Ricardo Barbosa; D'Ácri, Antônio Macedo; Martins, Carlos José; Lupi, Omar

doi:10.1111/jdv.13521

Cited by 7 publications

(12 citation statements)

References 5 publications

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“…Takeo et al hypothesized that calcium dysregulation may lead to epidermal infiltration by neutrophils and elevated serum levels of IL-8, two hallmarks of PP [ 94 ]. Annular PP was observed in an individual with Noonan syndrome, supporting a putative shared pathomechanism involving the RAS/MAPK signaling pathway [ 95 ].…”

Section: Pathogenesismentioning

confidence: 99%

Pustular Psoriasis: From Pathophysiology to Treatment

Genovese

Moltrasio

Cassano³

et al. 2021

Biomedicines

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Pustular psoriasis (PP) is a clinicopathological entity encompassing different variants, i.e., acute generalized PP (GPP), PP of pregnancy (impetigo herpetiformis), annular (and circinate) PP, infantile/juvenile PP, palmoplantar PP/palmoplantar pustulosis, and acrodermatitis continua of Hallopeau (ACH), which have in common an eruption of superficial sterile pustules on an erythematous base. Unlike psoriasis vulgaris, in which a key role is played by the adaptive immune system and interleukin (IL)-17/IL-23 axis, PP seems to be characterized by an intense inflammatory response resulting from innate immunity hyperactivation, with prominent involvement of the IL-36 axis. Some nosological aspects of PP are still controversial and debated. Moreover, owing to the rarity and heterogeneity of PP forms, data on prognosis and therapeutic management are limited. Recent progresses in the identification of genetic mutations and immunological mechanisms have promoted a better understanding of PP pathogenesis and might have important consequences on diagnostic refinement and treatment. In this narrative review, current findings in the pathogenesis, classification, clinical features, and therapeutic management of PP are briefly discussed.

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Section: Pathogenesismentioning

confidence: 99%

Pustular Psoriasis: From Pathophysiology to Treatment

Genovese

Moltrasio

Cassano³

et al. 2021

Biomedicines

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“…Catharino et al proposed that APP is possibly induced by RAS/MAPK signaling activation. This signaling pathway receives extracellular stimuli from cell surface receptors and acts as a molecular switch in the processes of cell proliferation, differentiation, survival, and death (6). Bachelez emphasizes that mutations in IL36RN, CARD14, and AP1S3 in these groups of diseases lead to an enhanced inflammatory cascade in several cellular subtypes including keratinocytes, and to the recruitment and activation of neutrophils and macrophages (17).…”

Section: Discussionmentioning

confidence: 99%

“…APP is a rare form of pustular psoriasis with a chronic relapsing course and a good prognosis. It is different from GPP because it has a more subacute and limited clinical course (6,7). In the literature, APP most often occurs in children, and the cases described involve siblings and twins (3,(8)(9)(10)(11)(12).…”

Section: Introductionmentioning

confidence: 99%

“…The clinical picture is characterized by erythematous lesions that are usually polycyclic, with the presence of small, sterile pustules on the circumference of the lesions and fine peeling. Eruptions extend circumferentially and disappear within a few weeks, sometimes leaving little hyperpigmentation (6,9,13). The lesions have a concentric arrangement: paler skin in the center or slight erythema, surrounded by a ring-shaped rash and by numerous pustules.…”

Section: Introductionmentioning

confidence: 99%

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Clinicopathologic retrospective analysis of annular pustular psoriasis

Owczarczyk‐Saczonek

Znajewska-Pander

Owczarek

et al. 2018

Acta Dermatovenerologica Alpina Pannonica Et Adriatica

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Annular pustular psoriasis (APP) is a rare form of pustular psoriasis with a chronic relapsing course and a good prognosis. The clinical picture is characterized by erythematous lesions, usually polycyclic, with the presence of small, sterile pustules on the circumference of the lesions and fine peeling. We present two cases of APP with diagnostic problems: a 65-year-old woman that suffered from intermittent APP with remission and exacerbation for many years, and an 83-year-old man with lesions that developed after atenolol treatment. In both cases, the patients were thought to have drug provocation, and therefore acute generalized exanthematous pustulosis (AGEP) was diagnosed. Only a thorough analysis of the course of the disease and histopathological examination allowed correct diagnosis. The clinical picture of APP is similar to AGEP, generalized pustular psoriasis (GPP), also known as von Zumbusch pustular psoriasis, and subcorneal pustular disease, and it requires accurate differential diagnosis.

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“…SHP2 missense mutations account for approximately 50% of the cases of Noonan syndrome (Keilhack et al, 2005), a common autosomal dominant disorder characterized by multiple, variably penetrant defects. Intriguingly, a 55-year-old woman with many cardinal physical features of Noonan syndrome also suffered simultaneously from annular pustular psoriasis (Catharino et al, 2016), suggesting a potential role of SHP2 in psoriasis. However, this has not been investigated either in vitro or in vivo .…”

Section: Introductionmentioning

confidence: 99%

Inhibition of SHP2 ameliorates psoriasis by decreasing TLR7 endosome localization

Zhu

Shao

Wei

et al. 2020

Preprint

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Psoriasis is a complex chronic inflammatory skin disease with unclear molecular mechanisms. Here, we identify Src homology-2 domain containing protein tyrosine phosphatase-2 (SHP2) as a novel accelerator of psoriasis development. Both genetic ablation of SHP2 in macrophages and pharmacological inhibition of SHP2 prevents the development of psoriasis-like skin inflammation in an imiquimod-induced murine model of psoriasis. Mechanistically, SHP2 promotes the trafficking of Toll-like receptor 7 (TLR7) from Golgi to endosome through its interaction with and dephosphorylation of TLR7 at Tyr1024, which promotes the ubiquitination of TLR7 and psoriasis-like skin inflammation. Importantly, SHP2 allosteric inhibitor SHP099 reduces the expression of pro-inflammatory cytokines in peripheral blood mononuclear cells from human patients with psoriasis. Collectively, our findings identify SHP2 as a novel regulator of psoriasis and suggest that SHP2 inhibition may be a promising therapeutic approach for psoriatic patients.

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Possible correlations between annular pustular psoriasis and Noonan syndrome

Cited by 7 publications

References 5 publications

Pustular Psoriasis: From Pathophysiology to Treatment

Pustular Psoriasis: From Pathophysiology to Treatment

Clinicopathologic retrospective analysis of annular pustular psoriasis

Inhibition of SHP2 ameliorates psoriasis by decreasing TLR7 endosome localization

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