Erythrodermic psoriasis (EP) is a rare and severe form of psoriasis characterized by erythema in 75–90% of the body surface1,2 with high morbidity and increased mortality and considered a dermatological emergency.

EP's prevalence is less than 3% of all cases of psoriasis.3 Although, its pathophysiology is largely unknown, it is thought to differ from that of plaque psoriasis (PP). EP may have a certain TH2 activation with Ig E, IL13, IL4 and IL10, while sharing TNF and IL-17A pathways with PP and genetics with pustular psoriasis, having found family mutations of CARD14 gene in EP.4 Alternatively, EP could represent a worsening of the other types of psoriasis (such as plaque or generalized pustular psoriasis).

EP patients can present systemic symptoms, such as fever, CHILLS, dehydration, arthralgia, asthenia and lymphadenopathy. Environmental triggers often precipitate erythrodermic flares, including steroid withdrawal, systemic infections, drug exposure such as lithium, and emotional stress.1

Treatment of EP is challenging and usually based on clinical experience, in part due to its low incidence and need for urgent management. Conventional treatments, such as glucocorticoid, cyclosporine, acitretin, and methotrexate are frequently ineffective and their discontinuation may cause flares. Recommendations for biologic therapy have limited evidence, but it seems to be well-tolerated and with positive results.5 Due to the need to obtain a rapid clinical response, the best therapies will be those with a faster onset of action, avoiding the more immunosuppressive agents given the high frequency of bacteraemia and sepsis in EP.4 Biologics as infliximab or IL-17 antagonist could be the first line, followed by IL-23 antagonist, anti-IL12/23 or other anti TNF.6 Interestingly, Th17 was found to be the second-most predominant T-cell type after Th2 in EP lesions, supporting the use of anti-IL-17 agents when rapid control is needed.1

We aimed to evaluate and compare the demographic characteristics, comorbidities and treatment prescription for EP with PP. To achieve this, we extracted data from the Biobadaderm from October 2008 to December 2021. The characteristics of the registry have been previously described.7

68 patients with inclusion diagnosis of EP were compared with 3930 patients with plaque psoriasis (PP). EP patients were older, had higher PASI and higher use of CsA when entering the cohort. No differences in comorbidities were observed, even when considering cancer and infection (Table 1).

Our most interesting finding has been a gradual reduction of EP cases included in the registry through the follow up time (Table 2). This may reflect the better disease control achieved recently in psoriatic patients due to advances in treatment. And it supports the idea that EP in some patients is a severe stage of other types of psoriasis, thus a greater control would result in a reduction of EP frequency.

When analysing the first treatment after entry in the cohort we found that the most prescribed treatments in EP compared with PP were Cyclosporine, Etanercept, Ustekinumab, Ixekizumab and Risankizumab (Table 1). When analysing all treatments used during follow up, the most frequently used in EP where Cyclosporine and anti-TNF due to their longer time of availability and that the majority of EP patients analyzed were included in the first eight years of the registry.

The limitation of our study is that in Biobadaderm, patients are classified with the diagnosis at the moment of inclusion, thus patients who developed EP after their inclusion in the registry were not analyzed. Moreover, treatment options changed during follow up period, which explains why the first treatment in several patients is no longer the current option for management of EP, as etanercept.

In conclusion, our study confirms that EP patients have a higher mean age, greater disease severity (higher base PASI and more frequent previous use of cyclosporine), and the decreasing frequency of this type of psoriasis.