China
Africa
Explore chapters and articles related to this topic
Psoriasis and lichen planus
Published in Rashmi Sarkar, Anupam Das, Sumit Sethi, Concise Dermatology, 2021
The role of topical corticosteroids in the treatment of psoriasis is limited owing to their side effect profile and rebound flare-up of the disease after stopping them. Life-threatening generalized pustular psoriasis can result after sudden withdrawal. They are useful for patients with flexural lesions for which other irritant preparations are not suitable. For the same reason, weak topical corticosteroids are also suitable for lesions on the genitalia and the face where potent topical corticosteroids cannot be used.Systemic steroids can be used ONLY in the following indications:Generalized pustular psoriasis of pregnancy/erythroderma: this is the ONLY definitive indication for using oral steroids.Persistent and uncontrolled erythrodermic psoriasis causing metabolic complications.Generalized pustular psoriasis if other drugs are contraindicated or not effective.Severe polyarthritis that could lead to irreversible joint damage.
Pustular psoriasis
Published in Biju Vasudevan, Rajesh Verma, Dermatological Emergencies, 2019
Santanu Banerjee, Neerja Saraswat
Pustular psoriasis can present in two main forms: localized and generalized. The generalized pustular form can manifest as a dermatological emergency and is associated with life-threatening complications. Generalized pustular psoriasis is described here.
Photochemotherapy
Published in Henry W. Lim, Nicholas A. Soter, Clinical Photomedicine, 2018
These conditions are difficult to treat with PUVA therapy alone (26). Recurrent phototoxicity and difficulty in differentiating between disease and phototoxicity complicate management of erythrodermic psoriasis. A low rate of success and a slow response are features of the therapy of generalized pustular psoriasis. For these reasons, combined treatment with etretinate or methotrexate plus PUVA therapy is preferable and successful in achieving clearing in most patients with these conditions. Once the disease is cleared, maintenance treatment with PUVA therapy alone is usually adequate.
Promising phase II biologics for future Crohn’s disease therapy
Published in Expert Opinion on Investigational Drugs, 2023
Pauline Wils, Silvio Danese, Laurent Peyrin-Biroulet
Intestinal fibrosis is a major complication of CD. In recent years, our knowledge about the mechanisms involved in intestinal fibrosis has greatly increased. Several cytokines are key mediators of intestinal fibrosis, including TGF-beta, IL-1 family (IL-1, IL-33, IL-36), IL-17 family, and TNFalpha family members (particularly the TNF-like cytokine 1A or TL1A) [47]. Therapeutics with anti-fibrotic action have shown promising results. IL-36 signaling promotes the secretion of pro-fibrotic mediators and is involved in epithelial inflammation. Its expression is increased in the intestinal mucosa of patients with IBD [48] and with fibro-stenotic lesions [49]. Antibodies inhibiting the IL-36 receptor (IL-36 R) may have an anti-fibrotic action. BI 655,130 (spesolimab) is a monoclonal antibody that blocks the action of the IL-36 R [50]. It has been previously investigated in UC [51] and is approved to treat generalized pustular psoriasis. Spesolimab was tested in subjects with fibro stenotic CD and symptoms of bowel obstruction (NCT05013385), however, the clinical trial was stopped due to the absence of clinical efficacy in the interim analyses. This molecule is currently being tested in phase II clinical trials in fistulizing CD (NCT03752970 and NCT04362254).
Pathogenesis-oriented therapy of psoriasis using biologics
Published in Expert Opinion on Biological Therapy, 2022
Wolf-Henning Boehncke, Nicolò Costantino Brembilla
It has to be admitted, that such strategies can only be considered ‘stratified approaches.’ To arrive in the age of truly personalized medicine, a diagnostic process analyzing each patient’s transcriptome/proteome will be needed. Given the impressive efficacy of current biologics, such an approach seems, however, only needed for a small proportion of patients not responding to such therapies. This may well result in the identification of diseases that share signs, but not pathways of psoriasis (e.g. certain types of pustular psoriasis). Consequently, other modes of action may be needed to treat such patients, for example, IL-1 inhibition – not approved for psoriasis – for certain patients with generalized pustular psoriasis. This may lead to a new classification of such diseases, based on pathogenesis rather than clinical signs and symptoms. Descriptive dermatology may finally be overcome.
Biological treatment for erythrodermic psoriasis
Published in Expert Opinion on Biological Therapy, 2022
Erythrodermic psoriasis (EP) is a severe subtype of psoriasis involving all or nearly all of the body surface area. It occurs in 1–2% of patients with psoriasis; however, approximately 30% of patients presenting with erythroderma have psoriasis as the underlying cause [1–3]. EP may be acute or chronic. Acute EP is characterized by sudden disease onset, often precipitated by triggering factors such as infection, drugs such as antimalarials, topical irritants, or withdrawal of corticosteroids or cyclosporine. Patients of acute erythroderma may be febrile and systemically ill. Complications of acute skin failure may be seen, including sepsis, hypothermia or hyperthermia, anemia, hypoalbuminemia, dehydration, and high-output cardiac failure. Untreated disease may result in mortality. Such patients require aggressive systemic treatment for disease control. Chronic EP results from gradual extension of plaque psoriasis where general condition is well preserved and overall prognosis is good. Primary EP refers to patients who develop erythroderma at presentation of disease. Secondary EP refers to erythroderma developing in a patient with preexisting psoriasis, either acutely or insidiously. Distinction between generalized pustular psoriasis and erythrodermic psoriasis is often arbitrary, given their frequent cooccurrence and overlapping clinical features.