Successful management of feline pemphigus foliaceus with pentoxifylline and topical hydrocortisone aceponate
The treatment regimen for feline pemphigus foliaceus (PF), an autoimmune disease caused by auto-antibodies against proteins of the desmosome junction, usually includes high doses of oral or parenteral immunosuppressive drugs, typically glucocorticoids. This case adds to a growing body of evidence that topical hydrocortisone aceponate is effective for the treatment of feline PF, and demonstrates the practical use of a non-invasive diagnostic method for histopathology when owners refuse a biopsy to support a clinical diagnosis of PF. Finally, this case highlights an international trend of owner-initiated treatment of feline infectious peritonitis (FIP) using unlicensed, unregistered drugs.
Introduction
Pemphigus foliaceus (PF), although rare in most species, is the most commonly reported autoimmune disease in cats (Bizikova & Burrows, 2019a; Scott et al., 2013). Most affected cats are middle-aged (5–8 years) with no clear breed or gender predisposition and typically present with yellow to brown, adherent crusting skin lesions involving the concave and convex surfaces of the pinnae, dorsal nose, claw folds and circumferentially around the nipples (Bizikova & Burrows, 2019a; Coyner et al., 2018). Pruritus can be variable (Bizikova & Burrows, 2019a; Coyner et al., 2018). Systemic signs are typically mild and non-specific. These may include fever, lethargy and anorexia (Bizikova & Burrows, 2019b; Jordan et al., 2019; Preziosi, 2019). A definitive diagnosis of feline PF requires histological documentation of epidermal and/or mural follicular pustules containing numerous acantholytic keratinocytes and non-degenerate neutrophils (Olivry, 2006; Preziosi et al., 2003). In addition, there should be compatible clinical signs.
Other causes for crusting and acantholysis, including pyoderma and dermatophytosis, should also be ruled out. Although indirect immunofluorescence to detect IgG anti-keratinocyte autoantibodies would be ideal to confirm a diagnosis of feline PF (Levy et al., 2020; Olivry, 2006), the diagnostic criteria described above are considered adequate (Bizikova & Burrows, 2019b; Peterson & McKay, 2010; Preziosi, 2019; Preziosi et al., 2003). The prognosis is considered good but most cats with PF require long-term immunosuppressive treatment (i.e., oral glucocorticoids, ciclosporin, chlorambucil, gold salts, etc.) (Coyner et al., 2018; Peterson & McKay, 2010; Preziosi, 2019). It's important to inform clients about the high relapse risk, either spontaneously or during treatment adjustments. The time until disease control can vary but is on average 3 weeks (Bizikova & Burrows, 2019b; Coyner et al., 2018; Preziosi et al., 2003).
In human medicine, drug-associated PF is subdivided into drug-triggered and drug-induced PF (Pile et al., 2021; Wolf et al., 1991). In the latter, there is a good chance of stopping medication without disease relapse after initial treatment and cessation of the offending drug. The former typically needs long-term treatment similar to spontaneous cases of PF (Wolf et al., 1991). There is evidence that the same classification for PF can be applied to companion animals (Bizikova et al., 2014; Oberkirchner et al., 2011). Various triggers reported in cats include drugs (doxycycline, itraconazole, lime sulphur, others), vaccination, neoplasia (thymoma) and infectious diseases (leishmaniosis) (Affolter & Tscharner, 1992; Imamichi, 2013; McEwan et al., 1987; Rufenacht et al., 2005).
Here we describe a successful therapeutic approach to PF in a cat with severe co-morbid disease, in which the administration of immunosuppressive doses of systemic glucocorticoids was considered contraindicated. A non-invasive technique to support our diagnosis was used, which may be useful when full thickness biopsies are not possible.
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Authors: Stefan Hobi, Julia A. Beatty, Jeanine R. Sandy, Vanessa R. Barrs
Source: https://onlinelibrary.wiley.com/
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