Acquired ichthyosis and false-positive hepatitis A serology as paraneoplastic phenomena in anaplastic lymphoma kinase-positive anaplastic large-cell lymphoma

Phillips, Alexandra; Parmar, Sheena Chantelle; Yakubu, Usman Kassim; Chin, Mei Fong

doi:10.1136/bcr-2020-240966

Cited by 1 publication

(1 citation statement)

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“…33 Several CD30 + NHLs have been associated with AI, including anaplastic large cell lymphoma (ALCL) with or without anaplastic lymphoma kinase (ALK) expression, primary cutaneous ALCL, peripheral T-cell lymphoma not otherwise specified and primary cutaneous T-cell lymphoma subtypes: mycosis fungoides (MF), ichthyosiform MF (IMF) and granulomatous slack skin disease. [34][35][36][37][38][39][40] Lymphomatoid papulosis, considered to be on the benign end of the spectrum of primary cutaneous CD30 + T-cell lymphoproliferative disorders, has also been reported with AI. 36,41,42 Morizane et al 38 followed a cohort of 106 patients with malignant lymphomas and found ichthyosiform eruption in nine patients-three with ALK-negative ALCL and six with MF.…”

Section: Pa R a N Eopl Astic Disor De R Smentioning

confidence: 99%

Acquired ichthyosis, asteatotic dermatitis or xerosis? An update on pathoetiology and drug‐induced associations

Park

Saeidian

Youssefian

et al. 2022

Acad Dermatol Venereol

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Acquired ichthyosis (AI) or conditions mimicking ichthyosis have been documented for well over a century. AI is limited to the skin, but can be the first presenting sign of an underlying disease or an adverse effect of select medications or environmental exposures. 1,2 Most heritable ichthyoses, with the exceptions of late-onset ichthyosis vulgaris (IV) and Refsum disease, typically manifest between the immediate postnatal period and 5 years of age. 2 AI, however, does not follow an obvious age distribution; rather, the appearance and disappearance of AI tend to coincide with onset and resolution of an inciting factor. Clinically, AI closely resembles IV with diffuse, symmetrically distributed, white-to-brown scales which can be confused with severe cases of xerosis or eczema (Figure 1a-c). 1 Histopathology of AI usually shows varying degrees of orthohyperkeratosis, a uniformly diminished or absent granular layer, and lack of dermal inflammation. 1,3 In patients with suspected AI, a detailed investigation into the clinical course typically does not yield personal or family history of ichthyosis, atopy, keratosis pilaris or other keratodermaassociated phenotypes seen with the heritable ichthyoses. 1,2 In this article, we provide an up-to-date overview of AI and the pathomechanisms suggested in the literature. While the associated clinical features in many cases of AI are unknown, detailed examples are provided for the medical conditions, medications and exposures with clinical importance. In

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