PUVA phototherapy-induced secondary amyloidosis in patients with mycosis fungoides: a rare adverse effect of phototherapy

Abstract

The cationic polymerization of cis, trans-2,5-dihydro-2,5-dimethoxy furan (DHMF) was studied in the presence of HClO 4 , in acetonitrile. Different reaction parameters were investigated such as initiator concentration and temperature with duration. Obtained polymers were soluble in dimethylsulfoxide (DMSO) and dimethylformamide (DMF) and the Mn value was calculated as 2700 g/mol by cryoscopy. The FT-IR and 1 H-NMR results indicate that the polymerization proceeds via ring opening. Thermal properties were studied by DSC and TGA.

Secondary Cutaneous Amyloidosis in a Patient with Mycosis Fungoides

“…A possible alternative mechanism of this case is amyloid formation through a cytotoxic effect of PUVA therapy. Secondary cutaneous amyloidosis was detected in five of 61 patients with mycosis fungoides simultaneously after PUVA by Zemheri et al 14 . The mechanism of PUVA is phototoxic reactions resulting from direct cellular damage caused by an inflammatory, non-immunological mechanism.…”

“…It is postulated that keratin tonofilaments undergo “filamentous degeneration” and keratinocytes “drop off” into the dermis forming amyloid 13 . A commonly accepted pathogenic theory of amyloidosis is that apoptotic basal keratinocytes (colloid bodies) release cytokeratins, which are covered with autoantibodies, phagocytized by macrophages, and enzymatically degraded into amyloid K (keratin-associated amyloid), which is a key feature of organ- limited cutaneous amyloidosis 13 14 .…”

“…PUVA primarily targets DNA, and other important targets of psoralens are specific receptors, such as epidermal growth factor receptor. More recently, PUVA therapy can induce programmed cell death (apoptosis) in skin infiltrating T-helper lymphocytes and keratinocytes, so it cause interface changes 10 11 14 . Lastly, we can also consider that amyloidosis might develop de novo without relation with mycosis fungoides or PUVA therapy.…”

Localized amyloidosis in usual-type vulvar intraepithelial neoplasia: High-risk HPV association and potential clinical significance. A series of 45 cases

“…It is postulated that keratin monofilaments undergo “filamentous degeneration,” and keratinocytes “drop off” into the dermis, forming amyloid ( Eto et al, 1984 ). One pathogenic theory proposes that apoptotic basal keratinocytes (colloid bodies) release cytokeratins covered with autoantibodies, phagocytized by macrophages, and enzymatically degraded into keratin-associated amyloid, a key feature of localized cutaneous amyloidosis ( Eto et al, 1984 , Zemheri et al, 2014 ).…”