Amyloid deposition after psoriasis therapy with psoralen and long-wave ultraviolet light

Greene, I.

doi:10.1001/archderm.115.10.1200

Cited by 10 publications

(4 citation statements)

References 0 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…In the present study, some of the colloid or amyloid-like bodies were demonstrated to be produced from the dropped-down degenerated cytoplasm of the keratinocyte into the papillary dermis. Similar amyloid-like bodies have been reported in normal-appearing skin of vitiligo (21), in PUVA-treated psoriatic skin (39,40), ultraviolet irradiated skin (24), and lichen and macular amyloidosis (24), In these conditions, it has been suggested that they derived from the degenerating epidermal cells. Such structures may thus represent a final common pathway in damaged cells.…”

Section: Discussionsupporting

confidence: 60%

Keratinocyte degeneration in human facial skin: Documentation of new ultrastructural markers for photodamage and their improvement during topical tretinoin therapy

Yamamoto

Bhawan

Hara

et al. 1995

Experimental Dermatology

View full text Add to dashboard Cite

We examined epidermal impairment in photodamaged Caucasian skin by light and electron microscopy and observed two types of degeneration of the basal and suprabasal keratinocytes. The first was an electron-lucent degeneration predominantly seen in the periphery of the cells. The marked lucent degeneration occurred in 14% of the basal and suprabasal keratinocytes, predominantly in cells immediately adjacent to melanocytes. In skin specimens with a large number of such damaged keratinocytes, bleb-like keratinocytic protrusions or electron-lucent intercellular structures were also seen. Many vacuolar structures were observed just under the dermoepidermal junction, occupying 9% of the junction length. These structures were produced by herniation of the degenerative portion of the basal and suprabasal keratinocytes, and appeared to be phagocytized by dermal macrophages. The vacuolar alterations in the basal layer and dermoepidermal junction previously reported at the light microscopic level probably represent these intercellular lucent structures, bleb-like protrusions and vacuole-like structures at the electron microscopic level. The second type, dark-staining keratinocytes, probably representing an extensive degenerative process, constituted 4% of the basal and suprabasal keratinocytes. After 12 months of topical tretinoin treatment, dramatic improvement of both degenerative processes of the keratinocytes was noted.

show abstract

Section: Discussionsupporting

confidence: 60%

Keratinocyte degeneration in human facial skin: Documentation of new ultrastructural markers for photodamage and their improvement during topical tretinoin therapy

Yamamoto

Bhawan

Hara

et al. 1995

Experimental Dermatology

View full text Add to dashboard Cite

show abstract

“…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.…”

Section: Discussionmentioning

confidence: 99%

“…Secondary cutaneous amyloidosis refers to clinically unapparent amyloid deposits within the skin in association with preexisting skin conditions or skin tumors, such as basal cell carcinoma, porokeratosis, seborrheic keratosis, solar elastosis, Bowen's disease, and mycosis fungoides 5 6 7 8 9 . It has also been reported following psoralen and ultraviolet A radiation (PUVA) therapy 10 11 . We report an interesting and rare case of secondary cutaneous amyloidosis that occurred in patient with mycosis fungoides who was treated with PUVA and narrow band ultraviolet B (UVB) therapy.…”

Section: Introductionmentioning

confidence: 99%

Secondary Cutaneous Amyloidosis in a Patient with Mycosis Fungoides

et al. 2017

View full text Add to dashboard Cite

Secondary cutaneous amyloidosis refers to clinically unapparent amyloid deposits within the skin in association with a pre-existing skin condition or skin tumors, such as basal cell carcinoma, porokeratosis, solar elastosis, Bowen's disease, and mycosis fungoides. A 70-year-old woman presented with a 6-month history of asymptomatic multiple yellowish plaques on both legs. She had been diagnosed with mycosis fungoides 7 years ago and was treated with psoralen and ultraviolet A radiation (PUVA) therapy, narrow-band ultraviolet B (UVB) therapy, and acitretin for 5 years. Finally, she reached complete remission of mycosis fungoides. However, new yellowish lesions started to appear 1 year after discontinuing the phototherapy. A physical examination revealed multiple yellowish plaques on both extremities. The plaques were well circumscribed and slightly elevated. All laboratory tests were normal. A biopsy specimen showed multiple nodular deposits of eosinophilic amorphous material in papillary dermis and upper reticular dermis. The deposits represented apple green birefringence on Congo red stain viewed under polarized light. Acellular small nodules in the upper dermis consisted of randomly oriented, non-branching, 6.67~12.7 nm thick amyloid fibrils on electron microscopy. We report an interesting and rare case of secondary cutaneous amyloidosis after narrow-band UVB therapy and PUVA therapy in a patient with mycosis fungoides.

show abstract

“…Ultraviolet (UV) A and particularly UVB can induce SCLE lesions in predisposed individuals, via different specific immunological mediators, most notably UV-induced cytokines, such as interleukins 1, 6 and tumor necrosis factor α [15, 16]. On the other hand, various authors reported amyloid in PUVA-treated skin and postulated an origin from PUVA-damaged keratinocytes [17, 18]. Furthermore, hypersensitivity to UVB with possible DNA repair defects has been suggested to be the cause of amyloidosis cutis dyschromica, a congenital form of primary cutaneous amyloidosis presenting as poikiloderma [19].…”

Section: Discussionmentioning

confidence: 99%

Poikilodermatous Subacute Cutaneous Lupus erythematosus

2003

View full text Add to dashboard Cite

Background: Subacute cutaneous lupus erythematosus (SCLE) is a distinct subset of lupus erythematosus with unique clinical, immunological and genetic features. Among the unusual variants of SCLE, there is a poikilodermic presentation. However, to date, only 1 case of poikilodermatous SCLE has been reported. Objective: Our goal was to summarize the clinical characteristics and course as well as the pathological, laboratory and immunofluorescence findings of 4 patients with poikilodermatous SCLE. Methods: A retrospective study was conducted including 54 patients diagnosed as having SCLE between 1980 and 2002. Results: Four patients (7.4%) had SCLE. All patients were alive, and none developed severe systemic involvement in up to 36 years (median, 24 years) after the onset of disease. The most noteworthy laboratory finding was the cutaneous deposition of amyloid. Conclusion: Poikilodermatous SCLE represents an uncommon variant within the clinicopathological spectrum of SCLE following a favorable course, in spite of extensive cutaneous involvement. Photosensitivity is the pathomechanism explaining, theoretically, the development of both poikiloderma and cutaneous amyloidosis in such cases.

show abstract

Amyloid deposition after psoriasis therapy with psoralen and long-wave ultraviolet light

Cited by 10 publications

References 0 publications

Keratinocyte degeneration in human facial skin: Documentation of new ultrastructural markers for photodamage and their improvement during topical tretinoin therapy

Keratinocyte degeneration in human facial skin: Documentation of new ultrastructural markers for photodamage and their improvement during topical tretinoin therapy

Secondary Cutaneous Amyloidosis in a Patient with Mycosis Fungoides

Poikilodermatous Subacute Cutaneous Lupus erythematosus

Contact Info

Product

Resources

About