Psychosocial Issues Associated with Breast Cancer-Related Lymphedema: a Literature Review.

PURPOSE OF REVIEW: Breast cancer-related lymphedema (BCRL) is a chronic disease affecting breast cancer survivors. The purpose of this article is to update the scientific literature regarding psychosocial issues associated with BCRL. RECENT FINDINGS: Reports describe economic burdens, social support, sexuality, BCRL patient-education needs, and interventions to reduce BCRL symptoms and improve QOL among women with breast cancer. The psychosocial impact of BCRL may differ between younger and older women which has implications for age-related interventions to reduce the adverse psychosocial experiences of women with BCRL. We did not locate studies reporting the psychosocial impact of BCRL on male breast cancer survivors. SUMMARY: More psychosocial-based interventions are needed that target the concerns of those with BCRL, including age-related needs, sexual concerns, body image, and social support. Future research is indicated to study the psychosocial impact of BCRL among men. Researchers may consider how pandemic-driven health care policies affect the psychosocial needs of those with BCRL.

Impaired Langerhans cell migration in psoriasis is due to an altered keratinocyte phenotype induced by interleukin-17.

BACKGROUND: Psoriasis is a common skin condition driven by increased expression of interleukin (IL)-17. Langerhans cells (LCs) are epidermal dendritic cells that regulate cutaneous immune responses. Within the uninvolved skin of patients with psoriasis, LCs display impaired migration from the epidermis. OBJECTIVES: To investigate the role of keratinocytes (KCs) in the regulation of LC function and the response of KCs to IL-17. METHODS: KCs were cultured from the uninvolved skin of patients with psoriasis and healthy individuals with or without IL-17 treatment and the conditioned medium examined for its ability to alter LC function in an ex vivo human skin explant model. Furthermore, we examined the effect of IL-17 on LC mobilization in psoriasis by neutralizing IL-17 in the same skin explant model. RESULTS: Conditioned medium from psoriasis KCs inhibited LC migration in healthy skin. Moreover, conditioned medium from healthy KCs treated with IL-17 also inhibited healthy LC migration. Finally, neutralizing IL-17 in psoriasis skin resulted in enhanced LC migration. CONCLUSIONS: Collectively, these data suggest that an altered KC secretome, driven by increased expression of IL-17, is responsible for impaired LC migration in the uninvolved skin of patients with psoriasis.

Guttate psoriasis is associated with an intermediate phenotype of impaired Langerhans cell migration.

BACKGROUND: An episode of guttate psoriasis can be an isolated event, can recur as guttate episodes, or develop into chronic plaque psoriasis (CPP). A previous study revealed that early-onset (before age 40 years) CPP is associated with inhibition of epidermal Langerhans cell (LC) migration. OBJECTIVES: To determine whether guttate psoriasis is also associated with abnormal LC mobilization. METHODS: Three groups of patients were recruited: current guttate episode (n = 5); guttate psoriasis progressed to CPP (n = 6); and resolved guttate psoriasis (n = 2). Biopsies were taken from uninvolved skin and LC migration was measured ex vivo using an epidermal explant model. RESULTS: Patients with a current episode of guttate psoriasis displayed epidermal LC migration, although the extent was significantly lower than in skin from healthy controls (P < 0·05). In contrast, in those patients in whom guttate psoriasis developed into CPP there was no mobilization of LC. Finally, in patients in whom guttate psoriasis had resolved, LC migration was normal. CONCLUSIONS: We have shown that guttate psoriasis is associated with an abnormality of LC mobilization, but a less marked inhibition compared with that seen in CPP. In resolved guttate psoriasis LC function returns to normal. These data provide further evidence that the pathogenesis of psoriasis is characterized by significant changes in epidermal LC function.