scholarly journals Two shades of malignancy in a psoriatic patient

2021 ◽  
Vol 12 (4) ◽  
pp. 436-438
Author(s):  
Meryam Chaabani ◽  
Kahena Jaber ◽  
Faten Rebhi
Keyword(s):  
Skin Cancer ◽  
Chronic Inflammation ◽  
Pustular Psoriasis ◽  
Psoriatic Patient ◽  
Non Melanoma Skin Cancer ◽  
Increased Risk ◽  
History Of ◽  
Melanoma Skin

Psoriasis is a chronic inflammation of the skin, affecting approx. 120 million people worldwide. The risk of developing skin cancer in psoriatic patients has been stressed, although with a significant amount of conflicting data in the literature. The most consistent findings suggest that psoriatic patients are at an increased risk of non-melanoma skin cancer. An increased risk of melanoma has not been well established. Herein, we report the case of a patient with a history of pustular psoriasis present since the age of ten, who developed an SCC and a melanoma, and discuss the etiopathology of this association.

Risk of Non-Melanoma Skin Cancer Following Hematopoietic Cell Transplantation and Voriconazole-Associated Risk

Blood ◽  
2016 ◽  
Vol 128 (22) ◽  
pp. 2249-2249
Author(s):  
Lawrence F. Kuklinski ◽  
Shufeng Li ◽  
Margaret R. Karagas ◽  
Bernice Y. Kwong ◽  
Wen-Kai Weng
Keyword(s):  
Multivariate Analysis ◽  
Skin Cancer ◽  
Cell Carcinoma ◽  
Median Time ◽  
Allogeneic Hct ◽  
Non Melanoma Skin Cancer ◽  
Increased Risk ◽  
History Of ◽  
Autologous Hct ◽  
Melanoma Skin

Abstract Introduction: Recipients of hematopoietic cell transplant (HCT) are at increased risk for secondary malignancy, most commonly non-melanoma skin cancer (NMSC) including cutaneous squamous cell carcinoma (SCC) and basal cell carcinoma (BCC) (Leisenring et al J Clin Oncol 2006).While both SCC and BCC are generally associated with low mortality, HCT recipients are more likely to develop clinically aggressive forms of disease associated with poorer prognosis and requiringchemoradiotherapy(Lott et al Transplantation 2010). Voriconazolehas been available since 2002 for the treatment of serious fungal infections, and has contributed to improved clinical outcomes in patients who undergo HCT. However,voriconazoleis associated with several known cutaneous toxicities including photosensitivity, and along with its metabolite,voriconazoleN-oxide, sensitizes keratinocytes to UVA light and may cause DNA damage and inhibition of repair mechanisms (Onaet alBr J Dermatol 2015). While the association betweenvoriconazoleuse and NMSC has been established in the solid organ transplant population (Singer et al J Heart Lung Transplant 2012), less is known about HCT patients. Therefore, we sought to determine the post-HCT risk of NMSC related tovoriconazoleuse. Methods: We performed a retrospective cohort study by exposure tovoriconazolefor allogeneic (n = 1370) and autologous (n = 1538) HCT recipients at Stanford University Medical Center between January 2003 and March 2015. Post-HCT incidence rates (IR) and hazard ratios (HR) were calculated based on first diagnosed NMSC after HCT. Multivariate analysis includedvoriconazoleexposure and known risk factors for NMSC including history of chronic graft-versus-host disease, age at transplant, sex, race, and history of NMSC. Results: The 10-year IR for NMSC in the overall HCT population was 14.1 (95% CI = 11.7 - 16.8) and time to incident NMSC ranged from 0.1 to 10.9 years post-transplant. Among allogeneic HCT recipients, 90 patients developed NMSC with a 10-year IR of 25.6 (95% CI = 20.6 - 31.5) (Table 1). The median time from HCT to first diagnosis of NMSC was 1.9 years (range 0.1 - 9.9 years). The 10-year IR for SCC was 19.7 (95% CI = 15.3 - 24.9) and 6.8 (95% CI = 4.4 - 10.2) for BCC (Table 1). NMSC occurred more often on the head and neck in the exposed cohort compared to the unexposed cohort (p = 0.020). In multivariate analyses, among allogeneic HCT recipients,voriconazoleuse was associated with an increased overall risk for NMSC (HR = 1.86, 95% CI = 1.18 - 2.92, p = 0.008) (Table 2). The association withvoriconazoleexposure was largely for SCC (HR = 2.12, 95% CI = 1.26 - 3.57, p = 0.005). Exposure tovoriconazoledid not appear to affect the risk for BCC (HR = 1.03, 95% CI = 0.43 - 2.46, p = 0.954). Among autologous HCT recipients, 34 developed NMSC with a 10-year IR of 6.3 (95% CI = 4.4 - 8.9) and a median time from HCT to diagnosis of 1.6 years (range 0.2 -10.9 years) (Table 1). The 10-year IRs among autologous HCT recipients for SCC and BCC respectively were 3.6 (95% CI = 2.2 - 5.9) and 2.1 (95% CI = 1.1 - 3.8) (Table 1). In the multivariate analysis, we found no relationship betweenvoriconazoleuse and risk for NMSC (HR = 0.93, 95% CI = 0.33 - 2.64, p = 0.887) (Table 3). Conclusion: There is a high rate of incident NMSC in the post-HCT setting with a wide range of times to diagnoses, and voriconazoleuse represents a novel factor that may contribute to increased risk for SCC in the allogeneic HCT population. Our data indicate that any history of exposure to voriconazolemay increase the risk of SCC, but not BCC, in allogeneic but not autologous HCT recipients. While other factors have greater impacts on HCT recipientsÕ risk of NMSC, the widely accepted use of voriconzaoleas either a prophylactic or therapeutic anti-fungal agent in HCT recipients makes it an important consideration in overall risk assessment.Regardless ofvoriconazole exposure, NMSC is prevalent in the post-HCT setting and there is a critical need for patient education and regular, vigilant surveillance by an experienced dermatologist to screen for and treat early skin cancer or precursor lesions. Disclosures No relevant conflicts of interest to declare.

Multiple primary melanoma in association with other personal and family history of cancers.

2021 ◽  
Vol 39 (15_suppl) ◽  
pp. e21559-e21559
Author(s):  
Xi Yang ◽  
Lilit Karapetyan ◽  
Na Bo ◽  
Hong Wang ◽  
Cindy Sander ◽  
...  
Keyword(s):  
Prostate Cancer ◽  
Family History ◽  
Skin Cancer ◽  
Cell Carcinoma ◽  
Primary Melanoma ◽  
Non Melanoma Skin Cancer ◽  
Skin Cancers ◽  
Increased Risk ◽  
History Of ◽  
Melanoma Skin

e21559 Background: Patients (PTs) with cutaneous melanoma are at increased risk of developing second primary melanoma and non-melanoma skin cancers. The primary aim of this study was to define the association between MPM and personal history of non-melanoma skin cancers and other non-skin cancers. The secondary aim was to evaluate the association between MPM and the presence of other cancers among first-degree relatives (FDRs). Methods: We performed a retrospective case-control study including cases with MPM and controls with single primary melanoma (SPM) from the University of Pittsburgh Cancer Institute Melanoma Center Biological Sample and Nevus Bank. The proportions and percentages of non-melanoma skin cancer, other non-skin cancer, 1st degree family history of melanoma, and 1st degree family history of other non-melanoma cancers were calculated separately for MPM and SPM groups. Fisher’s exact tests were performed to test whether MPM was associated with these variables. For each significant variable, a multivariable logistic regression model was used to test its association with MPM after adjusting for age, gender, melanoma staging, and smoking status. Results: In total, 311 PTs (39.2% men; median age at initial diagnosis 51years) were enrolled, including 194 with SPM (38.6%; 51) and 117 with MPM (39.8%; 48). 28 (9%) of PTs had squamous cell carcinoma (SCC), and 63 (20%) had basal cell carcinoma (BCC). The most common non-skin cancers in the whole cohort were prostate (4.8%), breast (3.8%), hematological (1.9%), colorectal (1.3%), and cervical cancers (1.3%). FDR history of melanoma, non-melanoma skin cancer, and other cancers were positive in 15.4%, 7.1% and 46.3% PTs, respectively. The most common non-skin cancers in FDRs were breast, prostate, lung, colorectal and hematological malignancies. In comparison to PTs with SPM, PTs with MPM were more likely to have SCC (14.5% vs 5.7%, p=0.013) but not BCC and other non-skin cancers. FDRs of PTs with MPM had higher prevalence of melanoma (23.1% vs 10.8%, p=0.005), prostate cancer (31.9% vs 5.3%, p=0.0002) but not other non-melanoma skin and non-skin cancers. In multivariate analysis the association remained significant between MPM and SCC (OR 2.7, 95% CI 1.1-6.6, p=0.032), FDR history of melanoma (OR 2.0, 95% CI 1.03-4.1, p=0.042), and FDR history of prostate cancer (OR 5.6, 95% CI 1.6-20.3, p=0.008). Conclusions: MPM is associated with higher prevalence of SCC and FDR history of melanoma and prostate cancer, but not BCC and other non-melanoma cancers in comparison to SPM.

scholarly journals Sunburn in Australian Men With a History of Non-Melanoma Skin Cancer

2003 ◽  
Vol 27 (3) ◽  
pp. 195-207 ◽  
Author(s):  
Torres Woolley ◽  
Petra G. Buettner ◽  
John B. Lowe
Keyword(s):  
Skin Cancer ◽  
Non Melanoma Skin Cancer ◽  
History Of ◽  
Melanoma Skin

A new hypothesis to explain skin cancer risk in kidney allograft recipients

2020 ◽  
pp. 239936932097212
Author(s):  
Davide Viggiano ◽  
Michael W Lee ◽  
Mariadelina Simeoni ◽  
Giovambattista Capasso ◽  
Anna Capasso
Keyword(s):  
Skin Cancer ◽  
Cell Carcinoma ◽  
Cancer Incidence ◽  
Calcineurin Inhibitors ◽  
Non Hodgkin Lymphoma ◽  
Non Melanoma Skin Cancer ◽  
Incident Cancer ◽  
Increased Risk ◽  
New Hypothesis ◽  
Melanoma Skin

Kidney transplant (KT) recipients have an increased risk for specific types of cancer. Some forms of incident cancer are similarly present in other diseases where T-cells are depleted, such as HIV-infection: specifically, non-Hodgkin lymphoma and Kaposi’s sarcoma. Conversely, other forms of highly incident cancers in KT patients, primarily non-melanoma skin cancer (squamous cell carcinoma and basal cell carcinoma), are specific to this condition. By comparing HIV-related cancers, general cancer incidence, and the association of immunotherapy with cancer incidence, we suggest that the high incidence of non-melanoma skin cancer seen in KT patients is mediated by off-target effects of calcineurin inhibitors in the skin, combined with a “permissive” cancer microinflammatory environment.

scholarly journals Abatacept initiation in rheumatoid arthritis and the risk of cancer: a population-based comparative cohort study

Rheumatology ◽  
2018 ◽  
Vol 58 (4) ◽  
pp. 683-691 ◽  
Author(s):  
François Montastruc ◽  
Christel Renoux ◽  
Sophie Dell’Aniello ◽  
Teresa A Simon ◽  
Laurent Azoulay ◽  
...  
Keyword(s):  
Cohort Study ◽  
Skin Cancer ◽  
Population Based ◽  
Cox Proportional Hazards ◽  
Non Melanoma Skin Cancer ◽  
Increased Risk ◽  
Significant Difference ◽  
Specific Cancer ◽  
Risk Of Cancer ◽  
Melanoma Skin

Abstract Objective To assess whether abatacept as initial biological DMARD (bDMARD) in the treatment of RA, when compared with other bDMARDs, is associated with an increased risk of cancer overall and by specific cancer sites (breast, lung, lymphoma, melanoma and non-melanoma skin cancer). Methods We performed a population-based cohort study among patients newly treated with bDMARDs within the US-based Truven MarketScan population and Supplemental US Medicare from 2007 to 2014. Cox proportional hazards models were used to estimate hazard ratios and 95% CIs of any cancer (and specific cancers) associated with initiation of abatacept, compared with initiation of other bDMARDs, adjusted for age and deciles of the propensity score. Results The cohort included 4328 patients on abatacept and 59 860 on other bDMARDs, of whom 409 and 4197 were diagnosed with any cancer during follow-up (incidence rates 4.76 per 100 per year and 3.41 per 100 per year, respectively). Compared with other bDMARDs, the use of abatacept was associated with an increased incidence of cancer overall (hazard ratioadjusted 1.17; 95% CI 1.06, 1.30). Analyses by specific cancer sites showed a significantly increased incidence of non-melanoma skin cancer (hazard ratioadjusted 1.20; 95% CI 1.03, 1.39), but no significant difference for other specific cancer sites. Conclusion The use of abatacept as first bDMARD in the treatment of RA was associated with a slight increased risk of cancer overall and particularly non-melanoma skin cancer, compared with other bDMARDs. This potential signal needs to be replicated in other settings.

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