Commentaries differentiation-regulating proteins during skin barrier repair. Br J Dermatol 2012; 166:1245–54. 13 Molin S, Merl J, Dietrich KA et al. The hand eczema proteome: imbalance of epidermal barrier proteins. Br J Dermatol 2015; 172:994–1001.
853
Conflicts of interest None declared. Department of Dermatology, Waikato Hospital, Waikato, Hamilton 3204, New Zealand E-mail: [email protected]
M. RADEMAKER
Growth of periocular basal cell carcinoma DOI: 10.1111/bjd.13529 ORIGINAL ARTICLE, p 1002 Since its first description in 1827 by Arthur Jacob, much has been learned about basal cell carcinoma (BCC). We now know that the lifetime risk for developing BCC, in an individual with Fitzpatrick skin type I or II, is 30–60%,1 making it the most common cancer in humans of European heritage. We understand that the risk of developing BCC is nonlinearly correlated to total ultraviolet exposure (10 000–35 000 h),2 which drives mutations of tumour suppressor genes such as p53 and patched homologue 1 (PTCH1). This has led to new and exciting targeted therapies such as itraconazole, vismodegib and other smoothened inhibitors.3 However, the answers to some of the simple questions, such as how quickly do BCCs grow, remain unclear. Traditionally it has been stated that BCCs grow slowly, yet clinically we have all seen BCCs with surprisingly fast growth rates. Although the study by Tan et al.4 in this issue of BJD, examined only periocular tumours, the growth rate was unexpectedly fast. In those tumours that increased in size after the initial biopsy, the mean growth rate was 146 mm length (22 mm2 in area) per 30 days. More worrisome was that the quickest tumour grew by 10 mm (168 mm2) per 30 days. While care must be taken in generalizing this study to other sites, it is likely that facial BCCs will grow at similar rates. The fact that one-third of the BCCs did not return to their original size after initial biopsy is not that reassuring, as the measurements were clinical dermoscopic margins, which may have underestimated histological margins, particularly for morphoeic BCCs. What are the clinical implications of these findings? A mean delay of 4 months (115 days, interquartile range 68–168) between diagnosis and definitive treatment is too long for eyelid BCCs, particularly for lesions 1 cm or longer at the time of diagnosis. Nonmelanoma skin cancer is already the most costly cancer for some healthcare systems.5 If resources become stretched, there is a risk that nonfatal cancers such as BCC will get deprioritized. These data may help direct the time frames of how quickly patients with eyelid (and probably facial) BCCs need to be seen and treated.
© 2015 British Association of Dermatologists
References 1 Miller DL, Weinstock MA. Nonmelanoma skin cancer in the United States: incidence. J Am Acad Dermatol 1994; 30:774–8. 2 Rosso S, Zanetti R, Martinez C et al. The multicentre south European study ‘Helios’. II: different sun exposure patterns in the aetiology of basal cell and squamous cell carcinomas of the skin. Br J Cancer 1996; 73:447–54. 3 Dreier J, Felderer L, Barysch M et al. Basal cell carcinoma: a paradigm for targeted therapies. Expert Opin Pharmacother 2013; 14:1307–18. 4 Tan E, Lin FPY, Sheck LHN et al. Growth of periocular basal cell carcinomas. Br J Dermatol 2015; 172:1002–7. 5 Brougham ND, Dennett ER, Tan ST. Non-melanoma skin cancers in New Zealand – a neglected problem. N Z Med J 2010; 123:59–65.
Fractional epidermal skin grafting DOI: 10.1111/bjd.13580 ORIGINAL ARTICLE, p 1021 Skin grafts can be obtained from several sources, both human and animal. Skin grafts can include all or a portion of the skin, including the epidermis and dermis.1 More recently, the use of skin substitutes, dermal fillers and tissue expanders has increased surgeons’ and dermatologists’ ability to cover skin defects resulting from burns, traumatic injury, chronic wounds or excision of cancerous lesions.2 The major sources of skin grafts are autografts, homografts and xenografts. Skin substitutes, dermal fillers and tissue expanders provide additional dermal or epidermal components (or both) for wound coverage and in order to stimulate wound healing. Autologous skin grafts are ideal because there is no risk of rejection due to incompatibility between donor and recipient. Autografts must be used to provide permanent coverage to replace allografts or xenografts, which provide only temporary coverage. Skin wounds often need reconstruction with autologous grafting or flap transplantation, which are associated with several comorbidities such as pain, risk of infection, discoloration and scarring at the donor site. Split-thickness skin grafting is also correlated with expensive operating procedures, which
British Journal of Dermatology (2015) 172, pp844–860
This document is a scanned copy of a printed document. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material.
853
Conflicts of interest None declared. Department of Dermatology, Waikato Hospital, Waikato, Hamilton 3204, New Zealand E-mail: [email protected]
M. RADEMAKER
Growth of periocular basal cell carcinoma DOI: 10.1111/bjd.13529 ORIGINAL ARTICLE, p 1002 Since its first description in 1827 by Arthur Jacob, much has been learned about basal cell carcinoma (BCC). We now know that the lifetime risk for developing BCC, in an individual with Fitzpatrick skin type I or II, is 30–60%,1 making it the most common cancer in humans of European heritage. We understand that the risk of developing BCC is nonlinearly correlated to total ultraviolet exposure (10 000–35 000 h),2 which drives mutations of tumour suppressor genes such as p53 and patched homologue 1 (PTCH1). This has led to new and exciting targeted therapies such as itraconazole, vismodegib and other smoothened inhibitors.3 However, the answers to some of the simple questions, such as how quickly do BCCs grow, remain unclear. Traditionally it has been stated that BCCs grow slowly, yet clinically we have all seen BCCs with surprisingly fast growth rates. Although the study by Tan et al.4 in this issue of BJD, examined only periocular tumours, the growth rate was unexpectedly fast. In those tumours that increased in size after the initial biopsy, the mean growth rate was 146 mm length (22 mm2 in area) per 30 days. More worrisome was that the quickest tumour grew by 10 mm (168 mm2) per 30 days. While care must be taken in generalizing this study to other sites, it is likely that facial BCCs will grow at similar rates. The fact that one-third of the BCCs did not return to their original size after initial biopsy is not that reassuring, as the measurements were clinical dermoscopic margins, which may have underestimated histological margins, particularly for morphoeic BCCs. What are the clinical implications of these findings? A mean delay of 4 months (115 days, interquartile range 68–168) between diagnosis and definitive treatment is too long for eyelid BCCs, particularly for lesions 1 cm or longer at the time of diagnosis. Nonmelanoma skin cancer is already the most costly cancer for some healthcare systems.5 If resources become stretched, there is a risk that nonfatal cancers such as BCC will get deprioritized. These data may help direct the time frames of how quickly patients with eyelid (and probably facial) BCCs need to be seen and treated.
© 2015 British Association of Dermatologists
References 1 Miller DL, Weinstock MA. Nonmelanoma skin cancer in the United States: incidence. J Am Acad Dermatol 1994; 30:774–8. 2 Rosso S, Zanetti R, Martinez C et al. The multicentre south European study ‘Helios’. II: different sun exposure patterns in the aetiology of basal cell and squamous cell carcinomas of the skin. Br J Cancer 1996; 73:447–54. 3 Dreier J, Felderer L, Barysch M et al. Basal cell carcinoma: a paradigm for targeted therapies. Expert Opin Pharmacother 2013; 14:1307–18. 4 Tan E, Lin FPY, Sheck LHN et al. Growth of periocular basal cell carcinomas. Br J Dermatol 2015; 172:1002–7. 5 Brougham ND, Dennett ER, Tan ST. Non-melanoma skin cancers in New Zealand – a neglected problem. N Z Med J 2010; 123:59–65.
Fractional epidermal skin grafting DOI: 10.1111/bjd.13580 ORIGINAL ARTICLE, p 1021 Skin grafts can be obtained from several sources, both human and animal. Skin grafts can include all or a portion of the skin, including the epidermis and dermis.1 More recently, the use of skin substitutes, dermal fillers and tissue expanders has increased surgeons’ and dermatologists’ ability to cover skin defects resulting from burns, traumatic injury, chronic wounds or excision of cancerous lesions.2 The major sources of skin grafts are autografts, homografts and xenografts. Skin substitutes, dermal fillers and tissue expanders provide additional dermal or epidermal components (or both) for wound coverage and in order to stimulate wound healing. Autologous skin grafts are ideal because there is no risk of rejection due to incompatibility between donor and recipient. Autografts must be used to provide permanent coverage to replace allografts or xenografts, which provide only temporary coverage. Skin wounds often need reconstruction with autologous grafting or flap transplantation, which are associated with several comorbidities such as pain, risk of infection, discoloration and scarring at the donor site. Split-thickness skin grafting is also correlated with expensive operating procedures, which
British Journal of Dermatology (2015) 172, pp844–860
This document is a scanned copy of a printed document. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material.
