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
854 Commentaries
must be performed in a hospital. Skin grafting can also be problematic in specific dermatological diseases, because of the potential for pathergy.3 For these reasons, much effort has been dedicated to finding exogenous graft materials such as artificial skin substitutes, cadaveric skin or xenografts; however, these materials can bring about only temporary wound coverage.4 Alternative wound closure technologies that reduce donor-site morbidity and that could be performed easily in an outpatient scenario would be very useful in wound care management. In this issue of BJD, Purschke et al.5 investigate a novel technique designed to obtain epidermal grafting for the treatment of vitiligo or difficult-to-heal wounds by using microepidermal suction blisters. The authors used two different methodological strategies (elastic surgical dressings and ‘blister array’) and tested these models for feasibility, ease of use, reliability, and preservation of viability of the epidermal graft. The most important finding of the study was that both strategies showed blister roof with an intact epidermis and with preserved cell viability, including epidermal basal cells, melanocytes and the underlying dermis. The second technique (‘blister array’) was found to be more user friendly, particularly with respect to the simultaneous steps of blister raising, blister capture onto the dressing scaffold and blister harvesting. In our opinion, this novel technique opens up a great opportunity for the practical and potential application of epidermal grafting in skin diseases such as vitiligo, difficult-toheal wounds and other disorders where a normal epidermis is lacking. The major advantages we have observed are the simple and automated harvesting procedure, a completely outpatient-based procedure not requiring anaesthesia, and rapid healing with less scarring of the donor site. Future improvements in the technique could include a different scaffold material for suction blisters in order to keep wound exudate under control. Conflicts of interest None declared. Department of Dermatology, Wound Healing Research Unit, University of Pisa, Via Roma 67, 56126 Pisa, Italy E-mail: [email protected]
M. ROMANELLI V. DINI
References 1 Zhang AY, Meine JG. Flaps and grafts reconstruction. Dermatol Clin 2011; 29:217–30. 2 Han G. State of the art wound healing: skin substitutes for chronic wound. Cutis 2014; 93:13–26. 3 Richmond NA, Lamel SA, Braun LR et al. Epidermal grafting using a novel suction blister-harvesting system for the treatment of pyoderma gangrenosum. JAMA Dermatol 2014; 150:999–1000.
British Journal of Dermatology (2015) 172, pp844–860
4 Dini V, Romanelli M, Piaggesi A et al. Cutaneous tissue engineering and lower extremities wounds (part 2). Int J Low Extrem Wounds 2006; 5:27–34. 5 Purschke M, Asrani FA, Sabir SA et al. Novel methods for generating fractional epidermal micrografts. Br J Dermatol 2015; 172:1021–28.
Sentinel lymph node biopsy for cutaneous squamous cell carcinoma: valuable or not valuable? DOI: 10.1111/bjd.13601 ORIGINAL ARTICLE, p 1029 The incidence of cutaneous squamous cell carcinoma (SCC) is still increasing, and this tumour has the potential to metastasize. The risk of metastasis is around 3–6%, but may increase to 20% in high-risk SCC.1 The challenge in daily practice is to identify high-risk SCC and to detect a metastasis as early as possible.2 In this issue of BJD, Krediet et al.3 report a retrospective study of 143 patients in which they evaluated risk factors for metastasis of SCC, and the value of sentinel lymph node biopsy (SLNB). They confirmed that sex, age, and tumour localization, diameter, thickness and differentiation are significant risk factors for metastasis.4 They performed SLNB in 17 patients with high-risk SCC, two of which were positive. Of the other 15 patients, six still developed a metastasis later on, despite a negative SLNB. One patient developed a metastasis in the lymph node region that was subjected to SLNB, while the other five developed a metastasis in a distant region or developed a systemic metastasis. In contrast, nine (71%) of the 126 patients without SLNB developed a metastasis. It appears that the patients selected for SLNB were indeed patients with high risk of metastasis in general, as eight (47%) of 17 developed a metastasis. The most commonly used tool to identify high-risk SCC is the T stage of the TNM (tumour, nodes, metastasis) classification. The T staging system is subject to periodic revision, most recently in 2009 by the Union for International Cancer Control and in 2010 by the American Joint Committee on Cancer. But still these staging systems are not satisfactory, and several alternative T staging systems have been studied and proposed, primarily based on the presence or absence of independent risk factors.5–7 Lymph node palpation, ultrasound, computed tomography (CT), magnetic resonance imaging (MRI) and positron emission tomography (PET) are currently the most frequently used methods for the detection of metastasis. Palpation has a sensitivity of 60–75%, with CT, MRI, PET and ultrasound being slightly better.8 However, there is no consensus as to which of these methods should be used at what time points and how frequently. In patients with high-risk SCC and negative imag© 2015 British Association of Dermatologists
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
854 Commentaries
must be performed in a hospital. Skin grafting can also be problematic in specific dermatological diseases, because of the potential for pathergy.3 For these reasons, much effort has been dedicated to finding exogenous graft materials such as artificial skin substitutes, cadaveric skin or xenografts; however, these materials can bring about only temporary wound coverage.4 Alternative wound closure technologies that reduce donor-site morbidity and that could be performed easily in an outpatient scenario would be very useful in wound care management. In this issue of BJD, Purschke et al.5 investigate a novel technique designed to obtain epidermal grafting for the treatment of vitiligo or difficult-to-heal wounds by using microepidermal suction blisters. The authors used two different methodological strategies (elastic surgical dressings and ‘blister array’) and tested these models for feasibility, ease of use, reliability, and preservation of viability of the epidermal graft. The most important finding of the study was that both strategies showed blister roof with an intact epidermis and with preserved cell viability, including epidermal basal cells, melanocytes and the underlying dermis. The second technique (‘blister array’) was found to be more user friendly, particularly with respect to the simultaneous steps of blister raising, blister capture onto the dressing scaffold and blister harvesting. In our opinion, this novel technique opens up a great opportunity for the practical and potential application of epidermal grafting in skin diseases such as vitiligo, difficult-toheal wounds and other disorders where a normal epidermis is lacking. The major advantages we have observed are the simple and automated harvesting procedure, a completely outpatient-based procedure not requiring anaesthesia, and rapid healing with less scarring of the donor site. Future improvements in the technique could include a different scaffold material for suction blisters in order to keep wound exudate under control. Conflicts of interest None declared. Department of Dermatology, Wound Healing Research Unit, University of Pisa, Via Roma 67, 56126 Pisa, Italy E-mail: [email protected]
M. ROMANELLI V. DINI
References 1 Zhang AY, Meine JG. Flaps and grafts reconstruction. Dermatol Clin 2011; 29:217–30. 2 Han G. State of the art wound healing: skin substitutes for chronic wound. Cutis 2014; 93:13–26. 3 Richmond NA, Lamel SA, Braun LR et al. Epidermal grafting using a novel suction blister-harvesting system for the treatment of pyoderma gangrenosum. JAMA Dermatol 2014; 150:999–1000.
British Journal of Dermatology (2015) 172, pp844–860
4 Dini V, Romanelli M, Piaggesi A et al. Cutaneous tissue engineering and lower extremities wounds (part 2). Int J Low Extrem Wounds 2006; 5:27–34. 5 Purschke M, Asrani FA, Sabir SA et al. Novel methods for generating fractional epidermal micrografts. Br J Dermatol 2015; 172:1021–28.
Sentinel lymph node biopsy for cutaneous squamous cell carcinoma: valuable or not valuable? DOI: 10.1111/bjd.13601 ORIGINAL ARTICLE, p 1029 The incidence of cutaneous squamous cell carcinoma (SCC) is still increasing, and this tumour has the potential to metastasize. The risk of metastasis is around 3–6%, but may increase to 20% in high-risk SCC.1 The challenge in daily practice is to identify high-risk SCC and to detect a metastasis as early as possible.2 In this issue of BJD, Krediet et al.3 report a retrospective study of 143 patients in which they evaluated risk factors for metastasis of SCC, and the value of sentinel lymph node biopsy (SLNB). They confirmed that sex, age, and tumour localization, diameter, thickness and differentiation are significant risk factors for metastasis.4 They performed SLNB in 17 patients with high-risk SCC, two of which were positive. Of the other 15 patients, six still developed a metastasis later on, despite a negative SLNB. One patient developed a metastasis in the lymph node region that was subjected to SLNB, while the other five developed a metastasis in a distant region or developed a systemic metastasis. In contrast, nine (71%) of the 126 patients without SLNB developed a metastasis. It appears that the patients selected for SLNB were indeed patients with high risk of metastasis in general, as eight (47%) of 17 developed a metastasis. The most commonly used tool to identify high-risk SCC is the T stage of the TNM (tumour, nodes, metastasis) classification. The T staging system is subject to periodic revision, most recently in 2009 by the Union for International Cancer Control and in 2010 by the American Joint Committee on Cancer. But still these staging systems are not satisfactory, and several alternative T staging systems have been studied and proposed, primarily based on the presence or absence of independent risk factors.5–7 Lymph node palpation, ultrasound, computed tomography (CT), magnetic resonance imaging (MRI) and positron emission tomography (PET) are currently the most frequently used methods for the detection of metastasis. Palpation has a sensitivity of 60–75%, with CT, MRI, PET and ultrasound being slightly better.8 However, there is no consensus as to which of these methods should be used at what time points and how frequently. In patients with high-risk SCC and negative imag© 2015 British Association of Dermatologists
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.
