692 Commentaries

specific chromophore. The added significance of pulse duration was recognized in the theory of selective photothermolysis, which relates optimal pulse duration to thermal relaxation time.1 There are now more or less widely accepted mechanisms with regard to laser–tissue interaction, via photochemical, photothermal, photomechanical or photoablative pathways.2 So it is tempting to believe that it is possible to predict the effects of different types of laser on each patient according to the target chromophore, taking due regard of skin pigmentation. However, anyone who has experience of laser treatment will know that this does not accord with reality. The assumed precision of the laser is partially lost when intense pulsed light (IPL) devices are used. IPLs are filtered broadband sources (usually a xenon flashlamp) that are widely used for cosmetic and dermatological treatments.3 Unlike a laser, an IPL does not emit monochromatic light and so its spectrum is not well defined. Surprisingly there are remarkably few publications showing calibrated emission spectra from IPLs. In one of the very few studies on this topic, it was shown that there was a drop in signal from one pulse to the next by as much as 19%.4 Moreover, the drop was wavelength dependent, e.g. 25% decrease at 600 nm compared with 14% at 900 nm. Even during a single pulse, there was a drop of 35% in output at 700 nm between the beginning and end of the pulse. This lack of precision of the IPL would tend to direct attention back towards the laser. Not surprisingly, practitioners are not very keen to report on cases that go wrong. It is refreshing therefore to read about complications of laser dermatological treatment as it shows that even experts, with extensive experience using light-based therapies, can and do have patients who develop complications.5 Some were due to equipment failure, e.g. bubbles in the cryogenic cooling liquid, but others were attributable to user error, e.g. scarring in a port-wine stain (PWS). It is well recognized that the threshold for damage varies significantly on different parts of the same PWS. For this reason, it is standard practice to perform test treatments on a few small areas of the lesion. Response is not entirely predictable. In this issue of the BJD another source of variation, hitherto overlooked, is highlighted.6 Most end users take it for granted that the energy delivered corresponds to the value shown on the console. Indeed, medical lasers in Europe should all meet the European manufacturing standard, which stipulates that the actual laser output measured in the operating plane shall not deviate from the set value by more than  20%.7 It is generally recognized that this is a fairly generous requirement that should not place manufacturers under any strain. So the finding that every laser tested had measured pulses outside the 20% tolerance is a cause for concern. One laser tested, a long-pulsed Nd:YAG laser, set at 385 J output, had a mean measured energy per pulse of only 106 J. These are lasers that had undergone a service within the past 6 months. This report calls into question the quality of the work undertaken by the laser servicing companies. It is standard practice in most clinics to perform test patches on selected sites prior to undertaking the full treatment. However, a difference of more than 10% between simulated test patches and the remaining treatment causes the authors to question the validity British Journal of Dermatology (2014) 171, pp687–695

of this practice. While recognizing the inconsistency in delivered energy, nonetheless, test patching should still be recommended practice as it helps to ensure that the starting dose is not likely to cause undue harm. Patients may fail to disclose previous prolonged steroid use or that they are currently taking a drug that is contra-indicated, such as isotretinoin. If laser or IPL treatment is to be considered as a credible branch of evidence-based medicine, it is essential that reliable data exist on delivered laser energies and IPL spectra. On the basis of this latest report, there is a significant gap between the treatment parameters that we think we are giving and what the device is actually delivering. Conflicts of interest None declared. The Photobiology Unit, Ninewells Hospital & Medical School, University of Dundee, Dundee DD1 9SY, U.K. E-mail: [email protected]

H. MOSELEY

References 1 Anderson RR, Parrish JA. Selective photothermolysis: precise microsurgery by selective absorption of pulsed radiation. Science 1983; 220:524–7. 2 Ross EV, Anderson RR. Laser–tissue interactions. In: Lasers and Energy Devices for the Skin (Goldman MP, Fitzpatrick RE, Ross EV, Kilmer SL, Weiss RA, eds), 2nd edn. Boca Raton, FL: CRC Press, 2013; 1–30. 3 Raulin C, Greve B, Grema H. IPL technology: a review. Lasers Surg Med 2004; 32:78–87. 4 Eadie E, Miller P, Goodman T, Moseley H. Time-resolved measurement shows a spectral distribution shift in an intense pulsed light system. Lasers Med Sci 2009; 24:35–43. 5 Willey A, Anderson RR, Azpiazu JL et al. Complications of laser dermatologic surgery. Lasers Surg Med 2006; 38:1–15. 6 Lister T, Brewin M. Variations in laser energy outputs over a series of simulated treatments. Br J Dermatol 2014; 171:806–12. 7 International Electrotechnical Committee. EN60601-2-22:2013, Medical Electrical Equipment – Part 2-22: Particular Requirements for Basic Safety and Essential Performance of Surgical, Cosmetic, Therapeutic and Diagnostic Laser Equipment. Geneva: IEC, 2013.

Malignancy behind chronic pruritus: the wolf in sheep’s clothing? DOI: 10.1111/bjd.13320 ORIGINAL ARTICLE, p 839 Pruritus is a common and frequent symptom of dermatoses. In its chronic form (with a duration of 6 weeks and longer), pruritus may occur not only in dermatoses but also in a broad variety of nondermatological diseases. In order to have a sys© 2014 British Association of Dermatologists

Commentaries 693

tematic approach to pruritus, the International Forum for the Study of Itch published a classification of underlying diseases, distinguishing chronic pruritus (CP) of dermatological, systemic, neurological, psychiatric, mixed or unknown origin.1 In the first three categories, CP may evolve from a malignant disease. For example, in cutaneous T-cell lymphoma (CTCL), especially erythrodermic and folliculotropic mycosis fungoides and Sezary syndrome, severe and therapy-refractory pruritus occurs in up to 66–88% of patients.2 Extracutaneous lymphoma has also been reported to induce CP, although less frequently than CTCL. In small cohort studies, 156% of patients with non-Hodgkin lymphoma (NHL) and 193% of patients with Hodgkin lymphoma (HL) reported generalized pruritus.3,4 Indeed, these two entities seem to be the major origin of CP in nondermatological malignancy. In a study investigating dermatological symptoms in 300 patients with confirmed internal malignancy, 10 (33%) patients reported having pruritus.5 All these patients had HL or NHL. CP is less frequent in solid malignancy and in neuropathic pruritus such as ependymoma in brachioradial pruritus. However, the common biofunctional understanding of pruritus is that it points to a not yet identified but potentially malignant disease type. Thus, pruritus is hypothesized to have an important alarm function that drives the diagnostic process.6 Based on this idea, several studies have analysed the diseases underlying CP in small- and medium-sized patient cohorts. Depending on selection bias, 2–26% of the investigated patients showed a malignancy.6 The large number of malignancies identified in patients with CP played a role in shaping the diagnostic recommendations incorporated in the current guideline,6 namely, that all patients with CP undergo cautious and comprehensive diagnostics, and furthermore, those with CP of unknown origin undergo repeat diagnostics at least every year in order to rule out malignancy. In their nationwide cohort study, Sigrun Johannesdottir et al.7 address the question of pruritus as a marker of undiagnosed cancer. Their retrospective analysis covered 33 years and > 12 000 patients with International Classification of Diseases (ICD) codes for pruritus, lichenification and prurigo and a median follow-up period of 6 years. It is possibly the largest European cohort analysed on this issue. A total of 1173 smoking- and alcohol-related cancers (n = 246, including lung carcinoma, n = 73), lymphoma (n = 78, among them NHL, n = 26; HL, n = 8), skin cancers (n = 119; among them basal cell carcinoma, n = 77) and solid cancers (n = 128; among them prostate cancer, n = 86) were detected in this cohort. Obviously, not all of these cancers are responsible for inducing CP as, for instance, skin neoplasms are not known to induce generalized CP. However, the total number of detected cancers was 13% higher than the expected Danish national cancer incidence rates. Thus, the standardized incidence ratio (SIR) for cancer in all patients was calculated to be 113, not much but slightly higher than expected. Interestingly, SIR was higher for HL (638) and NHL (226) and liver (323), breast (294) and thyroid gland cancer (208). Analysis of patient follow-up showed a dramatic overall decrease of SIR during © 2014 British Association of Dermatologists

the first 3 months from 258 (0–3 months) to 151 (4–12 months). After 10 years, the ratio of cancers was the same as that in the general population. The results are interesting, relevant and important for the medical care of patients with CP as they clearly show a dynamic favouring early diagnosis in patients with pruritus. However, the authors of this study face the limitation of not being able to obtain information from the ICD codes on the real duration of pruritus and whether there was unambiguous close historical association of pruritus to the development of cancer. Despite this, the study sheds new light on paraneoplastic pruritus and offers more rational guidance to the diagnostic processes in patients with CP. Conflicts of interest None declared. Competence Center for Chronic Pruritus, Department of Dermatology, University Hospital Mu¨nster, Mu¨nster, Germany E-mail: [email protected]

S . S T A€N D E R

References 1 St€ander S, Weisshaar E, Mettang T et al. Clinical classification of itch: a position paper of the International Forum for the Study of Itch. Acta Derm Venereol 2007; 87:291–4. 2 Vij A, Duvic M. Prevalence and severity of pruritus in cutaneous T cell lymphoma. Int J Dermatol 2012; 51:930–4. 3 Kumar SS, Kuruvilla M, Pai GS et al. Cutaneous manifestations of nonHodgkin’s lymphoma. Indian J Dermatol Venereol Leprol 2003; 69:12–15. 4 Rubenstein M, Duvic M. Cutaneous manifestations of Hodgkin’s disease. Int J Dermatol 2006; 45:251–6. 5 Rajagopal R, Arora PN, Ramasastry CV et al. Skin changes in internal malignancy. Indian J Dermatol Venereol Leprol 2004; 70:221–5. 6 Weisshaar E, Szepietowski JC, Darsow U et al. European guideline on chronic pruritus. Acta Derm Venereol 2012; 92:563–81. 7 Johannesdottir SA, Farkas DK, Vinding GR et al. Cancer incidence among patients with a hospital diagnosis of pruritus: a nationwide Danish cohort study. Br J Dermatol 2014; 171:839–46.

Patterns of vascular birthmarks: questions and clues DOI: 10.1111/bjd.13316 ORIGINAL ARTICLE, p 868 The dogma that port-wine stains (PWSs) associated with Sturge–Weber syndrome (SWS) occur in the distribution of the ophthalmic branch of the trigeminal nerve (V1) has been widely accepted. A modification of this distribution was proposed by Enjolras et al.1 in 1985. They proposed a ‘watershed’ British Journal of Dermatology (2014) 171, pp687–695

Malignancy behind chronic pruritus: the wolf in sheep's clothing?

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