Correspondence 837 Table 2 Themes that emerged following the interviews and comments made by patients Theme
Patients’ comments
Patients’ body image or self-image
Developed negative body image following the episode of drug reaction with eosinophilia and systemic symptoms. Patients refrained from participating in social activities and felt more self-conscious about wearing certain clothes Patients and their relatives felt very frightened, alarmed and upset about their physical appearance Felt depressed, tearful, isolated, frightened and anxious Experienced nightmares, flashbacks of the illness, intrusive thoughts and panic attacks Felt suicidal and that they were ‘going to die’ Concerned that their children were affected psychologically by the illness More meticulous in reading information leaflets and researching potential side-effects Patients’ relatives were more cautious about taking new medications Patients and their relatives lost confidence in healthcare professionals and hospitals
Psychological symptoms or mood disturbance
Fear of new medications
Attitude towards healthcare professionals
awareness of drug reactions and affected their trust in healthcare professionals. Seven (78%) patients felt depressed and anxious while five (56%) reported nightmares, intrusive thoughts and flashbacks lasting between 3 to 12 months. One patient sought psychological counseling via her general practitioner (GP) after the illness, two patients were already under psychiatric review for depression and two patients were referred to the liaison psychiatry team serving our department following the interviews. One patient had consulted her GP regarding intrusive thoughts, nightmares and tearfulness but was reassured and advised to ‘not be so hard on herself’. More worryingly, of the three patients who reported suicidal thoughts and panic attacks, only one received formal psychiatric input. The limitations of this study include the small sample size and recall bias. Additionally, patients with ongoing or previous psychological problems may be either more or less likely to participate than those without such issues. Nonparticipation may also represent the presence of psychological symptoms, thus this small study may underestimate the impact of this problem. Our study suggests that a significant proportion of patients experience psychological symptoms consistent with PTSD, anxiety and depression following DRESS. We would suggest that follow-up of patients should include systematic screening for PTSD, anxiety and depressive symptoms up to 12 months following DRESS in order to provide adequate psychological or psychiatric support. © 2014 British Association of Dermatologists
Dermatology Department, King’s College Hospital NHS Foundation Trust, London SE5 9RS, U.K. E-mail: [email protected]
T.T. LEW D. CREAMER J. MACKENZIE S.A. WALSH
References 1 Walsh SA, Creamer D. Drug reaction with eosinophilia and systemic symptoms (DRESS): a clinical update and review of current thinking. Clin Exp Dermatol 2011; 36:6–11. 2 Husain Z, Reddy BY, Schwartz RA. DRESS syndrome: part I. Clinical perspectives. J Am Acad Dermatol 2013; 68:693.e1–14. 3 Cuthbertson BH, Hull A, Strachan M, Scott J. Post-traumatic stress disorder after critical illness requiring general intensive care. Intensive Care Med 2004; 30:450–5. 4 Yu BH, Dimdale JE. Post-traumatic stress disorder in patients with burn injuries. J Burn Care Rehabil 1999; 20:426–33. 5 Butt TF, Cox AR, Lewis H, Ferner RE. Patient experiences of serious adverse drug reactions and their attitudes to medicines: a qualitative study of survivors of Stevens-Johnson syndrome and toxic epidermal necrolysis in the UK. Drug Saf 2011; 34:319–28. 6 Kardaun SH, Sidoroff A, Valeyrie-Allanore L et al. Variability in the clinical pattern of cutaneous side-effects of drugs with systemic symptoms: does a DRESS syndrome really exist? Br J Dermatol 2007; 156:609–11. 7 Zigmond AS, Snaith RP. The hospital anxiety and depression scale. Acta Psychiatr Scand 1983; 67:361–70. 8 Bjelland I, Dahl AA, Haug TT, Necklemann D. The validity of the hospital anxiety and depression scale. An updated literature review. J Psychosom Res 2002; 52:69–77. 9 Horowitz MJ, Wilner N, Alvarez W. The impact of event scale: a measure of subjective stress. Psychosom Med 1979; 41:209–18. 10 Sundin EC, Horowitz MJ. Impact of event scale: psychometric properties. Br J Psychiatry 2002; 180:205–9. Funding sources: none. Conflicts of interest: none declared.
Darier disease can be complicated by generalized cutaneous candidiasis: a case report DOI: 10.1111/bjd.13360 DEAR EDITOR, Darier disease (DD) is an autosomal dominant acantholytic genodermatosis caused by a mutation of the ATP2A2 gene.1 Patients with DD show enhanced susceptibility to bacterial or viral skin infections, in particular herpes simplex virus (HSV) type 1 and 2,2,3 varicella zoster virus (VZV)4 and cowpox virus.5 A 53-year-old woman had been suffering from extensive DD since the age of 5 years. Long-term treatment with acitretin (07 mg kg1), prophylactic aciclovir and emollients had resulted in stable disease with occasional flare-ups mostly involving her trunk. She did not present any cause of immuBritish Journal of Dermatology (2015) 172, pp805–840
838 Correspondence
nosuppression such as human immunodeficiency virus infection, diabetes or immunosuppressive treatment. She was hospitalized because of a week-long history of moderate fever and a flare-up of her skin condition, not improved by oral treatment with lincomycin. On admission, besides usual keratotic follicular papules, her back was scattered with multiple small-sized erosions, confluent on the lumbosacral region, forming a large belt-shaped, painful and pruriginous erosive area (Fig. 1). Neither vesicles, nor clinical evidence for impetiginization were identified. Routine laboratory investigations were unremarkable, except for an increased eosinophil count (098 9 109 L1), and C-reactive protein (62 mg L1). Procalcitonin, blood cultures and urinalysis were negative. Empirical treatment with valaciclovir (2 g daily) then intravenous aciclovir (15 mg kg1 daily) failed to improve the patient’s skin condition. Moreover, pretherapeutic surface samples collected from erosive areas were negative for HSV1, HSV2 and VZV. Based on documented skin colonization by Pseudomonas aeruginosa and methicillin-sensitive Staphylococcus aureus, intravenous antibiotic therapy with piperacillin plus tazobactam and ciprofloxacin was administered to the patient but did not result in any improvement. On the contrary, confluent erosive areas spread gradually to the whole trunk and to the proximal parts of the upper and
(a)
(c)
(d)
(b)
Fig 1. Clinical presentation at (a) admission to our department; (b) day 14, (c) day 21, (d) day 28 after admission. British Journal of Dermatology (2015) 172, pp805–840
lower limbs, to reach up to 60% of the total body surface, and became covered with white-coloured, curd-like exudates without pustules (Fig. 1). Skin pain required opiates. Meanwhile, our patient presented episodic low-grade febrile peaks. She became progressively bedridden and developed a major depressive disorder, and subsequent weight loss. Based on the clinical presentation, at day 30 after admission a specimen from the patient’s abdomen was collected for fungal analysis. Direct examination was positive for yeasts, later identified as Candida albicans on culture; fungal blood cultures were negative. Thus, our patient was treated by whole-body daily topical econazole ointment, in association with oral fluconazole 200 mg daily for 3 weeks after a loading charge of 400 mg. Thereafter, her skin gradually improved: almost all erosive areas healed within the first 2 weeks of antifungal treatment, except for the lumbosacral erosive region already noted on admission. The diffuse white-coloured exudates cleared. Opiates were tapered gradually, and the patient was discharged after 2 months of hospitalization. One month after she finished the antifungal treatment, her nutritional status was improved and no evidence of skin relapse was noted. To the best of our knowledge, the onset of generalized cutaneous candidiasis in a patient with DD has not been reported previously, contrary to dermatophyte infections.6 Classically, diffuse cutaneous candidiasis occurs either in newborns (due to vertical transmission), or in the course of Candida septicaemia in immunocompromised patients or drug users. In our patient, there was no evidence of immunosuppression. Moreover, it is unlikely that C. albicans secondary infection can be explained by haematogenous spread, because fungal blood cultures were negative and the patient’s elementary lesions included erosions, fissures and whitish curd-like exudates similar to those observed in localized candidiasis. There was no clinical evidence for extracutaneous involvement. Thus, we hypothesized that candidiasis arose primarily from the patient’s dyskeratotic skin (possibly from her chronic lumbosacral fissures) and later spread into the rest of her skin, in the same way as does HSV in the course of Kaposi varicelliform eruption in patients with chronic skin barrier damage, including patients with DD.2,3 No fungal sample collection was performed at the patient’s admission; thus, it cannot be excluded that C. albicans infection occurred later in the course of hospitalization. Antibiotic therapies administered before and during hospitalization may have promoted fungal dissemination. Also, it is likely that longterm treatment with acitretin, at doses higher than usually recommended in patients with DD, might have exerted deleterious effects by increasing skin barrier impairment. No specific therapeutic guidelines apply to patients with extensive, isolated skin candidiasis. In our patient, we decided to combine topical and systemic azole therapy. Fluconazole dosage was empirically adapted from the treatment standard of invasive systemic candidiasis, namely loading charge of 800 mg then 400 mg daily, for at least 2 weeks after a demonstrated negative blood culture result or clinical signs of improvement.7 © 2014 British Association of Dermatologists
News and Notices 839
In conclusion, physicians should consider the possibility of diffuse cutaneous candidiasis in patients with DD presenting unexplained and/or refractory flare-ups, and look for suggestive clinical signs among which are confluent erosions and/or whitish exudates. Given its moderate financial cost, systematic skin swab sampling for fungal analysis may be useful in any patient with DD exacerbation. 1
Department of Dermatology, Lyon 1 University, Centre Hospitalier Lyon Sud, 69495 Pierre Benite Cedex, France 2 Universite Claude Bernard Lyon 1, 43 Bd 11 Novembre 1918 BP 761, 69622 Villeurbanne Cedex, France Correspondence: Luc Thomas. E-mail: [email protected]
L. WEILER1 N. POULALHON1 S. DEBARBIEUX1 L. THOMAS1,2
2 Pantazi V, Potouridou I, Katsarou A et al. Darier’s disease complicated by Kaposi’s varicelliform eruption due to herpes simplex virus. J Eur Acad Dermatol Venereol 2000; 14:209–11. 3 Sais G, Jucgla A, Curc o N, Peyrı J. Kaposi’s varicelliform eruption with ocular involvement. Arch Dermatol 1994; 130:1209–10. 4 Kandasamy R, Hecker M, Choi M, Pile J. Darier disease complicated by disseminated zoster. Dermatol Online J 2009; 15:65. 5 Haase O, Moser A, Rose C. Generalized cowpox infection in a patient with Darier disease. Br J Dermatol 2011; 164:1116–18. 6 Tatnall FM, Sarkany I. Darier’s disease complicated by Trichophyton rubrum infection. Arch Dermatol 1986; 122:623. 7 Pappas PG, Kauffman CA, Andes D et al. Clinical practice guidelines for the management of candidiasis: 2009 update by the Infectious Diseases Society of America. Clin Infect Dis 2009; 48:503–35. Funding sources: no external funding. Conflicts of interest: none declared.
References 1 Sakuntabhai A, Ruiz-Perez V, Carter S et al. Mutations in ATP2A2, encoding a Ca2 + pump, cause Darier’s disease. Nat Genet 1999; 21:271–7.
News and Notices DOI: 10.1111/bjd.13731 95th Annual Meeting of the British Association of Dermatologists 7th–9th July 2015, Manchester The 95th Annual Meeting of the British Association of Dermatologists will be held at the Manchester Central, 7th–9th July 2015, organised by Prof Irene Leigh, BAD Academic Vice-President. Abstracts of papers and posters should be submitted for consideration by the Scientific Committee. Original communications will be allotted 15 min, which must include time for discussion. Online submission will be the only method of abstract submission available. Full instructions and the submission form can be accessed via the BAD website www.bad.org.uk/annualmeeting The closing date for the receipt of abstracts is Monday 12th January 2015 and the deadline will be adhered to strictly. Any abstracts received after this date will not be considered. The deadline for abstract submissions to any of the special interest group meetings will be Monday 9th February 2015. Poster submissions on the following topics are strongly encouraged: audit, medical education, and service delivery. Conference & Event Services, British Association of Dermatologists, 4 Fitzroy Square, London, W1T 5HQ, UK or email [email protected] Ó 2015 British Association of Dermatologists
I was born in Waterloo, Belgium; moved to Israel in 1981; received my MD and PhD degrees from the Hebrew University of Jerusalem; specialized in dermatology at the Rambam Medical Center, Haifa; spent a post-doc fellowship at Thomas Jefferson University, Philadelphia; and became Chair of the department of Dermatology at the Tel Aviv Medical center in 2008 and Full Professor at the Tel Aviv University in 2010. My research focuses on the genetic basis of skin diseases. It has been an honor and a special pleasure for me to serve the BJD as section editor for the past 9 years. I look forward to contributing to the transformation the journal goes through as its new Section Editor for Translational Research. Eli Sprecher Department of Dermatology and Laboratory of Molecular Medicine, Tel Aviv Sourasky Medical Center, Tel Aviv, Israel I studied medicine at Oxford University and also completed an Oxford DM doctorate. During my subsequent dermatology training in South Wales I was awarded one of the first U.K. Dermatology Clinical Trials Network registrar fellowships and undertook an MSc in medical education. On qualifying as a dermatologist I became a clinical academic at Cardiff University in 2011. My main clinical and research interest is hidradenitis suppurativa (HS) and, in 2014, I was awarded a 5 year NISCHR fellowship to investigate HS epidemiology. My ultimate goal is to conduct clinical trials in HS to improve patient care. British Journal of Dermatology (2015) 172, pp805–840
Patients’ comments
Patients’ body image or self-image
Developed negative body image following the episode of drug reaction with eosinophilia and systemic symptoms. Patients refrained from participating in social activities and felt more self-conscious about wearing certain clothes Patients and their relatives felt very frightened, alarmed and upset about their physical appearance Felt depressed, tearful, isolated, frightened and anxious Experienced nightmares, flashbacks of the illness, intrusive thoughts and panic attacks Felt suicidal and that they were ‘going to die’ Concerned that their children were affected psychologically by the illness More meticulous in reading information leaflets and researching potential side-effects Patients’ relatives were more cautious about taking new medications Patients and their relatives lost confidence in healthcare professionals and hospitals
Psychological symptoms or mood disturbance
Fear of new medications
Attitude towards healthcare professionals
awareness of drug reactions and affected their trust in healthcare professionals. Seven (78%) patients felt depressed and anxious while five (56%) reported nightmares, intrusive thoughts and flashbacks lasting between 3 to 12 months. One patient sought psychological counseling via her general practitioner (GP) after the illness, two patients were already under psychiatric review for depression and two patients were referred to the liaison psychiatry team serving our department following the interviews. One patient had consulted her GP regarding intrusive thoughts, nightmares and tearfulness but was reassured and advised to ‘not be so hard on herself’. More worryingly, of the three patients who reported suicidal thoughts and panic attacks, only one received formal psychiatric input. The limitations of this study include the small sample size and recall bias. Additionally, patients with ongoing or previous psychological problems may be either more or less likely to participate than those without such issues. Nonparticipation may also represent the presence of psychological symptoms, thus this small study may underestimate the impact of this problem. Our study suggests that a significant proportion of patients experience psychological symptoms consistent with PTSD, anxiety and depression following DRESS. We would suggest that follow-up of patients should include systematic screening for PTSD, anxiety and depressive symptoms up to 12 months following DRESS in order to provide adequate psychological or psychiatric support. © 2014 British Association of Dermatologists
Dermatology Department, King’s College Hospital NHS Foundation Trust, London SE5 9RS, U.K. E-mail: [email protected]
T.T. LEW D. CREAMER J. MACKENZIE S.A. WALSH
References 1 Walsh SA, Creamer D. Drug reaction with eosinophilia and systemic symptoms (DRESS): a clinical update and review of current thinking. Clin Exp Dermatol 2011; 36:6–11. 2 Husain Z, Reddy BY, Schwartz RA. DRESS syndrome: part I. Clinical perspectives. J Am Acad Dermatol 2013; 68:693.e1–14. 3 Cuthbertson BH, Hull A, Strachan M, Scott J. Post-traumatic stress disorder after critical illness requiring general intensive care. Intensive Care Med 2004; 30:450–5. 4 Yu BH, Dimdale JE. Post-traumatic stress disorder in patients with burn injuries. J Burn Care Rehabil 1999; 20:426–33. 5 Butt TF, Cox AR, Lewis H, Ferner RE. Patient experiences of serious adverse drug reactions and their attitudes to medicines: a qualitative study of survivors of Stevens-Johnson syndrome and toxic epidermal necrolysis in the UK. Drug Saf 2011; 34:319–28. 6 Kardaun SH, Sidoroff A, Valeyrie-Allanore L et al. Variability in the clinical pattern of cutaneous side-effects of drugs with systemic symptoms: does a DRESS syndrome really exist? Br J Dermatol 2007; 156:609–11. 7 Zigmond AS, Snaith RP. The hospital anxiety and depression scale. Acta Psychiatr Scand 1983; 67:361–70. 8 Bjelland I, Dahl AA, Haug TT, Necklemann D. The validity of the hospital anxiety and depression scale. An updated literature review. J Psychosom Res 2002; 52:69–77. 9 Horowitz MJ, Wilner N, Alvarez W. The impact of event scale: a measure of subjective stress. Psychosom Med 1979; 41:209–18. 10 Sundin EC, Horowitz MJ. Impact of event scale: psychometric properties. Br J Psychiatry 2002; 180:205–9. Funding sources: none. Conflicts of interest: none declared.
Darier disease can be complicated by generalized cutaneous candidiasis: a case report DOI: 10.1111/bjd.13360 DEAR EDITOR, Darier disease (DD) is an autosomal dominant acantholytic genodermatosis caused by a mutation of the ATP2A2 gene.1 Patients with DD show enhanced susceptibility to bacterial or viral skin infections, in particular herpes simplex virus (HSV) type 1 and 2,2,3 varicella zoster virus (VZV)4 and cowpox virus.5 A 53-year-old woman had been suffering from extensive DD since the age of 5 years. Long-term treatment with acitretin (07 mg kg1), prophylactic aciclovir and emollients had resulted in stable disease with occasional flare-ups mostly involving her trunk. She did not present any cause of immuBritish Journal of Dermatology (2015) 172, pp805–840
838 Correspondence
nosuppression such as human immunodeficiency virus infection, diabetes or immunosuppressive treatment. She was hospitalized because of a week-long history of moderate fever and a flare-up of her skin condition, not improved by oral treatment with lincomycin. On admission, besides usual keratotic follicular papules, her back was scattered with multiple small-sized erosions, confluent on the lumbosacral region, forming a large belt-shaped, painful and pruriginous erosive area (Fig. 1). Neither vesicles, nor clinical evidence for impetiginization were identified. Routine laboratory investigations were unremarkable, except for an increased eosinophil count (098 9 109 L1), and C-reactive protein (62 mg L1). Procalcitonin, blood cultures and urinalysis were negative. Empirical treatment with valaciclovir (2 g daily) then intravenous aciclovir (15 mg kg1 daily) failed to improve the patient’s skin condition. Moreover, pretherapeutic surface samples collected from erosive areas were negative for HSV1, HSV2 and VZV. Based on documented skin colonization by Pseudomonas aeruginosa and methicillin-sensitive Staphylococcus aureus, intravenous antibiotic therapy with piperacillin plus tazobactam and ciprofloxacin was administered to the patient but did not result in any improvement. On the contrary, confluent erosive areas spread gradually to the whole trunk and to the proximal parts of the upper and
(a)
(c)
(d)
(b)
Fig 1. Clinical presentation at (a) admission to our department; (b) day 14, (c) day 21, (d) day 28 after admission. British Journal of Dermatology (2015) 172, pp805–840
lower limbs, to reach up to 60% of the total body surface, and became covered with white-coloured, curd-like exudates without pustules (Fig. 1). Skin pain required opiates. Meanwhile, our patient presented episodic low-grade febrile peaks. She became progressively bedridden and developed a major depressive disorder, and subsequent weight loss. Based on the clinical presentation, at day 30 after admission a specimen from the patient’s abdomen was collected for fungal analysis. Direct examination was positive for yeasts, later identified as Candida albicans on culture; fungal blood cultures were negative. Thus, our patient was treated by whole-body daily topical econazole ointment, in association with oral fluconazole 200 mg daily for 3 weeks after a loading charge of 400 mg. Thereafter, her skin gradually improved: almost all erosive areas healed within the first 2 weeks of antifungal treatment, except for the lumbosacral erosive region already noted on admission. The diffuse white-coloured exudates cleared. Opiates were tapered gradually, and the patient was discharged after 2 months of hospitalization. One month after she finished the antifungal treatment, her nutritional status was improved and no evidence of skin relapse was noted. To the best of our knowledge, the onset of generalized cutaneous candidiasis in a patient with DD has not been reported previously, contrary to dermatophyte infections.6 Classically, diffuse cutaneous candidiasis occurs either in newborns (due to vertical transmission), or in the course of Candida septicaemia in immunocompromised patients or drug users. In our patient, there was no evidence of immunosuppression. Moreover, it is unlikely that C. albicans secondary infection can be explained by haematogenous spread, because fungal blood cultures were negative and the patient’s elementary lesions included erosions, fissures and whitish curd-like exudates similar to those observed in localized candidiasis. There was no clinical evidence for extracutaneous involvement. Thus, we hypothesized that candidiasis arose primarily from the patient’s dyskeratotic skin (possibly from her chronic lumbosacral fissures) and later spread into the rest of her skin, in the same way as does HSV in the course of Kaposi varicelliform eruption in patients with chronic skin barrier damage, including patients with DD.2,3 No fungal sample collection was performed at the patient’s admission; thus, it cannot be excluded that C. albicans infection occurred later in the course of hospitalization. Antibiotic therapies administered before and during hospitalization may have promoted fungal dissemination. Also, it is likely that longterm treatment with acitretin, at doses higher than usually recommended in patients with DD, might have exerted deleterious effects by increasing skin barrier impairment. No specific therapeutic guidelines apply to patients with extensive, isolated skin candidiasis. In our patient, we decided to combine topical and systemic azole therapy. Fluconazole dosage was empirically adapted from the treatment standard of invasive systemic candidiasis, namely loading charge of 800 mg then 400 mg daily, for at least 2 weeks after a demonstrated negative blood culture result or clinical signs of improvement.7 © 2014 British Association of Dermatologists
News and Notices 839
In conclusion, physicians should consider the possibility of diffuse cutaneous candidiasis in patients with DD presenting unexplained and/or refractory flare-ups, and look for suggestive clinical signs among which are confluent erosions and/or whitish exudates. Given its moderate financial cost, systematic skin swab sampling for fungal analysis may be useful in any patient with DD exacerbation. 1
Department of Dermatology, Lyon 1 University, Centre Hospitalier Lyon Sud, 69495 Pierre Benite Cedex, France 2 Universite Claude Bernard Lyon 1, 43 Bd 11 Novembre 1918 BP 761, 69622 Villeurbanne Cedex, France Correspondence: Luc Thomas. E-mail: [email protected]
L. WEILER1 N. POULALHON1 S. DEBARBIEUX1 L. THOMAS1,2
2 Pantazi V, Potouridou I, Katsarou A et al. Darier’s disease complicated by Kaposi’s varicelliform eruption due to herpes simplex virus. J Eur Acad Dermatol Venereol 2000; 14:209–11. 3 Sais G, Jucgla A, Curc o N, Peyrı J. Kaposi’s varicelliform eruption with ocular involvement. Arch Dermatol 1994; 130:1209–10. 4 Kandasamy R, Hecker M, Choi M, Pile J. Darier disease complicated by disseminated zoster. Dermatol Online J 2009; 15:65. 5 Haase O, Moser A, Rose C. Generalized cowpox infection in a patient with Darier disease. Br J Dermatol 2011; 164:1116–18. 6 Tatnall FM, Sarkany I. Darier’s disease complicated by Trichophyton rubrum infection. Arch Dermatol 1986; 122:623. 7 Pappas PG, Kauffman CA, Andes D et al. Clinical practice guidelines for the management of candidiasis: 2009 update by the Infectious Diseases Society of America. Clin Infect Dis 2009; 48:503–35. Funding sources: no external funding. Conflicts of interest: none declared.
References 1 Sakuntabhai A, Ruiz-Perez V, Carter S et al. Mutations in ATP2A2, encoding a Ca2 + pump, cause Darier’s disease. Nat Genet 1999; 21:271–7.
News and Notices DOI: 10.1111/bjd.13731 95th Annual Meeting of the British Association of Dermatologists 7th–9th July 2015, Manchester The 95th Annual Meeting of the British Association of Dermatologists will be held at the Manchester Central, 7th–9th July 2015, organised by Prof Irene Leigh, BAD Academic Vice-President. Abstracts of papers and posters should be submitted for consideration by the Scientific Committee. Original communications will be allotted 15 min, which must include time for discussion. Online submission will be the only method of abstract submission available. Full instructions and the submission form can be accessed via the BAD website www.bad.org.uk/annualmeeting The closing date for the receipt of abstracts is Monday 12th January 2015 and the deadline will be adhered to strictly. Any abstracts received after this date will not be considered. The deadline for abstract submissions to any of the special interest group meetings will be Monday 9th February 2015. Poster submissions on the following topics are strongly encouraged: audit, medical education, and service delivery. Conference & Event Services, British Association of Dermatologists, 4 Fitzroy Square, London, W1T 5HQ, UK or email [email protected] Ó 2015 British Association of Dermatologists
I was born in Waterloo, Belgium; moved to Israel in 1981; received my MD and PhD degrees from the Hebrew University of Jerusalem; specialized in dermatology at the Rambam Medical Center, Haifa; spent a post-doc fellowship at Thomas Jefferson University, Philadelphia; and became Chair of the department of Dermatology at the Tel Aviv Medical center in 2008 and Full Professor at the Tel Aviv University in 2010. My research focuses on the genetic basis of skin diseases. It has been an honor and a special pleasure for me to serve the BJD as section editor for the past 9 years. I look forward to contributing to the transformation the journal goes through as its new Section Editor for Translational Research. Eli Sprecher Department of Dermatology and Laboratory of Molecular Medicine, Tel Aviv Sourasky Medical Center, Tel Aviv, Israel I studied medicine at Oxford University and also completed an Oxford DM doctorate. During my subsequent dermatology training in South Wales I was awarded one of the first U.K. Dermatology Clinical Trials Network registrar fellowships and undertook an MSc in medical education. On qualifying as a dermatologist I became a clinical academic at Cardiff University in 2011. My main clinical and research interest is hidradenitis suppurativa (HS) and, in 2014, I was awarded a 5 year NISCHR fellowship to investigate HS epidemiology. My ultimate goal is to conduct clinical trials in HS to improve patient care. British Journal of Dermatology (2015) 172, pp805–840
