C. M. King
Royal Liverpool University Hospital
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Contact Dermatitis | 2009
Wolfgang Uter; Christiane Rämsch; Werner Aberer; Fabio Ayala; Anna Balato; Aiste Beliauskiene; Anna Belloni Fortina; Andreas J. Bircher; Jochen Brasch; M.M.U. Chowdhury; Pieter Jan Coenraads; Marielouise Schuttelaar; S. Cooper; Maria Teresa Corradin; Peter Elsner; John English; Manigé Fartasch; Vera Mahler; Peter J. Frosch; Thomas Fuchs; David J. Gawkrodger; Ana-Maria Gimènez-Arnau; C. Green; Helen L. Horne; Riitta Jolanki; C. M. King; Beata Kręcisz; Marta Kiec-Swierczynska; A.D. Ormerod; David Orton
Background: Continual surveillance based on patch test results has proved useful for the identification of contact allergy.
Contact Dermatitis | 2007
Cherng T. Jong; Barry N. Statham; C. Green; C. M. King; David J. Gawkrodger; Jane E. Sansom; John English; S. Mark Wilkinson; A.D. Ormerod; M.M.U. Chowdhury
Preservative sensitivity in the UK was last assessed in 2000. Given the changes in preservative usage, we have re‐evaluated our patch test data in order to detect any changes in the trend of sensitization. The results of patch testing using the extended British Contact Dermatitis Society Standard series were collected from 9 dermatology centres in the UK. Positive reactions to each of 10 preservative allergens were captured together with the MOAHFLA indices for each centre. In total, 6958 patients were tested during the period 2004–2005. The current data were compared with previously published data. Formaldehyde and methylchloroisothiazolinone/methyl‐isothiazolinone have the highest positivity rates at 2.0% and chloroxylenol the lowest at 0.2%. Parabens mix has the highest irritancy rate. Compared with the UK data in 2000, the positivity rate of imidazolidinyl urea (0.02 < P < 0.05) has significantly increased and that of methyldibromo glutaronitrile has significantly reduced (P < 0.001).
British Journal of Dermatology | 2014
H. Audrain; C. Kenward; C.R. Lovell; C. Green; A.D. Ormerod; Jane E. Sansom; M.M.U. Chowdhury; S. Cooper; G.A. Johnston; Mark Wilkinson; C. M. King; Natalie M. Stone; Helen L. Horne; C.R. Holden; S. Wakelin; D.A. Buckley
The oxidized forms of the fragrance terpenes limonene and linalool are known to cause allergic contact dermatitis. Significant rates of contact allergy to these fragrances have been reported in European studies and in a recent worldwide study. Patch testing to oxidized terpenes is not routinely carried out either in the U.K. or in other centres internationally.
Contact Dermatitis | 2002
P. D. Yesudian; C. M. King
Topical sunscreens are an essential armament for the protection of the human skin against acute and chronic adverse effects of solar radiation. All sunscreen groups have been reported to cause allergic reactions, which may be either contact or photocontact in nature (1). Contact urticarial reactions, however, are relatively rare (2). We report the occurrence of severe contact urticaria and anaphylaxis from benzophenone-3 (2-hydroxy 4methoxy benzophenone), a common sunscreen ingredient.
Contact Dermatitis | 2001
P. D. Yesudian; C. M. King
A 72-year-old woman presented with multiple Bowen’s disease on both shins, for which EfudixA cream was prescribed. She was instructed to use it 2¿ daily for 3 weeks and warned about its irritancy. Once the inflammation peaked, she was advised to stop using the cream for a week. She used the cream in this cyclical fashion (3 weeks on, 1 week off) for 5 months without any adverse effect. In the 7th cycle, she developed intense inflammation, more violent than previously encountered. FucibetA cream was commenced but led to further worsening. All treatment was stopped and patch testing performed.
Contact Dermatitis | 1993
N. Harowick; C. M. King
A 66-year-old man on haemodialysis for chronic renal failure (CRF) presented with widespread suberythrodermic eczema. 10 weeks previously, he had started erythropoietin EPO-P (Recormon®, Boehringer) 2000 units 3 x weekly subcutaneously (s.c.) for the anaemia of CRF. After 1 month, he had complained of generalized pruritus. 2 weeks later, he had developed an itchy maculopapular eczema. There was no local reaction at injection sites. His medications are listed in Table 1. Testosterone had been prescribed for its anabolic effect. There was no past or family history of atopy. Full blood count was normal, with no eosinophilia. Histology of i,nvolved skin showed a dermal infiltrate of ·lymphocytes, histiocytes, neutrophils and eosinophils, particularly around blood vessels, and foci of spongiosis and epidermal invasion by neutrophils and eosinophils, changes in keeping with drug-induced eczema. Patch testing was performed with the European standard series, a textile resins and dyes series, a series of topical corticosteroids, and aqueous EPO-p, 1000 u/ml. EPO was applied as reconstituted for injection, after tape stripping 15 x to enhance penetration. No reaction was obtained. Anti-EPO antibodies were assayed with a labelled EPO binding technique (1), and were not detected. Intradermal (i.d.) challenge with 100 units EPOp caused no immediate or delayed local reaction, but generalized pruritus developed 24 h after challenge. The patient was treated with potent topical corticosteroids as an inpatient, EPO and testosterone being discontinued. He improved rapidly, and maintained this improvement in spite of restarting testosterone. Rechallenge with EPO-IX (EPREX®, Cilag), 2000 units s.c., caused a relapse of dermatitis. This resolved on withholding further EPO.
British Journal of Dermatology | 2002
S. Sommer; S. M. Wilkinson; John English; David J. Gawkrodger; C. Green; C. M. King; S. Powell; Jane E. Sansom; S. Shaw
Summary Background Most studies investigating steroid allergy have been performed with tixocortol pivalate, hydrocortisone butyrate and budesonide. Betnovate® and Dermovate® are widely prescribed in the U.K. but little is known about the frequency of sensitization to them.
Contact Dermatitis | 1996
B. B. Tan; C. M. King
ably initially sensitized to sorbic acid in Biafine®, which he applied when first afflicted with perianal intertrigo, before the development of eczema. Sorbic acid is present naturally in several red fruits (cranberries, strawberries, currants), but may be synthesized for use as a preservative in certain foods (E200), or in medical or cosmetic products containing fatty acids or polyoxyethylene esters (3). In Europe, there is strict regulation of the sorbic aicd content of foods (4). Sorbic acid is mainly responsible for non-immunological contact urticaria of variable severity (5). Allergic contact dermatitis is also well-known, though less frequent (3). Its potential for allergic reaction to oral ingestion is less well-known, because sorbic acid is generally considered to be a harmless food additive (6). Reactivation of eczema in a patient sensitized to sorbic acid, provoked by the ingestion of cheese containing this preservative, has previously been reported (7). SHORT COMMUNICATIONS
Archive | 2008
Wolfgang Uter; Werner Aberer; Fabio Ayala; Aiste Beliauskiene; A. Belloni Fortina; Andreas J. Bircher; Jochen Brasch; M.M.U. Chowdhury; Pieter Jan Coenraads; Marie L. Schuttelaar; Peter Elsner; John English; Manigé Fartasch; Vera Mahler; Peter J. Frosch; Th. Fuchs; David J. Gawkrodger; Ana Giménez-Arnau; C. Green; Jeanne Duus Johansen; Torkil Menné; Riitta Jolanki; C. M. King; Beata Kręcisz; Marta Kiec-Swierczynska; Francesca Larese; A.D. Ormerod; David Orton; Tapio Rantanen; Thomas Rustemeyer
Contact Dermatitis | 1994
N. Hardwick; C. M. King