In-depth understanding of inflammatory skin diseases has greatly expanded during the last century. Clinical immunologists, dermatologists and immunobiologists paved the way for the rapidly expanding field of cutaneous immunology. Special forms of cutaneous inflammation are seen in so-called neutrophilic dermatoses and autoinflammatory skin diseases, both groups representing impressive examples of the fundamental diversity of innate immune diseases in human skin.1, 2 In domestic animals skin diseases mimicking neutrophilic dermatoses, for example, pustular and follicular disorders as well as various forms of acne have not been Iisted.3 In the following, we will focus on the micro invasion of neutrophils into epithelial structures (epidermis, hair follicles, sebaceous glands). The term 'neutrophilic dermatosis' (ND) was coined by dermatologists years before the discovery of autoinflammation. In 1991, Wallach4 collected several clinically heterogenous skin disorders, all of which showed neutrophils invading affected skin. Patients were presenting what was grossly called 'rash', acneiform papules-pustules, pustular lesions, neutrophilic plaques, subcorneal pustulosis, rare disorders such as Behcet's disease, and erythema elevatum diutinum. Further disorders included neutrophilic eccrine hidradenitis, bowel-associated dermatosis-arthritis syndrome, rheumatoid neutrophilic dermatitis, amicrobial pustulosis of the folds and generalized pustular psoriasis (Table 1).5 Also, non-healing ulcerous lesions as seen in pyoderma gangraenosum were listed. The histopathology of ND demonstrates predominance of neutrophils, near absence of dendritic cells, reduced B- and T-cell activation or autoantibodies as signs of adaptive immune reactivity. Overt signs of vasculitis are absent.6 FCAS, CINCA, TRAPS Blau syndrome In 1999, McDermott et al.7 described patients with recurrent fever and a multitude of symptoms due to genetic abnormalities or predisposition.8 The term autoinflammatory diseases (AID) was proposed for a series of clinical cases with an outstanding genetic defect and complexed clinical symptomatology.9-11 Signs of systemic inflammation dominated, and myeloid cells, for example, neutrophils, macrophages, mast cells and Langerhans cells played an important role. Because of clinical similarities and overlapping symptomatology, both ND and AID were recently proposed to be collectively called 'innate immune disorders' (showing various skin morphologies12). Considering the heterogeneity of clinical phenotypes collected under AID and ND, it is interesting to observe that a significant proportion of these disorders show cutaneous involvement. In a compilation of 26 autoinflammatory syndromes, Kalpana et al.13 identified a total of 18 entities demonstrating cutaneous changes. Surprisingly, half of these (n = 9) were pustular and acneiform lesions, while urticaria and urticaria-like rashes, various forms of exanthema, or disseminated papular or nodular inflammatory lesions were seen less often (n = 5). In eight autoinflammatory disorders listed by Hull et al.14 inflammatory changes in the deeper dermis were noted. The spectrum of clinical phenotypes included 'erysipeloid erythema' and urticaria-like maculopapular rash (FMF, HIDS), cold-induced urticaria (FCAS), urticaria-like plaques (CINCA), granulomatous rash (Blau syndrome), migratory erythema and (TRAPS13) (Table 1). In a carefully composed overview, Navarini et al.12 compared 22 diseases of the AID group with 18 ND disorders. Pustular lesions were described as common in all of the 18 ND patients, none were seen in AID.15 In recent reviews on AID and ND, epidermal and follicular alterations, namely pustules and acne, were noted as predominant cutaneous lesions.10-13 Acne lesions of variable severity are reported by Marzano et al.5 as constantly appearing features. Severe acne was commonly seen in combination with pyoderma gangraenosum (PG), pyogenic arthritis and suppurative hidradenitis (acne inversa). Next to skin changes, systemic disorders varied from arthritis, and intestinal and bone diseases (n = 9) often together with attacks of fever (n = 15). In a survey of monogenetic AID by Murphy and coworkers,15 pustules and acne lesions were seen more often as compared to urticaria and macular/papular rashes (Table 1). Taken together, predominant clinical skin lesions present in autoinflammatory and neutrophilic diseases include comedones, acneiforme and epidermal pustules and less frequent, urticarial rashes. Unfortunately, biopsy specimens sampled at the early stages of disease are rare. As revealed by gene expression profiles, Yang et al.16 recently observed a significant increase of neutrophils and activated mast cells as early as 48 h after onset of acne indicating neutrophilic microabscessing at the beginning. Early microfiltration of epidermis and follicular epithelia by myeloid cells at different sites may be noted to occur simultaneously. As an impressive example, SAPHO (Table 1) demonstrates follicular disease (plain acne at different degrees of severity including acne conglobata, acne fulminans, hidradenitis supp.), together with palmoplantar pustulosis in approximately 25% of patients.17-19 Interestingly PAPA appears as a nearly identical syndrome except that patients additionally are affected by pyoderma gangraenosum. In these syndromes, a pathogenetic principle (keratinocyte/epithelial-myeloid synergy (KMS))20 appears fundamental in expressing site-specific pathology: both epidermal (keratinocytes) and follicular epithelia are giving rise to either (epidermal) or (adnexal) chemoattraction of neutrophils. Neutrophilic microabscesses represent distinct cutaneous features in AID and ND. Initiation sites are (i) epidermis, forming pustules (or Munro abscesses) and (ii) follicle-bound neutrophilic microabscesses, generated in hair follicles or sebaceous gland ducts. A third group (iii) Table 1 includes exanthematous disorders, originating in the deeper dermis again dominated by neutrophilic infiltrates. These frequently resemble urticaria, often are associated with systemic disease and show genetic polymorphisms. Recurrent episodes of fever, and a variety of bone, gastrointestinal, mucous membrane, neurological and eye abnormalities4 heralding systemic diseases.15 Preferential comorbidity sites are musculo-skelettal sites, barrier organs. Clinical responses to dapsone, anakinra, TNFα- and IL-17- blockers are seen. During recent years, a growing number of neutrophilic dermatoses have widened our scope on the multiplicity of innate immune defence in human skin. Keratinocyte-myeloid synergism20 plays a principal role, periodicity with 'on-and-off' mechanisms. Microbial growth could play a role in determining secondary phenotypes, for example, folliculitis and papulo-pustules in acne, cysts, fistulae and non-healing ulcers in PG. Keratinocytes and follicular epithelial cells may act as sentinels, demonstrating susceptibility for microbial signals and danger molecules. Overreacting human skin pathology could be linked with the highly developed armentarium of antimicrobial defence provided by CIMADs as discussed by J. Schroeder.21 It needs to be seen to what extent antimicrobial immunity known in psoriasis drives immune hyper-responsiveness and in consequence also creates diseases. A significant number of closely related diseases now show a special expression of innate antimicrobial immune reactivity. None. The data that support the findings of this study are available from the corresponding author upon reasonable request.

Data results are available upon reasonable request to the corresponding author.

Pustules are among the most common lesions produced in human skin. Infections by pathogens and drug-induced reactions are frequent causes of pustule formation. In recent years immune-mediated pustular diseases have drawn attention. It is proposed to classify pustular diseases according to the initiating events and sites: purely epidermal pustules, follicular pustules or pustules noted in autoinflammatory syndromes. The unifying pathology in all of the three categories is a microinvasion of activated neutrophils into epidermal or adnexal epithelia. Formation of pustules involves established IL-17 / IL-23, IL-36 / IL-36RN driven pathology, or IL-1 /caspase-activated autoinflammation. Pathophysiology demonstrates an intriguing synergy of keratinocytes with neutrophils. This is called keratinocyte-myeloid synergy (KMS). Non-infectious pustules are formed by IFNα controlling the production of chemoattractants (IL-8, LTB4) or induced by IL-1-regulated inflammasomes and caspase/ IFNβ-induced chemotaxins. The presence of physical barriers, for example, cornified cell layers (str. corneum), is instrumental in establishing chemotactic gradients and blocking migrating neutrophils. In follicular KMS-driven pustular disorders, in contrast to epidermal pustules, neutrophil-mediated toxicity propagates lasting and expanding ulcerating diseases with increased levels of circulating immunoglobulin A (IgA). Complexed IgA is suggested to propagate ongoing pustular diseases. These are prerequisites essential for developing pustules in burdensome human skin diseases.

More often as compared to other barrier systems (gastrointestinal, urogenital, and respiratory linings) human skin over millions of years has been subject to fundamental changes in structure and function. When life on land started, the first changes consisted in the formation of a coherent impermeable stratum corneum. Two-legged locomotion was followed by loss of body hair and formation of sweat glands. Major changes took place after the agricultural revolution, investigating settlements with domestication of animals and plants. Living together after giving up nomadic life, hairless skin became a battlefield for pathogens, members of the skin microbiome, and arthropod visits. Human skin became exceptional in showing a boosted, highly developed immune system which is much more complex as compared to the "skins" of other species. A recently found skin disinfection system ("Cationic Intrinsically Disordered Antimicrobial Peptides, CIDAMPs") dates back to the origins of life and still is active in present-day integuments. As a skin-restricted and effective principle, keratinocyte- myeloid synergy (KMS) is recognized. As a consequence of such highly developed immune defense, the basic contributions of KMS - cells (keratinocytes, neutrophils, macrophages) in regulating innate immunity is emphasized. Antimicrobial peptides and chemokines became major keratinocyte products. The formation of impermeable str. corneum membrane has enabled KMS - cells to accumulate within upper skin levels and cause a special group of human skin diseases, pustular dermatoses.

JDDG: Journal der Deutschen Dermatologischen GesellschaftVolume 18, Issue 12 p. 1533-1533 Nachrufe Wolfram Sterry –in memoriam Enno Christophers, Corresponding Author echristophers@dermatology.uni-kiel.de Korrespondenzanschrift Prof. Dr. Dr. h.c. Enno Christophers Wulfshagen 11 24214 Tüttendorf E-Mail: echristophers@dermatology.uni-kiel.deSearch for more papers by this author Enno Christophers, Corresponding Author echristophers@dermatology.uni-kiel.de Korrespondenzanschrift Prof. Dr. Dr. h.c. Enno Christophers Wulfshagen 11 24214 Tüttendorf E-Mail: echristophers@dermatology.uni-kiel.deSearch for more papers by this author First published: 29 December 2020 https://doi.org/10.1111/ddg.14343_gRead the full textAboutPDF ToolsRequest permissionExport citationAdd to favoritesTrack citation ShareShare Give accessShare full text accessShare full-text accessPlease review our Terms and Conditions of Use and check box below to share full-text version of article.I have read and accept the Wiley Online Library Terms and Conditions of UseShareable LinkUse the link below to share a full-text version of this article with your friends and colleagues. Learn more.Copy URL Share a linkShare onEmailFacebookTwitterLinked InRedditWechat No abstract is available for this article. Volume18, Issue12December 2020Pages 1533-1533 RelatedInformation

Psoriasis may express as active severe disease or as mild stable disease. In particular, patients with active severe disease present systemic involvement, including comorbidities and increased values of parameters reflecting an active state of innate immunity. In contrast, patients with mild stable disease show a dominancy of acquired immunity. In this review article, we report the clinical aspects of disease manifestations of both active and quiescent psoriasis as well as the immunological aspects, as well as the impact on antimicrobial resistance. The activity of psoriasis is not captured in the present outcome measures for severity assessment. The present review suggests that incorporating disease activity may be important in the assessment of the efficacy of treatments.

Journal of the European Academy of Dermatology and VenereologyVolume 33, Issue 2 p. 260-262 Historical Perspectives Pioneers in dermatology and venereology: an interview with Prof. Enno Christophers E. Christophers, Corresponding Author E. Christophers echristophers@dermatology.uni-kiel.de Department of Dermatology, University of KielCorrespondence: E. Christophers. E-mail: echristophers@dermatology.uni-kiel.deSearch for more papers by this author E. Christophers, Corresponding Author E. Christophers echristophers@dermatology.uni-kiel.de Department of Dermatology, University of KielCorrespondence: E. Christophers. E-mail: echristophers@dermatology.uni-kiel.deSearch for more papers by this author First published: 11 February 2019 https://doi.org/10.1111/jdv.15436Read the full textAboutPDF ToolsRequest permissionExport citationAdd to favoritesTrack citation ShareShare Give accessShare full text accessShare full-text accessPlease review our Terms and Conditions of Use and check box below to share full-text version of article.I have read and accept the Wiley Online Library Terms and Conditions of UseShareable LinkUse the link below to share a full-text version of this article with your friends and colleagues. Learn more.Copy URL Share a linkShare onFacebookTwitterLinkedInRedditWechat No abstract is available for this article. Volume33, Issue2February 2019Pages 260-262 RelatedInformation

Polymorphonuclear leukocytes (PMNs) are highly motile mammalian cells, which tend to migrate to the sites of tissue injury or inflammation. In psoriasis the presence of large numbers of PMNs within the diseased epidermis is well recognized and has been repeatedly emphasized. In most studies on PMN chemotaxis randomized groups of patients with psoriasis were investigated. Of great importance appears to be the demonstration of chemotactic factors in psoriatic epidermis. Reasons for the enhancement of directed PMN migration with autologous serum in psoriasis could be based upon differences in enzyme liberation by psoriatic PMNs. Psoriasis is diagnosed by the morphology of the skin lesions rather than the biologic dynamics of the tissue changes leading to gross pathology. In addition to the identification of chemotactic factors it is of importance to study the factor(s) which inhibit or inactivate the additional chemotactic activity in the upper epidermis.

A 37-year-old Bulgarian woman presented with a three-year-history of multiple, reddish-purple, ulcerated plaques and nodules, distributed symmetrically over the extensor surfaces of the extremities and gluteal region (Figure 1 ). Upon examination of the oropharyngeal cavity, a large painful ulcer extending from the entire right tonsillar area into the soft palate was detected (Figure 1 ). The patient reported diffuse arthralgia and marked reduction of her general health with weakness and weight loss (BMI 16.0 kg/m 2 ). Laboratory investigations included differential blood count, renal and hepatic function, ferritin, transferrin, electrolytes, LDH, erythrocyte sedimentation rate (ESR), CRP, serological tests for viral and bacterial agents (including hepatitis B and C, HIV, CMV, EBV, QuantiFERON-TB and TPPA), dsDNA antibodies, antineutrophil cytoplasmic antibodies (ANCAs), anticardiolipin antibodies, lupus anticoagulant, cryoglobulins, rheumatoid factor, anti-Dsg1, anti-Dsg3, anti-BP180 and anti-BP230 antibodies. Results were all within the normal range. Normal or negative tests also included urinalysis and HLA typing for Behçet’s disease (HLA-B51). The only abnormal laboratory fi nding was an IgA monoclonal gammopathy, type IgA lambda as detected by immunofi xation. The patient underwent a bone marrow biopsy and plasma cell dyscrasia was excluded. Further diagnostic investigations including gastroscopy, colonoscopy, computed tomography (CT) of the neck, chest and abdomen, echocardiography and pulmonary function tests did not reveal any abnormalities. Skin biopsies from lesional plaques showed a perivascular and interstitial dermal infi ltrate consisting of neutrophils and, to a lesser extent, mononuclear cells and eosinophils (Figure 2 a). Signs of leukocytoclastic vasculitis with endothelial swelling, deposits of eosinophilic fi brinoid material and leukocytoclasia were seen (Figure 2 b). Biopsies were repeatedly taken from the tonsillar area. These all showed

JDDG: Journal der Deutschen Dermatologischen GesellschaftVolume 16, Issue 6 p. 817-818 Nachruf In Memoriam Professor Dr. Dr. h. c. mult. Otto Braun-Falco Enno Christophers, Corresponding Author Enno Christophers echristophers@dermatology.uni-kiel.de Korrespondenzanschrift Prof. Dr. Dr. h.c. Enno Christophers FRCP Wulfshagen 11 24214 Tüttendorf E-mail: echristophers@dermatology.uni-kiel.deSearch for more papers by this author Enno Christophers, Corresponding Author Enno Christophers echristophers@dermatology.uni-kiel.de Korrespondenzanschrift Prof. Dr. Dr. h.c. Enno Christophers FRCP Wulfshagen 11 24214 Tüttendorf E-mail: echristophers@dermatology.uni-kiel.deSearch for more papers by this author First published: 05 June 2018 https://doi.org/10.1111/ddg.13542Read the full textAboutPDF ToolsRequest permissionExport citationAdd to favoritesTrack citation ShareShare Give accessShare full text accessShare full-text accessPlease review our Terms and Conditions of Use and check box below to share full-text version of article.I have read and accept the Wiley Online Library Terms and Conditions of UseShareable LinkUse the link below to share a full-text version of this article with your friends and colleagues. Learn more.Copy URL Share a linkShare onFacebookTwitterLinkedInRedditWechat No abstract is available for this article. Volume16, Issue6June 2018Pages 817-818 RelatedInformation

JDDG: Journal der Deutschen Dermatologischen GesellschaftVolume 16, Issue 5 p. 616-619 Clinical Letter Erythema elevatum diutinum verbunden mit schwerer oropharyngealer Ulzeration und Pyoderma gangraenosum Rainer Hügel, Corresponding Author Rainer Hügel rainerhuegel@hotmail.com Universitätsklinik für Dermatologie und Venerologie, Medizinische Universität Graz, Österreich Korrespondenzanschrift Priv.-Doz. Dr. med. Rainer Hügel Universitätsklinik für Dermatologie Medizinische Universität Graz Auenbruggerplatz 8 8036 Graz, Österreich E-mail: rainerhuegel@hotmail.comSearch for more papers by this authorJochen Brasch, Jochen Brasch Klinik für Dermatologie, Venerologie und Allergologie, Universitätsklinikum Schleswig-Holstein, Campus Kiel, DeutschlandSearch for more papers by this authorIvelina Yordanova, Ivelina Yordanova Abteilung für Dermatologie und Venerologie, Medizinische Fakultät, Medizinische Universität Plewen, BulgarienSearch for more papers by this authorJohann Oltmann Schröder, Johann Oltmann Schröder Exzellenzzentrum Entzündungsmedizin, Universitätsklinikum Schleswig-Holstein, Campus Kiel, DeutschlandSearch for more papers by this authorAsita Fazel, Asita Fazel Klinik für Hals-, Nasen-, Ohrenheilkunde, Kopf- und Halschirurgie, Universitätsklinikum Schleswig-Holstein, Campus Kiel, DeutschlandSearch for more papers by this authorRegine Gläser, Regine Gläser Klinik für Dermatologie, Venerologie und Allergologie, Universitätsklinikum Schleswig-Holstein, Campus Kiel, DeutschlandSearch for more papers by this authorThomas Schwarz, Thomas Schwarz Klinik für Dermatologie, Venerologie und Allergologie, Universitätsklinikum Schleswig-Holstein, Campus Kiel, DeutschlandSearch for more papers by this authorEnno Christophers, Enno Christophers Klinik für Dermatologie, Venerologie und Allergologie, Universitätsklinikum Schleswig-Holstein, Campus Kiel, DeutschlandSearch for more papers by this author Rainer Hügel, Corresponding Author Rainer Hügel rainerhuegel@hotmail.com Universitätsklinik für Dermatologie und Venerologie, Medizinische Universität Graz, Österreich Korrespondenzanschrift Priv.-Doz. Dr. med. Rainer Hügel Universitätsklinik für Dermatologie Medizinische Universität Graz Auenbruggerplatz 8 8036 Graz, Österreich E-mail: rainerhuegel@hotmail.comSearch for more papers by this authorJochen Brasch, Jochen Brasch Klinik für Dermatologie, Venerologie und Allergologie, Universitätsklinikum Schleswig-Holstein, Campus Kiel, DeutschlandSearch for more papers by this authorIvelina Yordanova, Ivelina Yordanova Abteilung für Dermatologie und Venerologie, Medizinische Fakultät, Medizinische Universität Plewen, BulgarienSearch for more papers by this authorJohann Oltmann Schröder, Johann Oltmann Schröder Exzellenzzentrum Entzündungsmedizin, Universitätsklinikum Schleswig-Holstein, Campus Kiel, DeutschlandSearch for more papers by this authorAsita Fazel, Asita Fazel Klinik für Hals-, Nasen-, Ohrenheilkunde, Kopf- und Halschirurgie, Universitätsklinikum Schleswig-Holstein, Campus Kiel, DeutschlandSearch for more papers by this authorRegine Gläser, Regine Gläser Klinik für Dermatologie, Venerologie und Allergologie, Universitätsklinikum Schleswig-Holstein, Campus Kiel, DeutschlandSearch for more papers by this authorThomas Schwarz, Thomas Schwarz Klinik für Dermatologie, Venerologie und Allergologie, Universitätsklinikum Schleswig-Holstein, Campus Kiel, DeutschlandSearch for more papers by this authorEnno Christophers, Enno Christophers Klinik für Dermatologie, Venerologie und Allergologie, Universitätsklinikum Schleswig-Holstein, Campus Kiel, DeutschlandSearch for more papers by this author First published: 11 May 2018 https://doi.org/10.1111/ddg.13508_gAboutPDF ToolsRequest permissionExport citationAdd to favoritesTrack citation ShareShare Give accessShare full text accessShare full-text accessPlease review our Terms and Conditions of Use and check box below to share full-text version of article.I have read and accept the Wiley Online Library Terms and Conditions of UseShareable LinkUse the link below to share a full-text version of this article with your friends and colleagues. Learn more.Copy URL Share a linkShare onFacebookTwitterLinkedInRedditWechat Volume16, Issue5May 2018Pages 616-619 RelatedInformation

JDDG: Journal der Deutschen Dermatologischen GesellschaftVolume 15, Issue 7 p. 774-774 Nachrufe In memoriam Stefania Jabłon´ska 1920–2017 Enno Christophers, Corresponding Author Enno Christophers echristophers@dermatology.uni-kiel.de Kiel Korrespondenzanschrift Prof. Dr. med. Dr. h. c. Enno Christophers FRCP Tibarg 7–9 22459 Hamburg Tel. 040 / 58 51 82 E-mail: echristophers@dermatology.uni-kiel.deSearch for more papers by this authorGerd Plewig, Gerd Plewig MünchenSearch for more papers by this author Enno Christophers, Corresponding Author Enno Christophers echristophers@dermatology.uni-kiel.de Kiel Korrespondenzanschrift Prof. Dr. med. Dr. h. c. Enno Christophers FRCP Tibarg 7–9 22459 Hamburg Tel. 040 / 58 51 82 E-mail: echristophers@dermatology.uni-kiel.deSearch for more papers by this authorGerd Plewig, Gerd Plewig MünchenSearch for more papers by this author First published: 04 July 2017 https://doi.org/10.1111/ddg.13263Read the full textAboutPDF ToolsRequest permissionExport citationAdd to favoritesTrack citation ShareShare Give accessShare full text accessShare full-text accessPlease review our Terms and Conditions of Use and check box below to share full-text version of article.I have read and accept the Wiley Online Library Terms and Conditions of UseShareable LinkUse the link below to share a full-text version of this article with your friends and colleagues. Learn more.Copy URL Share a linkShare onFacebookTwitterLinkedInRedditWechat No abstract is available for this article. Volume15, Issue7July 2017Pages 774-774 RelatedInformation

JDDG: Journal der Deutschen Dermatologischen GesellschaftVolume 14, Issue 4 p. 448-448 Tagesnotizen Tagesnotizen Enno Christophers, Enno Christophers Kiel Peter Altmeier, BochumSearch for more papers by this author Enno Christophers, Enno Christophers Kiel Peter Altmeier, BochumSearch for more papers by this author First published: 29 March 2016 https://doi.org/10.1111/ddg.12968 Korrespondenzanschrift Prof. Dr. med. Dr. h. c. Enno Christophers Tibarg 7-9 22459 Hamburg E-mail: echristophers@dermatology.uni-kiel.de Read the full textAboutPDF ToolsRequest permissionExport citationAdd to favoritesTrack citation ShareShare Give accessShare full text accessShare full-text accessPlease review our Terms and Conditions of Use and check box below to share full-text version of article.I have read and accept the Wiley Online Library Terms and Conditions of UseShareable LinkUse the link below to share a full-text version of this article with your friends and colleagues. Learn more.Copy URL Share a linkShare onFacebookTwitterLinkedInRedditWechat No abstract is available for this article. Volume14, Issue4April 2016Pages 448-448 RelatedInformation

BACKGROUND:First studies have shown that juvenile psoriasis is associated with an increased prevalence of comorbidity.OBJECTIVES:We carried out a data analysis to characterise the profiles of comorbidity in children with psoriasis and atopic eczema.METHODS:Prevalence data were derived from the database of a German statutory health insurance company according to ICD-10 codes L40 (psoriasis) and L20 (atopic eczema) of children up to 18 years insured in 2009.RESULTS:Data sets included 1.64 million persons and 293,181 children. 1,313 children = 0.45% (0.42-0.47) had a diagnosis of psoriasis and 30,354 = 10.35% (10.24-10.47) had a diagnosis of atopic eczema. Obesity, hyperlipidaemia, arterial hypertension and diabetes were more often diagnosed in children with psoriasis in comparison to all children without psoriasis and to those with atopic eczema.CONCLUSION:Children with psoriasis and atopic eczema show different and specific patterns of comorbidity which should be detected early and treated adequately.

Journal Article Impact of early vs. late disease onset on treatment response to etanercept in patients with psoriasis Get access C.E.M. Griffiths, C.E.M. Griffiths Dermatology Centre Manchester Academic Health Science Centre Salford Royal Hospital University of Manchester M6 8HD Manchester U.K Search for other works by this author on: Oxford Academic Google Scholar E. Christophers, E. Christophers University of Kiel Kiel Germany Search for other works by this author on: Oxford Academic Google Scholar A. Szumski, A. Szumski Specialty Care Pfizer Inc Collegeville PA U.S.A Search for other works by this author on: Oxford Academic Google Scholar H. Jones, H. Jones Specialty Care Pfizer Inc Collegeville PA U.S.A Search for other works by this author on: Oxford Academic Google Scholar L. Mallbris L. Mallbris Specialty Care Pfizer Inc Collegeville PA U.S.A Search for other works by this author on: Oxford Academic Google Scholar British Journal of Dermatology, Volume 173, Issue 5, 1 November 2015, Pages 1271–1273, https://doi.org/10.1111/bjd.13865 Published: 01 November 2015