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July 2011

Double Trouble: Therapeutic Challenges in Patients With Both Juvenile Dermatomyositis and Psoriasis

Author Affiliations

Author Affiliations: Department of Dermatology (Drs Kim and Lio) and Division of Rheumatology, Children's Memorial Hospital (Dr Pachman), Northwestern University Feinberg School of Medicine, Chicago, Illinois; Center of Excellence in Clinical Immunology, Children's Memorial Research Center, Chicago (Ms Morgan and Dr Pachman); and Division of Pediatric Rheumatology, University of Oklahoma Health Sciences Center, Oklahoma City (Dr Jarvis).

Arch Dermatol. 2011;147(7):831-835. doi:10.1001/archdermatol.2011.49

Background Juvenile dermatomyositis (JDM) and psoriasis are inflammatory disorders that share interferon- α induced responses and dysregulation of cytokines, including tumor necrosis factor alpha. Although 13% of patients with JDM have a family history of psoriasis there is little information concerning children with JDM and psoriasis.

Observations We identified 3 children with both JDM and psoriasis. In 2 cases, psoriatic lesions occurred after the child's JDM symptoms had diminished following effective immunosuppressive therapy (high-dose intermittent intravenous methylprednisolone, methotrexate, and low dose oral corticosteroids). Patient 2, initially diagnosed as having psoriasis, was treated with prednisone and methotrexate but then developed classic JDM, which worsened following use of tumor necrosis factor alpha inhibitor and reduction of prednisone and methotrexate dosage. For each child, their history of JDM complicated the choice of therapy for psoriasis.

Conclusions Two therapies commonly used to treat psoriasis —phototherapy and tumor necrosis factor-alpha antagonists —must be used with caution in patients with both JDM and psoriasis owing to their potential to exacerbate clinical manifestations of JDM. We discuss the implications affecting treatment of children with these dual diagnoses and consider the pathophysiology linking these 2 conditions.

Juvenile dermatomyositis (JDM) is a vasculopathy associated with proximal muscle weakness and characteristic skin manifestations, including heliotrope sign over the eyelids, often with microvascular dilation, and Gottron's papules over extensor joint surfaces.1 Although JDM is the most common inflammatory myopathy of childhood, it is classified as a rare disease, with an incidence of 3.2 children per million in the United States.2 Photosensitivity, particularly to UV-B light,3 as well as a response to possible microbial antigens4-9 and other factors in the environment10 have all been implicated as potential triggers for development of idiopathic inflammatory myopathy in the setting of a genetically susceptible host.11-13 Although the etiology of JDM remains unknown, it is clear that disease pathophysiology involves the exuberant induction of interferon alpha (IFN- α) –induced genes,5,6 increased serum IFN- α activity early in the disease course,14 accompanied by localization of both IFN- α –induced proteins and mature plasmacytoid dendritic cells in the diagnostic muscle15 and skin biopsy specimens16 of children with untreated JDM. In addition, the inflammatory cytokine, tumor necrosis alpha (TNF- α) contributes to the inflammatory process.17-20

Psoriasis in childhood often occurs in the setting of a positive familial history and is an inflammatory disorder that primarily affects the skin. It is a disease of keratinocyte hyperproliferation typically characterized by well-defined erythematous papules and plaques with silvery scale. The true incidence of childhood psoriasis is unknown; however, psoriasis prevalence is estimated at 2.2% in the United States,21 and 31.5% of patients experience disease onset before age 16 years.22 As in JDM, despite many hypotheses, no specific etiology has been identified,23,24 and, similar to JDM, IFN- α has been implicated in psoriasis disease pathophysiology in association with activation of plasmacytoid predendritic cells.25 Review of over 304 cases of children with definite or probable JDM at our center has shown that approximately 13% of patients with JDM also have a family history of psoriasis by self-report,26 but review of the literature reveals only a few case reports of adults with a history of both conditions.27,28 Herein, we present the case histories of 3 children with both JDM and biopsy-proven psoriasis. We will discuss the pathophysiology of these illnesses and the challenges in managing these patients.


The following 3 case histories were obtained by retrospective medical chart review of children with inflammatory myopathy attending the Juvenile Myositis Clinic, examined by 1 investigator (L.M.P.) at Children's Memorial Hospital (CMH), Chicago, Illinois, using a standardized database format at the time of diagnosis.

The diagnosis of JDM was made using the criteria of Bohan and Peter in 1975.29 One of the 3 patients (case 1) met at least 3 criteria (plus the cutaneous eruption) of the following major criteria to make a “definite ” diagnosis of JDM: (1) symmetric, proximal muscle weakness; (2) positive findings from a muscle biopsy specimen for inflammation; (3) elevated serum skeletal-muscle enzyme levels (ie, creatine kinase, aldolase, aspartate aminotransferase, lactate dehydrogenase); (4) positive results from electromyography; and (5) pathognomonic dermatologic features of dermatomyositis (including heliotropic sign, periorbital edema, and Gottron's papules) (Table). In addition, all children had characteristic nail fold capillary changes on microscopy with loss of end row loops and capillary dilation.30,31 Decreased muscle strength and endurance was assessed by the Childhood Myositis Assessment Scale (CMAS)32 in cases 2 and 3 (it was not available when the diagnosis was made in case 1). Two patients (cases 2 and 3) met at least 2 (plus the “characteristic ” heliotrope sign and Gottron's papules) of the diagnostic criteria sufficiently to make a “probable ” diagnosis of JDM.

Table. Clinical Laboratory Information at Time of Juvenile Dermatomyositis (JDM) and Psoriasis Diagnosis
Table. Clinical Laboratory Information at Time of Juvenile Dermatomyositis (JDM) and Psoriasis Diagnosis
Table. Clinical Laboratory Information at Time of Juvenile Dermatomyositis (JDM) and Psoriasis Diagnosis

Report of cases

Case 1

An 8-year-old, previously healthy, untreated white girl with a family history of psoriasis and vitiligo presented with symmetrical, proximal muscle weakness and a heliotrope sign. Laboratory data, magnetic resonance imaging (MRI), and MRI-directed biopsy pathology were consistent with JDM. She was treated with intravenous methylprednisolone, 30.0 mg/kg, with a 1-g maximum dosage on several occasions until her muscle enzyme levels normalized, in conjunction with oral prednisone, 0.5 mg/kg/d, and did well, eventually discontinuing all steroid therapy after 2 years of treatment. She remained free of symptoms for 9 years. At age 18 years, she developed a new cutaneous eruption of thick, scaly, erythematous plaques on her legs and elbows. Otherwise, she had no JDM symptoms, evidence of activation on laboratory testing, or arthritis. Findings from a skin biopsy specimen confirmed these new skin lesions as psoriasis, and a trial of methotrexate by mouth was initiated. All of her other indicators of immune activation returned to normal limits. She improved with methotrexate and topical corticosteroids but continues to have significant plaque psoriasis.

Case 2

A 7-year-old, Native American/white girl with a family history of psoriasis was diagnosed as having the cutaneous manifestations of psoriasis. She was treated with topical agents, including fluocinolone acetonide, clobetasol propionate, fluocinonide, and hydrocortisone, with improvement. She then developed proximal small joint arthritis, which was partially responsive to oral prednisone and subcutaneous methotrexate. Ten months after the onset of her psoriasis cutaneous manifestations, she presented with periorbital edema, cutaneous erythema, and vascular changes typical of JDM, proximal muscle weakness, early fatigue, and elevated muscle enzyme levels consistent with a diagnosis of JDM. She was started on treatment with etanercept, but the oral steroid and methotrexate were tapered followed by worsening of her skin and muscle symptoms. She was referred to CMH for further evaluation. At CMH, findings from a skin biopsy specimen then confirmed that the predominate pattern was that of psoriasis, but there was also a concomitant increase in mucin, typical of cutaneous dermatomyositis (Figure). A muscle biopsy was not performed. Etanercept therapy was discontinued; she was given intermittent high-dose intravenous methylprednisolone, 30 mg/kg; low-dose (0.5 –mg/kg/d) oral prednisone, and subcutaneous methotrexate, 25 mg/M2; followed by mycophenolate mofetil, 20 mg/kg, divided every 12 hours, and cyclosporine to obtain a therapeutic blood level of 80 to 100 mg/mL with improvement in her symptoms.

Figure. Prominent dermal deposition of mucin, characteristic of juvenile dermatomyositis (JDM) in a child (case 3) with both JDM and psoriatic active lesions.

Figure. Prominent dermal deposition of mucin, characteristic of juvenile dermatomyositis (JDM) in a child (case 3) with both JDM and psoriatic active lesions.

Case 3

A 2-year-old, previously healthy, untreated white girl had an extensive family history of hypothyroidism, as well as systemic lupus erythematosus. She presented with Gottron's papules on the hands, dilated eyelid capillaries, palatal erythema, and nail fold capillary end row loops, which were both dilated and markedly decreased in number. A diagnosis of JDM was made when these cutaneous manifestations had been present for more than 6 months. The MRI images of the proximal muscles documented minimal involvement, and the CMAS was abnormal for her age. The child was given high-dose, intermittent methylprednisone supplemented with low-dose oral prednisone on the days she did not receive the intermittent methylprednisone, and subcutaneous weekly methotrexate, 25 mg/m2, with gradual tapering of the steroids, once her cutaneous symptoms improved. During this taper, the child developed numerous red, scaly papules and plaques on her scalp, face, chest, back, and legs. Findings from a biopsy of a lesion was diagnostic for psoriasis. She has responded to topical therapies, including mometasone ointment, alclometasone dipropionate ointment, and fluocinonide solution, and the psoriatic lesions have cleared. Currently, all medication has been discontinued and she is symptom free.


Despite the rarity of reports of patients with both dermatomyositis and psoriasis,27,28 we present the cases of 3 children with this dual diagnosis. It is significant that the type 1 interferon pathways are shared by both psoriasis and JDM and with a spectrum of autoimmune diseases.5,24,33 It is not known if the young age of the children in this report is an added risk factor, in addition to a strong family history that was positive for autoimmune disease, which facilitated the expression of both JDM and psoriasis.

There is ample evidence that TNF- α and interferon α/ β (IFN- α/ β) may play an important role in the pathogenesis of JDM.5,6,17-20 Patients with JDM have an increased frequency of the A polymorphism at the TNF- α-308 promoter region compared with controls.17 This polymorphism is associated with increased production of TNF- α by peripheral blood mononuclear cells in both the unstimulated and stimulated state, as well as resistance to therapy with resultant disease chronicity.17 Findings from muscle biopsy specimens from adult patients with dermatomyositis showed increased levels of TNF- α and its receptors,18 and TNF- α is produced by the muscle fibers themselves in children with JDM.19 One speculation is that viral or microbial antigen(s) may stimulate an IFN- α/ β –induced response, spreading to increase IFN- γ activity, which may be augmented by the local production of TNF- α.20 Though environmental and histocompatibility features seem be associated with JDM susceptibility, the TNF- α-308A polymorphism seems to be associated with disease severity and chronicity.17

The pathogenesis of psoriasis involves many of the same inflammatory pathways as JDM. In psoriasis, the IFN- γ, TNF- α, and IFN- α/ β signaling pathways were shown to be activated in the lesions of patients with psoriasis.26,34 In addition, psoriatic lesions contained plasmacytoid predendritic cells expressing high levels of IFN- α.35 These dendritic cells may also induce cytokines interleukin (IL)-23 and IL-20, which can activate T cells and keratinocytes, respectively. An imbalance of these cytokines is believed to disrupt the regulation of keratinocyte proliferation, leading to the hyperproliferation seen in psoriatic lesions.23

As suggested by the shared cytokine pathways in both JDM and psoriasis, there is a great deal of overlap between the treatment options available for these conditions. The topical steroids, systemic methotrexate, and cyclosporine used as successful treatment options for psoriasis36 can also be used effectively in patients with JDM,37 but currently, the usual dosage of these medications differ for JDM and psoriasis. The occurrence of both illnesses with similar pathways raises the distinct possibility of developing a single effective regimen for both clinical problems in the future. However, at the moment, there are 2 effective therapeutic approaches, discussed herein, that must be viewed with special consideration when treating patients with both psoriasis and JDM.

Phototherapy is the therapeutic use of UV radiation and is currently an integral treatment option for adult patients with moderate to severe psoriasis,38 and narrowband UV-B is well tolerated and effective in the pediatric population as well.39 A study of 68 pediatric patients with psoriasis showed a response —defined as a greater than 75% improvement in the cutaneous psoriasis —in over 90% of the patients.40 In another study of 20 children with psoriasis, 80% of patients sustained at least a 50% reduction in their Psoriatic Area Severity Index (PASI) score.41 Although phototherapy is generally reserved for older children and adolescents with widespread disease who have failed topical treatments, approximately 8% of children with psoriasis require phototherapy or systemic therapies.42

In contrast, children with JDM are advised to practice strict photoprotective behaviors owing to the sunlight's ability to aggravate the cutaneous features of JDM. Patients can experience worsening of their cutaneous inflammation and provocation of new skin lesions with sunlight exposure, particularly to UV-B light.3 Therefore, they are advised to avoid direct sunlight as well as artificial forms of UV light.

UV-B phototherapy is thus contraindicated in children with dual diagnoses of psoriasis and JDM. Though it is emerging as a useful and well-tolerated treatment for childhood psoriasis, the potentially detrimental effects it may have for those with JDM raise considerable concerns for patients with both diseases.

TNF- α is a proinflammatory cytokine associated with the pathophysiology of many inflammatory conditions, including psoriasis and JDM.43 Targeting this marker of inflammation, TNF- α antagonists have been used for management of a range of autoimmune diseases.44 Currently, 3 TNF- α antagonists are available for use in the pediatric population: infliximab, etanercept, and adalimumab.

Infliximab and etanercept have been reported (case reports) as successful therapies for children and adolescents with severe psoriasis.45-48 In psoriasis, TNF- α antagonists are used with the observation that elevated levels of serum and lesional TNF- α decrease following clinically effective psoriasis treatment. This suggests that the inflammatory effect of this cytokine is an important key to the progression of the disease, although it is well recognized that in some cases of psoriasis, inhibition of TNF- α is associated with florid disease flares,49 and in other instances, the development of a spectrum of autoimmune diseases.50

Although JDM is an inflammatory process also involving TNF- α, the safety and efficacy of TNF- α antagonists in these patients is questionable. Some case reports have described favorable clinical improvement in adult patients with dermatomyositis who have been treated with TNF- α antagonists51,52; however, there are also patients who showed exacerbation of disease with these agents. In a study of adult patients with refractory myopathies, 2 of 5 patients with polymyositis and 1 of 4 patients with dermatomyositis experienced disease flare with worsening muscle fatigue and increased creatine kinase levels after treatment with infliximab.53 In addition, in the same study, 2 of 3 patients enrolled in a myositis study who had initial improvement in disease symptoms actually had disease flares when infliximab was used as an extended treatment.53 In a case series of 5 adult patients with dermatomyositis treated with etanercept, all patients experienced worsening of their disease with muscle weakness and elevation of creatine kinase and lactate dehydrogenase levels.54

The mechanism of increased inflammation in some conditions treated with TNF- α antagonists is not established. A cross-regulatory suppression of TNF- α on the production of IFN- α has been proposed, which allows some IFN- α –associated autoimmune disorders to emerge or flare when patients are treated with TNF- α antagonists.55 Although the mechanism of interaction is not well defined, inhibitors of TNF- α may be useful to control the symptoms of psoriasis, once evidence of IFN- α activity has abated. This may be possible because serum IFN- α activity seems to be elevated for a relatively short time when there is active inflammation, but the levels of TNF- α seem to be elevated over time.14,56 The use of TNF- α antagonists, such as etanercept, is increasing in frequency in the population of pediatric patients with psoriasis. Clinical studies show efficacy and a relatively safe profile in children with moderate to severe psoriasis.48 However, owing to the potential for promoting a JDM flare, these TNF- α antagonists should be used with caution in patients with both psoriasis and JDM. Discussion of these therapies emphasizes the complications that may arise when treating patients with both psoriasis and JDM. It is clear that some modalities used to treat one disease may exacerbate the symptoms of the other. Clinicians who encounter and treat patients with both JDM and psoriasis should be aware of the potential risks associated with the use of UV-B therapy and TNF- α antagonists in these unique cases.

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Article Information

Correspondence: Lauren M. Pachman, MD, Center of Excellence in Clinical Immunology, Children's Memorial Research Center, 2300 Children's Plaza, Box 212, Chicago, IL 60614-3363 (pachman@northwestern.edu).

Accepted for Publication: December 25, 2010.

Published Online: March 21, 2011. doi:10.1001/archdermatol.2011.49

Author Contributions: All authors had full access to all of the data in the study and take responsibility for the integrity of the data and the accuracy of the data analysis. Study concept and design: Kim, Lio, and Pachman. Acquisition of data: Kim, Morgan, Jarvis, Lio, and Pachman. Analysis and interpretation of data: Kim, Morgan, Lio, and Pachman. Drafting of the manuscript: Kim and Pachman. Critical revision of the manuscript for important intellectual content: Morgan, Jarvis, Lio, and Pachman. Obtained funding: Pachman. Administrative, technical, and material support: Morgan. Study supervision: Lio. Patient identification: Jarvis.

Financial Disclosure: None reported.

Funding/Support: This study was supported in part by NIH/NIAMS R01 AR48289, the Cure JM Foundation, and the Macy's Miracle Foundation (to Dr Pachman).

Role of the Sponsors: The sponsors had no role in the design and conduct of the study; in the collection, analysis, and interpretation of data; or in the preparation, review, or approval of the manuscript.

Additional Contributions: Kelli Day provided expert technical support.

Feldman BM, Rider LG, Reed AM, Pachman LM. Juvenile dermatomyositis and other idiopathic inflammatory myopathies of childhood.  Lancet. 2008;371(9631):2201-221218586175PubMedGoogle ScholarCrossref
Mendez EP, Lipton R, Ramsey-Goldman R,  et al; NIAMS Juvenile DM Registry Physician Referral Group.  US incidence of juvenile dermatomyositis, 1995-1998: results from the National Institute of Arthritis and Musculoskeletal and Skin Diseases Registry.  Arthritis Rheum. 2003;49(3):300-30512794783PubMedGoogle ScholarCrossref
Dourmishev L, Meffert H, Piazena H. Dermatomyositis: comparative studies of cutaneous photosensitivity in lupus erythematosus and normal subjects.  Photodermatol Photoimmunol Photomed. 2004;20(5):230-23415379871PubMedGoogle ScholarCrossref
Mamyrova G, O ’Hanlon TP, Monroe JB,  et al; Childhood Myositis Heterogeneity Collaborative Study Group.  Immunogenetic risk and protective factors for juvenile dermatomyositis in Caucasians.  Arthritis Rheum. 2006;54(12):3979-398717133612PubMedGoogle ScholarCrossref
Tezak Z, Hoffman EP, Lutz JL,  et al.  Gene expression profiling in DQA1*0501+ children with untreated dermatomyositis: a novel model of pathogenesis.  J Immunol. 2002;168(8):4154-416311937576PubMedGoogle Scholar
Baechler EC, Bauer JW, Slattery CA,  et al.  An interferon signature in the peripheral blood of dermatomyositis patients is associated with disease activity.  Mol Med. 2007;13(1-2):59-6817515957PubMedGoogle ScholarCrossref
Pachman LM, Lipton R, Ramsey-Goldman R,  et al.  History of infection before the onset of juvenile dermatomyositis: results from the National Institute of Arthritis and Musculoskeletal and Skin Diseases Research Registry.  Arthritis Rheum. 2005;53(2):166-17215818654PubMedGoogle ScholarCrossref
Koch MJ, Brody JA, Gillespie MM. Childhood polymyositis: a case-control study.  Am J Epidemiol. 1976;104(6):627-631998610PubMedGoogle Scholar
Massa M, Costouros N, Mazzoli F,  et al.  Self epitopes shared between human skeletal myosin and Streptococcus pyogenes M5 protein are targets of immune responses in active juvenile dermatomyositis.  Arthritis Rheum. 2002;46(11):3015-302512428245PubMedGoogle ScholarCrossref
Vegosen LJ, Weinberg CR, O ’Hanlon TP, Targoff IN, Miller FW, Rider LG. Seasonal birth patterns in myositis subgroups suggest an etiologic role of early environmental exposures.  Arthritis Rheum. 2007;56(8):2719-272817665425PubMedGoogle ScholarCrossref
Cooper GS, Miller FW, Pandey JP. The role of genetic factors in autoimmune disease: implications for environmental research.  Environ Health Perspect. 1999;107:(suppl 5)  693-70010502533PubMedGoogle Scholar
Wedderburn LR, McHugh NJ, Chinoy H,  et al; Juvenile Dermatomyositis Research Group (JDRG).  HLA class II haplotype and autoantibody associations in children with juvenile dermatomyositis and juvenile dermatomyositis-scleroderma overlap.  Rheumatology (Oxford). 2007;46(12):1786-179118003662PubMedGoogle ScholarCrossref
Tomono N, Mori M, Nakajima S,  et al.  HLA-DRB1*15021 is the predominant allele in Japanese patients with juvenile dermatomyositis.  J Rheumatol. 2004;31(9):1847-185015338511PubMedGoogle Scholar
Niewold TB, Kariuki SN, Morgan GA, Shrestha S, Pachman LM. Elevated serum interferon-alpha activity in juvenile dermatomyositis: associations with disease activity at diagnosis and after thirty-six months of therapy.  Arthritis Rheum. 2009;60(6):1815-182419479879PubMedGoogle ScholarCrossref
Chen Y-W, Shi R, Geraci N, Shrestha S, Gordish-Dressman H, Pachman LM. Duration of chronic inflammation alters gene expression in muscle from untreated girls with juvenile dermatomyositis.  BMC Immunol. 2008;9:4318671865PubMedGoogle ScholarCrossref
Shrestha S, Wershil B, Sarwark JF, Niewold TB, Philipp T, Pachman LM. Lesional and nonlesional skin from patients with untreated juvenile dermatomyositis displays increased numbers of mast cells and mature plasmacytoid dendritic cells.  Arthritis Rheum. 2010;62(9):2813-282220506305PubMedGoogle ScholarCrossref
Pachman LM, Liotta-Davis MR, Hong DK,  et al.  TNF- α-308A allele in juvenile dermatomyositis: association with increased production of tumor necrosis factor alpha, disease duration, and pathologic calcifications.  Arthritis Rheum. 2000;43(10):2368-237711037898PubMedGoogle ScholarCrossref
De Bleecker JL, Meire VI, Declercq W, Van Aken EH. Immunolocalization of tumor necrosis factor-alpha and its receptors in inflammatory myopathies.  Neuromuscul Disord. 1999;9(4):239-24610399751PubMedGoogle ScholarCrossref
Fedczyna TO, Lutz J, Pachman LM. Expression of TNFalpha by muscle fibers in biopsies from children with untreated juvenile dermatomyositis: association with the TNFalpha-308A allele.  Clin Immunol. 2001;100:236-23911465953PubMedGoogle ScholarCrossref
Uzel G, Pachman LM. Cytokines in juvenile dermatomyositis pathophysiology: potential and challenge.  Curr Opin Rheumatol. 2003;15(6):691-69714569197PubMedGoogle ScholarCrossref
Stern RS, Nijsten T, Feldman SR, Margolis DJ, Rolstad T. Psoriasis is common, carries a substantial burden even when not extensive, and is associated with widespread treatment dissatisfaction.  J Investig Dermatol Symp Proc. 2004;9(2):136-13915083780PubMedGoogle ScholarCrossref
Raychaudhuri SP, Gross J. A comparative study of pediatric onset psoriasis with adult onset psoriasis.  Pediatr Dermatol. 2000;17(3):174-17810886746PubMedGoogle ScholarCrossref
Lowes MA, Bowcock AM, Krueger JG. Pathogenesis and therapy of psoriasis.  Nature. 2007;445(7130):866-87317314973PubMedGoogle ScholarCrossref
Yao Y, Richman L, Morehouse C,  et al.  Type I interferon: potential therapeutic target for psoriasis?  PLoS One. 2008;3(7):e273718648529PubMedGoogle ScholarCrossref
Farkas A, Tonel G, Nestle FO. Interferon-alpha and viral triggers promote functional maturation of human monocyte-derived dendritic cells.  Br J Dermatol. 2008;158(5):921-92918371115PubMedGoogle ScholarCrossref
Niewold T, Wu S, Smith M, Morgan GA, Pachman LM. Familial aggregation of autoimmune disease in juvenile dermatomyositis.  PediatricsIn PressGoogle Scholar
Pavlovi ć MD, Zecevi ć RD, Zolotarevski L. Psoriasis in a patient with dermatomyositis.  Vojnosanit Pregl. 2004;61(5):557-55915551809PubMedGoogle ScholarCrossref
Alekberova ZS, Balabanova RM, Agababov SV. Dermatomyositis associated with psoriasis [in Russian].  Ter Arkh. 1980;52(4):116-1197404325PubMedGoogle Scholar
Bohan A, Peter JB. Polymyositis and dermatomyositis (first of two parts).  N Engl J Med. 1975;292(7):344-3471090839PubMedGoogle ScholarCrossref
Smith RL, Sundberg J, Shamiyah E, Dyer A, Pachman LM. Skin involvement in juvenile dermatomyositis is associated with loss of end row nailfold capillary loops.  J Rheumatol. 2004;31(8):1644-164915290747PubMedGoogle Scholar
Christen-Zaech S, Seshadri R, Sundberg J, Paller AS, Pachman LM. Persistent association of nailfold capillaroscopy changes and skin involvement over thirty-six months with duration of untreated disease in patients with juvenile dermatomyositis.  Arthritis Rheum. 2008;58:571-57618240225PubMedGoogle ScholarCrossref
Lovell DJ, Lindsley CB, Rennebohm RM,  et al; Juvenile Dermatomyositis Disease Activity Collaborative Study Group.  Development of validated disease activity and damage indices for the juvenile idiopathic inflammatory myopathies, II: the Childhood Myositis Assessment Scale (CMAS): a quantitative tool for the evaluation of muscle function.  Arthritis Rheum. 1999;42(10):2213-221910524696PubMedGoogle ScholarCrossref
Delgado-Vega AM, Alarc ón-Riquelme ME, Kozyrev SV. Genetic associations in type I interferon related pathways with autoimmunity.  Arthritis Res Ther. 2010;12:(suppl 1)  S220392289PubMedGoogle ScholarCrossref
Lew W, Bowcock AM, Krueger JG. Psoriasis vulgaris: cutaneous lymphoid tissue supports T-cell activation and “type 1 ” inflammatory gene expression.  Trends Immunol. 2004;25(6):295-30515145319PubMedGoogle ScholarCrossref
Nestle FO, Conrad C, Tun-Kyi A,  et al.  Plasmacytoid predendritic cells initiate psoriasis through interferon-alpha production.  J Exp Med. 2005;202(1):135-14315998792PubMedGoogle ScholarCrossref
Leman J, Burden D. Psoriasis in children: a guide to its diagnosis and management.  Paediatr Drugs. 2001;3(9):673-68011688598PubMedGoogle ScholarCrossref
Reed AM, Lopez M. Juvenile dermatomyositis: recognition and treatment.  Paediatr Drugs. 2002;4(5):315-32111994036PubMedGoogle Scholar
Zanolli M. Phototherapy treatment of psoriasis today.  J Am Acad Dermatol. 2003;49(2):(suppl)  S78-S8612894130PubMedGoogle ScholarCrossref
Jury CS, McHenry P, Burden AD. Narrowband ultraviolet B (UVB) phototherapy in children.  Clin Exp Dermatol. 2006;31(2):196-19916487089PubMedGoogle ScholarCrossref
Ersoy-Evans S, Altaykan A, Sahin S, K ölemen F. Phototherapy in childhood.  Pediatr Dermatol. 2008;25(6):599-60519067863PubMedGoogle ScholarCrossref
Jain VK, Aggarwal K, Jain K, Bansal A. Narrow-band UV-B phototherapy in childhood psoriasis.  Int J Dermatol. 2007;46(3):320-32217343596PubMedGoogle ScholarCrossref
al-Fouzan AS, Nanda A. A survey of childhood psoriasis in Kuwait.  Pediatr Dermatol. 1994;11(2):116-1198041649PubMedGoogle ScholarCrossref
Victor FC, Gottlieb AB. TNF-alpha and apoptosis: implications for the pathogenesis and treatment of psoriasis.  J Drugs Dermatol. 2002;1(3):264-27512851985PubMedGoogle Scholar
Sfikakis PP. The first decade of biologic TNF antagonists in clinical practice: lessons learned, unresolved issues and future directions.  Curr Dir Autoimmun. 2010;11:180-21020173395PubMedGoogle Scholar
Papoutsaki M, Costanzo A, Mazzotta A, Gramiccia T, Soda R, Chimenti S. Etanercept for the treatment of severe childhood psoriasis.  Br J Dermatol. 2006;154(1):181-18316403117PubMedGoogle ScholarCrossref
Hawrot AC, Metry DW, Theos AJ, Levy ML. Etanercept for psoriasis in the pediatric population: experience in nine patients.  Pediatr Dermatol. 2006;23(1):67-7116445417PubMedGoogle ScholarCrossref
Menter MA, Cush JM. Successful treatment of pediatric psoriasis with infliximab.  Pediatr Dermatol. 2004;21(1):87-8814871337PubMedGoogle ScholarCrossref
Paller AS, Siegfried EC, Langley RG,  et al; Etanercept Pediatric Psoriasis Study Group.  Etanercept treatment for children and adolescents with plaque psoriasis.  N Engl J Med. 2008;358(3):241-25118199863PubMedGoogle ScholarCrossref
Collamer AN, Battafarano DF. Psoriatic skin lesions induced by tumor necrosis factor antagonist therapy: clinical features and possible immunopathogenesis.  Semin Arthritis Rheum. 2010;40(3):233-24020580412PubMedGoogle ScholarCrossref
Ramos-Casals M, Brito-Zer ón P, Mu ñoz S,  et al.  Autoimmune diseases induced by TNF-targeted therapies: analysis of 233 cases.  Medicine (Baltimore). 2007;86(4):242-25117632266PubMedGoogle ScholarCrossref
Efthimiou P, Schwartzman S, Kagen LJ. Possible role for tumour necrosis factor inhibitors in the treatment of resistant dermatomyositis and polymyositis: a retrospective study of eight patients.  Ann Rheum Dis. 2006;65(9):1233-123616476710PubMedGoogle ScholarCrossref
Hengstman GJ, van den Hoogen FH, van Engelen BG. Treatment of dermatomyositis and polymyositis with anti-tumor necrosis factor-alpha: long-term follow-up.  Eur Neurol. 2004;52(1):61-6315240986PubMedGoogle ScholarCrossref
Dastmalchi M, Grundtman C, Alexanderson H,  et al.  A high incidence of disease flares in an open pilot study of infliximab in patients with refractory inflammatory myopathies.  Ann Rheum Dis. 2008;67(12):1670-167718272672PubMedGoogle ScholarCrossref
Iannone F, Scioscia C, Falappone PC, Covelli M, Lapadula G. Use of etanercept in the treatment of dermatomyositis: a case series.  J Rheumatol. 2006;33(9):1802-180416960940PubMedGoogle Scholar
Palucka AK, Blanck JP, Bennett L,  et al.  Cross-regulation of TNF and IFN-alpha in autoimmune diseases.  Proc Natl Acad Sci U S A. 2005;102(9):3372-337715728381PubMedGoogle ScholarCrossref
Pachman LM, Niewold T, Shrestha S, Morgan GA, Sullivan C. TNF- α levels and IFN- α activity in children with juvenile dermatomyositis (JDM) are associated and modified by etanercept.  Clin Immunol. 2009;131:(suppl)  S158Google ScholarCrossref