Successful Treatment of Pansclerotic Morphea with Imatinib Mesylate in a Pediatric Patient
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1 Case Report Successful Treatment of Pansclerotic Morphea with Imatinib Mesylate in a Pediatric Patient Taylor A. Banks 1, Virginia Steen 2, Ildy Katona 3, Olcay Y. Jones 4 1 Division of Allergy and Immunology, Walter Reed National Military Medical Center, Bethesda; 2 Division of Rheumatology, Georgetown University Hospital, Washington, DC; 3 Department of Pediatrics, Uniformed Services University of the Health Sciences, Bethesda; 4 Department of Pediatrics, Walter Reed National Military Medical Center, Bethesda, USA Corresponding Author: Olcay Y. Jones, WRNMMC, Division Pediatric Rheumatology, 8901 Wisconsin Ave, America Building 4th floor, Bethesda, USA olcay.jones@gmail.com Received: Jan 09, 2013 Accepted: Jan 16, 2013 Ann Paediatr Rheum 2013; 2:43-49 DOI: /apr Abstract Juvenile localized scleroderma ( JLS) is a childhood condition consisting of a number of subtypes, the most severe of which is pansclerotic morphea. This disease process manifests with both significant cutaneous and extra-cutaneous findings and is associated with severe morbidity and mortality. We present the case of a seven year-old female with pansclerotic morphea who had a limited initial response to a variety of immunosuppresants including corticosteroids, methotrexate and cyclophosphamide. Addition of imatinib mesylate, an N-demethylated piperazine derivative (CGP74588), resulted in marked and consistent improvement and eventual resolution of her condition. While reported in a few case reports in the adult population, to our knowledge, this is the first successful use of imatinib mesylate in a pediatric patient as a component of combination therapy to treat pansclerotic morphea. Key words: Gleevac, imatinib mesylate, pansclerotic morphea, panmorphea, juvenile localized scleroderma Introduction Juvenile localized scleroderma (JLS) is a childhood condition characterized by thickening of the skin. A variety of clinical subtypes have been described, differentiated by the size, shape, and location of skin involvement as well as the presence or absence of extra-cutaneous manifestations. These forms include linear scleroderma, plaque morphea, en coup de sabre and pansclerotic or generalized morphea [1-3]. JLS is a rare condition with a reported incidence of 3.4 cases per million. JLS is regarded as an autoimmune disease with unknown etiology or genetic risk factors [4]. In some cases incidental associations were reported involving po-
2 Pansclerotic morphea treated with imatinib mesylate 44 tential physical, environmental or infectious triggers affecting genetically inclined children. These include trauma, previous infection of Borrelia Burgdorferi, and chronic venous insufficiency [5]. Such inciting events are thought to provoke an immune response resulting in excessive production of TGF-β and PDGF coupled with activation of fibroblasts and upregulation of collagen production as well as increased serum cytokines (interleukin [IL] 2, 6, and 8) [4,6,7]. Additionally, nearly half of pansclerotic morphea patients demonstrate anti-histone antibodies and many are positive for anti-dna topoisomerase IIα autoantibodies [4,6-8]. Pansclerotic morphea represents the most severe form of JLS and accounts for approximately 7% of cases and is associated with a female to male ratio of 4:1 [1,5,9,10]. Clinically, it often presents with a sudden eruption of multiple large plaques on the truck and extremities that progress over extensive areas of skin, while sparing the fingers and toes. Unlike systemic scleroderma, these children do not develop Raynaud s or acrosclerosis but show extensive induration and hyperpigmentation from full thickness changes in cutaneous and subcutaneous layers. Pansclerotic morphea has also been observed to have extra-cutaneous manifestations including arthritis and a restrictive-pattern of lung disease [1,2,5,11]. The literature on the natural history of pansclerotic morphea is limited but emphasizes a guarded prognosis with severe disability and mortality [3,4,11]. In the series reported by Diaz- Perez et.al, 13 of 14 pansclerotic morphea patients, some of whom demonstrated lung involvement (n=5), progressed in disease severity or died despite ongoing immunosuppressive treatment [12]. In addition to its greater clinical impact, the pansclerotic morphea subtype is often the most resistant to treatment. The proposed, but nebulous, immunologic basis of pansclerotic morphea has guided treatment, which has remained broad in scope. We present our experience with a multifaceted therapeutic approach in a pediatric patient, including the use of imatinib mesylate. Imatinib mesylate (Gleevec) is an N-demethylated piperazine derivative (CGP74588), which acts as a tyrosine kinase inhibitor with additional inhibitory effect on CD117 (c-kit receptor), transforming growth factor-β (TGF-β), and platelet-derived growth factor (PDGF) [13,14]. While imatinib mesylate has seen extensive use in chronic myelogenous leukemia (CML) and gastrointestinal stromal tumors (GIST), only recently has interest risen in its use to treat scleroderma [15-19]. The resistance of pansclerotic morphea to previous treatment options and recent use of imatinib mesylate in adult-onset systemic scleroderma patients prompted our use of this targeted agent [15-17]. Case report A seven-year-old white female presented to Walter Reed National Military Medical Center with a three week history of fatigue, emotional lability, edematous face, hands, and feet, as well as an erythematous rash on the abdominal wall. She was previously in good health and just returned from an uneventful vacation in Germany. Fever, headaches, arthralgias, myalgia, chest and GI concerns were all absent. On exam, the rash over the abdominal wall consisted of two discrete round patches located in the right upper and left middle quadrants, measuring about 5cm in diameter each. The rash was diffusely erythematous, non-pruritic, non-painful, and had a flat and thickened texture. No scaling was present and there were no signs to suggest an insect bite in the vicinity. There were no other mucocutaneous findings, Raynaud s sign, or hair or nail changes. Initial laboratories included a CBC with WBC of 7.4 x109/l, hemoglobin and hematocrit of 12 and 36.1, respectively and platelet count of 416. The differential was significant only for eosinophilia (absolute eosinophil count, AEC) to 1.3 x109/l (18%) that peaked at 1.9 x109/l (25%) in repeat CBCs in the next two weeks before returning to within normal limits (AEC<300x109/L ) at 6 weeks. Serum chemistries, liver enzymes, and urinalysis were normal. MRI of the lower extremities was normal without any signs of inflammation in the fascia. Serology, including ANA, antibodies to extractable nuclear antigens, Scl 70, and centromere, was negative. An extensive infectious disease work-up, including Borrelia antibody titer and DNA PCR, was negative. Pathology review on a full thickness skin biopsy was compatible with morphea (Figure 1). Based on the biopsy results and clinical course, a diagnosis of pansclerotic morphea was established. Her clinical course in the following 3 months time was marked by rapid deterioration. Initially, the two morphea DOI: /apr
3 45 Banks TA et al. patches on the torso coalesced, followed by spread of indurated skin centrally to peripherally, affecting the entire torso in a circumferential manner. These same skin changes then spread to the neck, upper thighs and arms, and finally down to the dorsum of the hands and feet, sparing the fingers and toes. The progression of skin changes was symmetric and involved both a enlargement of the affected area and continuous worsening of skin thickening, producing a wood-like quality. These lesions led to fixed flexion contractures of degrees at the hips, knees, shoulders, and elbows in spite of intensive, daily physical therapy. The ankles were noted to just return to neutral and the wrists only achieved passive dorsiflexion to 30 degrees. Pulmonary function testing (PFT) demonstrated a restrictive pattern with FVC 63% predicted, FEV1 64% predicted, FEV1/FVC 91%, and her DLCO was markedly reduced at 55% predicted. A subsequent high-resolution chest CT revealed an approximately 30% reduction in lung-volume without ground glass appearance or other parenchymal changes. An echocardiogram was normal. A prolonged and intensive treatment course was embarked upon as summarized in Figure 2. The patient (weight 21 kg) was initially started on combination treatment of prednisone (2mg/kg/day, maximum 42 mg/day) and weekly subcutaneous methotrexate (maximum 25mg/ dose) within three weeks of presentation. This therapy had a negligible effect on the rapid progression of her disease process. Two months into her course, she was given a 3-day burst of high dose methylprednisolone (20mg/kg/dose). At four months time, it was decided to intensify the immunosuppressive regimen due b Figure 1. Low (a) and high-powered (b) views of the patient s skin biopsy demonstrating a sclerosing pattern, with homogenization of the papillary dermis and thickening of the collagen bundles within the mid-deep dermis. The collagen encroaches on eccrine sweat glands and extends into the superficial portion of the subcutis. Inflammatory cells including occasional eosinophils lightly populate these expanded septa. An inflammatory infiltrate comprised mostly of lymphocytes and plasma cells, with a minor component of eosinophils surround eccrine glands and extends into the interstitial dermis. While eosinophils are present, this histological pattern does not suggest eosinophilic fasciitis. Images and histological interpretation courtesy of the Dermatopathology Division at Walter Reed National Military Medical Center. Figure 2. Summary of the patient s treatment course, with month 0 representing initial presentation. Monthly pulses of cyclophosphamide began two months prior to imatinib mesylate and continued monthly for six months. Imtainib mesylate is represented in blue with total daily dosing (100mg twice daily, initially). Oral prednisone (red line) was started at 2mg/kg/day and weaned initially rapidly and then much more gradually over the patient s course. Finally, methotrexate is represented in green and while weaned over time, it was maintained throughout much of the patient s course. Annals of Paediatric Rheumatology Year 2013 Volume:2 Issue:
4 Pansclerotic morphea treated with imatinib mesylate 46 a b Figure 3. (a) depicts the patient a few months after diagnosis. Note the skin discoloration, thickening, and contractures, the latter prevented the patient from completely extending her legs. (b) depicts the patient at month 60, several months after discontinuing all treatment. Trace residual discoloration of the skin is visible. to the findings on PFTs, severe contractures, very poor quality of life, and a high risk for long-term disability and growth failure. This was outlined in a step-wise fashion with an endpoint of commitment to immunoablation and hematopoietic stem cell transplant (HSCT). First, she was started on monthly IV cyclophosphamide along with monthly IV solumedrol. At six months, imatinib mesylate (100mg orally, twice daily) was added to her regimen. Supportive measurements included UVA light-box treatments (10.3 minutes to both anterior and posterior planes every other day), multivitamin, calcium, vitamins E and D, fish oil and folic acid supplements and meticulous physical therapy with deep-tissue massage. At 9 months, her skin texture began to show improvement. She completed six doses of monthly IV cyclophosphamide treatment (4.5 grams in total, 5grams/meter2), which allowed a slow, but steady, wean from corticosteroids. Over the next 3 years time, her skin gradually improved, following a symmetric pattern. Similar to her initial presentation, this steady resolution started from her torso, then extended to her extremities. Although the skin improvement was continuous, it was greatest during the first 6 months of imatinib in the presence of co-treatment with cyclophosphamide, high doses of prednisone, methotrexate and intensive physical therapy. At the conclusion of three years of treatment, her skin changes and joint contractures had completely resolved. Throughout her course, she did not develop any signs of systemic scleroderma or overlap syndrome, in that there was no Raynaud s sign, periungual capillary changes, weakness, or changes in GI motility or renal function. Her PFTs improved with DLCO of 83% at 6 months and DLCO of 97% at 2 years. The treatment was gradually weaned starting with steroids, followed by imitinab and finally methotrexate. She has been off treatment for 12 months and continues to be in remission. Overall the treatment was well tolerated. The patient reported a few minor adverse effects attributable to imatinib including: 1) the development of intermittent muscle cramps, 6 months into the treatment, mostly involving lower extremities and alleviated by a slight modification of the imatinib dose, 2) fluctuating muscle enzymes (ALT, AST, LDH and aldolase) up to two times institutional norms in the setting of a repeat MRI of the thighs, which did not show any signs of fasciitis or myositis, 3) Borderline low WBC (4 to 5 x109/l) throughout the course without infectious complications [20]. There was no nausea, rash, allergic or infectious complications. She is now at 60 months in her follow-up and her growth has remained stable, tracking at the 4th percentile for weight and the 15th percentile for height. Discussion Pansclerotic morphea is a severe disease, associated with significant risk for morbidity and mortality. Treatment has been hampered by the intensity and wide extent of the skin changes and the poor understanding of the disease s underlying pathogenesis. To our knowledge, the patient presented is the first pediatric patient to achieve a full recovery using imatinib mesylate as a component of a therapeutic regimen. The levels of immunosuppression used was greater than that described in the published literature [21]. While it may challenge the boundaries of comfort levels within the subspecialty traditions, tightly tailored treatment was necessary given the patient s fulminant course and the specter of permanent morbidity and poor quality of life. The choices of immunosuppressive regimens were selected carefully for complementary qualities and included prednisone and methotrexate, mainstays of JLS treatment [21]. Introduction of new agents was stepwise, DOI: /apr
5 47 Banks TA et al. as much as possible, allowing time for assessment. The multiagent approach targeted different aspects of the disease process including those engendered by fibroblasts, lymphocytes and innate immune system components. Our multi-agent approach was inspired based on the preclinical models, in which it is clearly evident that in scleroderma there is a diverse set of mechanisms involved in disease pathogenesis. For instance, while Tsk mice with fibrillin 1 gene mutation have thickened skin attributed to altered extracellular matrix, increased levels of TGF-β, and direct stimulation of fibroblast, DBA mice exposed to bleomycin develop skin fibrosis as a result of robust inflammation and indirect stimulation of fibroblasts. Interestingly, studies have shown imitinib to be efficacious in both models, through its direct inhibition of fibroblasts [16]. It is not clear in our patient if imatinib alone would have been sufficient. Given the lack of clear guidance from the literature, a commitment to the mainstays of treatment and cyclophosphamide remained our first option. Sfikakis first reported the compassionate use of imitanib in a severe systemic scleroderma patient with skin, lung and GI involvement who failed to achieve long term remission after 36 doses of IV cyclophosphamide during 7 years of her disease course. Similar to our experience, the response was rapid, with softening of skin within 6 months time. The decision to use imatinib mesylate was based on its successful use in a few case reports in systemic scleroderma, resulting in the reversal of skin as well as pulmonary pathology, and its safety profile in patients with CML and GISTs [14-16,22]. Imatinib s mechanism of action involves competitive binding of the ATP-binding site, inhibiting enzymatic tyrosine kinase activity [23]. This leads to downstream effects on TGF-β and separate action on PDGF receptors [17,24]. These targets in turn represent principal regulators of extracellular matrix (ECM) production by activated dermal fibroblasts [13,23]. Through this dual inhibition, the excessive effects of activated fibroblasts are halted and reversed. The reversal of fibrosis is postulated to represent a decrease in synthesis of new ECM relative to its ongoing degradation, rather than a direct increase in such degradation [16]. By shifting this balance, imatinib provides a means to selectively induce reversal of fibrosis through specifically targeted pathways. The observation in our patient that skin changes were symmetrical and progressed from central to peripheral suggests such an ongoing dynamic and reciprocal relationship between the immune system and resident tissue. There is no known treatment proven to be highly efficacious for skin changes in scleroderma, and for some, HSCT has been regarded as the only viable approach for remission that was supported with the results of recent clinical trials. HSCT removes specific immune memory and therefore immune damage, but it remains as a serious commitment with attendant risks of morbidity and mortality [25]. In our hands, it was considered as an exit strategy held in reserve. The child was subject to careful titration of immune suppression without causing immune ablation. This approach not only halted the disease progression, but also reversed the skin pathology. Pansclerotic morphea can often present patients and their families with a grim prognosis. As demonstrated by our case, the impact on quality of life can be quite severe. This case exemplifies that there is a need for developing new treatment protocols to achieve intensified immunosuppression compared to that of current practice. As noted in recent publications, such developments will require a refined definition of disease remission not only by clinical judgment, but also by laboratory parameters involving immune system populations and functions. As observed in our patient, careful titration of immune suppression without reaching complete ablation of immune memory was effective in allowing target tissue recovery. Careful risk-benefit assessment and tailored treatment is essential for such patients, particularly in a growing child with severe and life threatening autoimmune and inflammatory conditions. Acknowledgements: The authors would like to acknowledge the contribution made by Drs. Paul Reed, Cassandra Carr, Navin Arora, Aizen Marrogi and Ms. Nona Cedrone in the care of our patient. The authors would also like to extend their most sincere thanks for the steadfast, gracious, and generous participation and assistance of our patient and her family as well as to recognize their indomitable spirits throughout her treatment. The authors received no funding in preparation of this article and have no corporate affiliations. Annals of Paediatric Rheumatology Year 2013 Volume:2 Issue:
6 Pansclerotic morphea treated with imatinib mesylate 48 Disclaimer: The views expressed in this article are those of the authors and do not reflect the official policy of the Department of the Navy, Department of Defense, or U.S. Government. References 1. Zulian F, Vallongo C, Woo P, Russo R, Ruperto N, Harper J, et al. Localized Scleroderma in childhood is not just a skin disease. Arthritis and Rheumatism. 2005; 52: Zulian F, Athreya BH, Laxer R, Nelson AM, Feitosa de Oliveira SK, Punaro MG, et al. Juvenile localized scleroderma: clinical and epidemiological features in 750 children. An international study. Rheumatology. 2006; 45: Wollina U, Looks A, Uhlemann C, Wollina K. Correspondence: Pansclerotic Morphea of Childhood Followup over 6-years. Pediatric Dermatology. 1999; 16: Takehara K, Sato S. Localized scleroderma is an autoimmune disorder. Rheumatology. 2005; 44: Laxer RM, Zulian F. Localized scleroderma. Current Opinion in Rheumatology. 2006; 18: Uziel Y, Feldman B, Krafchik BR, Yeung RSM, Laxer R. Methotrexate and corticosteroid therapy for pediatric localized scleroderma. Journal of Pediatrics. 2000; 136: Zulian F. New developments in localized scleroderma. Current Opinion in Rheumatology. 2008; 20: Zulian, F. Systemic sclerosis and localized scleroderma in childhood. Rheumatic Disease Clinics of North America. 2008; 34: Kaplan Mariana J. Localized Fibrosing Disorders- Linear Scleroderma, Morphea and Regional Fibrosis. E-medicine: overview. Accessed on December 21, Haber PL. Clinical manifestations of Scleroderma. Pediatrics in Review. 1995; 16: Doede T, Wollina U, Hindermann W, Schier F, Bondartschuk M. Pansclerotic Morphea in childhood: a case report. Pediatric Surgery International. 2003; 19: Diaz-Perez JL, Connolly SM, Winkelmann RK. Disabling pansclerotic morphea of children. Archives of Dermatology. 1980; 116: De Kogel CE, Schellens JHM. Imatinib. The Oncologist. 2007; 12: Barr RD. Imatinib mesylate in children and adolescents with cancer. Pediatric Blood Cancer. 2010; 55: Sfikakis PP, Gorgoulis VG, Katsiari CG, Evangelou K, Kostopoulos C, Black CM. Imatinib for the treatment of refractory, diffuse systemic sclerosis. Rheumatology. 2008; 47: Akhmetshina A, Venalis P, Dees C, Busch N, Zwerina J, Schett G, et al. Treatment with Imatinib prevents fibrosis in different preclinical models of systemic sclerosis and induces regression of established fibrosis. Arthritis and Rheumatism. 2009; 60: Distler JHW, Jungel A, Huber LC, Schulze-Horsel U, Zwerina J, Gay RE, et al. Imatinib Mesylate reduces production of extracellular matrix and prevents development of experimental dermal fibrosis. Arthritis and Rheumatism. 2007; 56: Bibi Y, Gottlieb AB. A potential role for imatinib and other small tyrosine kinase inhibitors in the treatment of systemic and localized sclerosis. Journal of the American Academy of Dermatology. 2008; 59: Lazar J, Poonawalla T, Teng JMC. A case of sclerodermatous graft-versus-host disease responsive to imatinib therapy. Pediatric Dermatology. 2011; 28: Spiera RF, Gordon JK, Mersten JN, Magro CM, Mehta M, Wildman HF, et al. Imatinib mesylate (Gleevec) in the treatment of diffuse cutaneous systemic sclerosis: results of a 1-year, phase IIa, single-arm, open-label clinical trial. Annals of the Rheumatic Diseases. 2011; 70: Li SC, Torok KS, Pope E, Dedeoglu F, Hong S, Jacobe HT, et al. Development of consensus treatment plans for juvenile localized scleroderma: a roadmap toward comparative effectiveness studies in juvenile localized scleroderma. Arthritis Care and Research. 2012; 64: Van Daele PLA, Dik WA, Thio HB, van Hal PT, van Laar JA, Hooijkaas H, et al. Is imatinib mesylate a promising drug in systemic sclerosis. Arthritis and Rheumatism. 2008; 58: Distler JHW, Distler O. Intracellular tyrosine kinases as novel targets for anti-fibrotic therapy in systemic sclerosis. Rheumatology. 2008; 47:v10-v11. DOI: /apr
7 49 Banks TA et al. 24. Chung L, Fiorentino DF, Benbarak MJ, Adler AS, Mariano MM, Paniagua RT, et al. Molecular framework for response to imatinib mesylate in systemic sclerosis. Arthritis and Rheumatism. 2009; 60: Burt RK, Milanetti F. Hematopoietic stem cell transplantation for systemic sclerosis: history and current status. Current Opinion in Rheumatology. 2011; 23: Kroft EB, Berkhof NJ, van de Kerkhof PC, Gerritsen RM, de Jong EM. Ultraviolet A phototherapy for sclerotic skin diseases: A systemic review. Journal of American Academic Dermatology. 2008; 59: Annals of Paediatric Rheumatology Year 2013 Volume:2 Issue:
Citation The Journal of dermatology, 37(1), available at
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