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• W1944143323 abstract "Dear Editor, A 52-year-old woman was admitted to our department because of a progressive thickening and tightening of the skin for 2 months. Seven months ago, she was diagnosed as having infiltrating ductal carcinoma on the left breast. Eight courses were designed for her treatment. The interval of the polychemotherapy was 3 weeks. She was given modified radical mastectomy and polychemotherapy with epirubicin (60 mg, day 1 and day 2, infusion), cyclophosphamide (800 mg, day 1, infusion) and docetaxel (DOC) 100 mg/m2 (day 1, infusion) according to the recommended therapeutic schedule. Two weeks after the third course of chemotherapy, mild erythema on the face, neck, arms and hands presented. With continued chemotherapy, incapacity in finger flexion and difficulty in opening her mouth was noticed after treatment with the sixth course. After eight courses of chemotherapy, she experienced marked edema of the arms, lower legs and trunk, with progressive thickening and tightening of the skin and progressive esophagus dysphagia. On examination, the patient revealed prominent tightening and stiffness of the skin in flexion contractures of the distal interphalangeal joints and edema of the dorsum of the hands (Fig. 1a). Moderate flexion and extension restrictions were observed bilaterally in her ankles (Fig. 1b). The skin of the lower legs, trunk and proximal extremities was also involved. In particular, the skin of her left chest was stiff and unmovable (Fig. 1c). Approximately 60% of her body surface area was involved. Hyperpigmentation was also observed on the tightened skin. Raynaud's phenomenon on her hands was observed. As assessed by modified Rodnan skin score (MRSS), the cutaneous involvement was severe (36, grade 3).1, 2 Laboratory examination of peripheral blood was non-suspicious, including negative findings from assays for anti-nuclear antibody (ANA), anti-centromere antibodies,anti-Scl-70, extractable nuclear antigen and rheumatoid factor, except for erythrocyte sedimentation rate (ESR) which was 34 mm in the first hour. Chest radiography, electrocardiograph and echocardiography thoracic computed tomography scan were normal. Radiographs of the hands and feet revealed no absorption of the terminal phalanges or areas of punctate subcutaneous calcification. A skin biopsy from her left forearm showed diffused dermal fibrosis with collagen bundles which extended to the underlying subcutis, an absence of pilar adnexal structures, and a slightly lymphocytic perivascular infiltration without mucin deposition. This was consistent with a diagnosis of scleroderma. After cessation of DOC, prednisone (30 mg/day), d-penicillamine (125 mg/day) and enalapril (10 mg/day) were administrated. Half a year later, regression of the skin tightness over the chest, abdomen and thighs was observed. However, the tightening and stiffness on the extremities were persistent. It was difficult for the patient to walk or make a fist. Dermal fibroblasts were cultured as previously described.3, 4 Fibroblasts were treated with DOC at concentrations ranging from 0 nmol/L to 10.0 nmol/L (four wells per condition) in the medium (Dulbecco's modified Eagle's medium with 10% fetal bovine serum) for 48 h. Western blot was assayed according to previous protocols.4 Anti-type I collagen antibody (Abcam, Cambridge, UK), anti-fibronectin (FN) antibody, anti-connective tissue growth factor (CTGF) antibody, anti-plasminogen activator inhibitor 1 (PAI-1) antibody (Santa Cruz Biotechnology, Sant Cruz, CA, USA) and anti-β-actin antibody (Cell Signaling Technology, Beverly, MA, USA) were probed. The levels of each protein were normalized to β-actin. At the concentrations of 0.1 and 0.5 nmol/L, DOC did not change the level of type I collagen, FN and CTGF. However, type I collagen was upregulated by DOC at the concentrations of 2.0, 5.0 and 10.0 nmol/L, and no obvious difference was observed between them. The induction effect was statistically significant over the concentration of 2.0 nmol/L of DOC (P < 0.01). The protein level of FN was significantly upregulated by DOC at the concentrations of 5.0 and 10.0 nmol/L, as compared with blank control (P < 0.01). CTGF was also stimulated by DOC at the concentration of 2.0 nmol/L (P < 0.01) and reached a relatively stable level at 5.0 and 10.0 nmol/L. No difference of PAI-1 was observed between the DOC-treated and untreated groups (P = 0.38). (Fig. 2). This report describes a case of progressive diffuse scleroderma in a patient who had received an adjuvant systemic chemotherapy, including DOC, epirubicin and cyclophosphamide for the treatment of breast cancer. To our knowledge, no case of scleroderma was reported after administration of epirubicin and cyclophosphamide. Moreover, cyclophosphamide is a choice for early diffuse fibrotic skin disease5 and interstitial lung disease(ILD).6 Therefore, scleroderma in this case was probably caused by DOC, not epirubicin or cyclophosphamide. DOC is one of the most common anticancer agents against a wide range of cancers, including breast cancer.7 Scleroderma-like side-effects have been reported, but the mechanisms underpinning it are not well understood.8, 9 It is well known that over-produced extracellular matrix play a critical role in the pathogenesis of fibrosis.10 Our results showed that at a low concentration, DOC did not change the level of type I collagen, FN or CTGF. However, at a relatively high concentration, DOC prominently upregulated these protein levels. PAI-1 was not changed by DOC in the dermal fibroblasts. These data suggest that DOC may induce fibrosis through regulating the production of type I collagen, FN and CTGF, but not PAI-1. This study was supported by grants from Zhejiang Provincial Natural Science Foundation of China (Outstanding Youth Science Foundation, LR13H110001). The authors declare that there are no conflicts of interest." @default.
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• W1944143323 date "2015-07-14" @default.
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• W1944143323 title "Docetaxel-induced scleroderma: a case report and its role in the production of extracellular matrix" @default.
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• W1944143323 doi "https://doi.org/10.1111/1756-185x.12697" @default.
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