Rosaceiform Dermatitis with Follicular Demodex after Treatment of Facial Atopic Dermatitis with 1% Pimecrolimus Cream
Rosaceiform Dermatitis with Follicular Demodex after Treatment of Facial Atopic Dermatitis with 1% Pimecrolimus Cream
复制标题
玫瑰状%20皮炎%20with%20毛囊%20蠕形螨%20after%20治疗%20of%20面部%20特应性%20皮炎%20with%201%%20吡美莫司%20霜
作者：
J. Lübbe;Lisette Stucky;J. Saurat
205腹部皮肤，有一些半球形丘疹，直径5-20毫米；其他的是直径几厘米的斑块病变，首次发现是在 20 个月前（图 1）。胸部、上下背部和上臂也可见半球形病变，有的与腹部相似，有隆起的丘疹，有的为皮下、结节状；这些病变孤立地位于正常皮肤区域，并对称分布在双侧。此外，右大腿后侧有一个凸起的病变（直径3厘米）。所有病变均无症状且自发发生，受影响区域没有已知的皮肤损伤史。体格检查未发现系统性硬化症或相关硬斑病的体征。发病 5 个月后，对其中一个腹部丘疹（直径 7 毫米）进行活检，进行组织学研究，结果显示表皮正常，真皮内有结节区域，胶原纤维轻微增厚，血管周围淋巴细胞轻微浸润，偶尔有非脱颗粒肥大细胞。附件组织未见硬化或炎症浸润。没有观察到粘多糖沉积。活检伤口愈合，形成肥厚性疤痕。当患者来到我们诊所时（发病后 20 个月），我们对靠近现有活检疤痕的斑块进行了第二次活检。该活组织检查显示明显的真皮硬化，胶原束增厚（图 2），马森染色加剧了这种情况。免疫组织化学研究（Dako®，丹麦）显示，在第二次活检和第一次活检储存的材料中，细胞外基质蛋白生腱蛋白和纤连蛋白水平适度升高。体格检查、动脉张力、甲襞毛细血管镜检查和心电图均正常。血常规和尿常规分析、红细胞沉降率、蛋白图、血清 IgG、IgA、IgM 和 IgE 水平、肌酐清除率和蛋白尿（24 小时尿液）也均正常。可检测到抗核抗体（用 Hep-2 细胞检测）（滴度 1:100），核仁染色均匀。未检测到抗 DNA 和抗 ENA 抗体。我们同样没有检测到梅毒抗体（RPR 和 TPHA）。在这两种情况下，对 2 个独立血液样本进行伯氏疏螺旋体抗体测试，结果显示 ELISA 中显示 IgM，但没有 IgG 抗体，酶联荧光测定中既没有 IgM 也没有 IgG 抗体，并且免疫印迹（通过 IgM 或 IgG 抗体）没有识别伯氏疏螺旋体蛋白 p100、BmpA 或 OspA；尿液中伯氏疏螺旋体的 PCR 检测同样呈阴性；我们将这些结果解释为阴性（即 ELISA 中 IgM 假阳性）。所有病例的胸部放射线检查、骨骼系列和上消化道系列均正常。肺功能同样正常。鉴于这些发现，我们开始每周 4 次 PUVA 治疗，同时每天早上用卡泊三醇局部治疗腹部病变，睡前用 0.05% 丙酸氯倍他索局部治疗。 4个月后停止治疗，此时大腿病灶无变化，背部病灶仅中度消退，但胸部、手臂和腹部病灶的厚度和稠度明显减少，第一次活检的增生性疤痕完全消退，第二次活检的疤痕保持平坦。治疗结束两个月后，我们没有观察到任何进一步的变化；治疗结束后5个月，胸部病变完全消失，包括色素沉着过度，但左乳房出现了一个新的结节（直径4毫米），并且两个活检疤痕均显示轻微肥厚。 7个月后，大部分腰部病变和许多手臂病变消失，而腹部和上背部病变则保持不变。文献中模糊地使用术语“结节性”和“瘢痕疙瘩性”硬皮病来命名这种疾病[1]。此外，其多变的临床表现也引发了人们的疑问：皮下病变病例是否与凸起病变病例不同。本病例没有显示任何相关硬皮病的迹象，最合适的名称似乎是“纤维化反应”[1]。
205 the skin of the abdomen, some hemispherical papules, 5–20 mm in diameter; others were plaque lesions of several centimetres in diameter, first noted 20 months previously (fig. 1). Hemispherical lesions, some raised papules similar to those observed on the abdomen, others subcutaneous and nodular, were also observed on the thorax, upper and lower back and upper arms; these lesions were located in isolation in areas of normal skin and were distributed bilaterally and symmetrically. Additionally, a single raised lesion (diameter 3 cm) was present on the posterior aspect of the right thigh. All lesions were asymptomatic and had arisen spontaneously, with no known history of skin damage in the affected area. Physical examination did not reveal signs of systemic sclerosis or associated morphea. Histological study of a biopsy of one of the abdominal papules (diameter 7 mm), taken 5 months after onset, had revealed a normal epidermis and a nodular area in the dermis showing slight thickening of collagen fibres, slight perivascular lymphocyte infiltration and occasional non-degranulated mastocytes. Adnexal tissue did not show sclerosis or inflammatory infiltration. Mucopolysaccharide deposits were not observed. The biopsy wound healed forming a hypertrophic scar. When the patient came to our clinic (20 months after onset), we performed a second biopsy of a plaque close to the existing biopsy scar. This biopsy showed marked dermal sclerosis with thickened collagen bundles (fig. 2) accentuated with Masson’s stain. Immunohistochemical studies (Dako®, Denmark) revealed moderately raised levels of the extracellular matrix proteins tenascin and fibronectin, in both the second biopsy and stored material from the first biopsy. Physical examination, arterial tension, nail fold capillaroscopy and electrocardiography were normal. Also normal were routine blood and urine analyses, erythrocyte sedimentation rate, proteinogram, serum levels of IgG, IgA, IgM and IgE, creatinine clearance and proteinuria (in 24-hour urine). Antinuclear antibodies (as detected with Hep-2 cells) were detectable (titre 1:100), with homogeneous nucleolar staining. Anti-DNA and anti-ENA antibodies were not detectable. We likewise did not detect syphilis antibodies (RPR and TPHA). Tests of 2 independent blood samples for antibodies to Borrelia burgdorferi in both cases showed IgM but not IgG antibodies in ELISA, neither IgM nor IgG antibodies in an enzyme-linked fluorescent assay and no recognition in immunoblots (by either IgM or IgG antibodies) of the B. burgdorferi proteins p100, BmpA or OspA; PCR testing for B. burgdorferi in urine was likewise negative; we interpreted these results as negative (i.e. false-positive for IgM in ELISA). Radiography of the thorax, a bone series and an upper gastro-intestinal series was in all cases normal. Pulmonary function was likewise normal. In view of these findings, we commenced treatment with PUVA 4 times weekly, together with topical treatment of the abdominal lesions with calcipotriol every morning and 0.05% clobetasol propionate before bed. The treatment was discontinued after 4 months, by which time the thigh lesion remained unchanged and the back lesions had subsided only moderately, but the thickness and consistency of the chest, arm and abdominal lesions was markedly reduced, with full subsidence of the hypertrophic scar of the first biopsy, and the scar of the second biopsy remaining flat. Two months after the end of treatment we did not observe any further changes; 5 months after the end of treatment the chest lesions had disappeared entirely, including the hyperpigmentation, but a new nodule (diameter 4 mm) had arisen on the left breast, and both biopsy scars showed slight hypertrophy. By 7 months later, most of the lower back lesions and many of the arm lesions had disappeared, while the abdominal and upper back lesions remained unchanged. The terms ‘nodular’ and ‘keloidal’ scleroderma have been used indistinctly in the literature for naming this disorder [1]. Also, its variable clinical manifestations have led to question whether cases with subcutaneous lesions are different from cases with raised lesions. The present case did not show any indications of associated scleroderma, and the most appropriate name would appear to be ‘fibrosing reaction’ [1].