嗜酸性蜂窝织炎

报告1例嗜酸性蜂窝织炎.患者男,36岁.双下肢红斑时有痒痛半个月.外周血嗜酸性粒细胞2.55×109/L(分类0.263),骨髓嗜酸性粒细胞0.125,FIP1L1/PDGFRα融合基因(-),骨髓组织病理示嗜酸性粒细胞相对增生活跃.皮损组织病理检查:真皮及皮下组织浅层小血管内皮细胞肿胀,不同程度纤维素样变性、坏死直至阻塞,周围见大量嗜酸性粒细胞反应性浸润,呈火焰状,其间有少量淋巴细胞.诊断:嗜酸性蜂窝织炎.予甲泼尼龙和抗组胺药等治疗后皮损消退.     

嗜酸性蜂窝织炎

报告1例嗜酸性蜂窝织炎(Wells综合征).患者女,48岁.躯干反复出现水肿性红斑、斑块伴瘙痒6个月余.组织病理显示:真皮内大量嗜酸性粒细胞浸润,并町见胶原变性,形成火焰现象.诊断为嗜酸性蜂窝织炎.     

嗜酸性蜂窝织炎

报告1例嗜酸性蜂窝织炎.患者女,42岁.躯干出现水肿性红斑、结节伴瘙痒1月余.皮肤科检查:右侧腹部、臀部可见大片水肿性红斑、结节,界限较清,皮损形态不规则,触之有浸润感,触之较韧,无明显鳞屑.右侧腹部皮损组织病理检查示:真皮中下层大量嗜酸性粒细胞浸润,形成火焰现象,诊断:嗜酸性蜂窝织炎.     

呈带状损害的嗜酸性蜂窝织炎1例

患者男,62岁。左背部出现带状皮疹3月余。皮肤科情况:左背部可见一带状斑块,质韧。外周血和骨髓的嗜酸性粒细胞增多。皮损组织病理示真皮胶原间、真皮血管和附属器周围可见致密的淋巴细胞和嗜酸性粒细胞浸润。诊断:嗜酸性蜂窝织炎。     

皮损内注射复方倍他米松治疗Wells综合征一例

报告1例61岁女性患者,右前臂结节、斑块伴瘙痒1年。皮损组织病理示:真皮中下层见大量淋巴细胞及嗜酸粒细胞浸润,部分胶原束内可见嗜酸粒细胞脱颗粒形成"火焰"现象。诊断:Wells综合征(嗜酸性蜂窝织炎)。皮损内注射糖皮质激素治疗3个月后皮损消退,随访6个月未见复发。     

Well’s综合征1例

报告1例Well's综合征。患者女,31岁。四肢反复出现皮疹,伴瘙痒、疼痛1年余,加重1月。组织病理示:真皮内大量嗜酸性细胞浸润,并可见火焰现象。诊断为嗜酸性蜂窝织炎(Well's综合征)。     

嗜酸性蜂窝织炎一例

<正>嗜酸性蜂窝织炎又称Wells综合征,是一种原因不明的皮肤病,特征性的临床表现为类似蜂窝织炎的坚硬斑块,常常伴有外周血嗜酸粒细胞升高,皮损组织病理表现为嗜酸粒细胞浸润及特殊的"火焰征"。该病较为少见,现将诊治的1例报道如下。临床资料患者,女,39岁。双下肢暗褐色斑片、结节伴瘙痒5年。5年前,患者无明显诱因双下肢出现散在性暗褐色斑片、结节伴瘙痒,无发热、关节疼痛及其他全身症状,在当地医院就诊,行相关检查示嗜酸粒细胞升高(0.78×10     

Wells综合征1例

Wells综合征，又名嗜酸性蜂窝织炎（eosinophilic cellulitis），是一种病因不明、反复发作的炎症性疾病。现将我们所见1例报道如下。     

Wells综合征一例

42岁女性患者,全身反复出现红斑、水疱及脓疱,伴瘙痒3年,加重1个月。外周血嗜酸粒细胞绝对值4.83×10~9/L,分类28.4%。皮损组织病理示:真皮内大量嗜酸粒细胞浸润,并可见胶原变形,形成"火焰征"。诊断:嗜酸性蜂窝织炎(Wells综合征)。给予甲泼尼龙等治疗后皮损消退。     

Wells综合征1例

患者女,38岁。右臀部红斑肿热伴关节酸痛3个多月,加重并反复寒战发热1个月。皮肤组织病理检查：炎症性肉芽肿,血管周围见嗜酸性粒细胞浸润及局灶性胶原纤维坏死。诊断：嗜酸性蜂窝织炎（Wells综合征）。     

Eosinophilic Fasciitis Occurring Four Weeks after the Onset of Dialysis in a Renal Failure Patient

BACKGROUND: Eosinophilic fasciitis is a rare, scleroderma-like disease that usually affects the extremities of young to middle-aged males. The disease may cause flexion contractures and limit joint mobility and is associated with peripheral eosinophilia. The fascia, by definition, is infiltrated with mononuclear cells and typically with eosinophils. Eosinophilic fasciitis may be separated from another sclerodermatous disorder, linear scleroderma, by its response to systemic corticosteroids. The etiology is unclear but eosinophilic fasciitis has numerous disease associations. However, it has not previously been associated with renal failure and hemodialysis. OBJECTIVE: This article reports a case of eosinophilic fasciitis occurring four weeks following the onset of hemodialysis. METHODS: The clinical and histologic features confirmed the diagnosis of eosinophilic fasciitis. He was treated with systemic corticosteroids with good response. CONCLUSION: This is the first reported patient who developed eosinophilic fasciitis in close temporal relationship with the start of hemodialysis. While eosinophilic fasciitis may be coincidental with a common disorder, namely, renal failure, it is interesting to note that hemodialysis patients often have immune-regulation abnormalities and peripheral eosinophilia.     

32例幼年黄色肉芽肿临床与病理分析

 目的:归纳总结幼年黄色肉芽肿的临床及组织病理特点。方法:回顾性分析2011年12月-2019年12月我院确诊的32例幼年黄色肉芽肿患儿的临床资料和组织病理学检查结果。结果:32例患儿皮损多表现为头面部、躯干、四肢黄色或黄褐色丘疹、结节,也可表现为红色或暗红色,有1例伴皮肤外症状。皮损组织病理特点可分为3种类型：早期（占12.50%）,可见大量组织细胞浸润,散在多核巨细胞、淋巴细胞、少量嗜酸性细胞浸润;成熟期（占78.12%）,可见典型泡沫细胞、多核巨细胞及Touton巨细胞;消退期（占9.38%）,可见梭形细胞,少许组织细胞及多核巨细胞。免疫组化结果为CD68（+）、CD1a（-）、Langerin（-）及S-100（-）。结论:临床上根据典型皮损特点及病理表现一般可诊断幼年黄色肉芽肿,但临床上有必要行病理检查以帮助减少误诊率。     

Eosinophilic cellulitis and dermographism

A 26-year-old man presented with a history of intermittent erythematous plaques on his hands and legs. A peripheral blood eosinophilia was noted. Histopathologic examination showed numerous eosinophils and characteristic flame figures. The clinical presentation and histopathologic alterations are consistent with the diagnosis of Wells' syndrome, which is also known as eosinophilic cellulitis. Wells' syndrome is a rare condition of unclear etiology. We discuss its diagnosis and possible association with other conditions that manifest peripheral eosinophilia.     

Unexplained hypereosinophilia and the need for cytogenetic and molecular genetic analyses

BACKGROUND: Idiopathic hypereosinophilic syndrome (HES) is a diagnosis made after the exclusion of other causes of eosinophilia. However, differentiation of idiopathic HES from eosinophilic leukemia is sometimes difficult. In some cases, these diagnoses can be differentiated by cytogenetic or molecular findings, as illustrated in the patients described herein. OBSERVATIONS: We describe 3 patients with HES and associated pruritus; 1 patient also had recurrent lesions of eosinophilic cellulitis. All 3 patients were initially diagnosed as having idiopathic HES, but after evaluation and demonstration of molecular abnormalities, they were classified as having eosinophilic leukemia. CONCLUSIONS: Patients with a diagnosis of idiopathic HES should be evaluated for cytogenetic or molecular genetic abnormalities. These abnormalities can establish a diagnosis of chronic eosinophilic leukemia and may provide clues for emerging therapies.     

Eosinophilic cellulitis presented with semicircular pattern

Eosinophilic cellulitis (Wells' syndrome) is a rare condition of unknown etiology and pathogenesis. It is characterized by erythematous plaques and a histological picture of dermal eosinophilic infiltration with "flame figures". The typical clinical presentation of eosinophilic cellulitis is mildly pruritic cellulite-like plaques. Urticarial, vesiculo-bullous, nodular and papulonodular variants were also reported. Herein, we describe a patient with annular and semicircular manifestations of eosinophilic cellulitis. It was treated successfully with low-dose cyclosporine A treatment.     

Wells syndrome

A rare eosinophilic dermatosis, Wells syndrome, also referred to as eosinophilic cellulitis, is characterized by great clinical variability. Typical findings include infiltrated erythematous plaques arising on the extremities. Lesions initially resemble erysipelas/cellulitis, however, they do not improve with antibiotic treatment. Eosinophilic cellulitis is a diagnosis of exclusion that may only be made over the course of the disease, taking into account clinical and characteristic histological findings (flame figures). Although multiple potential triggers have been proposed, the exact etiology remains unresolved. Involvement of abnormal Th2 cells, IL‐5, and activated eosinophilic granulocytes suggest a nonspecific hypersensitivity response to exogenous or endogenous stimuli. Corticosteroids may have a beneficial effect on the chronic, recurrent course frequently observed. The disease is often self‐limiting, healing without sequelae. Given that transitions to hematological and oncological disorders have been observed, patients should be closely followed up.     

Eosinophilic Panniculitis

A 39-year-old obese female patient with borderline diabetes mellitus who developed multiple, tender, and hard nodules on the lower abdominal wall is described. The histological features were characterized by mixed panniculitis, showing massive eosinophilic infiltration and fibrosis in the septae and many foam cells in the parenchymal area of subcutaneous tissues. The eruption regressed gradually during the course of diet therapy for diabetes mellitus and obesity. Although the etiology is diverse and nonspecific, eosinophilic panniculitis seems to be a unique histopathological reaction pattern characterized by massive eosinophilic infiltration into subcutaneous tissues.     

Eosinophilic Cellulitis (Wells' Syndrome)

Abstract: Two patients with eosinophilic cellulitis are reported and 22 additional cases from the literature are reviewed. Cutaneous lesions are variable in appearance and may be confused with cellulitis, urticaria, insect bites, or contact dermatitis. Microscopically, there is a dense dermal infiltrate of eosinophils. Subsequently, granulomatous features with characteristic "flame figures" become apparent. Peripheral eosinophilia is common. The etiology of eosinophilic cellutitis is unknown, although a hypersensitivity mechanism is suspected. Treatment with systemic corticosteroids is frequently effective, but the disease Is often characterized by relapses that can occur for several years.     

Acral keratosis with eosinophilic dermal deposits: a distinctive clinicopatholgic entity or colloid milium redux?

AIMS: The differential diagnosis of acral keratoses is broad. Encompassing a variety of infectious, heritable and degenerative disorders, emphasis upon the clinical setting and histologic subtlety are often required to arrive at the correct diagnosis. Herein, we report on a series of adult patients who presented with agminated or solitary papules of the distal finger found on histologic examination to contain amorphous eosinophilic deposits. RESULTS: The eosinophilic deposits were found in close proximity to the overlying epithelium and devoid of apoptotic keratinocytes, plasma cells, or vascular thickening reminiscent of amyloidosis or hyalinosis cutis. Special and immunostains yielded eosinophilic material that was elastin and Protein P negative. Despite a similar histomorphologic appearance to colloid milium, typical clinical features of this entity were not present. CONCLUSION: The etiologic significance of this condition is unknown. Potential sources of the material and a discussion of the differential diagnosis follow.     

Rapidly growing squamous cell carcinoma.

BACKGROUND: Squamous cell carcinoma (SCC) may present with a history of rapid growth. Although multiple subtypes have been described regarding histologic characteristics and etiology, the subset of rapidly growing squamous cell carcinomas (RGSCC) has not been described. OBJECTIVE: To evaluate and describe the clinical and histologic characteristics of squamous cell carcinomas that grow rapidly. METHODS: Recorded clinical data and biopsies of 26 lesions with a history of rapid growth and histologically diagnosed as SCC were reviewed. RESULTS: Rapidly growing SCC occurred most commonly on the head and neck, followed by hands and extremities, and had an average duration of 7 weeks before diagnosis. The average size of the lesions was 1.29 cm and nearly 20% occurred in immunosuppressed patients. CONCLUSIONS: Some SCCs may grow rapidly. The reason for the rapid growth is not clear and several hypotheses are discussed including immunosuppression and viral etiology. These lesions should be treated aggressively as their behaviour and prognosis are not yet well described.