Spindle cell lipoma (SCL) in the scrotum is a very rare presentation with only a few cases reported in the literature. The most common sites for this benign lesion are the neck, shoulder, and back. We present a 72-year-old male patient with painless swelling on the left half of the scrotum with a histopathological diagnosis of SCL.

Background: Palpable migratory arciform erythema is clinically characterized by sharply circumscribed, infiltrated erythematous patches that tend to spread irregularly, resulting in arciform morphologic features. The histopathologic features are characterized by a patchy inflammatory perivascular and periadnexal T-lymphocytic infiltrate throughout the dermis. The disease runs a chronic course and is rarely described in the literature.Observation: Three middle-aged patients of both sexes had palpable migratory arciform erythema with 1, several, or multiple lesions on the trunk. There was a dense perivascular and periadnexal, predominantly lymphocytic infiltrate of the reticular dermis without any interstitial distribution of inflammatory cells. Absence of mucin deposits and plasma cells was a striking feature. The immunohistochemical profile showed an infiltrate dominated by T cells of polyclonal origin. In addition, polyclonal B cells and histiocytes were present in small, numbers. In all 3 cases, oral antibacterial treatment resulted in a complete (2 patients) or temporary (1 patient) resolution of skin lesions.Conclusions: Palpable migratory arciform erythema shows distinctive differences in clinical and pathological features and treatment in contrast to other diseases with cutaneous lymphocytic infiltrates, including lymphocytic infiltration of Jessner and Kanof. Therefore, it is likely a distinct disease entity.

Twenty cases of cutaneous follicular lymphoid hyperplasia with monotypic plasma cells are presented in a clinicopathologic study on 18 patients. The plaque-like or nodular lesions were solitary in 10 and multiple in eight patients. Immunohistochemistry showed well-defined B- and T-cell areas. Sheets of monotypic plasma cells occurred either interfollicularly or adjacent to the sclerotic stroma, with expression of IgG/kappa in 14 and IgG/lambda in six cases. In one patient with multiple lesions, one sample contained polyclonal plasma cells, whereas the other specimen showed light chain restriction. In another patient, disease recurred with a polytypic cutaneous plasma cell infiltrate. Polymerase chain reaction (PCR) revealed clonal immunoglobulin heavy chain gene rearrangements in eight of 13 cases, which was confirmed by Southern blot analysis in three samples. Clonal T-cell receptor chain gene rearrangements were not detected. Disease progression to overt malignant lymphoma did not occur within the follow-up period of up to 12 years, but recurrent disease was seen in three patients. Our data indicate that cutaneous lymphoid hyperplasia with monotypic plasma cells is a biologically distinct clinicopathological entity.

Adenoid cystic carcinoma of the skin is one of the rarest sweat gland tumours. We have studied two cases of adenoid cystic sweat gland carcinoma clinically, histologically and immunohistochemically. One tumour was located on the occiput of an 18-year-old male patient, while the other developed on the back of a 49-year-old woman. Histologically, both carcinomas were characterized by basaloid tumour cells showing the typical adenoid-cystic growth pattern. The cells were arranged in solid, cribriform, tubular and cystic aggregates, which were surrounded by mucoid, Alcian blue material. Immunohistochemically, the tumour cells showed coexpression of cytokeratins typical of stratified epithelia (CK1/5/10/14) and cytokeratins of the simple epithelial type, namely CK7, CK8, CK18, and CK19. Coexpression of these cytokeratins is usually observed in normal fetal sweat glands, but not in adult sweat glands.

Although myoepithelial cells are detectable in many benign sweat gland tumours, little is known about their role in sweat gland carcinomas. To specifically demonstrate myoepithelial cells, paraffin sections from 46 sweat gland carcinomas were stained, using a standard avidin-biotin-peroxidase complex method, with the monoclonal alpha-smooth muscle actin antibody 1A4. Myoepithelial cells were not found in adenoid cystic eccrine carcinoma (n = 2), malignant nodular hidradenoma (n = 2), porocarcinoma (n = 4), extramammary Paget's disease (n = 12), sclerosing sweat duct carcinoma (n = 4) or in adenosquamous-mucoepidermoid carcinoma (n = 1). In contrast, myoepithelial cells were demonstrated in two of eight apocrine adenocarcinomas, one of six mucinous eccrine carcinomas and two of seven eccrine adenocarcinomas. In all these tumours myoepithelial differentiation was found in peripheral cells of solid tumour islands, or in basal cells of tubular structures. However, in most areas of the tumours, myoepithelial layers were discontinuous. Cells in the centre of solid tumour nodules, and luminal cells of tubular structures, were negative for alpha-smooth muscle actin. In analogy to breast tumours, in which malignancy and invasiveness correlate with scattered or absent myoepithelial cells, we suggest that disrupted myoepithelial layers in sweat gland carcinomas may be interpreted as a loss of the invasion barrier.

The coexpression of cytokeratin and vimentin intermediate filaments has been immunohistochemically evaluated in 124 benign and malignant sweat gland tumors of various types in comparison to normal sweat glands. In addition, all neoplasms have been stained by an antibody to alpha‐smooth muscle actin. Epithelial cells reacted with the pan‐cytokeratin antibody lu‐5. In normal sweat glands, vimentin immunoreactivity was restricted to myoepithelial cells and to some cells of the coiled duct. In benign sweat gland tumors (n=88), coexpression of vimentin and alpha‐smooth muscle actin was frequently found in basal cells of neoplasms considered to differentiate towards the secretory coil of the eccrine or apocrine gland. These included eccrine spiradenoma, apocrine cystadenoma, hidradenoma papilliferum, syringocystadenoma papilliferum, and cylindroma. Thus, in these tumors, vimentin‐reactive cells corresponded to myoepithelial cells. Vimentin‐positive cells were also found in 14 of 36 sweat gland carcinomas, including 1 case of sclerosing sweat duct carcinoma, 1 case of porocarcinoma, 4 cases of eccrine adenocarcinoma, 1 case of mucinous eccrine carcinoma, and 5 cases of apocrine adenocarcinoma. Co‐expression of vimentin and alpha‐smooth muscle actin was observed in some cells of eccrine and apocrine adenocarcino‐mas. Therefore, in these neoplasms, some vimentin‐positive cells appear to represent myoepithelial cells. In contrast, vimentin‐positive cells in all other malignant tumors did not express alpha‐smooth muscle actin. Our results indicate that coexpression of cytokeratin and vimentin may be frequently found in a variety of benign and malignant sweat gland tumors. In the majority of these neoplasms, vimentin‐positive cells correspond to myoepithelial cells. Because vimentin is not specific for myoepithelial cells, additional stains for alpha‐smooth muscle actin should be performed to prove the myoepithelial nature of vimentin‐positive cells.

Cutaneous metastasis from gastric carcinoma is uncommon. We describe a patient with a metastasis from gastric carcinoma to a congenital melanocytic nevus. The diagnosis was confirmed by positive immunohistochemical staining for cytokeratin 20 and lack of cytokeratin 7.

Brooke-Spiegler syndrome is an autosomal dominantly inherited disease characterized by the development of multiple trichoepitheliomas and cylindromas. Among other neoplasms that may also occur in Brooke-Spiegler syndrome are basal cell carcinomas and spiradenomas. Spiradenomas and cylindromas have so many features in common that they have been regarded as variants of the same neoplasm. This assumption was supported by the occurrence of both types of lesions in Brooke-Spiegler syndrome. We report a case of Brooke-Spiegler syndrome in which spiradenomas were found in the immediate vicinity of trichoepitheliomas and in continuity with follicles. Because of the embryonic relationship between follicles and apocrine glands, these features indicate that spiradenomas are apocrine neoplasms. We conclude that Brooke-Spiegler syndrome is an inherited disease that affects the folliculosebaceous apocrine unit.

ever,now that effective treatment has been found, it is essential that pyodermagangrenosum starting in infancy at the site of OPT injection be recognized as the marker for this syndrome.The pathologic findings in the aorta included granulation tissue, giant cells, plasma cells, and neutrophils.lA review of the synovial pathologyfrom the first patient showed the same features, as pictured in the original report.The two described cases may not fully define all features of the syndrorne.f

One hundred and two cases of benign sweat gland tumors of the skin were studied for the presence of myoepithelial cells specifically identified by a monoclonal antibody to alpha-smooth muscle actin on paraffin-embedded tissues. The monoclonal antibody gave a positive result in 12 of 12 cases of cylindroma, 14 of 16 cases of spiradenoma, 2 of 2 cases of apocrine tubular adenoma (papillary eccrine adenoma), 5 of 5 cases of apocrine hidrocystoma, 5 of 5 cases of hidradenoma papilliferum, and in 10 of 10 cases of syringocystadenoma papilliferum. Rare myoepithelial cells were detected in only 1 of 10 cases of mixed tumor, apocrine type. There was no immunoreactivity for alpha-smooth muscle actin in eccrine hidrocystoma (2 cases), mixed tumor of eccrine type (2 cases), syringoma (7 cases), hidroacanthoma simplex (1 case), eccrine poroma (14 cases), clear cell hidradenoma (15 cases), and in 1 case of eccrine syringofibroadenoma. Our data support the concept that myoepithelial cells are seen in most sweat gland tumors considered to differentiate toward the secretory coil of the normal sweat gland. In contrast, myoepithelial cells are absent in tumors showing differentiation toward the excretory (ductal) component of the gland.

1 Department of Dermatology, University of Munich, Germany. 2 Department of Dermatology, University of Zagreb, Yugoslavia. 3 Department of Pathology, Kantonsspital St. Gallen, Switzerland.

This report describes a 50-year-old male patient with fibroma of tendon sheath. The tumour had grown rapidly, and clinical examination of it led to the suspicion of a giant cell tumour of tendon sheath and a vascular glomus tumour. Microscopical investigation then allowed diagnosis of the tumour as a fibroma of tendon sheath, which was characterized by spindle-shaped and stellate-shaped fibroblasts, a fibrocollagenous, partly myxoid stroma, and slit-like vessels. Immunohistochemically, most tumour cells expressed vimentin and smooth muscle actin, but not desmin. Thus, fibroma of tendon sheath can be regarded as a synovial tumour with myofibroblastic differentiation. Histologically, fibroma of tendon sheath must be differentiated from other tumours, such as giant cell tumour of tendon sheath and histiocytoma, but also from nodular fasciitis and sarcomas.

Four mucinous sweat gland carcinomas were examined for the distribution of cytokeratin (CK) polypeptides using immunohistochemical techniques on paraffin‐embedded sections. All the tumour specimens reacted with monoclonal antibodies to CK 7, CK 8, CK 18 and CK 19. Antibodies to CK 1, CK 1/2/10/14, CK 1/5/10/11, CK 13, CK 14 and CK 20 did not stain any of the carcinomas. The results add additional support to the notion that mucinous sweat gland carcinoma represents a tumour histogenetically related to the eccrine secretory coil. Furthermore, the absence of CK 20 might significantly contribute to the differentiation of this tumour from cutaneous metastases from gastrointestinal carcinomas.