Cutaneous Hodgkin's disease: an immunohistochemical analysis

Studies of skin involvement in Hodgkin's disease are infrequent in the literature. In particular, immunophenotypic analyses of specific cutaneous infiltrates have been performed in only a few cases. We analyzed the clinical, histological and immunohistochemical features of specific cutaneous manifestations of Hodgkin's disease comparing histologic and immunophenotypic aspects of skin lesions with those of the nodal counterpart. Seven patients with Hodgkin's disease of the lymph nodes and specific cutaneous lesions, where both nodal and skin biopsies were available for histologic and immunohistochemical analyses, were included in this study. Immunohistochemical stains were performed with a 3-step immunoperoxidase technique on routinely-fixed, paraffin-embedded tissue sections. All 7 patients had nodular sclerosis Hodgkin's disease of the lymph nodes. In the skin, clinical presentations included reddish-brown papules, plaques, nodules and ulcerated tumors. Histologic examination of cutaneous lesions showed features consistent with nodular sclerosis Hodgkin's disease in 6 cases and unclassifiable Hodgkin's disease in one. Reed-Sternberg cells and lacunar cells were present in 4 cases (57.1%). Immunohistochemical analysis of Hodgkin's and Reed-Sternberg cells revealed a constant positivity for CD30 (BerH2) and negativity for CD45 (LCA) in both the lymph nodes and the skin. Staining with CD15 (M1) revealed positivity in 7/7 nodal samples and 5/7 skin biopsies. Cytoplasmic expression of immunoglobulin light chains (both lambda and kappa) was observed in one cutaneous case. The accompanying infiltrate was mostly composed of T-lymphocytes admixed with variable numbers of monocytes/macrophages and eosinophils. Our results indicate that the histology of cutaneous specific manifestations of Hodgkin's disease correlates with that of the nodal counterpart in most cases. Classical Reed-Sternberg cells, however, can be detected only in a proportion of the cutaneous lesions. Although the immunophenotype of Hodgkin cells and Reed-Sternberg cells in the lymph nodes and the skin is similar, CD15-negativity of Reed-Sternberg cells can be observed in cutaneous infiltrates of Hodgkin's disease.     

Histologic features of cutaneous sinus histiocytosis (Rosai-Dorfman disease): study of cases both with and without systemic involvement

Sinus histiocytosis with massive lymphadenopathy (Rosai-Dorfman disease) is a systemic proliferation of cells that resemble the sinus histiocytes of lymph nodes. Whereas initial reports highlighted the often striking cervical adenopathy, more than 40% of patients have extranodal involvement. Cutaneous lesions are the most common form of extranodal disease, but cases that present as cutaneous disease without lymph node involvement are rare. We examined biopsies from three patients with cutaneous lesions of sinus histiocytosis, none of whom had detectable systemic involvement, and compared them to those of two patients whose lymph nodes were involved by the disease. The histology of skin lesions in all five cases showed dense nodular or diffuse infiltrates of "histiocytes," emperipolesis of lymphocytes, neutrophils, and plasma cells. "Histiocytes" were present in lumens of dilated lymphatics. At the peripheries of the lesions were lymphoid aggregates and thick-walled vessels surrounded by plasma cells. Staining with anti-S-100 protein antibody showed marked cytoplasmic positivity in the "histiocytes" in each case. The only features that differed among the two groups were the presence of pseudoepitheliomatous hyperplasia and infiltrates of eosinophils in one case in which the disease was limited to the skin. We believe that cutaneous sinus histiocytosis can be specifically diagnosed by skin biopsy. Because cutaneous sinus histiocytosis may be unfamiliar to general pathologists, dermatopathologists, and dermatologists, cases limited to the skin may be under-recognized.     

Lymphomatoid papulosis and Hodgkin's disease: Are they related?

Two different characteristic types of lymphomatoid papulosis (type A and type B) can be histologically distinguished, that represent the ends of a spectrum. In the present report, two patients are described. One patient with both lymphomatoid papulosis type A and type B lesions for more than 25 years developed Hodgkin's disease (nodular sclerosing type) in the para-aortic and para-iliac lymph nodes. Histologic examination of the skin lesions in the second patient, who had Hodgkin's disease (nodular sclerosing type) in many supradiaphragmatic lymph nodes, showed the characteristic features of lymphomatoid papulosis type A. These findings, together with the results of recent immunohistochemical investigations showing many similarities between the large atypical cells in lymphomatoid papulosis type A lesions and Reed-Sternberg cells in Hodgkin's disease, support the view that lymphomatoid papulosis type A and Hodgkin's disease are closely related conditions. The results of recent studies indicate a close relationship between lymphomatoid papulosis type B and the early stages of mycosis fungoides. Accordingly, the possible relationship between lymphomatoid papulosis types A and B, mycosis fungoides, and Hodgkin's disease is discussed.     

Lymphomatoid papulosis followed by large-cell lymphoma: immunophenotypical and genotypical analysis

The immunophenotype and genotype of atypical cells in skin and lymph node infiltrates were investigated in a patient with lymphomatoid papulosis (LyP) complicated by anaplastic large-cell lymphoma of the lymph nodes. The large atypical cells in both skin and lymph nodes displayed an almost identical immunophenotype, i.e. CD30+ and CD25+. Southern blot analysis for T-cell receptor beta-chain gene rearrangement revealed an identical gene configuration in DNA extracted from skin and lymph node. Our results strongly support the hypothesis that clonal populations of T cells arising in cutaneous LyP lesions may undergo malignant transformation, spread into regional lymph nodes, and give rise to secondary malignant lymphomas, such as anaplastic large-cell lymphoma.     

以环形红斑为初发表现的T淋巴母细胞性淋巴瘤的临床研究

目的 的降雨 例罕见的以环形红斑为初发表现的成人T淋巴母细胞性淋巴瘤。方法 对其临床,组织病理,免疫组化,分子生物学和各种特殊的实验室检查进行研究。结果 颈部,腹股沟肿大数10个淋巴结,全身百余个环形红斑,胸部CT示;前上纵隔占位性淋巴瘤表现。胸水中找到异形细胞。骨髓片示;淋巴瘤累及骨髓,外周血中未发现瘤细胞。淋巴结结构破坏,瘤细胞弥漫分布,呈“满天星”图像。部分瘤细胞浸润,部分向表皮性,可见Pautrier微脓肿,少数淋巴样细胞细胞核呈曲核型,与淋巴结的瘤细胞相似;免疫组化示：LCA,CD43,UCHL-1均阳性,TdT阴性,原位杂交示EBER1/2在淋巴结组织中呈最性;皮肤组织中呈阴性。结论 此例为首例报告罕见的以环形红斑为初发表现的T淋巴母细胞性淋巴瘤。     

Primary cutaneous T-cell-rich B-cell lymphoma and Hodgkin's disease in a patient with Gardner's syndrome

A 50-year-old patient, suffering from familial polyposis (Gardner's syndrome), initially presented with several nodules on his left arm. Histological examination revealed primary cutaneous T-cell-rich B-cell lymphoma (TCRBCL). Staging procedures failed to detect any systemic involvement. Three years after total excision of the tumours, the patient presented with a non-specific dermatitis, enlarged axillary lymph nodes and splenomegaly. Histological and immunohistochemical examination of lymph node and spleen biopsy specimens resulted in the diagnosis of Hodgkin's disease (HD) of the nodular sclerosis type. Sequence analysis of single cells micromanipulated from skin and from lymph node lesions indicated that both lymphoma infiltrates were derived from the same precursor germinal centre B-cell clone. This is a case showing a clonal relationship between TCRBCL and HD, providing support to the B-cell origin of Hodgkin and Reed-Sternberg cells.     

The clinical picture and therapy of nodular mastocytosis

The authors review the literature data on and describe 6 cases of nodular mastocytosis presenting as multiple blending nodes. The patients (2 girls and 4 boys aged under 4) have developed a disseminated process with multiple nodes up to 3.0-3.5 cm in diameter colored brownish or yellowish, mostly with a smooth surface, localized on the hairy part of the head, trunk, and limbs. Some nodes blended to form larger foci of lesions, particularly on the back and in large skin folds. In 5 patients the diagnosis has been confirmed histologically. No visceral or systemic abnormalities have been revealed. Enlarged (pea-size) inguinal and cubital lymph nodes have been detected in one child. Zaditen therapy has been fairly effective.     

A CASE OF PLASMACYTOSIS WITH MULTIPLE PECULIAR ERUPTIONS

A 32-year-old man had been in good health until he noticed painful swelling of the lymph nodes in the left occipital region in spring of 1975. Half a year later, multiple, infiltrating erythematous or nodular lesions appeared on the anterior chest and then spread over almost his entire body except for the lower extremities. These skin lesions were reddish brown to purplish brown in color, and irregular in shape and size. All of his superficial lymph nodes were palpable, and pain was felt on pressure. No other systemic symptoms were noted. Laboratory findings showed polyclonal gammopathy; total protein, 9.6 g/dl; IgG, 4,900 mg/dl; IgA, 590 mg/dl and an increased erythrocyte sedimentation rate of 92 mm/hr. A skin biopsy revealed prominent perivascular proliferation of plasma cells and follicular hyperplasia in the dermis. Lymph node biopsy also revealed proliferation of plasma cells in both the paracortical area and medulla. No neoplastic growth was recognized. These pathological findings and polyclonal hypergammaglobulinemia were consistent with reactive plasmacytosis. The patient is now under observation, and the skin lesions and systemic lymphadenopathy have not been changed. This peculiar B-cell proliferative disorder was discussed in relation to other diseases.     

Purely cutaneous Rosai-Dorfman disease present for 19 years

BACKGROUND: Rosai-Dorfman disease is a non-Langerhans histiocytosis chiefly affecting lymph nodes sites. In rare cases, it presents in the form of isolated skin lesions, without adenopathy, in which case it is a benign disease that regresses spontaneously within our number of months and years. PATIENTS AND METHODS: An 83 year-old man presented with multiple red-brown nodular lesions on the upper part of the body that had been progressing over a period of 19 years. Histological examination showed infiltrate characteristic of Rosai-Dorfman disease, with numerous dermal foci of histiocytes expressing protein S100 but not expressing CD1a on immunohistochemical analysis, as well as emperipolesis. The lymph nodes sites were unaffected, and the remainder of the clinical and laboratory examinations were normal, indicating a purely cutaneous form of the disease. Treatment with isotretinoin was ineffective and the lesions continued to spread gradually, being treated from time to time with CO2 laser or cryotherapy. DISCUSSION: Our case is atypical in terms of clinical presentation since it involved diffuse nodular lesions. The disease course was also unusual in that no spontaneous regression was observed even after 19 years.     

Immunohistochemical detection of interferon-gamma-producing cells in dermatophytosis

Skin lesions of dermatophytosis are thought to be a result of a T cell-dependent inflammatory response that is mediated by various cytokines. We examined whether IFN-gamma-positive cells (as expression of Th1 response) were present in the skin lesions of dermatophytosis in situ by immunohistochemical techniques. Mixtures of CD4-positive T cells and CD8-positive T cells were found to be present in the dermal infiltrates of the lesions. Considerable numbers of CD1a-positive cells were detected in the upper dermis and epidermis. A marked accumulation of CD68-positive cells was found in the upper dermis. IFN-gamma-positive cells were present in the upper dermis of the lesions. The pattern of IFN-gamma staining appeared to be intracellular in mononuclear lymphoid cells. The staining was considered to be highly specific because it could be completely blocked by preabsorption with recombinant IFN-gamma. Our data support the hypothesis that the skin lesions of dermatophytosis may be associated with a Th1 response. Th1 response, which is characterized by IFN-gamma release, is thought to be involved in the host defense against dermatophytes and to reflect cutaneous reaction in dermatophytosis.     

Dendrocyte population in cutaneous and extracutaneous Kaposi's sarcoma.

In order to investigate the hypothesis that the spindle cells of Kaposi's sarcoma originate from dendrocytes, we stained 22 cases of cutaneous and extracutaneous Kaposi's sarcoma for the presence of factor XIIIa. We selected eight lesions from the skin, five from the oral mucosa, four from gastrointestinal mucosa, three from lymph nodes, and one each from esophagus and conjunctiva for this study. The majority of cutaneous and lymph node Kaposi's sarcoma lesions had a considerable number of dendrocytes admixed with the spindle tumor cells. Of the five oral mucosal lesions only three showed a focal presence of dendrocytes. No dendrocytes were observed in the lesions biopsied from the gastrointestinal mucosa, esophagus, and conjunctiva. Our findings suggest that the proliferation of dendrocytes seen within the lesions of Kaposi's sarcoma in the skin and lymph nodes probably represents a nonspecific host response in organs where they are normally present, and it is unlikely that they constitute the neoplastic cells of Kaposi's sarcoma.     

The role of chemokines in allergic contact dermatitis

Chemokines are important mediators of immune-mediated skin diseases. Allergic contact dermatitis (ACD) is the most thoroughly investigated T cell-mediated disorder because of the ability to easily reproduce the lesions in humans and the availability of an excellent mouse model. Migration of dendritic cells from the skin to lymph nodes is absolutely required for induction of hapten sensitization, and depends upon expression of CCR7 by mature dendritic cells and SLC in the lymph nodes. During expression of ACD, recruitment of T lymphocytes is driven by chemokines exposed on the surface of endothelial cells or released by activated resident skin cells such as mast cells, fibroblasts and keratinocytes. Chemokines are produced in a coordinated and sequential manner, with IL-8 and RANTES induced by TNF-alpha during early stages, and MCP-1, IP-10, Mig, I-TAC, I-309 and MDC induced by IFN-gamma during later stages. Infiltrating monocytes, dendritic cells and T cells are additional sources of chemokines for further leukocyte accumulation. Distinct T cell subsets express different chemokine receptors, with type 2 cells mostly attracted by eotaxin, MDC, TARC and I-309, and type 1 cells sensitive to IP-10, Mig, I-TAC, RANTES and MIP-1beta. MCP-1 is effective on both subsets. T regulatory cells, which inhibit dendritic cell function and are probably involved in the termination of ACD, are sensitive to MCP-1, MIPs and TARC, but express high levels of CCR8 and are more specifically attracted by I-309. Targeting chemokines and chemokine receptors may offer new opportunities for therapeutic interventions in ACD and other chronic inflammatory skin diseases.     

EC-SOD suppresses contact hypersensitivity in mouse skin by impairing Langerhans cell migration

Extracellular superoxide dismutase (EC-SOD) is primarily a tissue enzyme and has been implicated in the modulation of inflammatory response. The biological role of EC-SOD in skin, however, has rarely been investigated. In this study, we aim to explore the effects of EC-SOD on the inflammatory response in skin by evaluating the contact hypersensitivity response (CHS) in EC-SOD transgenic mice. Transgenic mice with skin-specific expression of EC-SOD were sensitized and challenged with 2,4,6-trinitro-1-chlorobenzene (TNCB), followed by measurement of ear swelling. EC-SOD transgenic mice showed significantly reduced CHS responses compared with wild-type mice. Histological evaluation of the challenged ears of EC-SOD transgenic mice revealed diminished infiltration of inflammatory cells with a failure to induce expression of inflammatory cytokines, such as tumor necrosis factor-alpha and IFN-gamma, on sensitization and challenge with TNCB. Furthermore, Langerhans cell migration to lymph nodes was impaired in EC-SOD transgenic mice. These results indicate that EC-SOD downregulates CHS through inhibition of the inflammatory response, suggesting a possible therapeutic regimen in inflammatory skin diseases.     

套细胞淋巴瘤伴皮肤虫咬样反应一例

【摘要】 患者男,74岁,确诊套细胞淋巴瘤5年,躯干、四肢丘疱疹伴瘙痒10个月就诊。皮疹瘙痒剧烈,给予抗组胺药物对症治疗不能缓解。体检：躯干、四肢皮肤见散在绿豆至黄豆大小红色丘疹及丘疱疹,部分表面见浅表结痂,以双上肢皮损为主,颈部、双侧腹股沟可触及肿大淋巴结,约2 cm × 1 cm。颈部淋巴结病理示,正常淋巴结结构完全破坏,中等大淋巴样细胞呈结节状或弥漫增生浸润,免疫组化示CD20（+++）,CD79α（+++）, Bcl-2（++）,细胞周期蛋白D1（+++）,CD5（++弱）,CD43（++）,Bcl-6（++）, PAX-5（+++）,κ（+++）,λ（±） ,Ki-67（10% ~ 30%+不均）。皮损组织病理及免疫组化：表皮大致正常,真皮浅中层血管、附属器周围见以中等大小淋巴样细胞为主的团灶状浸润,其间散在嗜酸性粒细胞;免疫组化：CD3（部分+）,CD5（弥漫性+）,CD20（部分+）,细胞周期蛋白D1（部分+）,Ki-67（10% +）。根据临床资料、淋巴结及皮损组织病理及免疫组化,诊断为套细胞淋巴瘤伴皮肤虫咬样反应。     

Cutaneous composite lymphoma of mycosis fungoides and Hodgkin lymphoma: Response to sequential therapy

Composite lymphoma is defined as two or more morphologically and immunophenotypically distinct lymphoma clones that occur in the same tissue site. The occurrence of cutaneous composite lymphoma (CCL) is extremely rare. Here we report a unique case of CCL consisting of Hodgkin lymphoma (HL) and mycosis fungoides (MF). Our patient presented with longstanding erythematous plaques on the skin and later developed axillary lymph node enlargement. Histopathologically, the skin lesions were characterized by a dense dermal lymphocytic infiltrate with prominent epidermotropism of pleomorphic T-cells, consistent with typical MF. Nonetheless, scattered large atypical cells resembling Reed-Sternberg (R-S) cells were interspersed among these atypical T-cells in the deep dermis. Immunophenotyping suggested a HL origin of these R-S cells. Monoclonality of T-cell receptor beta gene was detected in the skin, monoclonal immunoglobulin heavy chain gene rearrangement was identified in these R-S cells microdissected from the deep dermis, confirming the origin from HL. The lymph node biopsy showed nodular sclerosis classic Hodgkin lymphoma. Therefore, CCL of HL and MF, with lymph node HL was diagnosed. The lesions of this patient responded to a sequential treatment to HL and MF. Being aware of this rare CCL facilitates correct diagnosis and proper clinical management.     

Necrobiotic xanthogranuloma associated with paraproteinemia and non-Hodgkin's lymphoma developing into chronic lymphocytic leukemia: the first case reported in the literature and review of the literature

A 56-year-old married female presented in May 1998 with a 5-month history of xanthelasma of the eyelids, followed 4 months later by two enlarged lymph nodes of the left side of the neck and three of the left axilla. At the same time, she developed xanthomatous patches on the face, neck, and shoulders (Fig. 1). The cutaneous lesions were xanthomatous nodules and plaques, affecting the periorbital regions. Later, the whole face was affected, followed by ulcerated lesions on the scalp, chest, back, and extremities (Fig. 2). The skin lesions became painful, pruritic, ulcerated tumors (Fig. 3). In July 1998, computed tomography (CT) scans of the chest and abdomen with contrast medium showed pretracheal, bilateral axillary, right retrochural, paracaval, aortocaval, and para-aortic lymph node enlargement. These findings were suggestive of lymphoma. CT scan also showed slight heterogeneous hypodensity in the upper part of the right lobe of the liver, suggesting fatty infiltration. The spleen, pancreas, and suprarenal glands appeared normal. One cervical and two left axillary lymph nodes were excised. They revealed total replacement of the nodular architecture by a diffuse proliferation of mature lymphoid cells having small nuclei and a crumbled chromatin pattern, and very rare mitosis. It was concluded from the lymph node biopsies that these changes were typical of non-Hodgkin's lymphoma, diffuse and small cell type, of low-grade malignancy. A bone marrow aspirate showed a marrow heavily infiltrated by lymphoid cells with some immaturity. The megakaryopoiesis was adequate. Trephine biopsies showed similar changes. Iron stores appeared to be absent. The bone marrow picture was consistent with diffuse, well-differentiated non-Hodgkin's lymphoma, developing into chronic lymphocytic leukemia (CLL). Endoscopy showed antral-type gastric mucosa exhibiting mild chronic gastritis. Skin biopsy from a fresh lesion on the back showed a diffuse inflammatory cell infiltrate with collections of histiocytic cells. It also showed necrobiotic foci, surrounded by mixed inflammatory cells, dark palisaded foamy histiocytes, and a few Touton giant cells. These findings are compatible with necrobiotic xanthogranuloma (NXG) (Figs 4 and 5). Blood film showed normochromic, normocytic erythrocytes with anisopoikilocytotic leukocytes and normal platelets. The sedimentation rate was 90 mm in the first hour. The blood picture also showed monoclonal IgG paraprotein (3170 mg/dL) of the kappa light chain type. The patient was treated by the oncologist for her lymphoma, and was given Cytoxan, prednisolone, endoxan, Leukeran, and melphalan. She showed an excellent response to pulsed treatment with steroids (60 mg prednisolone orally daily for 5 days, repeated every month for 6 months). She also responded to Leukeran at a dose of 5 mg daily for 5 days every month for 6 months, and showed regression in the size of the lymph nodes. The treatment of her skin lesions was unsatisfactory in spite of the fact that she was given cyclosporine and both systemic and topical corticosteroids.     

Pathology of post-kala-azar dermal leishmaniasis: a light microscopical, immunohistochemical, and ultrastructural study of skin lesions and draining lymph nodes

BACKGROUND: Whereas the clinical manifestations and treatment of post-kala-azar dermal leishmaniasis (PKDL) have been adequately described before, the pathology received little attention, particularly the African form of PKDL which shows some clinical differences from the disease in India. Therefore, our aim was to characterize the pathology and the immunohistopathology in PKDL lesions and correlate the histopathological findings with the clinical features of the disease. METHODS: Biopsies of skin lesions were examined for histopathological changes in formalin-fixed tissues and for cell phenotypes and adhesion molecules by immunohistochemistry. RESULTS: The epidermis showed various changes in different combinations. The dermis was infiltrated by lymphocytes and macrophages, but plasma cells were scanty or absent. The majority of cells were CD3 T cells, with a preponderance of CD4 over CD8 cells. Degenerating basal keratinocytes expressed HLA-DR, ICAM-1 and Leishmania antigen and closely interacted with CD4 T cells. Regional lymph nodes showed hyperplasia of the B- and T-cell zones. Conclusions: The inflammatory reaction in PKDL lesions is in response to Leishmania parasites and/or antigen. The majority of cells are CD4 T cells. Degeneration of the basal keratinocytes is probably due to the action of cytotoxic CD4 T cells interacting with leishmania-expressing epidermal cells. Ismail A, Gadir AFA, Theander TG, Kharazmi A, El Hassan AM. Pathology of post-kala-azar dermal leishmaniasis: a light microscopical, immunohistochemical, and ultrastructural study of skin lesions and draining lymph nodes.     

Metastatic extramammary Paget's disease treated with paclitaxel and trastuzumab combination chemotherapy

In the treatment of metastatic breast cancer, trastuzumab, a recombinant monoclonal antibody against human epidermal growth factor receptor 2 (HER2), is effective when tumor cells overexpress HER2 protein. Although some cases of extramammary Paget's disease (EMPD) also express HER2 protein, no case of EMPD has been reported to be treated with trastuzumab. A 75-year-old man who suffered from EMPD of the scrotum and inguinal region underwent a local excision and lymph node dissection. Tumor cells invaded the dermis and lymph nodes. Although he was postoperatively treated with adjuvant chemotherapies, metastatic skin lesions appeared and spread over his left thigh, rapidly and widely. Tumor cells disseminated along lymph vessels in the dermis and overexpressed HER2 protein. We administered paclitaxel and trastuzumab according to a protocol for HER2-positive metastatic breast cancers. The skin metastasis dramatically decreased during the regimen and a histopathological examination showed that most of HER2-positive tumor cells diminished. Six months later, metastases were found in the central nervous system (CNS), but no other metastases were found in the skin, visceral organs or lymph nodes. Trastuzumab and paclitaxel-combination with the assessment of central nervous system lesions should be considered as an option for the treatment of HER2-positive EMPD.     

Necropsy and ultrastructural findings in histiocytic medullary reticulosis

In a case of histiocytic medullary reticulosis with protracted course and necrotic skin lesions, histological study revealed infiltration of the fat tissue by atypical rcticulohistiocytic cells, areas of asso-ciated fat necrosis and vascular lesions. Autophagocytosis (phagocytosis of erythrocytes, erythroblasts, platelets, lymphoid cells, and nuclear debris) was found in biopsy specimens of the subcutaneous in-filtrates, lymph nodes, and bone marrow, and in necropsy specimens of skin, iliac mesenteric lymph nodes, bone marrow, liver, spleen, and suprarenal glands. Electron microscopy of various viscera showed abnormal histiocytic cells containing multiple phagocytosed erythrocytes and other blood cells in different stages of destruction and digestion. Multi-membranous bodies also were present. Defective lysosomal degradation of intracytoplasmatic ceroids in this condition is postulated.     

Inflammatory cells in skin lesions of scabies

Cell infiltrates of biopsy specimens from nodular or papulovesicular skin lesions of seven patients with scabies were characterized by α-naphthyl acetate esterase (ANAE) staining and immunoperoxidase labelling. T lymphocytes were the dominant cells in the dermal inflammatory infiltrates of both nodular and papulovesicular lesions. Their mean proportion in the deeper dermal infiltrates was 64% and in the papillary infiltrates 42%. However, they were few in number around the burrows in the epidermis. In contrast, macrophages were frequent in the epidermis and papillary dermis, where they accounted for 47% and 25% respectively of all mononuclear cells. Immunoperoxidase staining revealed immunoglobulin-positivc plasma cells (from 1% to 10%, of all mononuclear cells) only in the dermal infiltrates of nodular lesions. IgE-positive plasma cells were encountered in all four specimens. These results emphasize the importance of macrophages in scabies infestation and suggest that a local IgE-mediated antibody response may occur in nodular lesions of scabies.