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Notes: Background. Cutaneous manifestations of myeloid leukemia can be specific or nonspecific. The study was designed to determine the prevalence and histologic appearance of cutaneous lesions in patients with myeloid leukemia and various myeloproliferative disorders. Methods. The histologic changes of cutaneous lesions in 52 patients with myelodysplastic syndrome, polycythemia vera, and myeloid, myelomonocytic, or monocytic leukemia are presented in this study. Results. Two types of cellular infiltrates were identified. In the first group, the most common pattern was a diffuse involvement by the leukemic cells through the entire dermis with preservation of a “grenz zone” in the superficial dermis. Two cases exhibited a Kaposi's sarcoma-like pattern, with prominent slit-like blood-filled spaces lined by myeloblasts against a fibrocellular stroma. The second group of lesions was characterized by dense, neutrophilic dermal infiltrates resembling acute neutrophilic dermatosis (Sweet's syndrome) or pyoderma gangrenosum. In two of these cases, scattered immature blast cells admixed with the mature neutrophilic elements were identified. Conclusions. Awareness of these different morphologic features and application of special stains are of value in the evaluation of suspicious cutaneous infiltrates in patients with myeloid leukemia and various myeloproliferative disorders.

Notes: : Circumscribed dermal hypermelanosis refers to a group of cutaneous disorders with circumscribed blue, blue-grey, slate-grey, or blue-black pigmentation. Dermal Melanocyte deposition (melanocytosis) and melanin in mdcrophages (melaninosis) are observed histopathologically. This group of disorders can be differentiated clinically from brown epidermal hypermelanosis by examination using Wood's light. The microscopic, histochemical, immunofluorescent, and ultrastructural findings in three cases of erythema dyschromicum Persians supports its classification in the group of circumscribed dermal melanosis. Damage to epidermal basal cells gives rise to a caseade of events producing the’ ashen-gray color. The epidermal melanocytes in this disorder are morphologically distinctive and increased in number. Ultrastructurally, a direct interaction between melanocytes and lymphocytes's seen resulting in vacuolar degeneration of the dermalepidermal junction, with resultant incontinence of pigment. The dermal depth to which the pigment-containing macro-phages may extend is greater than that found in post-inflammatory hyperpigmentation. perhaps because of involvement of the appendageal structures.

Notes: : The substitution of glucose-antiglucose oxidase complex (GAG) for peroxidase antiperoxidase (PAP) in the Sternberger three-layer unlabeled antibody method avoids the problems associated with the use of the chromogen 3,3, diaminobenzidine (DAB). The blue final reaction product obtained using the GAG complex is not obscured by melanin granules, which is often the case when using the PAP-DAB combination. The replacement of PAP with GAG complexes facilitates the detection of melanocytes in melanoma and blue nevi. The absence of endogenous glucose oxidase in mammals provides for greater image contrast, which is not possible using alternative chromogens and immunoperoxidase.

Notes: The patient was a 77-year-old male former smoker, with history of several basal cell carcinomas (BCCs) in sun-protected areas around the waistline, who presented with another small ulceration on the anterior right upper scrotum near the base of the penis. BCC was suspected clinically and the lesion was treated with cryosurgery. The tumor recurred, became raised, and began to bleed. On examination, it was found to be a 3 cm × 4 cm, raised, light and dark gray variegated lesion with fissures, crusted bloody scale, and necrosis. There were no other penile, testicular, or scrotal lesions or masses. There was no regional lymphadenopathy. An excisional biopsy was performed. It showed nodular BCC surrounded by a cellular proliferation of round histiocytic cells with convoluted, lobulated and reniform nuclei and abundant cytoplasm (〈link href="#f1"〉Fig. 1). The histiocytic proliferation was associated with numerous eosinophils. Histological features and immunohistochemical phenotype, including expression of CD1a and S-100 antigens by histiocytic cells, were all consistent with Langerhans cell histiocytosis. As expected, BCC expressed keratin.〈figure xml:id="f1"〉1〈mediaResource alt="image" href="urn:x-wiley:00119059:IJD2178:IJD_2178_f1"/〉(a) Low magnification (×40) view of the scrotal tumor showing nodular basal cell carcinoma surrounded by a cellular zone of Langerhans cell proliferation. (b) Langerhans cells showed typical irregular reiniform nuclei with convoluted outlines and were associated with eosinophilic infiltrate (×400). In immunohistochemical studies, they expressed (c) S-100 and (d) CD1A antigens (both ×400)The patient had no history of exposure to ionizing radiation, chemotherapy, immunosuppressive medications, prior lymphoma or other malignancy. However, he spent 4 years on a ship loading coal into the furnace of a steam engine, during which he slept in adjacent quarters that were covered with coal dust. Additionally, he had a several-year history of occupational skin exposure to machine oil, oil refinery waste, sulfur waste, hydraulic fluid, and asbestos. He also reported a history of nude sunbathing. His current medical problems include pleural asbestosis, poorly controlled type II diabetes, and congestive heart failure. His past dermatologic history includes intertrigo, onychomycosis, and an unknown skin lesion removed from the face 40 years ago. Recent clinical follow-up and imaging studies, including chest X-ray and bone scan, showed no evidence of visceral lesions, lytic bone lesions, or other signs of systemic involvement by Langerhans cell histiocytosis. The scrotal lesion was re-excised and the patient remains disease-free more than 1 year after the diagnosis.

Notes: The rare presentation of choriocarcinoma as a cutaneous metastasis in a 23-year-old male is reported. Histological and immunohistochemical analysis of the biopsy material demonstrated two distinct cell populations, syncytiotrophoblasts and cytotrophoblasts, with syncytiotrophoblasts strongly positive for human chorionic gonadotropin antigen. Subsequent clinical evaluation revealed a testicular tumor with metastases to lungs, brain, liver and kidney and increased serum levels of human chorionic gonadotropin. The patient died shortly alter diagnosis due to complications of metastatic disease despite chemotherapy.

Notes: Abstract:  Mutations in β-catenin are present in benign pilomatrixomas. β-catenin is a downstream effector in the WNT-signalling pathway, acting as a signal for differentiation and proliferation. Mutations in CTNNB1, the gene encoding β-catenin, are present in a wide variety of benign and malignant neoplasms. We examined β-catenin in a series of pilomatrix carcinomas (15 cases) by using immunohistochemistry and DNA sequencing of exon 3 from CTNNB1, and compared these to a series of benign pilomatrixomas (13 cases). All 11 pilomatrix carcinomas available for examination showed nuclear localization of β-catenin and mutations in exon 3 similar to those demonstrated in benign pilomatrixomas. Two of 11 pilomatrix carcinomas showed significant nuclear accumulation of p53, whereas this was absent in all 13 benign pilomatrixomas. Expression of nuclear cyclin D1 was similar in both benign pilomatrixomas and pilomatrix carcinomas. Clinical follow-up from the 15 malignant cases reported in this study and by others indicates that wide excision offers superior control of local recurrence, compared to simple excision. Immunohistochemical and molecular analysis of β-catenin reveals that both pilomatrix carcinomas and benign pilomatrixomas harbour mutations in β-catenin. This implies a common initial pathogenesis and is compatible with the proposition that pilomatrix carcinomas may at least on occasion arise from their benign counterparts.

Notes: A carcinosarcoma of the skin in a 74–year-old man is reported. The epithelial clement consisted of a highly anaplastic basal cell carcinoma with focal keratinization. The mesenchymal component included elements of fibrosarcoma, chondrosarcoma, osteogenic sarcoma, and synovial sarcoma. This is, to our knowledge, the second reported case of carcinosarcoma arising in the skin.

Notes: Statistical analysis of research results provides powerful tools for understanding the data from projects. A prospective review of the statistical methods utilized in 100 consecutive articles in the recent literature relevant to dermatopathology was performed. The majority of papers, 75%, did not contain statistical analyses. A wide variety of methods were utilized in the papers that did have statistical analyses including methods in the following categories: t-test. contingency tables, multiple regression, multiple comparisons, nonparametric tests, life tables, and survival tests. Nine of the 25 papers utilizing statistical analysis had problems in the methods. These problems included treating categorical data as a continuous variable, multiple comparisons, subgroup analysis, and discordance of statistics and conclusions. It is important to understand the underlying assumptions of statistical methods to use the appropriate tets. These are tools of the trade for dermatopathology investigators.

Notes: Mast cell participation in immune responses, tumor progression, and vascularization has been studied extensively in vitro. In situ investigation of mast cells in routinely processed tissues is hampered by difficulty in reliable detection of mast cells. We studied the tissue density of mast cells using a morphometric point-counting technique in 1 μm-thick, Giemsa-stained, tissue sections from epon-embedded samples of skin biopsies. This technique has been demonstrated to be an accurate and reproducible method for determining mast cell density.Mast cell density in 15 cases of invasive melanoma was compared to that of 9 cases of benign melanocytic nevi and 4 cases of melanoma in situ. Mast cell density was greatest in invasive melanoma (mean density = 0.61 vol.%). The mean density of mast cells in nevi and in situ melanoma was 0.33 and 0.5 respectively. Six of 15 cases of melanoma had mast cell densities 〉 0.6, whereas mast cell density did not exceed 0.6 in any cases of melanoma in situ or benign melanocytic nevi (p 〈 0.02). Our findings confirm an increase in mast cell tissue density in some cases of invasive melanoma when compared to mast cell density in benign nevi and in situ melanoma.