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Biomedical subjects

B R Smoller

Publications and source records attributed to B R Smoller.

At least 127 records · Page 7Linked to original sources
PubMed1992

Acute cutaneous graft versus host disease: a clinicopathologic and immunophenotypic study.

Acute graft versus host disease (GVHD) is a major complication of bone marrow transplantation. This study was undertaken to characterize the histopathologic alterations in early lesions of GVHD and to improve our understanding about the disease process. Histopathologic and immunoperoxidase studies of skin tissue were carried out in 20 patients of GVHD. Sixty percent had grade II histopathologic changes in the skin, grade I and III changes were observed in 35% and 5% respectively. Follicular involvement could be observed in all cases beyond grade I. Immunoperoxidase study revealed OPD4 (+) (T-helper) cells in dermis and OPD4 (-) (probably cytotoxic/suppressor) cells in epidermis.

Acute Disease↗
PubMed1992

Porokeratosis in immunosuppressed and nonimmunosuppressed patients.

Porokeratosis is an uncommon, inherited, autosomally dominant disorder. In the last decade association of porokeratosis and immunosuppression has been observed. In this study we carried out a comparative study between immunosuppressed and nonimmunosuppressed porokeratosis cases. We found that 9 out of 20 cases of porokeratosis were associated with organ transplantation/immunosuppression. Clinicopathologic study revealed that the pattern of disease is alike both in immunosuppressed and nonimmunosuppressed patients. Our observations indicate that immune modulation could be a factor in the genesis of porokeratosis.

Adult↗
PubMed1992

Mucoepidermoid carcinoma metastatic to the skin. An histologic mimic of a primary sweat gland carcinoma.

Mucoepidermoid carcinomas are tumors that usually arise from salivary glands and have a characteristic histologic pattern of atypical squamous cells showing focal mucin production. Mucoepidermoid carcinomas are uncommon neoplasms that metastasize most commonly via lymphatic and hematogenous channels. We report what we believe to be the first case of a mucoepidermoid carcinoma arising from a sublingual salivary gland with metastasis to a distant site on the skin. The patient is a 58-year-old black woman who was initially diagnosed with a high grade mucoepidermoid carcinoma of the salivary glands of the tongue. Approximately 18 months after presentation, and 6 months following surgery, chemotherapy, and radiation therapy, the patient noted a firm nodule on her flank. Biopsy showed malignant squamous epithelium. Periodic acid-Schiff and alcian blue stains revealed focal mucin production. The histologic differential diagnosis included an eccrine carcinoma, mucin-producing adenocarcinoma with squamous differentiation, a primary cutaneous adenosquamous (mucoepidermoid) carcinoma and a malignant mixed tumor of the skin. Clinical correlation was essential in making the correct diagnosis. While mucoepidermoid carcinomas only uncommonly show distant metastasis, and even less frequently involve the skin, this entity should be included in the differential diagnosis of mucin-producing neoplasms in the skin.

Carcinoma↗
PubMed1992

Skin malignancies in the elderly. Diagnosable, treatable, and potentially curable.

Cutaneous malignancies are the most common tumors seen in the elderly population. They are often easily diagnosed while still in an early and potentially curable state. Basal cell carcinoma is the most frequently seen malignant neoplasm, followed by squamous cell carcinoma and malignant melanoma. Correct diagnosis depends on complete physical examination of the skin by health-care personnel who have been trained to recognize these lesions and appropriate referral to dermatologists or other experts in skin cancer.

Aged↗
PubMed1992

A case of Woringer-Kolopp disease with Ki-1 (CD30) + cytotoxic/suppressor cells.

BACKGROUND: Woringer-Kolopp (W-K) disease is a rare, localized, histologically malignant, but clinically indolent lymphoproliferative disorder. Most authors have regarded W-K disease as a variant of mycosis fungoides. However, a recent case suggests that W-K disease may represent a spectrum of lymphoproliferative disorders that may not be related to mycosis fungoides. OBSERVATIONS: A patient with a 40-year history of localized cutaneous eruption characterized by markedly atypical epidermotropic lymphocytes was seen at Stanford (Calif) University Hospital. The lymphocytes were predominantly CD30+ cytotoxic/suppressor T cells, an immunophenotype not previously described in W-K disease. Genotype analysis revealed a clonal rearrangement. CONCLUSIONS: The findings in our patient, along with a review of all cases previously reported in the literature, suggest that W-K disease may be an entity with a uniform clinical and histologic presentation, but one with marked immunophenotypic heterogeneity of the malignant-appearing atypical cells. Some cases showed immunophenotypic similarities to mycosis fungoides. However, in almost half of the reviewed cases, including the one presented here, the immunophenotypic differences exceeded the similarities.

Aged↗
PubMed1992

Extramammary Paget's disease: diagnosis and disease pattern.

Extramammary Paget's disease is a rare cutaneous disorder. We report the clinical and histochemical features of five such cases. In all the cases studied, the lesions were located on the perineum of elderly women. None of the cases showed malignant proliferation invading the dermis. Recent observations suggest that extramammary Paget's disease is a disease of the apocrine glands. Immunoreactants to identify apocrine glands have been developed and can be used to confirm the diagnosis of extramammary Paget's disease.

Anus Neoplasms↗
PubMed1992

Ki-1 (CD30) expression in differentiation of lymphomatoid papulosis from arthropod bite reactions.

Lymphomatoid papulosis (LP) is an uncommon cutaneous T-cell lymphoproliferative disorder that can mimic arthropod bite reactions clinically and histologically. Erythematous, crusted papules and nodules occur mainly on extremities of young adults and, when biopsied, display a superficial and deep perivascular infiltrate characterized by atypical lymphocytes and scattered eosinophils. Arthropod bite reactions may show an identical histologic pattern. It has been suggested that up to 10% of patients with LP will eventually develop lymphoma. We examined biopsies from 10 cases of LP and six cases of arthropod bite reactions diagnosed by clinical history and prolonged follow-up, with BerH2, an antibody directed against the Ki-1 antigen (CD30) and found it to be useful in helping distinguish between the two entities. All cases of LP examined showed scattered Ki-1-positive large, atypical lymphocytes in the dermis. In the arthropod bite reactions, there was virtually no staining with BerH2 antibody. This suggests that the abnormal activated T-cells, which comprise the cellular infiltrate in LP, are not present in arthropod bite reactions.

Adult↗
PubMed1992

T lymphocytes expressing HECA-452 epitope are present in cutaneous acute graft-versus-host disease and erythema multiforme, but not in acute graft-versus-host disease in gut organs.

Lymphocytes in formalin-fixed skin biopsies from patients with cutaneous acute graft-versus-host disease (aGVHD) were studied with HECA-452 (an antibody recognizing lymphocytes with skin-homing properties) and a panel of antibodies recognizing pan-B (L26 [CD20]), pan-T (L60 [CD43] and A6 [CD45RA]), and T-helper subset (OPD4) antigens in paraffin sections. Biopsies from patients with erythema multiforme (EM) were similarly studied for comparison. In both conditions, T lymphocytes stained by OPD4 were predominantly confined to the dermis, whereas those stained by HECA-452 were concentrated in the epidermis; however, there was considerable variation between cases, and overlap between findings in the dermis and epidermis. Lymphocytes similarly studied in paraffin sections of liver, salivary gland, and gut affected by aGVHD were essentially unreactive with HECA-452, although they were largely stained by pan-T markers and showed some comparable reactivity with OPD4. The findings suggest that aGVHD of the skin is mediated by a different set of lymphocytes than in gut organs, and may have a similar immunologic mechanism to EM.

Acute Disease↗
PubMed1991

Detection of cytokine-induced protein gamma-immune protein-10 (gamma-IP10) in atypical melanocytic proliferations.

gamma-Immune protein-10 (gamma-IP10) is a cytokine whose expression has been shown to be induced by interferon-gamma. It is a member of a group of closely related cytokines (e.g., interleukin 8 and platelet factor 4) with chemotactic properties. gamma-IP10 has been detected in keratinocytes, lymphocytes, monocytes, and endothelial cells in immunologically mediated processes, such as positive tuberculin skin tests, and in growth-activated keratinocytes, such as in psoriasis. Keratinocytes in normal epidermis do not produce gamma-IP10. We tested the hypothesis that keratinocytes adjacent to dysplastic nevi and melanomas would produce gamma-IP10, perhaps as part of an immune response to a tumor, and that this response would not be seen in ordinary melanocytic nevi. We used an affinity-purified, polyclonal rabbit anti-gamma-IP10 antibody to examine 10 nevi with moderate to severe histologic dysplasia, one superficial spreading melanoma, and 10 compound melanocytic nevi with no features of dysplasia. As predicted, keratinocytes surrounding all of the cytologically atypical melanocytic lesions displayed strong staining with gamma-IP10. There was no staining of keratinocytes adjacent to ordinary melanocytic nevi. The observed keratinocyte staining with gamma-IP10 may be related to a host immune response to antigenically abnormal cells.

Cytokines↗
PubMed1991

Fixed drug eruptions: evidence for a cytokine-mediated process.

Fixed drug eruptions (FDE) are immunologic reactions to drugs which produce erythematous plaques or blisters that characteristically recur at the same cutaneous sites with repeated antigenic challenges. While a detailed pathogenesis of these lesions remains obscure, T-lymphocyte infiltration has been documented repeatedly. In this study, we tried to determine if FDE were mediated, at least in part, by cytokines, such as gamma-interferon. We examined biopsies from 6 cases of clinically well-documented FDE with an HLA-DR antibody, LN3, and an antibody to gamma IP-10 (IP-10), a protein expressed by keratinocytes, monocytes, lymphocytes and endothelial cells following exposure to gamma-interferon. We found staining of the dermal lymphocytes with anti-HLA-DR antibody in all 6 cases examined. Keratinocytes and endothelial cells showed only focal staining at the antibody concentrations used. In addition, there was keratinocyte staining with the IP-10 antibody at all levels of the epidermis, with accentuation in areas of blister formation. There was more intense staining of keratinocytes with the IP-10 antibody in cases with accumulations of HLA-DR positive lymphocytes in the dermis. We believe that these findings are consistent with the hypothesis that FDE represent cell-mediated immunologic responses to a variety of antigens, and further, that the histologic alterations can be explained, at least in part, by a cytokine-mediated process.

Adult↗
PubMed1991

Pigmented purpuric eruptions: immunopathologic studies supportive of a common immunophenotype.

Traditionally, the pigmented purpuric eruptions (PPE) have been subdivided into four histologic categories, based upon variations in histologic pattern and clinical morphologies. In recent years, it has become apparent that the lesions behave similarly, and this family of eruptions has become grouped under the term PPE. The pathogenesis of these eruptions is largely unknown. In this study, we examined 13 examples of the histologic and clinical subtypes of the PPE with a panel of hematolymphoid immunophenotypic markers, in hopes of better understanding the pathogenesis of these curious eruptions. All lesions examined showed a predominantly T cell infiltrate composed of a mixture of OPD4 (CD4) positive and OPD4 negative cells. B cells were rare. Macrophages did not comprise a significant component of the infiltrate. The staining pattern was relatively constant, independent of the histologic pattern (i.e., Schamberg's vs. Gougerot-Blum, etc) of the PPE. Our results suggest that PPE are a group of related eruptions which may have a common pathogenesis. It seems likely that the vascular damage and erythrocyte extravasation are secondary to a localized cell-mediated immunologic event.

Adolescent↗
PubMed1991

HMB-45 monoclonal antibody recognizes an inducible and reversible melanocyte cytoplasmic protein.

HMB-45 is a monoclonal antibody directed against human melanoma cells and which stains epidermal and dermal melanoma cells, the junctional components of common and dysplastic melanocytic nevi, and melanocytes in fetal skin. In addition, melanocytes in a variety of reactive conditions have been shown to label with HMB-45, as have dermal melanocytes within Spitz and dysplastic nevi. No melanocytes in normal adult epidermis or in the dermis of common nevi have stained with HMB-45. In order to better understand the properties of this antibody, and of the melanocytes that react with it, we stained cultured human melanocytes grown in a variety of conditions. Melanocytes from human foreskins were grown for 2-3 weeks in MCDB 153 medium supplemented with insulin, epidermal growth factor, and bovine pituitary extract as a mixed population of keratinocytes and melanocytes. Some cells were transferred to basal medium MCDB 153 (unsupplemented) for periods ranging from 3-5 days, and a subset of these were returned to growth-factor supplemented medium. In all cases, S100 staining was used to confirm the presence of melanocytes. Melanocytes grown in complete medium showed strong granular cytoplasmic staining with HMB-45. Cells transferred to basal medium showed a markedly diminished staining intensity which was reversible within 3 days upon return of the cells to complete medium. The findings suggest that expression of the protein recognized by HMB-45 may be related to a growth factor present in complete medium, but missing from basal MCDB 153.(ABSTRACT TRUNCATED AT 250 WORDS)

Antibodies, Monoclonal↗
PubMed1991

Benign cutaneous polyarteritis nodosa. Relationship to systemic polyarteritis nodosa and to hepatitis B infection.

Benign cutaneous polyarteritis nodosa has been described as having a benign course in contrast to that of systemic classic polyarteritis nodosa. We tested the hypothesis that this histologic distinction is false by reviewing nine consecutive cases with the histologic diagnosis of benign cutaneous polyarteritis nodosa. Our study revealed that on follow-up, seven (78%) of nine cases had evidence of involvement of at least one organ other than the skin, with the kidney being the organ most commonly involved. Four (44%) of nine patients had serologic evidence of hepatitis B infection, one had cryoglobulinemia, and one had polyclonal hypergammaglobulinemia associated with acquired immunodeficiency syndrome. We conclude that benign cutaneous polyarteritis nodosa is not necessarily benign and is closely related to systemic polyarteritis nodosa.

Adult↗
PubMed1991

Relationship of factor XIIIa-positive dermal dendrocytes to Kaposi's sarcoma.

The histogenesis of Kaposi's sarcoma (KS) has been the subject of controversy, much of which has centered around whether the spindle cells of KS are derived from vascular endothelium or from lymphatics. Recently, some investigators have speculated that the spindle cells of KS are derived from dermal dendrocytes, a population of mononuclear dendritic cells normally present in the papillary and upper reticular dermis. These cells have been shown to proliferate in response to a variety of stimuli and have been reported to express the plasma proenzyme factor XIIIa. We examined immunohistochemically sections fixed in formaldehyde solution and embedded in paraffin from 20 tumor-stage, 15 patch-stage, and 15 plaque-stage lesions of KS with antibodies directed against factor XIIIa, factor VIII-related antigen, Ulex europaeus lectin, and LN3 (anti-HLA-DR) to investigate the relationship of dermal dendrocytes to KS in general and to try to clarify the histogenesis of this tumor. Our results revealed that the dermis of patch- and plaque-stage KS lesions contains an increased number of factor XIIIa-positive dermal dendrocytes compared with normal dermis and that some of these cells are spindle shaped. Many of the spindle cells in patch- and plaque-stage lesions of KS, however, are negative for factor XIIIa. The cells lining the slitlike spaces and some spindle-shaped cells in close proximity to the vascular spaces stain for factor VIII-related antigen and for Ulex europaeus lectin. LN3 labeled many cells resembling macrophages within the lesions and in papillary dermis. Less than 25% of the dendritic cells within the lesions and in the adjacent dermis expressed both factor XIIIa and LN3. Tumor-stage lesions showed focal but unequivocal staining of the spindle cells for factor VIII-related antigen and Ulex europaeus lectin. Tumor spindle cells were negative for factor XIIIa. Factor XIIIa-positive dendrocytes were plentiful in the uninvolved dermis and were aggregated around the periphery of the tumor nodules. The expression of factor VIII-related antigen and Ulex europaeus lectin by the spindle cells of nodular KS, and their lack of expression of factor XIIIa, suggests that the spindle-shaped tumor cells in all stages of KS are derived from endothelial cells and not from dermal dendrocytes. Dermal dendrocytes appear to undergo hyperplasia in response to KS of all stages. In patch- and early plaque-stage KS lesions, dermal dendrocytes are near factor VIII-related antigen-positive spindle cells and tumor vessels. The mechanism reactive dermal dendrocyte hyperplasia in KS remains obscure.

Dendritic Cells↗
PubMed1990

Neurofibromas and neurotized melanocytic nevi are immunohistochemically distinct neoplasms.

Neurofibromas are often clinically, as well as histologically, indistinguishable from completely neurotized melanocytic nevi. We tested the hypothesis that immunologic markers would differentiate the perineural fibroblasts and Schwann cells of neurofibromas from the neurotized cells of melanocytic origin. We examined eight partially neurotized acquired melanocytic nevi, three partially neurotized congenital melanocytic nevi, and five neurofibromas, with antibodies directed against S-100 protein, Leu-7(HNK-1), glial fibrillary acid protein (GFAP), and myelin-basic protein (MBP). A histologic diagnosis of neurofibroma was based on identification of a dermal proliferation of spindle-shaped cells with wavy nuclei, in a background of loose reticulated collagen. Neurotized nevi were diagnosed upon recognition of scattered nests of type A or B nevus cells, surrounded by basement membrane, present in the papillary dermis of lesions otherwise indistinguishable from neurofibromas. The congenital nevi were all large melanocytic nevi known to be present at birth. S-100 stained the majority of neoplastic cells in all neurofibromas, neurotized acquired nevi, and neurotized congenital nevi. Neurofibromas showed focal staining for Leu-7, GFAP, and MBP. In contrast, neurotized acquired and congenital nevi failed to express these markers. We believe that Leu-7, GFAP, and MBP may be helpful in differentiating neurofibromas from completely neurotized melanocytic nevi. The differences in the immunohistochemical profiles of neurofibromas and neurotized nevi support the concept that these neoplasms are histogenically distinct, despite their similar histologic appearance.

Antigens, Differentiation↗