Biomedical subjects
P E LeBoit
Publications and source records attributed to P E LeBoit.
Compare your diagnosis. Xanthogranuloma, seborrheic keratosis associated with mycosis fungoides, Kikuchi's disease.
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Chromosomal gains and losses in primary cutaneous melanomas detected by comparative genomic hybridization.
The analysis of genetic changes in primary cutaneous melanoma has been limited by the need for fixation for diagnostic purposes. However, comparative genomic hybridization is able to analyze such specimens. We have applied comparative genomic hybridization to 32 primary melanomas to discover and map genomic regions with aberrant DNA copy numbers. The analysis was performed on native, nonamplified DNA extracted from manually dissected tumor sections. Loss of chromosome 9 was detected in 81% of the tumors, most commonly affecting the p arm. Additional common losses occurred on chromosomes 10 (63%), 6q (28%), and 8p (22%). Gains in copy number involved chromosomes 7 (50%), 8 (34%), 6p (28%), 1q (25%), 20 (13%), 17 (13%), and 2 (13%). Amplifications indicating areas harboring potential oncogenes were seen at 4q12, 5p14.3-pter, 7q33-qter, 8q12-13, 11q13.3-14.2, and 17q25. Correlations among the regions with copy number changes indicate that losses of chromosomes 9 and 10 occur early on in melanoma progression, whereas gains of chromosome 7 occur later. This sequence of events was further substantiated by an intratumoral comparison of copy number changes in areas with radial and vertical growth phase patterns. The overall pattern of regions affected by copy number changes is consistent with cytogenetic data from metastatic melanoma; however, the frequencies of involvement differ, providing further insight into the course of genetic events.
Hormone-induced acneiform eruption in human immunodeficiency virus disease.
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Subacute radiation dermatitis from fluoroscopy during coronary artery stenting: evidence for cytotoxic lymphocyte mediated apoptosis.
A patient with fluoroscopy-induced subacute radiation dermatitis is described. Her biopsy specimen showed vacuolar change and necrotic keratinocytes with lymphocytes in direct apposition, or "satellitosis". Lymphocytes in the dermis and infiltrating the epidermis were predominantly CD8+ and a number of the lymphocytes stained for TIA-1, a cytotoxic granule protein in T-cells and natural killer cells, that appears to be involved in the induction of apoptosis. Our findings suggest cytotoxic lymphocyte mediated apoptosis is involved in the pathogenesis of subacute radiation dermatitis.
You mean it, but do you say it?
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Eosinophilic globules in spitz nevi: no evidence for apoptosis.
Eosinophilic globules are commonly found in Spitz nevi and can be of help in the differential diagnosis with melanoma. Despite their use as a diagnostic marker, there are conflicting concepts concerning the mechanism of the formation of these globules. Because pyknotic nuclei are often present in the cells surrounding the globules, many believe that apoptotic cell death of keratinocytes and melanocytes is an important mechanism in their formation. We studied nine Spitz nevi containing 21 eosinophilic globules for apoptotic cell death around and within Kamino bodies using the TUNEL method (TdT-mediated dUTP-x nick end-labeling method). In none of the cases were positive cells seen in the vicinity of the globules. Single apoptotic cells were found only sporadically in the melanocytes of the neoplasms (one to four per section) and were scattered throughout the entire lesion. The absence of apoptosis-specific labeled cells in the vicinity of eosinophilic globules and the rare occurrence of positive stained cells in other parts of the tumors makes apoptotic cell death unlikely to be relevant in the formation of eosinophilic globules.
Light microscopic criteria for the diagnosis of early vulvar lichen sclerosus: a comparison with lichen planus.
Lichen sclerosus (LS) and lichen planus (LP) are two conditions frequently affecting genital skin whose clinical and histologic distinction can be difficult. Both diseases can feature solitary genital lesions with bandlike lymphocytic infiltrates. We reviewed 68 cases of vulvar LS to find sections that contained a transition from a lichenoid interface reaction to pathognomonic LS (i.e., marked papillary dermal sclerosis or edema), and in these nine cases we studied routinely and specially stained sections, as well as sections stained with a panel of antisera to lymphoid antigens, and compared the findings with those in six cases of genital LP. We assumed that changes at the periphery of a lesion of LS mirror findings seen in early lesions. The features that we found more commonly in the inflammatory phase of LS included a psoriasiform lichenoid pattern (100% LS, 0% LP), basilar epidermotropism (78% LS, 0% LP), loss of papillary dermal elastic fibers (100% LS, 33% LP), basement membrane thickening (44% LS, 0% LP), and epidermal atrophy (33% LS, 0% LP). Features found more commonly in LP included many cytoid bodies (0% LS, 100% LP), wedge-shaped hypergranulosis (11% LS, 100% LP), basal squamatization (22% LS, 100% LP), and pointed rete ridges (11% LS, 83% LP). We did not detect any significant differences in the immunohistochemical features of the infiltrates. Taken together, these histologic features comprise light microscopic criteria for the diagnosis of early vulvar LS and its differentiation from LP.
Molecular epidemiology of bartonella infections in patients with bacillary angiomatosis-peliosis.
BACKGROUND: Bacillary angiomatosis and bacillary peliosis are vascular proliferative manifestations of infection with species of the genus bartonella that occur predominantly in patients infected with the human immunodeficiency virus. Two species, B. henselae and B. quintana, have been associated with bacillary angiomatosis, but culture and speciation are difficult, and there has been little systematic evaluation of the species-specific disease characteristics. We studied 49 patients seen over eight years who were infected with bartonella species identified by molecular techniques and who had clinical lesions consistent with bacillary angiomatosis-peliosis. METHODS: In this case-control study, a standardized questionnaire about exposures was administered to patients with bacillary angiomatosis-peliosis and to 96 matched controls. The infecting bartonella species were determined by molecular techniques. RESULTS: Of the 49 patients with bacillary angiomatosis-peliosis, 26 (53 percent) were infected with B. henselae and 23 (47 percent) with B. quintana. Subcutaneous and lytic bone lesions were strongly associated with B. quintana, whereas peliosis hepatis was associated exclusively with B. henselae. Patients with B. henselae infection were identified throughout the study period and were epidemiologically linked to cat and flea exposure (P< or =0.004), whereas those with B. quintana were clustered and were characterized by low income (P=0.003), homelessness (P = 0.004), and exposure to lice (P= 0.03). Prior treatment with macrolide antibiotics appeared to be protective against infection with either species. CONCLUSIONS: B. henselae and B. quintana, the organisms that cause bacillary angiomatosis-peliosis, are associated with different epidemiologic risk factors and with predilections for involvement of different organs.
Persistent pigmented purpuric dermatitis and mycosis fungoides: simulant, precursor, or both? A study by light microscopy and molecular methods.
Mycosis fungoides (MF) can present with purpuric lesions, and rare patients who seemed to have persistent pigmented purpuric dermatitis (PPPD) have developed MF. We recently encountered two patients referred to our cutaneous lymphoma clinic who had PPPD rather than MF and two others who appeared to have both conditions, leading us to explore the histologic similarities of these diseases. We examined specimens from 56 patients with PPPD to determine the frequency of MF-like histologic configurations, namely, the psoriasiform lichenoid, psoriasiform spongiotic lichenoid, and atrophic lichenoid patterns. We also noted the degree of spongiosis, epidermotropism, papillary dermal fibrosis, lymphocytic atypia, and epidermal hyperplasia, the number of extravasated erythrocytes and siderophages, and the distribution of lymphocytic infiltrate within the epidermis. In 29 of 56 patients, there were patterns typically seen in MF. PPPD can feature lymphocytes aligned along the epidermal side of the dermoepidermal junction, with few necrotic keratinocytes, as can MF. Papillary dermal edema occurred frequently in PPPD but not in MF, while lymphocytes in MF but not PPPD had markedly atypical nuclei and had ascended into the upper spinous layer. Given these similarities, we tested for clonality of the T-cell population using a polymerase chain reaction assay for gamma-chain rearrangements. Clonal populations were present in three of three and one of two specimens from patients with both PPPD and MF, but also in 8 of 12 specimens typical of lichenoid patterns of PPPD. These findings raise the possibility that the lichenoid variants of PPPD are biologically related to MF.
That "admitting- you're wrong stuff".
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Microcystic adnexal carcinoma with extensive sebaceous differentiation.
We report two cases of microcystic adnexal carcinoma showing extensive sebaceous differentiation. Multiple cellular nests and strands within a moderately sclerotic stroma involving the full thickness of the dermis were observed. Clusters of basaloid cells with extensive sebaceous differentiation were present. Foci of sebaceous ductal differentiation were observed in the more superficial areas. Neither strikingly atypical cells nor mitotic figures were present. Perineural invasion was present in the deep areas of both tumors. Clinically, the lesions were solitary whitish-pink papules with a central dell on the faces of 2 men (aged 78 and 73 years old). We propose a relationship between these tumors and other cytologically bland but locally aggressive adnexal carcinomas. Sebaceous differentiation itself in a poorly circumscribed neoplasm does not indicate conventional extraocular sebaceous carcinoma. We propose a simple classification of locally aggressive adnexal carcinomas that takes into account the full range of adnexal differentiation that can occur in such lesions.
Basal cell carcinoma with thickened basement membrane: a variant that resembles some benign adnexal neoplasms.
Because cutaneous basal cell carcinoma (BCC) is such a common malignancy, its unusual histologic manifestations are important. We identified a variant of BCC in which thickened basement membranes surround aggregations of neoplastic epithelial cells. Thickened basement membranes of similar appearance have previously been observed in benign cutaneous adnexal neoplasms, in basaloid monomorphic adenomas of the salivary gland and in other benign conditions, such as folliculocentric basaloid proliferation. We identified nine BCCs that otherwise met standard criteria, but which also had thick basement membranes surrounding some of the aggregations, and examined them by routine and histochemical staining. The cases included BCC with nodular, micronodular, and infiltrating patterns. Two neoplasms were composed largely of clear cells, suggesting, together with the thickened membranes, outer root sheath differentiation. CD34, which labels keratinocytes of the outer root sheath, marked only the epithelial cells of one of these cases. The thickened membranes were stained by periodic-acid Schiff with and without diastase (PAS-D) and by antibodies to type IV collagen and laminin, with slightly different staining patterns. Intraepithelial droplets within aggregations stained with PAS-D and type IV collagen antibodies. Thickened basement membranes therefore can occur in most of the common growth patterns of BCC. The absence of CD34 staining of epithelial cells in most cases makes it problematic at this time to prove that the thickened membranes indicate trichilemmal differentiation. BCC with thick basement membranes can closely mimic benign neoplasms, such as cylindroma and trichilemmoma, from which they can be distinguished in routinely stained sections. The presence of a continuous thick basement membrane around aggregates of epithelial cells does not in and of itself distinguish between benign and malignant cutaneous epithelial neoplasms.
Localized chronic fibrosing vasculitis of the skin: an inflammatory reaction that occurs in settings other than erythema elevatum diutinum and granuloma faciale.
Erythema elevatum diutinum (EED) and granuloma faciale (GF) are chronic, localized forms of cutaneous leukocytoclastic vasculitis that result in patterned (storiform or concentric) fibrosis. EED often occurs in systemically ill patients as bilaterally symmetrical plaques, papules, or nodules, often over the dorsa of joints. GF occurs as one or a few plaques on the face. Eosinophils and plasma cells are prominent in GF, whereas neutrophils are plentiful in EED. Rarely, extrafacial lesions accompany facial ones in GF, and there are a few reports of upper respiratory tract masses with GF-like histologic features. We report on eight patients with solitary cutaneous lesions with histologic features similar to those of EED or GF, but whose clinical picture was not that of either disease. One, whose histology resembled GF, had a large multinodular dermal and subcutaneous mass that persisted despite attempted resection. Unusual histologic findings in other cases included storiform fibrosis with dense infiltrates of plasma cells, branching nerve fascicles admixed with EED-like changes, and EED-like areas adjacent to zones mimicking a sclerotic fibroma. Chronic fibrosing venulitis can be seen outside the stereotypic settings of GF and EED and is an inflammatory reaction pattern that does not signify a specific diagnosis. Because of transitions between EED or GF-like areas and those of patterned sclerosis with plasma cell-rich infiltrates, we believe that some "inflammatory pseudotumors" of the skin, and perhaps of other sites could be the result of localized vasculitis.
Are primary cutaneous immunocytoma and marginal zone lymphoma the same disease?
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Disseminated recurrent papular B-cell pseudolymphoma.
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An immunohistochemical analysis of radiation fibroblasts.
A commonly recognized feature of chronic radiation dermatitis is the presence of mesenchymal cells with large atypical nuclei known as radiation fibroblasts. Little is known about their lineage or potential for neoplastic transformation. To investigate these properties, we examined 16 biopsy specimens in which radiation fibroblasts were present with antisera to mesenchymal determinants (FXIIIa, CD34, HHF-35), a proliferation marker (Ki-67), and a tumor-suppressor protein that is overexpressed in many cancers (p53). Radiation fibroblasts were largely negative for the markers of lineage that we employed - only 2 of 16 specimens showed strong expression of FXIIIa, with weak expression in another case. Scattered radiation fibroblasts expressed CD34 in one case. HHF-35 (muscle specific actin) stained small, dendritic cells in the superficial dermis, but not radiation fibroblasts. P53 was not detected within radiation fibroblasts in any of our cases, but was overexpressed by endothelial cells in 2 cases. Ki-67 stained rare endothelial and interstitial cells but not radiation fibroblasts. Radiation fibroblasts are immunophenotypically distinct from dermal dendrocytes and myofibroblasts. They appear to be non-cycling cells, and do not express high levels of p53 despite their marked nuclear atypia. Their phenotype argues against their possible role as progenitors of atypical fibroxanthoma (AFX) and dermatofibrosarcoma protuberans (DFSP) which are associated with ionizing radiation-induced skin damage.
Spitz's nevi with halo reaction: a histopathologic study of 17 cases.
Halo reactions to melanocytic nevi are a well-recognized phenomenon. In contrast, halo reactions to Spitz's nevi have been reported only infrequently. Halo reactions may cause misdiagnosis of an otherwise benign nevus as melanoma because inflammatory cells sometimes obscure the architectural features of the underlying nevus, and may induce cytologic atypia. For Spitz's nevus where the distinction between malignancy and benignancy is already challenging, halo reactions compound the problem. We describe 17 examples of Spitz's nevus with halo reaction, and compare their immunohistochemical features with those of "ordinary" halo nevi. Only 2 of 17 lesions demonstrated clinically apparent halos. Clinical follow-up was available for 12 of 17 cases. None of the 12 has persisted at the biopsy site or metastasized after an average 3.6-year follow-up period. Junctional, compound, intradermal, and combined types of Spitz's nevi were represented. All were characterized by symmetrical lymphocytic infiltrates which permeated the full thickness of the nevus, including junctional nests. Combined Spitz's nevi constituted more than one-half of examples in this series (9/17 cases). The combined Spitz's nevus included a combination of Spitz's nevus with either an ordinary (common, banal) nevus or a superficial congenital type nevus. In these combined Spitz's nevi, the lymphocytic response was often directed exclusively to the Spitz's nevic component. Important distinguishing features from malignant melanoma arising in a pre-existing nevus included symmetry and lateral circumscription of the spitzoid component, no large expansile-appearing aggregates of melanocytes, a decrease in size of nests with increasing dermal depth, a lack of mitotic figures among melanocytes at the base, and a symmetrical and diffusely permeative lymphocytic response. Although the combined Spitz's nevus with halo reaction sometimes appeared asymmetrical at scanning magnification, each component of the combination was symmetrical, when examined independently. Probably because of reactive atypia, nuclear maturation with progressive descent into the dermis was sometimes absent. There were no obvious differences in immunohistochemical staining patterns among 4 Spitz's nevi with halo reaction, 5 regressing melanomas, and 5 benign halo nevi when stained with antibodies to S100, HMB-45, OPD4, CD8, TIA-1, CD1a, CD68, and Ki-67.