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Biomedical subjects

J Andrew Carlson

Publications and source records attributed to J Andrew Carlson.

36 records · Page 2Linked to original sources
PubMed2003

Sclerosing lipogranuloma of the orbit after periocular steroid injection.

PURPOSE: To report the clinical and histopathologic findings of a large sclerosing lipogranuloma of the orbit arising after a sub-Tenon's corticosteroid injection. DESIGN: Interventional case report and review of the literature. METHODS: A complete ocular and systemic evaluation was performed on a 81-year-old patient, who developed a large orbital mass subsequent to a periocular corticosteroid injection producing proptosis, ptosis, and ocular motility impairment. The lesion was biopsied and submitted for histopathologic analysis. MAIN OUTCOME MEASURES: Orbital, computed tomography, and histopathologic findings. RESULTS: Histopathologic examination revealed lipogranulomatous inflammation. Specifically, this type of reaction was consistent with a diagnosis of sclerosing lipogranuloma. CONCLUSIONS: It is extremely rare to find a large granulomatous orbital lesion arising subsequent to a periocular corticosteroid injection. Only one case has been reported in the English-language literature to date. It is important to include this type of lesion in the differential diagnosis of an orbital mass seen after the injection of periocular corticosteroids.

Aged↗
PubMed2003

Bednár tumor associated with dermal melanocytosis: melanocytic colonization or neuroectodermal multidirectional differentiation?

BACKGROUND: Neuroectodermal differentiation or melanocytic colonization are the opposing theories of histogenesis for the Bednár tumor or pigmented dermatofibrosarcoma protuberans (DFSP). OBSERVATION: A 31-year-old African-American woman presented with a 2-cm blue-black shoulder nodule of 1-year duration. Punch biopsy revealed a CD34+, Factor XIIIa-DFSP, harboring numerous, pigmented spindle S100+, Mart-1+ and HMB-45+ cells. Subsequent wide excision demonstrated pigmented dendritic and spindled cells widely scattered throughout the dermis of the 3-cm excisional margins and punch biopsy specimens of normal skin from both shoulders. This latter process was interpreted as dermal melanocytosis (nevus of Ito). The dermal pigmented spindle cells were Mart-1+ and CD34-, and were associated with non-pigmented CD34+, cytologically banal spindle cells, which were more numerous in the excisional margins than the contralateral shoulder. CONCLUSION: Reported herein is a singular case of Bednár tumor associated with dermal melanocytosis. Although the coexistence of these processes implicates colonization of the DFSP by constituent dermal melanocytes, the mixed immunophenotype (CD34+ or Mart-1+ cells) of dispersed dermal spindle cells hints at the possibility of a common cell of origin: the putative neuromesenchymal cell. In effect, the Bednár tumor could represent one part of a spectrum of neural crest-derived dermal tumors that includes dermal melanocytosis, cellular blue nevus and conventional DFSP.

Adult↗
PubMed2003

Chronic vulvar purpura: persistent pigmented purpuric dermatitis (lichen aureus) of the vulva or plasma cell (Zoon's) vulvitis?

BACKGROUND: Lichen aureus is localized variant of persistent pigmented purpuric dermatitis that typically affects the legs and can be associated with delayed hypersensitivity reactions or vascular abnormalities. Plasma cell vulvitis (Zoon's vulvitis) is a rare condition that frequently contains hemosiderin deposits and is suspected to be a mucosal reaction pattern due to variety of insults, most often local irritation or trauma. CASE REPORT: A 50-year-old female with longstanding complaints of spotting, vulvar dryness, irritation, and dyspareunia presented with circumscribed, purpuric, erythematous vulvar patches. Past estrogen cream treatment evoked symptoms of discomfort. On biopsy, siderophages and extravasated red blood cells were found in conjunction with a lichenoid, lymphocyte and plasma cell infiltrate, and dilated dermal and intraepithelial vessels. CONCLUSIONS: Reported herein is an unusual vulvar dermatosis that is best classified as a localized variant of persistent pigmented dermatosis (lichen aureus) but overlaps clinically and histologically with Zoon's vulvitis. This constellation of findings may represent a site-specific mucosal reaction to an erosive process that could either be inflammatory (hypersensitivity reaction) and/or traumatic in nature.

Chronic Disease↗
PubMed2003

Tumor doubling time of cutaneous melanoma and its metastasis.

Tumor doubling time, estimated using clinical data, is one factor used to determine who will benefit from surgery for patients with pulmonary metastatic melanoma. Reported herein are the tumor doubling times of four primary cutaneous melanomas in which the diagnosis of melanoma had been delayed, and their metastases (3 of 4). The median/mean tumor doubling times for primary melanoma and metastatic melanoma was 94/144 days (range 50-377) and 33/64 days (range 8-212), respectively. By paired t test, metastatic tumor doubling time was significantly faster than primary tumor doubling time (P = 0.01). Extrapolating the growth curves of metastatic melanoma to the point of onset of metastasis revealed that dissemination of tumor cells occurred well before first clinical presentation and symptoms in two cases, and in one case, during the interval between clinical presentation and complete excision of the primary. At the opposite pole, extrapolated growth curves for slow tumor doubling time melanoma demonstrated that long-term follow up (>10 years) is required to determine whether patients have been cured of melanoma or not. Overall, these estimates of melanoma tumor doubling time validate the concept of tumor progression, reinforce the tenet of early detection and curative excision, and can explain the phenomenon of late onset of metastases, respectively.

Adult↗
PubMed2003

Recurrent solitary reticulohistiocytoma of the eyelid.

A healthy 13-year-old female presented with a 5-month history of an enlarging red-brown, firm lower eyelid mass associated with loss of eyelashes. An excisional biopsy revealed a well-circumscribed nodule composed of coalescing nests of epithelioid cells, rare multinucleated cells, and vacuolated macrophages and spindle cells. Additional studies revealed a positive vimentin and alpha(1)-antitrypsin, and negative S100 protein and Factor XIIIa immunophenotype. This constellation of clinicopathologic features is diagnostic of solitary reticulohistiocytoma, but also shows overlap with xanthogranuloma, a common childhood histiocytosis. Reticulohistiocytoma should be considered in the differential diagnosis of eyelid tumors and has the potential for local recurrence. Diffuse cutaneous reticulohistiocytosis or multicentric reticulohistiocytosis should be considered if similar cutaneous lesions with or without symptoms of arthritis are present, respectively.

Adolescent↗
PubMed2003

Malignant melanoma 2003: predisposition, diagnosis, prognosis, and staging.

The incidence and mortality of melanoma has seemed to level off for certain groups after a steady increase during the last 50 years. This trend is suspected to be secondary to education efforts aimed at prevention and better detection and removal of thin, biologically benign melanomas. Since no effective systemic therapies exist for metastatic melanoma, early detection and removal of thin melanomas offer the best chance of cure. For thicker melanomas, sentinel lymph node biopsy has improved the accuracy of staging and prognostic evaluation. However, approximately one third of patients diagnosed with metastatic melanomas present without previous regional lymph node metastases. As the genomic understanding of melanoma's pathogenesis grows, new methods likely will be developed to more accurately identify the people at risk for melanoma, those who have high-risk melanomas, and those who have disseminated disease. We review current and potential biomarkers useful for the screening for and prevention, diagnosis, staging, and prognosis of melanoma.

Cytodiagnosis↗
PubMed2003

Biomarkers in melanoma: predisposition, screening and diagnosis.

Melanoma's incidence and mortality for certain groups has appeared to level off after a steady increase over the last half century. This trend is suspected to be due to better detection and removal of thin, biological early melanomas. However, to date, no prospective evidence exists to clearly demonstrate the efficacy of prevention and early detection in decreasing melanoma mortlity. Nonetheless, many studies suggest that both self-assessment of risk factors or clinician examination can identify a proportion of patients at highest risk for melanoma who may benefit from behavior modification (primary prevention) and routine screening (secondary prevention). Compromising these goals is the fact that neither the clinical or histologic diagnosis of melanoma is 100% accurate. Clinical diagnosis of melanoma, based on evaluation of a skin lesion's color and shape, correlates best with the experience of the clinician. Ancillary technologies have been developed to improve clinical accuracy of suspicious skin lesions but a subset of melanomas exist that do not fall in the spectrum of the 'ABCDE' guidelines commonly used for melanoma identification. Similarly, at the histologic level (the 'gold standard' of diagnosis), overlap exists between benign and malignant melanocytic proliferations leading to both over and underdiagnosis of melanoma. A better understanding of melanoma's pathogenesis has identified disease-related biomarkers that may more reliably differentiate a melanocytic nevus from melanoma. In this paper, we review current and novel, potentially more accurate, biomarkers and supplementary technologies that can be used for the prevention, screening and diagnosis of melanoma.

Animals↗
PubMed2003

Biomarkers in melanoma: staging, prognosis and detection of early metastases.

Currently, melanoma remains a surgical disease since early detection and excision of thin melanomas offers the best chance of a cure. Despite intensive clinical investigation, no effective systemic therapies exist for metastatic melanoma. Sentinel lymph node biopsy has greatly aided the staging and prognostic evaluation of primary cutaneous melanoma, however, approximately a third of patients diagnosed with metastatic melanomas present without prior regional lymph node involvement. Additional prognostic biomarkers exist which help determine the risk of advanced melanoma but the accuracy for each current marker is less than 100%. A greater understanding of the biology of melanomas and the development of new methods to identify patients with early (subclinical) metastatic disease may allow for selective and more effective therapy for patients at-risk for advanced disease. In this paper, current and novel potentially more accurate biomarkers for the staging and prognostic evaluation of melanoma patients, and for the detection of subclinical metastases are reviewed.

Biomarkers, Tumor↗
PubMed2002

Melanocytic proliferations associated with lichen sclerosus.

OBJECTIVES: To describe the clinicopathologic features of melanocytic proliferations associated with lichen sclerosus (LS) and to compare these findings with those in controls. DESIGN: Cohort study. SETTING: Academic and private practice dermatology and dermatopathology services. PATIENTS: Cases of melanocytic proliferations associated with LS and consecutive controls with persistent (recurrent) melanocytic nevi, persistent malignant melanomas, and compound melanocytic nevi. MAIN OUTCOME MEASURES: Diagnostic criteria and disease recurrence. RESULTS: Eleven patients, all female, with a mean age of 40 years (range, 8-83 years), presented with pigmented lesions clinically suspected to be malignant melanoma or atypical melanocytic nevi affecting the vulva (7 patients), perineum (3 patients), or chest (1 patient). Lichen sclerosus was first identified in the biopsy specimen and subsequently confirmed clinically. In 10 cases, a melanocytic nevus was superimposed on LS (overlying or entrapped by sclerosis), whereas LS was found at the periphery of vulvar malignant melanoma. After complete excision, no recurrences have been reported for the melanocytic nevi in LS (mean follow-up, 29 months; range, 4-60 months). Compared with control lesions, the LS melanocytic nevi most closely resembled persistent melanocytic nevi and could be distinguished from persistent malignant melanoma histologically. Melanocytes, nevoid or malignant, proliferating contiguously with fibrotic or sclerotic collagen, contained abundant melanin, diffusely expressed HMB-45, and had a higher Ki-67 labeling index than ordinary melanocytic nevi. However, persistent malignant melanoma exhibited mitotic figures, significantly higher Ki-67 labeling index, and deep dermal HMB-45 expression compared with LS melanocytic nevi and persistent melanocytic nevi. CONCLUSIONS: Melanocytic nevi occurring in LS have features in common with persistent melanocytic nevi and can mimic malignant melanoma. An "activated" melanocytic phenotype is seen in LS melanocytic nevi, implicating a stromal-induced change.

Adolescent↗
PubMed2002

Solitary spindle-cell xanthogranuloma of the eyelid.

PURPOSE: To describe a rare presentation of a solitary spindle-cell xanthogranuloma in a 3-year-old boy with a 6-month history of a right upper lid soft tissue lesion. DESIGN: Interventional case report. METHODS: An excisional full-thickness biopsy of the right upper lid was performed. Histologic examination and immunohistochemistry of the specimen were performed. RESULTS: Histopathologic evaluation revealed a well-demarcated nodule arising from the tarsus that contained a storiform array of spindle cells admixed with numerous multinucleated giant cells (some Touton type) and lymphocytes. The spindle cells labeled with antibodies to Factor XIIIa, CD68, lysozyme, Mac 387, and vimentin. The multinucleate giant cells labeled with CD68, lysozyme, and vimentin. Findings were consistent with the diagnosis of solitary spindle-cell xanthogranuloma. CONCLUSIONS: Spindle-cell xanthogranuloma resembles juvenile xanthogranuloma and fibrous histiocytoma (dermatofibroma) and should be considered in the differential diagnosis of spindle-cell tumors of the eyelid and periocular region. If similar lesions are noted elsewhere, the diagnosis of progressive nodular histiocytoma should be considered.

Biomarkers↗
PubMed2002

Anaplastic neoplasms arising from basal cellcarcinoma xenotransplants into SCID-beige mice.

BACKGROUND: An animal model for the study of basal cell carcinoma (BCC) is required to better understand its biology. Several attempts to grow BCC in immuno-incompetent animals have been only modestly successful. METHODS: To test the ability of BCC to grow in a mouse with complete and severe immuno-incompetence, 14 individual BCC were transplanted into the subcutaneous tissue of 18 SCID-beige mice (T, B and natural killer cell deficient). Light microscopy and immunophenotypic analyses were performed on primary BCC and first and seventh passage tumors. RESULTS: Transplantation of three BCC yielded rapidly growing anaplastic tumors for a tumor take of 18% (3/18). SCID-beige mice without tumor growth had mostly scars or epidermoid cysts at the transplant sites. The three patients whose BCC gave rise to the anaplastic tumors were significantly older than those without tumor growth (87 vs. 64, p = 0.001), but they did not differ with respect to BCC type or general health. These three anaplastic tumors were histologically and immunophenotypically similar, being composed of dyscohesive, pleomorphic cells that expressed vimentin and smooth muscle actin. In the first passage mice these tumors were locally invasive, tumor-forming nodules associated with an expansion of donor inflammatory cells (T and B lymphocytes and plasma cells), rare remnants of BCC epithelium and epidermoid cysts. By the seventh passage, the tumors were homogenous and metastasized widely throughout the mice. Changing transplantation location to the dermis to wound environment or supplementing the tumor with BCC-derived fibroblasts did not alter the phenotype or growth rate in SCID-beige mice. Anaplastic tumors also grew easily in SCID mice (T and B cell deficient). However, transplantation of the anaplastic tumors into normal mice (CB-17) or less severely immunodeficient mice (NCr and Balb/c: T and natural killer cell deficient) did not allow for growth. Furthermore, tumor growth could not be maintained in vitro. CONCLUSION: Empirically, these data suggest that BCC has the potential to become an aggressive metastatic neoplasm, given the right immune and stromal environment. Moreover, a functional B lymphocyte system appears to prevent this growth. As human lymphocytes also engraft in SCID-beige mice, the original host immune response could be responsible for the lack of tumor growth in the majority of xenografts. Furthermore, the anaplastic and metastatic phenotype of these BCC derived neoplasms may be the experimental equivalent of metastatic BCC and BCC associated with carcinosarcoma.

Anaplasia↗
PubMed2002

Actin-binding protein fascin expression in skin neoplasia.

BACKGROUND: Fascin containing actin bundles provide mechanical support to cellular protrusions and stress fibers. In cancers, some malignant cells (e.g. subsets of breast and ovarian carcinomas) express fascin. In skin cancer, the role of fascin is unknown. METHODS: Cases of 61 keratocytic neoplasms, 35 melanocytic neoplasms, nine extramammary Paget's disease (four with adenocarcinoma) and five sarcomas (angiosarcoma and atypical fibroxanthoma) were examined by immunohistochemistry, using monoclonal antihuman fascin antibody, clone 55 k-2 (Dako Corporation, Carpinteria, CA, USA). RESULTS: Fascin labeled all sarcomas and all keratinocytic neoplasms except for pagetoid pattern Bowen's disease. The regions of most intense fascin labeling were seen in the basal cells of infiltrative tumor margins. A minority of Merkel cell carcinomas exhibited weak or absent immunoreactivity. All melanocytic nevi except for some junctional nests of dysplastic melanocytic nevi expressed fascin. However, pagetoid cells of melanoma in situ and epithelioid cells of invasive melanoma weakly expressed or did not express fascin, whereas melanoma cells exhibiting spindle cell morphologies labeled intensely with fascin. Lastly, all cells of extramammary Paget's disease and most associated adenocarcinomas cells did not or were faintly labeled by fascin antibodies. Decreased or absent fascin expression was significantly associated with skin cancers with a high risk for metastasis (e.g. melanoma) vs. those with a low risk (e.g. basal cell carcinoma) (24% vs. 100% with > 50% immunoreactivity; p = 0.0001, chi-squared test). CONCLUSION: Fascin is expressed by skin tumors that locally infiltrate and replace surrounding tissues indicating a role for fascin in cell adhesion, cell motility and invasiveness. No or weak fascin expression is exhibited by cancers with pagetoid intraepidermal spread and by invasive tumors with a high risk of metastasis. Downregulation or loss of fascin's actin-bundling properties, probably associated with disorganization of cell-cell and cell-matrix contacts, may be a crucial step in the progression from locally invasive to widely disseminating cancers.

Actins↗
PubMed2002

Low CD7 expression in benign and malignant cutaneous lymphocytic infiltrates: experience with an antibody reactive with paraffin-embedded tissue.

Loss of CD7 expression by neoplastic lymphocytes is considered a distinguishing characteristic of mycosis fungoides (MF) and cutaneous T-cell lymphoma. Reports to date examining for the CD7 immunophenotype in MF have been performed on fresh-frozen tissue. In this study, we used a paraffin-reactive antibody directed against CD7 to determine its range of expression in MF and to compare these results with those in controls. Examining 22 cases of MF and 61 controls, we found minimal CD7 expression by lymphocytes in MF and in a few cases of benign inflammatory dermatosis (BID). The lowest mean CD7 counts (as a percentage of total lymphocytes) were found in MF (patch stage: 5% +/- 5%, range: 0-10; plaque and tumor stages: 15% +/- 5%, range: 5-25), and these counts were significantly lower than those for BID (35% +/- 20%, range: 5-80; p = 0.001). By logistic regression analysis, low CD7 expression (<10% lymphocytes labeling) had sensitivity and positive predictive values of 80% and 72%, respectively, and specificity and negative predictive values of 93% and 96%, respectively, for the diagnosis of patch stage MF. False-positive results were found for spongiotic dermatitis. Moreover, spongiotic dermatitides exhibited a progressive decrease in mean CD7 counts from acute to subacute to chronic stages (50% versus 35% versus 30%, respectively). In conclusion, minimal CD7 expression is a specific finding for MF. Benign inflammatory infiltrates can also show low CD7 expression, however, which rarely matches that of patch stage MF. Progressive loss of CD7 expression in BID is the likely consequence of expansion of antigen-selected CD3+CD4+CD7- T cells. These inflammatory CD4+CD7- T cells may represent the physiologic counterpart to the neoplastic lymphocyte of MF.

Antibodies, Neoplasm↗
PubMed2002

Possible mechanisms of hypopigmentation in lichen sclerosus.

Lichen sclerosus (LS) shares with vitiligo a milky-white appearance. By biopsy, pathognomonic dermal sclerosis readily distinguishes LS from vitiligo and other causes of leukoderma. To determine what the mechanism of hypopigmentation is in LS, we examined samples from LS cases for alterations in melanin content (Fontana-Masson stain) and melanocyte number (HMB-45 [PMEL-17/gp100], Mel-5 [TRP-1], Mart-1 [Melan A]) and compared these findings with those in controls of normal skin, acute scars, vitiligo, and lichen planus (LP; a common inflammatory cause of hyperpigmentation). The degree and extent of melanization found in LS overlapped with that in acute scars showing predominantly hypomelanized keratinocytes, with that in LP containing regions with numerous melanophages, and with that in vitiligo exhibiting focal regions of keratinocytes devoid of melanin pigment. By hematoxylin-eosin staining and immunocytochemistry for Mel-5 and Mart-1, LS had a lower mean count of melanocytes than acute scars, LP, and normal skin per 200 basal keratinocytes. In addition, a few LS cases had a significant loss of melanocytes comparable to that of vitiligo. Surprisingly, Mart-1 identified rare melanocytes in 67% of vitiligo cases and a significantly larger pool of melanocytes in LS and controls other than those labeled by Mel-5. Furthermore, LP and evolving lesions of LS contained the highest Mart-1 counts. HMB-45-immunoreactive melanocytes were found in the majority of acute scars and in LP and late-stage LS lesions at significantly lower levels than Mel-5- and Mart-1- labeled melanocytes, but they were not found in vitiligo or normal skin. We propose that several mechanisms may play a role in the production of leucoderma in LS: 1) decreased melanin production; 2) block in transfer of melanosomes to keratinocytes; and 3) melanocyte loss. The latter finding may be the pathogenic connection (lichenoid dermatitis of LS triggering an autoimmune reaction to melanocytes) that underlies the documented association of LS with vitiligo.

Antigens, Neoplasm↗
PubMed2002

Vulvar malignant melanoma associated with human papillomavirus DNA: report of two cases and review of literature.

Oncogenic human papillomavirus (HPV) types such as HPV 16 are known to play a crucial role in the development of anogenital carcinomas. The etiology of anogenital malignant melanoma is unknown. We report two case of vulvar malignant melanoma in which multiple HPV types including HPV 16 and putative novel HPV types (alb-1, alb-2, alb-7, and alb-10) were identified by degenerated nested polymerase chain techniques (polymerase chain reaction) in both the malignant melanoma and surrounding skin. One melanoma was associated with lichen sclerosus, and the other, with melanoma in situ and pigmented vulvar squamous papillomatosis. These melanomas harbored HPV types alb-7, and HPV 16 as well as alb-1, respectively. HPV types 16, 20, 21, 36, alb-2, and AJ001060 were detected in vulvar skin affected by lichen sclerosus. Vulvar squamous papillomatosis harbored HPV types 28 and alb-10. HPV 16 was physically integrated into the host genome in lichen sclerosus skin and possibly in the melanoma associated with pigmented vulvar squamous papillomatosis. Twenty-two percent (4 of 18) of normal control specimens from skin tumor excisions were found to harbor HPV DNA (HPV types 3, 54, and alb-7); none of these control samples harbored multiple HPV DNA. These findings of multiple HPV DNA and integrated HPV 16 in skin associated with vulvar malignant melanoma indicate that HPV may play a role in the development of vulvar malignant melanoma. The role of HPV could be either direct through infection of melanocytes or indirect as a cofactor with free radicals in chronic fibroinflammatory vulvar disorders such as lichen sclerosus.

Aged↗
PubMedDate not supplied

Cutaneous vasculitis: diagnosis and management.

Vasculitis is histologically defined as inflammatory cell infiltration and destruction of blood vessels. Vasculitis is classified as primary (idiopathic, eg, cutaneous leukocytoclastic angiitis, Wegener's granulomatosis) or secondary, a manifestation of connective tissue diseases, infections, adverse drug eruptions, or a paraneoplastic phenomenon. Cutaneous vasculitis, manifested as urticaria, purpura, hemorrhagic vesicles, ulcers, nodules, livedo, infarcts, or digital gangrene, is a frequent and often significant component of many systemic vasculitic syndromes such as lupus or rheumatoid vasculitis and antineutrophil cytoplasmic antibody-associated primary vasculitic syndromes such as Churg-Strauss syndrome. In most instances, cutaneous vasculitis represents a self-limited, single-episode phenomenon, the treatment of which consists of general measures such as leg elevation, warming, avoidance of standing, cold temperatures and tight fitting clothing, and therapy with antihistamines, aspirin, or nonsteroidal anti-inflammatory drugs. More extensive therapy is indicated for symptomatic, recurrent, extensive, and persistent skin disease or coexistence of systemic disease. For mild recurrent or persistent disease, colchicine and dapsone are first-choice agents. Severe cutaneous and systemic disease requires more potent immunosuppression (prednisone plus azathioprine, methotrexate, cyclophosphamide, cyclosporine, or mycophenolate mofetil). In cases of refractory vasculitis, plasmapheresis and intravenous immunoglobulin are viable considerations. The new biologic therapies that work via cytokine blockade or lymphocyte depletion such as tumor alpha inhibitor infliximab and the anti-B-cell antibody rituximab, respectively, are showing benefit in certain settings such as Wegener's granulomatosis, antineutrophil cytoplasmic antibody-associated vasculitis, Behçet's disease, and cryoglobulinemic vasculitis.

Anti-Inflammatory Agents, Non-Steroidal↗