The Experts below are selected from a list of 1689 Experts worldwide ranked by ideXlab platform
Carole Mcarthur - One of the best experts on this subject based on the ideXlab platform.
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Salivary Gland disease in hiv aids and primary sjogren s syndrome analysis of collagen i distribution and histoPathology in american and african patients
Journal of Oral Pathology & Medicine, 2003Co-Authors: William J. Castellani, Nida J. Luangjamekorn, Matthew Mclaughlin, Paul Howard, Antonio Subtildeoliveira, Charlene W.j. Africa, Carole Mcarthur, Charles M. Cobb, Steven GustafsonAbstract:Background: Salivary Gland disease (SGD) in HIV/AIDS is clinically and histopathologically very similar to Sjogren's Syndrome (SS), although the mechanism of tissue damage is unknown. The aim of this study is to determine the prevalence of SGD in primary SS and in HIV/AIDS in USA and in West African patients, and to seek distinguishing histopathologic features that may help to elucidate underlying mechanisms. Methods: Histologic sections of minor Salivary Glands from 164 HIV-positive and -negative patients from Cameroon and the US, and from 17 US patients with primary SS, were evaluated following Salivary Gland biopsy for inflammatory changes. To confirm the presence of fibrosis, collagen I, which is the most abundant collagen type, was assessed immunohistochemically in H&E-stained sections. Results: Forty-eight per cent of patients with HIV from Cameroon had severe SGD, while it was only in 6% of patients from the US. Patients with HIV in the US had less fibrosis and collagen I deposits than Cameroonians. Seventy-six per cent of US HIV-positive patients had received anti-retroviral therapy, while none of the African patients had. SS and AIDS patients had a tendency for lymphocytes to locate in a perivascular rather than in a periductal distribution. Conclusions: The prevalence of SGD and the presence of fibrosis and collagen I in Cameroonians with HIV is significantly higher than in HIV-positive American patients, and is similar to US patients with primary SS. The impact of patient selection, anti-retroviral therapy, and pathogenic mechanisms on Salivary Gland Pathology is discussed.
Steven Gustafson - One of the best experts on this subject based on the ideXlab platform.
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Salivary Gland disease in hiv aids and primary sjogren s syndrome analysis of collagen i distribution and histoPathology in american and african patients
Journal of Oral Pathology & Medicine, 2003Co-Authors: William J. Castellani, Nida J. Luangjamekorn, Matthew Mclaughlin, Paul Howard, Antonio Subtildeoliveira, Charlene W.j. Africa, Carole Mcarthur, Charles M. Cobb, Steven GustafsonAbstract:Background: Salivary Gland disease (SGD) in HIV/AIDS is clinically and histopathologically very similar to Sjogren's Syndrome (SS), although the mechanism of tissue damage is unknown. The aim of this study is to determine the prevalence of SGD in primary SS and in HIV/AIDS in USA and in West African patients, and to seek distinguishing histopathologic features that may help to elucidate underlying mechanisms. Methods: Histologic sections of minor Salivary Glands from 164 HIV-positive and -negative patients from Cameroon and the US, and from 17 US patients with primary SS, were evaluated following Salivary Gland biopsy for inflammatory changes. To confirm the presence of fibrosis, collagen I, which is the most abundant collagen type, was assessed immunohistochemically in H&E-stained sections. Results: Forty-eight per cent of patients with HIV from Cameroon had severe SGD, while it was only in 6% of patients from the US. Patients with HIV in the US had less fibrosis and collagen I deposits than Cameroonians. Seventy-six per cent of US HIV-positive patients had received anti-retroviral therapy, while none of the African patients had. SS and AIDS patients had a tendency for lymphocytes to locate in a perivascular rather than in a periductal distribution. Conclusions: The prevalence of SGD and the presence of fibrosis and collagen I in Cameroonians with HIV is significantly higher than in HIV-positive American patients, and is similar to US patients with primary SS. The impact of patient selection, anti-retroviral therapy, and pathogenic mechanisms on Salivary Gland Pathology is discussed.
J K C Chan - One of the best experts on this subject based on the ideXlab platform.
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advances in Salivary Gland Pathology
Histopathology, 2007Co-Authors: W Cheuk, J K C ChanAbstract:This review summarizes the new findings on Salivary Gland Pathology under the following categories: immunohistochemistry; molecular genetics; newly recognized tumour types; known tumour entities with new findings; and progression of Salivary Gland tumours. In the application of immunohistochemistry, CD117 can aid in highlighting the luminal cell component of various Salivary Gland tumours, whereas p63 or maspin can aid in highlighting the abluminal cell component. A high Ki67 index remains the most useful marker to predict adverse outcome in Salivary Gland carcinoma. Specific chromosomal translocations are recognized in pleomorphic adenoma (with translocation involving PLGA1 or HMGA2 gene) and mucoepidermoid carcinoma (with MECT1–MAML2 gene fusion). Newly recognized entities include: sclerosing polycystic adenosis (with recent molecular evidence supporting its neoplastic nature), sclerosing mucoepidermoid carcinoma with eosinophilia, keratocystoma, adenoma with additional stromal component (lymphadenoma, lipoadenoma and adenofibroma), cribriform adenocarcinoma of the tongue and signet ring adenocarcinoma of minor Salivary Gland. Known tumour entities with new findings include: Salivary duct carcinoma (with newly recognized mucinous, micropapillary and sarcomatoid variants), intraductal carcinoma (with controversies in terminology), mucoepidermoid carcinoma (with newly proposed grading parameters and oncocytic variant), epithelial–myoepithelial carcinoma (with newly recognized morphological variants), small cell carcinoma (with most cases being related to Merkel cell carcinoma), extranodal marginal zone B-cell lymphoma (with specific chromosomal translocation) and chronic sclerosing sialadenitis (being a component of IgG4-related sclerosing disease). Progression of Salivary Gland tumours can take the form of malignant transformation of a benign tumour, progression from low-grade to high-grade carcinoma, dedifferentiation, or stromal invasion of an in situ carcinoma.
W Cheuk - One of the best experts on this subject based on the ideXlab platform.
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advances in Salivary Gland Pathology
Histopathology, 2007Co-Authors: W Cheuk, J K C ChanAbstract:This review summarizes the new findings on Salivary Gland Pathology under the following categories: immunohistochemistry; molecular genetics; newly recognized tumour types; known tumour entities with new findings; and progression of Salivary Gland tumours. In the application of immunohistochemistry, CD117 can aid in highlighting the luminal cell component of various Salivary Gland tumours, whereas p63 or maspin can aid in highlighting the abluminal cell component. A high Ki67 index remains the most useful marker to predict adverse outcome in Salivary Gland carcinoma. Specific chromosomal translocations are recognized in pleomorphic adenoma (with translocation involving PLGA1 or HMGA2 gene) and mucoepidermoid carcinoma (with MECT1–MAML2 gene fusion). Newly recognized entities include: sclerosing polycystic adenosis (with recent molecular evidence supporting its neoplastic nature), sclerosing mucoepidermoid carcinoma with eosinophilia, keratocystoma, adenoma with additional stromal component (lymphadenoma, lipoadenoma and adenofibroma), cribriform adenocarcinoma of the tongue and signet ring adenocarcinoma of minor Salivary Gland. Known tumour entities with new findings include: Salivary duct carcinoma (with newly recognized mucinous, micropapillary and sarcomatoid variants), intraductal carcinoma (with controversies in terminology), mucoepidermoid carcinoma (with newly proposed grading parameters and oncocytic variant), epithelial–myoepithelial carcinoma (with newly recognized morphological variants), small cell carcinoma (with most cases being related to Merkel cell carcinoma), extranodal marginal zone B-cell lymphoma (with specific chromosomal translocation) and chronic sclerosing sialadenitis (being a component of IgG4-related sclerosing disease). Progression of Salivary Gland tumours can take the form of malignant transformation of a benign tumour, progression from low-grade to high-grade carcinoma, dedifferentiation, or stromal invasion of an in situ carcinoma.
Allan H Ropper - One of the best experts on this subject based on the ideXlab platform.
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positive Salivary Gland biopsy sjogren syndrome and neuropathy clinical implications
Muscle & Nerve, 2003Co-Authors: Kenneth C Gorson, Allan H RopperAbstract:The relationship between neuropathy and Sjogren syndrome has been predicated largely on sicca symptoms or serological abnormalities rather than Salivary Gland Pathology. We reviewed consecutive neuropathy patients who had had a lip biopsy to identify features of the neuropathy that were associated with a positive lip biopsy suggesting Sjogren syndrome. Twenty of 54 neuropathy patients were biopsy positive; 13 had a painful or nonspecific sensory neuropathy and only 4 were ataxic. Sicca symptoms were not associated with a positive biopsy (P = 0.14). Serological abnormalities were found more often in the biopsy-positive group (P = 0.008), but anti-Sjogren syndrome A or B (anti-SSA or SSB) antibodies were detected in only 30%. There were no other clinical or electromyographic (EMG) features associated with a positive biopsy. From this experience, we conclude that: (1). most patients with neuropathy and a positive lip biopsy for Sjogren syndrome have a painful, distal, sensory axonal neuropathy; (2). there are no clinical or EMG features that are predictive of a positive lip biopsy; (3). ataxic neuropathy is uncommon; and (4). the lack of sicca symptoms or anti-SSA or SSB antibodies in patients with neuropathy does not exclude Sjogren syndrome based upon Salivary Gland Pathology.
