Publications (12) View all
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Article: Plasmacytoid Dendritic Cells in Lymph Nodes of Patients With Human Immunodeficiency Virus.
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ABSTRACT: Circulating plasmacytoid dendritic cells (PDC) decrease in human immunodeficiency virus (HIV) infection, either from loss or redistribution to lymph nodes (LN). Limited animal and human studies variably showed increased or decreased nodal PDC. CD123 immunostaining was performed on 28 archived LN biopsies (20 reactive) from 25 HIV patients. PDC clustering was graded (1: none; 2: rare small; 3: medium-sized, loose; and 4: large tight clusters) and correlated with HIV-lymphadenitis stage, blood CD4 counts, time since HIV diagnosis, and treatment duration. Increased PDC clustering was seen with decreasing CD4 counts (P=0.001), shorter treatment duration (P=0.0268), and advancing HIV-lymphadenitis stage (P=0.06). No correlation with time since HIV diagnosis was noted. To our knowledge, this is the first human study assessing relationship of nodal PDC in HIV to CD4 counts, treatment duration, and lymphadenitis pattern. Our findings suggest that PDC redistribute to LN with advancing immunodeficiency and stage of HIV infection.Applied immunohistochemistry & molecular morphology: AIMM / official publication of the Society for Applied Immunohistochemistry 04/2012; · 1.63 Impact Factor -
Article: Acute monoblastic leukemia with abnormal granules and disseminated intravascular coagulation: diagnostic pitfalls.
Rebecca Pohlmann, Parul BhargavaAmerican Journal of Hematology 09/2009; 84(11):773-5. · 4.67 Impact Factor -
Article: Utility of fascin and JunB in distinguishing nodular lymphocyte predominant from classical lymphocyte-rich Hodgkin lymphoma.
Parul Bhargava, Liron Pantanowitz, Geraldine S Pinkus, Jack L Pinkus, Michele E Paessler, Michele Roullet, Shiva Gautam, Adam Bagg, Marshall E Kadin[show abstract] [hide abstract]
ABSTRACT: Nodular lymphocyte-predominant Hodgkin lymphoma (NLPHL) and lymphocyte-rich classical Hodgkin lymphoma (LRCHL), although clinically and morphologically similar, differ biologically and in prognosis. Immunolabeling of Reed-Sternberg (RS) cells in LRCHL and lymphocytic and/or histiocytic variants (L&H cells) in NLPHL is often required to help distinguish between the 2 variants. Our aim was to evaluate fascin (a distinct 55-kd actin-bundling protein) and JunB (an activator protein-1 family transcription factor) to differentiate NLPHL from LRCHL. A total of 35 archival cases of NLPHL (n = 24) and LRCHL (n = 11) from adults and children were studied. Slides were reviewed for all cases and clinical, morphologic, and immunohistochemical features were evaluated. Each case was immunostained for fascin and JunB, and immunoreactivity of RS cells, L&H cells, and background lymphocytes were recorded. Whereas occasional L&H cells were weakly positive for fascin in 3 out of 24 (12.5%) cases of NLPHL, RS cells in LRCHL were positive for fascin in 11 out of 11 (100%) cases with a strong cytoplasmic staining pattern. JunB was positive in 10 out of 24 (41.7%) of NLPHL cases, and 11 out of 11 (100%) of LRCHL cases, showing a stippled and/or diffuse nuclear staining pattern. In addition to L & H Cells, JunB also stained small background lymphocytes, particularly in areas of progressively transformed germinal centers of NLPHL. Either stains when tested alone, if negative, or with rare L&H cell weak positivity for fascin, is indicative of NLPHL. The L&H cells of NLPHL cases were negative for concomitant staining in 24 out of 24 (100%) cases. Concomitant positive staining of classic RS cells for fascin and JunB was found in 11 out of 11 (100%) of LRCHL cases. Although fascin positivity alone supports the diagnosis of LRCHL, concomitant positivity offers stronger support and is less likely to lead to a false conclusion if aberrant fascin staining were to be encountered in a case of NLPHL. Staining for fascin and JunB provides a basis for distinguishing NLPHL from LRCHL and offers an alternative to other antibody profiles.Applied immunohistochemistry & molecular morphology: AIMM / official publication of the Society for Applied Immunohistochemistry 06/2009; 18(1):16-23. · 1.63 Impact Factor -
Article: Detection of JC virus DNA and proteins in the bone marrow of HIV-positive and HIV-negative patients: implications for viral latency and neurotropic transformation.
Chen S Tan, Bruce J Dezube, Parul Bhargava, Patrick Autissier, Christian Wüthrich, Janice Miller, Igor J Koralnik[show abstract] [hide abstract]
ABSTRACT: We sought to determine the prevalence of JC virus (JCV) in bone marrow samples from human immunodeficiency virus (HIV)-positive and HIV-negative patients and to determine whether bone marrow is a site of latency and neurotropic transformation of JCV, the agent of progressive multifocal leukoencephalopathy (PML). We collected bone marrow aspirates, archival bone marrow samples, and blood and urine samples from 75 HIV-negative and 47 HIV-positive patients without PML as well as bone marrow and urine or kidney samples from 8 HIV-negative and 15 HIV-positive patients with PML. Samples were tested for JCV DNA by quantitative polymerase chain reaction and for JCV protein expression by immunohistochemical analysis. JCV regulatory regions (RRs) were characterized by sequencing. JCV DNA was detected in bone marrow samples from 10 (13%) of 75 and 22 (47%) of 47 of the HIV-negative and HIV-positive patients without PML, respectively, compared with 3 (38%) of 8 and 4 (27%) of 15 of the HIV-negative and HIV-positive patients with PML. JCV DNA (range, 2-1081 copies/microg of cellular DNA) was detected in multiple leukocyte subpopulations of blood and bone marrow samples. JCV large T antigen, but not VP1 capsid protein, was expressed in bone marrow plasma cells. Bone marrow JCV RR sequences were similar to those usually found in the brains of patients with PML. Bone marrow is an important reservoir and a possible site of neurotropic transformation for JCV.The Journal of Infectious Diseases 04/2009; 199(6):881-8. · 6.41 Impact Factor -
Article: Medical mystery: A 71-year-old man with pancytopenia--the answer.
Julia M Braza, Parul BhargavaNew England Journal of Medicine 01/2009; 359(26):2845-6; discussion 2846. · 53.30 Impact Factor