Subramanian Yegappan

Publications (2)11.65 Total impact

• Article: Cytomegalovirus in the perilymphatic fluid.

  Paul W Bauer, Mojgan Parizi-Robinson, Peter S Roland, Subramanian Yegappan
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  ABSTRACT: The incidence of congenital cytomegalovirus (CMV) infection is approximately 1% of neonates. Ninety percent of congenitally infected infants are "asymptomatic;" they have no signs or symptoms at birth. The prevalence of congenital CMV in the profoundly deaf population and the pathogenesis of deafness from CMV are unknown. The objective of this study is to determine whether CMV can be demonstrated and quantified in perilymphatic fluid of patients with congenital CMV infection and sensorineural hearing loss (SNHL) using a quantitative real-time polymerase chain reaction (QRTPCR). Prospective case series. Perilymphatic fluid was collected at the time of cochlear implantation from children with known or radiologic evidence of congenital CMV infection and analyzed for the presence of CMV using QRTPCR. Blood was collected and analyzed for CMV using QRTPCR, serology, and culture. CMV was quantified in perilymphatic fluid and compared with that present in the patient's blood. Perilymphatic fluid and blood was collected from six children. QRTPCR was positive for CMV in the perilymphatic fluid of four patients. Blood analyzed with QRTPCR, and culture was negative in all patients. CMV can be demonstrated and quantified in perilymphatic fluid using QRTPCR. Refinements in our technique and sampling of perilymphatic fluid from a large population of children with congenital SNHL and unknown etiology can determine the prevalence of CMV-mediated profound HL.
  The Laryngoscope 03/2005; 115(2):223-5. · 1.75 Impact Factor
• Article: Unusual immunophenotype of CD8+ T cells in familial hemophagocytic lymphohistiocytosis.

  Nitin J Karandikar, Steven H Kroft, Subramanian Yegappan, Beverly B Rogers, Victor M Aquino, Kyung-Mi Lee, Vinay Kumar, F Javier Guenaga, Elaine S Jaffe, Daniel C Douek, Robert W McKenna
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  ABSTRACT: Familial hemophagocytic lymphohistiocytosis (FHL) is an inherited, fatal disorder of infancy. We report here a 17-day-old female infant who presented with high fever, hepatosplenomegaly, hypertriglyceridemia, hypofibrinogenemia, thrombocytopenia, and liver failure. Leukocytosis was detected with circulating "atypical" lymphoid cells. Flow cytometric studies revealed expanded subpopulations of CD8+ T cells with unusual immunophenotypic features, including a subset that lacked CD5 expression. A liver biopsy showed hemophagocytic lymphohistiocytosis with exuberant infiltrates of CD8+ T cells that lacked perforin. Mutational studies revealed a 666C-->A (H222Q) missense mutation in the perforin gene. T-cell receptor studies on flow-sorted T-cell subpopulations revealed no evidence of monoclonality. Analysis of T-cell receptor excision circle levels indicated long proliferative history in the aberrant CD8+ T-cell subsets. This case provides an instructive example of uncontrolled reactive proliferation of CD8+ T cells in FHL, resulting in atypical morphology and unusual immunophenotypic features that might suggest malignancy in other clinical settings.
  Blood 11/2004; 104(7):2007-9. · 9.90 Impact Factor