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CMV retinitis in an HIV-infected patient on prolonged and effective highly active antiretroviral therapy (HAART)
Abstracts
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CMV Immune Response- Posters G3-26 CMV retinitis in an HIV-infected patient on prolonged and effective highly active antiretroviral therapy (HAART) ADRIANA WEINBERG University of Colorado Health Sciences Center, CO, USA The incidence of CMV disease in HIV-infected patients has dramatically decreased using HAART. Patients who develop CMV retinitis on HAART are failing therapy or do so during the first 3 months of HAART, presumably before immune reconstitution has occurred. We identified a case of CMV retinitis that occurred after 2 years of effective HAART. This HIV-infected male reached CD4 < 50 cells//ll in August 1995. He developed left eye CMV retinitis in June 1996, while CD4 number was < 50 cells//~l. The patient was successfully treated with parenteral GCV. In Feb 1997, with CD4 = 100 cells/,ul on HAART, he developed bilateral CMV retinitis that responded well to parenteral GCV followed by maintenance oral GCV. The second and third recurrences (left and then right eye) occurred in June and Dec 1998, respectively, while the patient was on oral GCV, had CD4 = 374 and 443 cells//Jl, respectively, and plasma HIV RNA < 5,000 copies/ml. The etiology of the last recurrence was confirmed by vitreous CMV PCR. Both episodes responded to intra-ocular GCV implants. CMV-specific cell-mediated immunity (CMI) was assessed by lymphocyte proliferation, responder cell frequency and induced cytokine production. At presentation and 3 weeks after the implant, CMV-specific CMI was not detected. In contrast, CMV plasma PCR, which was positive at diagnosis, became negative after 3 weeks. Eight weeks post-therapy CMI and PCR results will be presented. This case illustrates the lack of reconstitution of CMV-specific CMI. Implications for pathogenesis and clinical management of opportunistic infections will be discussed.
G3-27 Low anti-HCMV IgG level as a consequence of transient hypogammaglobulinemia in infected premature infants BOGUMILA MILEWSKA-BOBULA The Children's Memorial Health institute, Warsaw, Poland Twenty infants with symptomatic HCMV congenital infection born 25 to 40 weeks of gestational age were hospitalised between March 1996 and June 1998. The diagnosis was confirmed by detection of specific IgM and IgG antibodies (by ELISA) and HCMV-DNA by PCR in C-SF, serum and urine (before and after treatment). Other laboratory examinations (eg. serum total protein level with fractions) were performed. Canciclovir in doses 5,0 - 7,5mg/kg twice daily, as an intravenous infusion was given for 3 to 6 weeks. RESULTS: In 6 infants born prematurely and in 2 term babies, specific IgG antibody concentration was 32 to 183 i.u.; in 7 of them specific IgM were present. In all 8 cases serum concentration of gammaglobulin fraction was low, it ranged from 3,48 to 4,99 g/I. After antiviral treatment, serum concentration of IgG increased (219 to 922 i.u.) except in one child with prolonged hypogammaglobulinemia; specific IgM were not detected in any of the cases except one. No IVIG were given during therapy. CONCLUSIONS: The low concentration of specific IgG antibodies in infants with congenital HCMV infection was probably the effect of immature immunologic response of infected preterm babies. In congenitally infected premature infants it is indicated to evaluate total levels of immunoglobulins in serum beside the examination of specific antibodies.
143
CMV Immune Response- Posters G3-26 CMV retinitis in an HIV-infected patient on prolonged and effective highly active antiretroviral therapy (HAART) ADRIANA WEINBERG University of Colorado Health Sciences Center, CO, USA The incidence of CMV disease in HIV-infected patients has dramatically decreased using HAART. Patients who develop CMV retinitis on HAART are failing therapy or do so during the first 3 months of HAART, presumably before immune reconstitution has occurred. We identified a case of CMV retinitis that occurred after 2 years of effective HAART. This HIV-infected male reached CD4 < 50 cells//ll in August 1995. He developed left eye CMV retinitis in June 1996, while CD4 number was < 50 cells//~l. The patient was successfully treated with parenteral GCV. In Feb 1997, with CD4 = 100 cells/,ul on HAART, he developed bilateral CMV retinitis that responded well to parenteral GCV followed by maintenance oral GCV. The second and third recurrences (left and then right eye) occurred in June and Dec 1998, respectively, while the patient was on oral GCV, had CD4 = 374 and 443 cells//Jl, respectively, and plasma HIV RNA < 5,000 copies/ml. The etiology of the last recurrence was confirmed by vitreous CMV PCR. Both episodes responded to intra-ocular GCV implants. CMV-specific cell-mediated immunity (CMI) was assessed by lymphocyte proliferation, responder cell frequency and induced cytokine production. At presentation and 3 weeks after the implant, CMV-specific CMI was not detected. In contrast, CMV plasma PCR, which was positive at diagnosis, became negative after 3 weeks. Eight weeks post-therapy CMI and PCR results will be presented. This case illustrates the lack of reconstitution of CMV-specific CMI. Implications for pathogenesis and clinical management of opportunistic infections will be discussed.
G3-27 Low anti-HCMV IgG level as a consequence of transient hypogammaglobulinemia in infected premature infants BOGUMILA MILEWSKA-BOBULA The Children's Memorial Health institute, Warsaw, Poland Twenty infants with symptomatic HCMV congenital infection born 25 to 40 weeks of gestational age were hospitalised between March 1996 and June 1998. The diagnosis was confirmed by detection of specific IgM and IgG antibodies (by ELISA) and HCMV-DNA by PCR in C-SF, serum and urine (before and after treatment). Other laboratory examinations (eg. serum total protein level with fractions) were performed. Canciclovir in doses 5,0 - 7,5mg/kg twice daily, as an intravenous infusion was given for 3 to 6 weeks. RESULTS: In 6 infants born prematurely and in 2 term babies, specific IgG antibody concentration was 32 to 183 i.u.; in 7 of them specific IgM were present. In all 8 cases serum concentration of gammaglobulin fraction was low, it ranged from 3,48 to 4,99 g/I. After antiviral treatment, serum concentration of IgG increased (219 to 922 i.u.) except in one child with prolonged hypogammaglobulinemia; specific IgM were not detected in any of the cases except one. No IVIG were given during therapy. CONCLUSIONS: The low concentration of specific IgG antibodies in infants with congenital HCMV infection was probably the effect of immature immunologic response of infected preterm babies. In congenitally infected premature infants it is indicated to evaluate total levels of immunoglobulins in serum beside the examination of specific antibodies.