No abstract

RESUMENCaso clínico: Se describe una mujer de 16 años con epilepsia severa que desarrolló una hemianopsia homónima izquierda después de tomar topiramato 125 mg durante 12 semanas y una mujer epiléptica de 24 años que presentó una maculopatía bilateral después de tomar 150 mg de topiramato durante 8 semanas. Discusión: Se identifican dos reacciones oculares adversas al topiramato. Ambas precisan retirar el tratamiento, aunque la maculopatía por topiramato es irreversible.Palabras clave: Topiramato, hemianopsia homóni-ma, maculopatía. COMUNICACIÓN CORTA ABSTRACTCase reports: We describe 2 patients who developed ocular side effects during treatment with topiramate. One was a 16-year-old woman with generalized seizures who developed a homonymous hemianopia after using topiramate 125 mg per day for 12 weeks, and the other was a 24-year-old epileptic female who developed a bilateral maculopathy after using topiramate 150 mg per day for 8 weeks. Discussion: We identified two severe ocular adverse reactions from topiramate. Both reactions necessitated discontinuing the treatment, but the topiramate-associated maculopathy was irreversible (Arch Soc Esp Oftalmol 2006; 81: 345-348).

Fusion of CD4+ cells by HIV-1 envelope proteins (Env) is a mechanism of virus spread and cell damage. Production of antibodies able to influence cell-cell fusion in vivo may affect the course of the infection. The effect of sera from 49 HIV-1-positive patients was tested on an in vitro fusion assay using Env-expressing and normal Jurkat T cells labelled with DiI and DiO dyes, and flow cytometry for quantification of cell-cell fusion. Sera varied in their activity on fusion: 69?4 % inhibited, 24?5 % had no effect and 6?1 % enhanced cell fusion. Fusion activity correlated positively with the CD4 + T-cell count and inversely with the viral load. Removal of IgG or IgM from sera reduced or eliminated inhibition and enhancing activities, respectively. Antibodies with inhibitory activity predominate in early and intermediate stages of infection, whereas loss of inhibition or enhancement of fusion correlates with progression to AIDS.Human immunodeficiency virus type 1 (HIV-1) frequently induces cell-cell fusion with syncytia formation in cultures of CD4 + T cells. Syncytia formation result from the interaction between infected cells expressing the virus envelope glycoprotein (Env) on their surface and neighbouring uninfected CD4+ cells (Lifson et al., 1986;Sodroski et al., 1986). Cell-cell fusion may have an important pathogenic role in vivo. HIV-1-infected giant multinucleated cells are frequently detected in the lymph nodes of asymptomatic and AIDS patients, and have been proposed as virus reservoirs (Budka 1986; Frankel et al., 1996;Koenig et al., 1986). Syncytium-inducing viruses (usually requiring CXCR4 as a co-receptor) associate with an increased rate of CD4 + T-lymphocyte depletion in patients and progression to AIDS (Blaak et al., 2000; Connor et al., 1993;Miedema et al., 1994). Peptides that interfere with virus-cell fusion decrease viral loads in humans (Kilby et al., 1998;Lazzarin et al., 2003). Furthermore, the membrane fusing ability of Env from a simian-human immunodeficiency virus chimera was determinant for CD4 + T-cell depletion in macaques (Etemad-Moghadam et al., 2001). Cell fusion is a significant cause of cell death in vitro, mainly by apoptosis triggered by aberrant initiation of mitosis (Castedo et al., 2002; Ferri et al., 2000;Laurent-Crawford et al., 1991). The magnitude of CD4 + cell-cell fusion events can be significant in lymphoid tissues, where there is close contact between cells (Amendola et al., 1996). On the other hand, cell-to-cell HIV-1 transmission without formation of syncytia, likely involving localized fusion events at cell contact points was proposed as a mechanism of transmission between individuals, and an important route of viral spread (Gupta et al., 1989;Phillips, 1994;Sato et al., 1992). Recently, it was shown that virus strains highly efficient in cell-to-cell transmission and with a syncitium-inducing phenotype are selected in an in vitro model of the rapid T-cell turnover known to occur during HIV-1 infection (Gummurulu et al., 2000).Inhibition of pathogenic cell-cell ...

Our data indicate that peginterferon alpha-2b plus ribavirin treatment produces significant changes in HCV dynamics that can be detected as early as 48 h after the first dose of peginterferon alpha-2b and that these changes are useful in predicting response to therapy in CHC patients.

No abstract