Risk factors and disease associations in people living with idiopathic intracranial hypertension.

INTRODUCTION: Idiopathic intracranial hypertension is a neurological condition characterized by a raised intracranial pressure and papilledema, leading to chronic headaches and visual disturbances. By recognizing modifiable risk factors and deploying evidence-based interventions, healthcare providers have the potential to mitigate the burden of the disease and improve patient outcomes. AREAS COVERED: It is well known that the condition occurs in predominantly pre-menopausal females who live with obesity particularly in the context of recent weight gain. This review discusses what risk factors may contribute to the metabolic underpinnings of cerebrospinal fluid dysregulation. There are a number of disease associations that are important to screen for as they can alter management. EXPERT OPINION: There is emerging evidence to suggest that idiopathic intracranial hypertension is a systemic metabolic disease and it is unknown what are all the risk factors are that precipitate the condition. Targeting certain hardwired risk factors is unachievable. However, as recent weight gain has been identified as a predominant risk factor for the development of the disease and relapse, modification of body weight should be the primary aim of management. Insightful research into the involvement of the neuroendocrine axis driving cerebrospinal fluid dysregulation now has the potential for the development of therapeutic targets.

Antiretroviral therapy corrects HIV-1-induced expansion of CD8+ CD45RA+ CD2-) CD11a(bright) activated T cells.

BACKGROUND: HIV infection decreases thymic output and induces chronic T-cell activation. OBJECTIVE: To examine the reconstitution of naive and activated T cells. METHODS: Extended immune phenotyping of CD4(+) and CD8(+) T-cell subsets was combined with T-cell receptor rearrangement excision circle (TREC) levels and measures of T-cell receptor repertoire perturbations in CD8(+) T-cell subpopulation to define the global effect of HIV-1 on T-cell dynamics. Evaluations before and after therapy were performed in HIV-infected children and compared with those in healthy individuals. RESULTS: Ten HIV-infected children and adolescents with a broad range of pretherapy CD4(+) T-cell counts were compared with healthy individuals. Pretherapy late activated CD8(+) T cells (CD3(+)CD8(+)CD45RA(+)CD27(-)CD11a(bright) cells) were expanded among HIV-infected subjects. Successful antiretroviral therapy increased the proportion of naive T cells (CD3(+)CD4(+)CD45RA(+)CD27(+)CD28(+) and CD3(+)CD8(+)CD45RA(+)CD27(+)CD11a(dim) cells), with a significant decrease in late activated CD8(+) T cells. The proportion of naive CD4(+) and CD8(+) T cells significantly predicted log(10) TREC copies/10(6) PBMCs in infected children and healthy control subjects, with a negative correlation in late activated CD8(+) T cells and activated CD4(+) T cells. Treatment re-established Gaussian distributions and decreased oligoclonal expansion within the Vbeta repertoire of CD8(+)CD45RA(+) T cells, but compared with that seen in healthy children, the proportion of late activated CD8(+) T cells remained increased. CONCLUSION: HIV infection strikingly shifts the proportion of naive and late activated CD45RA(+)CD8(+) T cells. Homeostasis within this T-cell population reflects TREC levels and the extent of T-cell receptor Vbeta perturbations.