Hypertriglyceridemia and low high-density lipoprotein (HDL)-cholesterol (HDL-C) may contribute to a presumed accelerated risk for cardiovascular disease in HIV-infected individuals. We evaluated the effect of omega-3 fatty acid treatment on triglycerides, low-density lipoprotein (LDL)-C, HDL-C, and HDL subpopulations. Forty-one HIVseropositive subjects with hypertriglyceridemia ( ‡ 150 mg/dl) on active antiretroviral therapy were enrolled in this placebo-controlled, double-blind, randomized, crossover trial comparing the effects of omega-3 fatty acid treatment (1.9 g EPA and 1.5 g DHA) on triglycerides, LDL-C, HDL-C, and HDL subpopulations. An independent sample t-test was used to assess the study start to posttreatment change for all components. After omega-3 fatty acid treatment, triglyceride levels decreased 63.2 -86.9 mg/dl ( p < 0.001). No significant changes in total cholesterol, LDL-C, or HDL-C were found. Within HDL subpopulations, significant changes were seen in the most atheroprotective HDL particles, a-1, which increased by 2.5 -5.6 mg/dl ( p < 0.05), and prea-1, which increased by 0.6 -1.0 mg/dl ( p < 0.001). Prea-3, a presumably atherogenic HDL particle, decreased by 0.5 -0.9 mg/dl ( p < 0.01). Omega-3 fatty acid treatment significantly lowered triglyceride levels in HIV-positive patients with moderate hypertriglyceridemia. While no study-wide improvements in LDL-C or HDL-C were detected, the HDL subpopulation profile changed in a beneficial way suggesting more cardioprotection after treatment.

Introduction. Varicella zoster virus (VZV) encephalomyelitis with cranial nerve involvement is rare. Characteristically it is preceded by a rash and primarily presents in the immunocompromised. The spectrum of VZV neurologic disease is extensive and it is not uncommon to present without rash. We report the case of an elderly otherwise immunocompetent patient who presented with diverse manifestations of VZV CNS infection all occurring without rash. Case Report. A 78-year-old man presented with 1 week of progressive paraparesis and sensory loss, malaise, and fevers. MRI of the neuraxis demonstrated numerous enhancing lesions: intramedullary, leptomeningeal, pachymeningeal, and cranial nerves. Cerebrospinal fluid (CSF) showed a white blood cell count of 420/μL with elevated protein (385 mg/dL). CSF VZV qualitative PCR was positive and CSF VZV immunofluorescence assay detected IgM antibody, confirming the diagnosis of VZV encephalomyelitis. Clinical and radiological improvement was observed after intravenous acyclovir treatment. Conclusion. This is a rare report of an immunocompetent patient with extensive VZV encephalomyelitis. We highlight the importance of considering this diagnosis even in the absence of the characteristic rash, and the potential risk of premature discontinuation of antiviral therapy once HSV has been excluded. Prompt recognition and treatment can dramatically reduce morbidity and mortality in patients.