Patients with systemic lupus erythematosus (SLE) have accelerated atherogenesis. A recent study suggested that Chlamydia pneumoniae infection might also be a contributing factor in the development of atherogenesis in patients with SLE. The objective of this study was to investigate the possible association of C. pneumoniae infection with markers of atherosclerosis in adolescents with SLE compared with age-matched healthy controls. History and exam focused on cardiovascular risk factors were obtained from 20 patients with SLE and 20 age- and sex-matched controls. Laboratory studies included serum lipid profile and high-sensitivity C-reactive protein (hsCRP). Detection of C. pneumoniae in peripheral blood mononuclear cells (PBMCs) and in nasopharyngeal swab specimens was performed. Carotid Intima-Media Thickness (CIMT) was determined by sonography in all subjects. C. pneumoniae DNA was not detected in PBMCs of any of the patients or controls. Nasopharyngeal cultures were also negative for C. pneumoniae in all patients. CIMT was slightly higher in the SLE group (0.48 +/- 0.049) compared with controls (0.454 +/- 0.041, p = 0.29). There was no significant difference between the two groups in body mass index, blood pressure, hsCRP, and serum cholesterol (total, LDL and HDL). Serum triglycerides were higher in the lupus group (p = 0.03). Children and adolescents with SLE might have accelerated atherosclerosis; however, we did not observe an association with C. pneumoniae infection in this population.

Temperature excursions in real-world conditions may be less detrimental than previously suggested. Freezing and limited heat excursions did not result in epinephrine degradation. Refrigeration of epinephrine appears to reduce degradation. However, the effect of extreme temperatures, particularly freezing, on autoinjectors is not sufficiently well established. More research in needed at clinically relevant high temperatures, with limited exposure to heat, and involving autoinjector devices.

Elevated serum immunoglobulin E (IgE) and increased prevalence of atopy is reported in patients infected with human immunodeficiency virus (HIV). The elevated serum IgE may be attributed to polyclonal stimulation of B cells or IgE production against allergens, viruses, fungi and bacteria. This study investigates the prevalence of atopy in perinatally HIV-infected children, and the relationships between serum IgE (and other serum immunoglobulins) with atopy, CD4+ cell count and HIV-disease stage. Serum immunoglobulin levels, epicutaneous skin test for common aeroallergens, clinical Centers for Disease Control and Prevention (CDC) classification, CD4+ cell counts and allergy history were extracted from the charts of perinatally HIV-infected children on highly active antiretroviral therapy. The prevalence of atopy (52%) and the pattern of aeroallergen sensitivity were comparable with the US pediatric population. Serum IgE levels did not correlate with clinical disease stage. However, in non-atopic patients, serum IgE levels increased with disease progression (p = 0.02). There was an inverse relationship between the prevalence of elevated serum IgE levels and atopy with progression of disease (p = 0.019). Serum IgE did not correlate with atopy, CD4+ cell count, or duration of HIV infection or levels of serum immunoglobulins. This is the first study to show no increased prevalence of atopy in perinatally HIV-infected children compared with the general population. In advanced stages of HIV, elevated serum IgE may be specific for antigens other than those known as allergens.

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