A systematic review of epinephrine degradation with exposure to excessive heat or cold.

BACKGROUND: Epinephrine is a lifesaving drug in the treatment of anaphylaxis and cardiac resuscitation. Current US storage recommendations are for controlled room temperature (20°C-25°C), with excursions permitted from 15°C to 30°C. Maintaining epinephrine within this required range is challenging, particularly for patients carrying autoinjectors and during storage in emergency vehicles. OBJECTIVE: To study epinephrine degradation with extreme temperature exposure for epinephrine concentrations used in anaphylaxis and cardiac resuscitation. METHODS: We searched the literature for all studies of epinephrine in sealed syringes, vials, or ampules in concentrations between 1:1,000 and 1:10,000, that measured epinephrine in samples exposed to temperatures above and/or below the recommended storage temperature compared with control samples. RESULTS: Nine studies were included. Heat exposure resulted in epinephrine degradation but only with prolonged exposure. Constant heat resulted in more degradation. None of the studies that evaluated epinephrine exposure to extreme cold found significant degradation. None of the studies evaluating the effects of real-world temperature fluctuations detected significant degradation. Only 2 small studies (1 evaluating heat and 1 freezing) involved autoinjectors, and all 40 devices tested fired correctly. CONCLUSION: 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.

Correlation of plasma complement split product levels with allergic respiratory disease activity and relation to allergen immunotherapy.

BACKGROUND: Allergens, including dust mite and grass pollen, and mast cell tryptase are known to generate the complement split products (CSPs) C5a and C3a, which can then trigger allergic inflammation. The relation of these anaphylatoxin levels to clinical allergic disease responses is not known. OBJECTIVE: To evaluate the relationship of plasma CSP levels to allergic respiratory disease variables in an adult cohort. METHODS: A cross-sectional survey was used to assess the association of plasma C5a desArg and C3a desArg levels with clinical allergic respiratory disease variables. Furthermore, a time course of the effect of routine allergen immunotherapy on plasma CSP levels and cutaneous and pulmonary responses was determined. RESULTS: Adult plasma C5a desArg levels correlate with asthma severity as determined by a physician (P = .01) and by Asthma Quality of Life Questionnaire scores (P < .01). Change in plasma C5a desArg levels 1 hour after immunotherapy is associated with baseline rhinoconjunctivitis symptom severity (P = .03), change in total mean wheal diameter (P = .05), and total dust mite dosage (P = .04). Change in plasma C3a desArg levels 3 hours after immunotherapy correlates with change in total mean wheal diameter induced by dust mite (P = .01). Change in plasma CSP levels after immunotherapy did not correlate with change in spirometric outcome. CONCLUSIONS: Plasma C5a desArg levels reflect allergic respiratory disease severity as assessed by physicians and correlate with Asthma Quality of Life Questionnaire scores. Changes in CSP levels after immunotherapy reflect cutaneous allergic responses, especially to dust mite allergen.

Absence of Chlamydia pneumoniae and signs of atherosclerotic cardiovascular disease in adolescents with systemic lupus erythematosus.

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.

IgE and atopy in perinatally HIV-infected children.

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.

Prevalence of viral and mycobacterial co-infections in perinatally HIV-infected children.

The progression of HIV disease may be affected by co-infection with other viruses. This study investigates the prevalence of Epstein-Barr virus (EBV); cytomegalovirus (CMV); herpes simplex virus (HSV) types 1 and 2; hepatitis A, B, and C (HA, HB, HC); and tuberculosis in perinatally HIV-infected children. Electrochemiluminescence Immunoassay (EIA) against EBV, CMV, HSV 1 and 2, HAV HBV HCV, and skin testing with purified protein derivative was performed on 45 perinatally HIV-infected children. CMVwas positive in 51%, EBVin 93.3%, HSV-1 in 62.2%, HSV-2 in 48.9%, HAV in 15.6%, HBVand HCV in 6.7% and PPD in 0%. HSV-2 prevalence was higher in females and Hispanics. The prevalence of CMV, EBV HSV-1, and tuberculosis was equivalent to rates reported in the general population. Prevalence of HSV-2 was significantly higher than in the general population (p < 0.001). Higher rates of HSV-2 infection and hepatitis may be secondary to high maternal co-infection rate and subsequent vertical transmission.