Login to your account

Username *
Password *
Remember Me

Blog With Right Sidebar

    Vous êtes ici :  
  1. Accueil
  2. Blog With Right Sidebar

Mother to child transfer of IgG and IgA antibodies against Dermatophagoides pteronyssinus.

There is strong evidence from animal models that placental and/or breast milk-mediated transfer of maternal allergen-specific IgG prevents allergic immune responses in the progeny. Both human and animal data also point to IgA as having an important regulatory role. In contrast, little is known about maternal transfer of IgG and IgA specific for respiratory allergens in humans. Dermatophagoides pteronyssinus (Der p) is an indoor allergen that is a major cause of asthma worldwide.

We analyzed maternal to child Der p-specific IgG and IgA transfer in a cohort of 77 paired maternal and child samples. We found Der p-specific IgG and its IgG1, IgG2 and IgG4 subclasses in all cord blood samples. Except for IgG1, cord levels were higher in newborns from atopic mothers (n=29) compared to non-atopic mothers (n=48). Der p-specific IgA was found in all colostrum samples and levels were independent of maternal atopic status. Notably, anti-Der p IgG was also found in colostrum and levels were higher in atopic mothers.

We believe that our work is a critical first step in the identification of early factors that may impact asthma development and should guide the development of clinical studies that assess whether Der p-specific IgG and IgA protect children from allergy as demonstrated in animal models.

Allergy blood testing: A practical guide for clinicians.

Blood tests are available that measure levels of immunoglobulin E (IgE) against specific allergens such as foods, inhalants, medications, latex, and venoms.

These tests can confirm the diagnosis of an allergic disorder, supplementing a clinical history consistent with an immediate allergic reaction. They are particularly useful when skin testing cannot or should not be performed.

The Effects of Cause of Death Classification on Prognostic Assessment of Patients With Pulmonary Embolism.

Although previous studies have provided evidence that the majority of deaths following an acute pulmonary embolism (PE) directly relate to the PE, more recent registries and cohort studies suggest otherwise.

Methods: We assessed the cause of death during the first 30 days after the diagnosis of acute symptomatic PE in a consecutive series of patients. We also assessed the prognostic characteristics of the simplified Pulmonary Embolism Severity Index (sPESI) and cardiac troponin I (cTnI) obtained at the time of PE diagnosis.

Results: During the first 30 days after diagnosis, 127 of the 1,291 patients died (9.8%; 95% confidence interval [CI], 8.2 -11.5%). Sixty patients (4.6%; 95% CI, 3.5-5.8%) died from definite or possible PE, and 67 (5.2%; 95% CI, 4.0-6.4%) died from other causes (cancer 25, infection 18, hemorrhage 7, heart failure 7, chronic obstructive pulmonary disease 5, renal failure 1, seizures 1, unknown 3). The sPESI predicted all-cause (odds ratio [OR] 5.97; 95% CI, 1.74-20.54, P < 0.01) and PE-associated mortality (OR 8.79; 95% CI, 1.12-68.79; P = 0.04). cTnI only predicted PE-associated mortality (adjusted OR 2.39; 95% CI, 1.25 to 4.57; P < 0.01). For all-cause mortality, the sPESI low-risk strata had a negative predictive value of 98.8% (95% CI, 97.4-100%) in comparison to 91.3% (95% CI, 88.9-93.6%) for the cTnI.

Conclusions: Within the first 30 days after the diagnosis of acute symptomatic PE, death due to PE and death due to other causes occur in a similar proportion of patients. As cTnI only predicted PE-associated mortality, low-risk sPESI had a higher negative predictive value for all-cause mortality compared to cTnI.

Selection of disease-specific biomarkers by integrating inflammatory mediators with clinical informatics in AECOPD patients: a preliminary study.

Systemic inflammation is a major factor influencing the outcome and quality of patient with chronic obstructive pulmonary disease (COPD) and acute exacerbations (AECOPD). Due to the inflammatory complexity, a great challenge is still confronted to optimize the identification and validation of disease-specific biomarkers.

The present study aimed at developing a new protocol of specific biomarker evaluation by integrating proteomic profiles of inflammatory mediators with clinical informatics in AECOPD patients, understand better their function and signal networks.

Methods: Plasma samples were collected from healthy non-smokers or patients with stable COPD (sCOPD) or AECOPD on days 1 and 3 of the admission and discharging day (day 7-10). Fouty chemokines were measured using a chemokine multiplex antibody array. Clinical informatics was achieved by a Digital Evaluation Score System (DESS) for assessing severity of patients. Chemokine data was compared among different groups and its correlation with DESS scores was performed by SPSS software.

Results: Of 40 chemokines, 30 showed significant difference between sCOPD patients and healthy controls, 16 between AECOPD patients and controls, and 13 between AECOPD patients and both sCOPD and controls, including BTC, IL-9,IL-18Bpa, CCL22,CCL23, CCL25, CCL28, CTACK, LIGHT, MSPa, MCP-3, MCP-4 and OPN. Of them, some had significant correlation with DESS scores.

Conclusion: There is a disease-specific profile of inflammatory mediators in COPD and AECOPD patients which may have a potential diagnostics together with clinical informatics of patients. Our preliminary study suggested that integration of proteomics with clinical informatics can be a new way to validate and optimize disease-special biomarkers.

Interactions between HIV infection and chronic obstructive pulmonary disease: Clinical and epidemiological aspects.

INTRODUCTION: an association between HIV infection and chronic obstructive pulmonary disease (COPD) has been observed in several studies.

Objective and methods: we conducted a review of the literature linking HIV infection to COPD, focusing on clinical and epidemiological data published before and during widespread highly active antiretroviral therapy (HAART).

RESULTS: Interactions between HIV infection and COPD appear to be influenced by multiple factors. In particular, the bronchopulmonary tract can be damaged by HIV infection, the immunodeficiency it induces, and the resulting increase in the risk of pulmonary infections. In addition, the prevalence of smoking and intravenous drug use is higher in HIV-infected populations, also increasing the risk of COPD. Before the advent of HAART, respiratory tract infections probably played a major role. Since the late 1990s and the widespread use of HAART, the frequency of opportunistic infections has fallen but new complications have emerged as life expectancy has increased.

CONCLUSION: given the high prevalence of smoking among HIV-infected patients, COPD may contribute significantly to morbidity and mortality in this setting.

Search

Search