Immediate hypersensitivity to chlorhexidine appears to be common but underreported in the UK. We recommend that centres investigating patients with reactions during anaesthesia and surgery should routinely include testing for chlorhexidine allergy.
The role of anaerobic bacteria in ventilator-associated pneumonia (VAP) has been little investigated. In this study we analyzed the incidence of anaerobes in patients with a first episode of bacteriologically documented VAP (> 10(3)CFU/ml), using protected specimen brushes (PSB). We particularly took care to preserve anaerobic conditions during transport and the microbiological procedure. Two groups were considered: group A with anaerobic bacteria recovered from PSB, with or without anaerobes, and group B with aerobic bacteria only. One hundred and thirty patients were included, 30 (23%) in group A, and 100 (77%) in group B. The main anaerobic strains isolated were Prevotella melaninogenica (36%), Fusobacterium nucleatum (17%), and Veillonella parvula (12%). Univariate analysis demonstrated that patients in group A were younger than those in group B (p < 0.05) and their simplified acute physiologic score was higher (p < 0.02). The percentage of patients receiving antibiotics before PSB did not differ significantly between group A (57%) and group B (35%). VAP with anaerobes occurred more often in patients orotracheally intubated than nasotracheally intubated (p < 0.02). Episodes of VAP involving anaerobic bacteria occurred more often in the first five days (early VAP) than after the fifth day (late VAP) (p < 0.05). The 3-mo mortality rate was similar in the two groups, but death occurred earlier in group B (p < 0.01). Multivariate analysis demonstrated that presence of altered level of consciousness (p = 0.0002), higher simplified acute physiologic score (p = 0.003), and admission to the medical ICU (p = 0.02) were the factors independently predisposing to the development of VAP with anaerobes.
This study provides evidence that testing for gastric parietal cell antibodies is an appropriate screening test for pernicious anaemia, with intrinsic factor antibodies reserved for confirmatory testing or in patients with other autoantibodies that mask the GPC pattern; B12 levels are not related to autoantibody status.
Therapeutic regimens of intravenous immunoglobulin are currently based on actual body weight. The relationship between immunoglobulin dose and serum IgG level in relation to body size was retrospectively explored in patients on replacement therapy. Data were collected as part of a national audit on immunoglobulin therapy in patients with common variable immunodeficiency. 107 patients received immunoglobulin titrated to optimum effect. Correlations were sought between body mass index, trough IgG levels, infusion frequency and total annual dose. The mean (±SD) trough IgG level was 8.4±1.6 g/L and annual immunoglobulin dose received was 456.8±129.4 g. There was no relationship between annual dose and trough IgG level, regardless of infusion frequency, or adjustment for weight or body mass index. These results support the clinical practice of immunoglobulin prescription by clinical outcome rather than fixed dose by body weight. Future studies exploring immunoglobulin efficacy should include treatment arms with dosages based on both ideal and actual body weight, as ideal body weight-based prescribing would save significant amounts of product.
Use of a 1st percentile globulin fraction improved early detection of hypogammaglobulinaemia. This is a useful adjunct to alert clinicians to unsuspected hypogammaglobulinaemia but should not replace immunoglobulin measurement. Patients with globulin fraction below the first percentile should be reviewed for possible hypogammaglobulinaemia.
SummaryThe considerable clinical heterogeneity of patients with common variable immunodeficiency disorders (CVID) shares some similarity with bonemarrow failure disorders such as Diamond-Blackfan anaemia (DBA) and Shwachman-Diamond syndrome (SDS), now recognized as defects in ribosome biogenesis or ribosomopathies. The recognition of a patient with DBA who subsequently developed CVID lends support to our previous finding of a heterozygous mutation in the SBDS gene of SBDS in another CVID patient, suggesting that ribosome biogenesis defects are responsible for a subset of CVID. Genetic defects in the ribosomal translational machinery responsible for various bone marrow failure syndromes are recognized readily when they manifest in children, but diagnosing these in adults presenting with complex phenotypes and hypogammaglobulinaemia can be a challenge. In this perspective paper, we discuss our clinical experience in CVID patients with ribosomopathies, and review the immunological abnormalities in other conditions associated with ribosomal dysfunction. With genetic testing available for various bone marrow failure syndromes, our hypothesis that ribosomal abnormalities may be present in patients with CVID could be proved in future studies by testing for mutations in specific ribosomal genes. New knowledge might then be translated into novel therapeutic strategies for patients in this group of immunodeficiency disorders.
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