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Immediate adverse reactions to anaesthetics have an immune mechanism in more than 50% of the cases. They are mainly due to muscle relaxant drugs. A prospective evaluation of tryptase, histamine and serotonin for diagnosing anaphylaxis to anaesthetics was performed over 2 years. The sensitivity of each marker was at 60-70% and it reached 80% when combining tryptase and histamine. Specific IgE have been already observed in serum from patients allergic to muscle relaxant, thiopentone, morphine, phenoperidine, propofol and radio-contrast media. However, the recent progress in the identification of drug epitopes by Sepharose-solid drug phase IgE radioimmunoassay has to be reconsidered as non-specific binding of hydrophobic drugs such as propofol to hydrophobic serum IgE has been observed recently in patients with drug allergy. In addition, association of drugs such as propofol and muscle relaxant may potentiate the mediator release by a non-elucidated mechanism. [ABSTRACT FROM AUTHOR]

Drug hypersensitivity reactions ( DHRs) are a matter of great concern, both for outpatient and in hospital care. The evaluation of these patients is complex, because in vivo tests have a suboptimal sensitivity and can be time-consuming, expensive and potentially risky, especially drug provocation tests. There are several currently available in vitro methods that can be classified into two main groups: those that help to characterize the active phase of the reaction and those that help to identify the culprit drug. The utility of these in vitro methods depends on the mechanisms involved, meaning that they cannot be used for the evaluation of all types of DHRs. Moreover, their effectiveness has not been defined by a consensus agreement between experts in the field. Thus, the European Network on Drug Allergy and Drug Allergy Interest Group of the European Academy of Allergy and Clinical Immunology has organized a task force to provide data and recommendations regarding the available in vitro methods for DHR diagnosis. We have found that although there are many in vitro tests, few of them can be given a recommendation of grade B or above mainly because there is a lack of well-controlled studies, most information comes from small studies with few subjects and results are not always confirmed in later studies. Therefore, it is necessary to validate the currently available in vitro tests in a large series of well-characterized patients with DHR and to develop new tests for diagnosis. [ABSTRACT FROM AUTHOR]

Background/Objectives:Carotenoids are potentially malabsorbed in patients with chronic pancreatitis (CP). The aims of this study were: (1) to determine the prevalence of low levels of each of the major carotenoids in subjects with CP; (2) to compare carotenoids in CP subjects with or without vascular disease and (3) to test the effect of an increase in dietary lycopene intake in patients with low plasma lycopene concentration.Subjects/Methods:Simultaneous determination of carotenoids was done in 80 patients with CP and 20 healthy subjects, using high-performance liquid chromatography. Of the CP patients who had low lycopene concentration, 22 (<120 μg/l) had to consume daily 40 g tomato paste (approximately 24 mg lycopene).Results:Of these patients, 84.7% had at least one carotenoid deficiency and 27.5% had more than four carotenoid deficiencies. Low plasma concentrations in β-carotene and lycopene were correlated, in CP group, with a low body mass index (BMI), a low low-density lipoprotein (LDL) cholesterol concentration, alcohol consumption and current smoking status, whereas low plasma concentration in β-cryptoxanthine was correlated with a low BMI, a low LDL cholesterol concentration and alcohol consumption. Lycopene concentration was decreased in patients with vascular disease (171±197 vs 99±72 μg/l; P=0.02). After an intervention period of 8±2 months, lycopene concentration increased from 67.5±30 to 121.8±102 μg/l (P=0.025).Conclusion:Carotenoid concentrations are dramatically decreased in CP, especially lycopene in CP patients with vascular disease. Despite malabsorption, it is possible to increase lycopene plasma concentration by increasing heated tomato consumption. [ABSTRACT FROM AUTHOR]

Background The interaction of ribavirin, an inosine monophosphate dehydrogenase inhibitor, with azathioprine metabolism, potentially leading to myelotoxicity, remains unexplored. Aim To underline the interaction of ribavirin, an inosine monophosphate dehydrogenase inhibitor, with azathioprine metabolism, potentially leading to myelotoxicity. Methods The medical records of eight patients who developed severe pancytopenia following concomitant use of azathioprine and ribavirin were retrospectively reviewed. Results Bone marrow suppression reached nadir after a mean interval of 4.6 ± 1.6 weeks following HCV therapy initiation in seven patients. At the time of pancytopenia, the mean platelet count was 69.75 ± 82.8 × 10−3/mm3, mean haemoglobin level 7.75 ± 1.3 g/dL and mean neutrophil count 0.45 ± 0.26 × 10−3/mm3. All patients had normal thiopurine methyltransferase genotype. In two patients, a prospective monitoring of azathioprine metabolites was available. Myelotoxicity was accompanied by elevated total methylated metabolite levels (16 500 and 15 000 pmol/8 × 108 erythrocytes) with a concomitant decrease in 6-tioguanine nucleotide levels; 1 month after azathioprine, pegylated interferon alfa and ribavirin were discontinued and full blood count returned to normal in both patients. No haematological toxicity occurred after the reintroduction of peginterferon plus ribarivin or azathioprine alone in eight patients. Conclusion Collectively, the benefit/risk ratio favours avoidance of inosine monophosphate dehydrogenase inhibitors in purine analogue-treated patients with normal thiopurine methyltransferase activity, a situation frequently encountered in clinical practice. [ABSTRACT FROM AUTHOR]

Presents a letter to the editor on severity of ulcerative colitis in central China.