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We report a case of spuriously 'normal' haemoglobin A(1c) (HbA(1c)) result due to misidentification of HbG Taipei as HbA(o) by the Variant II built-in retention time algorithm. The defect was circumvented effectively by the implementation of a chromatographic system specific internal quality control mechanism for peak identity verification. HbA(1c) and estimated average glucose results were corrected from 4.7% to 8.2%, and 4.9 to 10.5 mmol/L, respectively. The results were consistent with the patient's concurrent and previous fasting blood glucose concentrations and existence of diabetes mellitus dermopathy, indicating poor glycaemic control. A review of currently available analytical systems showed that other than mass spectrometry, HbA(1c) measurements by these systems were generally affected by the presence of haemoglobin variants. The same haemoglobin variant may affect different analytical systems differently, resulting in the deviation of HbA(1c) results from the true value to different extents. Including the analytical principle of HbA(1c) measurement in the laboratory report can avoid inappropriate comparison of results obtained by different analytical systems. Moreover, since individual haemoglobinopathy may affect the degree of glucose binding to haemoglobin in a different way, this uncertainty limits the general application of same decision cut-off of established guidelines for glycaemic control monitoring. Adoption of an individualized monitoring system based on the critical difference or reference change value of HbA(1c) can be considered. [ABSTRACT FROM AUTHOR]

The emergence of pandemic (H1N1) 2009 virus highlighted the need for enhanced surveillance of swine influenza viruses. We used real-time reverse-transcription PCR-based genotyping and found that this rapid and simple genotyping method may identify reassortants derived from viruses of Eurasian avian-like, triple reassortant-like, and pandemic (H1N1) 2009 virus lineages. [ABSTRACT FROM AUTHOR]

Background: Age-related skewing of X-chromosome inactivation leading to glucose-6-phosphate dehydrogenase (G6PD) deficiency in elderly women in a population with prevalent G6PD gene mutations was investigated.Methods: G6PD activity was measured biochemically. G6PD mutations were detected by polymerase chain reaction (PCR) and allele-specific extension, and analyzed by matrix-assisted laser desorption ionization-time of flight (MALDI-TOF) mass spectrometry and Sequenom MassARRAY. X-chromosome inactivation was quantified by semiquantitative PCR for the HUMARA gene, before and after HpaII digestion.Results: In 173 women (median age: 90 years; range, 80-107 years), 18 heterozygotes for G6PD mutations were identified. Three heterozygotes were G6PD deficient, owing to skewed X-chromosome inactivation affecting the wild-type allele. Fifteen heterozygotes, with skewing apparently affecting the mutant alleles, had normal but significantly lower G6PD levels. At 1.73%, G6PD deficiency was significantly more frequent than expected from population screening at birth.Conclusion: Due to skewed X-chromosome inactivation, elderly women in populations with prevalent G6PD mutations are at risk of G6PD deficiency. [ABSTRACT FROM AUTHOR]