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There are many causes of interference in immunoassays causing erratic patient results. A method-specific interference due to antiruthenium antibodies in Roche free thyroxine (fT4) and free triiodothyronine (fT3) assays has been described previously. As a result, a new generation fT4 assay has been introduced by Roche. We describe six cases of interference due to antiruthenium antibodies, where in four cases interference in the Roche thyroid-stimulating hormone (TSH) assay was found as well. This raised the question as to whether other assays on this platform would also give incorrect results in patients with antiruthenium antibodies. Interference due to antiruthenium antibodies was suspected because of discrepancies between clinical presentation and/or TSH, fT4 and fT3 results. Samples of these six patients were reanalysed in Roche Diagnostics Laboratory, where it was demonstrated that the found discrepancies were indeed caused by interfering antiruthenium antibodies. Subsequently, these patients were asked to donate some blood once more for further evaluation, and three subjects agreed to participate. Their plasma was used to assay 18 analytes on Modular E and on a ruthenium-independent platform. The results were compared taking into account the known differences between distinct methods. As expected, significant interference was found in TSH. Also, in the new generation fT4 assay, ruthenium-induced interference was still present. However, the other assays, both competitive and immunometric, did not show clear interference. We therefore conclude that although antiruthenium antibodies theoretically can interfere in all assays on the Modular E platform, this kind of interference is found in the thyroid hormone assays, without marked interference in the other assays.

Hepatitis C virus (HCV) infection often persists in association with chronic hepatitis. Different factors have been proposed to determine the clinical outcome of HCV infection. The aim of this study was to examine three different factors of HCV infection among injecting drug users. Nineteen untreated HCV seroconverters were tested longitudinally for the presence of HCV RNA by reverse transcriptase (RT) PCR, and results were quantified by the branched-DNA (bDNA) assay. HCV genotypes were determined with the first sample taken after HCV seroconversion. To assess the natural course of infection, serum alanine aminotransferase (ALT) levels were measured at three stages in every individual. The concordance between bDNA and RT-PCR was 98.9%. Three distinct patterns were found, according to the HCV RNA load after seroconversion during a mean follow-up period of 5 years (range, 1 to 8 years). HCV genotype 1a was predominant (52.6%). There was a significant increase in serum ALT levels (mean 55.5 U/liter) in the early phase of HCV infection, compared with basal serum ALT levels before HCV seroconversion and at the end of the follow-up period. Three distinct HCV RNA load profiles were found, without apparent relationship to genotype and serum ALT levels in the first 5 years of HCV infection.

We studied the predictive power at admission of troponin T and myoglobin and compared them with that of CK and CK-MB activity and ECG in 290 consecutive patients admitted for evaluation of a suspected AMI. The likelihood ratio for an ischaemic ECG at admission < 4 h (between 4 and 12 h) after onset of chest pain was 2.85 (1.92), for a inconclusive ECG 1.53 (1.98) and for a normal ECG 0.27 (0.35). In patients admitted < 4 h after onset of chest pain, the likelihood ratio for abnormal and normal myoglobin concentrations (8.06 and 0.67) was considerably better for detection of AMI as defined by the WHO criteria than for the other markers, including the ECG. In patients admitted 4-12 h after onset of chest pain, the likelihood ratios for abnormal and normal myoglobin concentrations were 4.88 and 0.42; for troponin T 3.11 and 0.31; for CK activity 3.44 and 0.49 and for CK-MB activity 4.08 and 0.54 respectively. The sensitivity for troponin T (64%) was better than that of the other markers but its specificity (74%) was worse, because in patients with unstable angina troponin T was frequently elevated (37%). Stepwise logistic regression analysis showed that the best predictors of AMI within 4 h after onset of chest pain were the ECG and myoglobin and between 4-12 h after onset of chest pain the ECG, CK-MB activity and myoglobin.