Interference by antiruthenium antibodies in the Roche thyroid-stimulating hormone assay.

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 re-analysed 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.

Patients' representations of their end-stage renal disease: relation with mortality.

BACKGROUND: Self-regulation theory explains how patients' illness perceptions influence self-management behaviour (e.g. via adherence to treatment). Following these assumptions, we explored whether illness perceptions of ESRD-patients are related to mortality rates. METHODS: Illness perceptions of 182 patients participating in the NECOSAD-2 study in the period between December 2004 and June 2005 were assessed. Cox proportional hazard models were used to estimate whether subsequent all-cause mortality could be attributed to illness perception dimensions. RESULTS: One-third of the participants had died at the end of the follow-up. Mortality rates were higher among patients who believed that their treatment was less effective in controlling their disease (perceived treatment control; RR = 0.71, P = 0.028). This effect remained stable after adjusting for sociodemographic and clinical variables (RR = 0.65, P = 0.015). CONCLUSIONS: If we consider risk factors for mortality, we tend to rely on clinical parameters rather than on patients' representations of their illness. Nevertheless, results from the current exploration may suggest that addressing patients' personal beliefs regarding the effectiveness of treatment can provide a powerful tool for predicting and perhaps even enhancing survival.

Unexpected prolonged extreme hypocalcaemia and an inadequate PTH response in a patient with metastatic breast carcinoma.

Although hypercalcaemia is often encountered during the course of malignant disease, hypocalcaemia appears to be rather rare. We describe a 37-year-old patient with metastatic carcinoma of the breast, who developed extreme hypocalcaemia (as low as 0.75 mmol calcium per litre) after chemotherapy. This is caused by a combination of hungry-bone syndrome and an insufficient parathyroid response. The latter may be the result of a direct toxic effect of chemotherapy on parathyroid hormone (PTH) synthesis possibly in combination with microscopic tumour infiltration in the parathyroid glands. Correction of the extreme hypocalcaemia over a period of 100 days by oral and intravenous calcium supplementation, corresponding to a total of 352 gram elemental calcium (1/3 of the total body calcium), resulted in gradual symptomatic relief. The possible mechanisms for these findings are discussed and the literature is briefly reviewed.