Objective To investigate serum cardiac troponin I, a sensitive marker of cardiac rnyocyte damage, in normal pregnancy and pregnancies complicated by hypertension with and without significant proteinuria.Design Prospective cross sectional study.Setting University hospital delivery suite.Sample Serum samples obtained from women in normal pregnancy and in pregnancies complicated by hypertension with and without significant proteinuria.Method Women with hypertension in pregnancy (at least two readings of systolic blood pressure > 140 mmHg and diastolic blood pressure > 90 mmHg) (n = 26) and norrnotensive women (n = 43) were included in the study. Serum cardiac troponin I was measured using Beckman Access immunoassay.Main outcome measure Serum cardiac troponin I level in the pregnancies complicated by hypertension (with and without significant proteinuria) compared with the levels measured in normotensive women.Results The median serum cardiac troponin I level in pregnancies complicated by hypertension was 0.11 8 ng/mL (n = 26) which was significantly greater than that measured in samples obtained from normotensive women in pregnancy (0.03 ng/n&; n = 43) (P < O@OOl). There were higher median serum cardiac troponin I levels in hypertensive women with sigdicant proteinuria (0.155 ng/mL; n = 6), compared with those without proteinuria (0.089 ng/nL; n = 20; P = 0.03).Conclusion Serum cardiac troponin I is elevated in women with hypertensive disorders of pregnancy indicating some degree of cardiac myofibrillary damage in these disorders.

Fifty sporadic colorectal carcinomas diagnosed in 1991 were analysed for microsatellite instability at four loci. Five of 50 (10 per cent) tumours showed replication errors (RERs) at two or more loci and were classed as RER‐positive (RER+). A further five showed RERs at one locus only. A significant association (Fisher exact test) was found between RER+ tumours and location in the proximal colon, exophytic shape, size >5 cm, histological margin, lymphoid reaction, and near‐diploid DNA content. There was no significant difference for age, sex, grade, mucin production, p53 protein overexpression or Duke's stage. There was no significant difference in survival as measured over a 60‐month follow‐up period. The findings, though limited by the small case numbers involved, show an association between RER positivity in sporadic colorectal tumours and certain clinico‐pathological features. They do not suggest a better clinical outcome for sporadic RER+ tumours. Copyright © 1999 John Wiley & Sons, Ltd.

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The use of continuous fetal heart rate (FHR) recordings to monitor fetal well-being during labor is standard clinical practice in developed countries. Little is known about the relationship, if any, that exists between these FHR abnormalities and the fetal cardiac musculature and function. The aim of this study was to investigate umbilical artery serum levels of cardiac troponin I, a sensitive and specific marker of myocardial necrosis, and N-terminal pro-brain natriuretic peptide (pro-BNP), a sensitive marker of left ventricular dysfunction, in relation to FHR abnormalities. Umbilical artery blood samples were taken from 27 cases immediately after delivery of the infant. There was evidence of significant FHR abnormalities in 11 of these cases (group 2) and the FHR recording was normal in 16 cases (group 1). The mean N-terminal pro-BNP level in umbilical artery serum in group 2 was 413 fmol/L (SEM = 85) and in group 1 was 223 fmol/L (SEM = 28)(p = 0.022). There was no significant difference observed in cardiac troponin I levels between the two groups. Umbilical artery serum N-terminal pro-BNP is elevated in association with fetal heart rate abnormality in the late stage of labor. This finding suggests that some degree of cardiac compromise accompanies FHR abnormality.

Nitrofurantoin is a synthetic nitrofuran commonly used for the treatment and prophylaxis of urinary tract infections. We describe the case of a 75-yr-old woman who was taking nitrofurantoin as prophylaxis against recurrent urinary tract infections, and who subsequently developed pulmonary and hepatic toxicity. We postulate that a breakdown product of the drug or the drug itself complexed to an endogenous peptide is presented by the class I HLA antigen on the hepatocyte cell membrane, inducing cytotoxic T cell activation and subsequently, hepatocyte death.