Elevated tumour marker: an indication for imaging?

INTRODUCTION: The purpose of this study was to evaluate the utility of imaging examinations in patients with elevated tumour markers when (a) the tumour marker is not validated for as a primary diagnostic test; (b) the patient had no personal history of cancer and (c) the patient had no other imaging indication. MATERIALS AND METHODS: Patients without known cancer who had abnormal carcinoembryonic antigen, CA19-9, CA125 and/or CA15-3 serology over a one-year period were included. A retrospective medical record review was performed to assess the number of these cases who underwent imaging because of 'elevated tumour marker' in the absence of a clinical indication for imaging. The number and result of these imaging studies were evaluated. RESULTS: Eight hundred and nineteen patients were included. Of those, 25 patients (mean age: 67.8 [range 41-91] y), were imaged to evaluate: 'elevated tumour marker'. They underwent 29 imaging studies (mean [+/-standard deviation (SD)] per patient = 1.2 [+/-0.4]), and had 42 elevated tumour marker serology tests (mean [+/-SD] per patient = 1.7 [+/-0.7]). Four patients had >1 imaging test. No patient had an imaging study which diagnosed a malignancy or explained the elevated tumour marker. CONCLUSION: The non-judicious use of tumour markers can prompt further unnecessary investigations including imaging. In this study, there was no positive diagnostic yield for imaging performed for investigation of 'elevated tumour marker'. 'Elevated tumour marker', in the absence of a known underlying malignancy, should not be considered an independent indication for imaging.

Introduction of an NT-proBNP assay to an acute admission unit--a 2-year audit.

BACKGROUND: The differential diagnosis of dyspnoea is difficult due to the low predictive value of clinical and laboratory parameters. The elevated levels of NT-proBNP in congestive heart failure may improve diagnostic accuracy. We have evaluated the effect of the introduction of an NT-proBNP assay on hospital length of stay (LOS) and mortality. METHODS: There were 11,853 AMAU patient episodes in the 22 months study period (March 2005-Dec 2006). An NT-proBNP assay was requested in 657 (5.5%) of these. Comparison between categorical variables such as diagnosis, NT-proBNP testing, LOS, and in-hospital mortality was made using Chi-square tests. Literature review suggested that an NT-proBNP cut-off >or=5000 ng/L should predict acute in-patient mortality. Logistic regression analysis was used to examine the association between such an elevated NT-proBNP level and outcomes. RESULTS: Of the 396 patients with NT-proBNP <5000 ng/L, 8.1% died compared with 22.5% of the 178 patients dying with values >or=5000 ng/L (p<0.0001). An NT-proBNP >or=5000 ng/L was predictive of both LOS >or=9 days (odds ratios (OR) 1.54 (95% CI 1.06, 2.24: p=0.02) and LOS >or=14 days (OR=1.87 (95% CI 1.29, 2.71: p=0.0009). NT-proBNP requests increased over time, from 2.6% to 8.2% of all patients; the result fell in the diagnostic range for CHF in 60% of requests. CONCLUSION: The introduction of an NT-proBNP was reflected in an appropriate but rapidly increasing pattern of requests from clinicians. High NT-proBNP levels predicted in-hospital mortality and longer LOS in an acute medical population.

Impact of vitamin E and C supplementation on serum adhesion molecules in chronic degenerative aortic stenosis: a randomized controlled trial.

BACKGROUND: An inflammatory component has been identified in degenerative aortic stenosis (AS). The combination of vitamins E and C has been shown to have anti-inflammatory properties. The aim of this study was to determine the impact of the combination of vitamins C and E or vitamin C only on serum levels of cell adhesion molecules and C-reactive protein in patients with chronic degenerative AS, with or without concomitant coronary artery disease. METHODS AND RESULTS: One hundred patients with asymptomatic or mildly symptomatic moderate AS were randomized in 2:2:1 format in an open-label trial. Forty-one patients received vitamin E (400 IU) and vitamin C (1000 mg) daily, 39 patients received vitamin C (1000 mg) only, and 20 patients were followed as controls. Serum intracellular adhesion molecule (ICAM-1), E selectin, P selectin, vascular-cellular adhesion molecule (VCAM-1), C-reactive protein, and alpha-tocopherol (vitamin E) were measured by enzyme-linked immunosorbent assay at baseline and 6 months postsupplementation. Half of the patients from each of the 2 active groups were followed for further 6 months to determine any changes after cessation of therapy. In the vitamin E and C, group there was reduction in serum ICAM-1 (298 +/- 12 to 272 +/- 12 ng/mL at 6 months, P = .0015) with a return to base line 6 months after cessation of therapy. In the vitamin C only group, there was a reduction in serum P selectin (134 +/- 10 to 118 +/- 10 ng/mL at 6 months, P = .033). All the inflammatory markers were unchanged in control group over 6 months of follow-up. CONCLUSION: Vitamin E and C supplementation had modest anti-inflammatory effect in chronic degenerative AS. The clinical relevance of this would require further clarification.

Vitamin E modulation of C-reactive protein in smokers with acute coronary syndromes.

Acute coronary syndromes are characterized by the expression of proinflammatory cytokines such as C-reactive protein (CRP). Sustained upregulation of inflammatory markers is associated with an adverse prognosis. Vitamin E is known to have significant anti-inflammatory properties and has been associated with a reduction in cardiovascular events in some studies of high-risk patients. The mechanism of benefit remains controversial. We conducted a randomized, double-blind placebo controlled trial of vitamin E 400 IU daily for 6 months in 110 patients with acute coronary syndromes. Serum samples were collected at enrollment and at 2, 4, and 6 months. CRP, interleukin-6 and the soluble cell adhesion molecules were measured. Vitamin E levels increased significantly in the treatment group (from 31 micromol/l at baseline to 51 micromol/l, p <.0001) and were unchanged in the placebo group (32 micromol/l at baseline to 34 micromol/l, p = NS). CRP levels fell in both the vitamin E group and the placebo group over the treatment period (from 17.2 +/- 2.9 to 6.1 +/- 0.8 mg/l and from 21.5 +/- 4.9 to 5.9 +/- 0.9 mg/l, p = NS for the difference between active and placebo groups). However, vitamin E treatment was associated with significantly lower 6 month CRP levels in smokers versus smokers on placebo (4.7 +/- 0.71 mg/l vs. 8.26 +/- 1.5 mg/l, p =.02). Vitamin E reduces CRP levels in smokers with acute coronary syndromes for up to 6 months after hospitalization.