Relationships between disease activity and serum and fecal biomarkers in patients with Crohn's disease.

BACKGROUND & AIMS: The quantitative relationships between instruments and assays that measure clinical, endoscopic, and biologic disease activity in patients with Crohn's disease are poorly characterized. This study evaluated the correlations between the Crohn's Disease Activity Index (CDAI), the Simple Endoscopic Score for Crohn's Disease (SES-CD), serum high-sensitivity C-reactive protein (hsCRP) (both phenotype and genotype) and interleukin-6 (IL-6), and fecal calprotectin and lactoferrin. METHODS: A total of 164 patients with Crohn's disease undergoing colonoscopy were enrolled. The CDAI and SES-CD scores, serum hsCRP and IL-6, CRP and IL-6 genotypes, and fecal calprotectin and lactoferrin were measured. RESULTS: There were no significant associations between the CDAI and SES-CD scores (Spearman rank correlation coefficient, 0.15) or between the CDAI scores and the serum concentrations of hsCRP and IL-6, or the fecal concentrations of calprotectin and lactoferrin. In contrast, the serum hsCRP and IL-6 concentrations and the fecal calprotectin and lactoferrin concentrations were significantly higher in patients with more severe endoscopic disease activity (SES-CD score > 7 points) (P < .001 for all comparisons). The CRP 717 mutant homozygote and heterozygote status was associated with significantly lower concentrations of hsCRP (P = .02). There was a trend toward higher hsCRP concentrations in the CRP 286 heterozygous adenine mutant-type mutant genotype, but this did not reach statistical significance. CONCLUSIONS: Serum and fecal biomarker concentrations are associated with endoscopic but not clinical disease activity in patients with Crohn's disease. Stimulated hsCRP concentration is affected significantly by select genetic polymorphisms.

3-yr-follow-up of topical corticosteroid treatment for eosinophilic esophagitis in adults.

BACKGROUND: Eosinophilic esophagitis (EE) is a clinicopathologic syndrome comprising isolated eosinophilic inflammation of the esophagus, with symptoms of dysphagia, and possibly, reflux. It was initially described in children, and in recent years, there is a heightened awareness in adults. The etiology is not completely understood. The treatments include dietary manipulation, topical corticosteroids, systemic corticosteroids, Montelukast, and endoscopic dilation. In adults, there are no randomized trials demonstrating the efficacy of any particular treatment, and no prospective studies describing the natural history of the disease following treatment. METHODS: We performed an interval follow-up of patients treated with a swallowed corticosteroid inhaler. We contacted 51 adult patients who were diagnosed with EE and treated with a swallowed corticosteroid inhaler between September 1, 1999, and May 31, 2003. All patients had received 6 wk of treatment with fluticasone 220 mEq/puff, four puffs swallowed twice daily for 6 wk. RESULTS: Thirty-two patients replied (63%) with a mean follow-up duration of 3.3 yr. Ninety-one percent of patients reported recurrent symptoms; a mean of 8.8 months after treatment was completed. Sixty-nine percent of patients repeated treatment with the steroid inhaler at least once. CONCLUSIONS: It appears that EE is a chronic remitting disorder that requires more than one topical steroid treatment course.

Noninvasive diagnosis of biopsy-proven cardiac amyloidosis.

OBJECTIVES: This study analyzed the utility of electrocardiographic (ECG) and echocardiographic findings in the diagnosis of amyloidosis proven by endomyocardial biopsy. BACKGROUND: Cardiac amyloidosis is associated with characteristic ECG and echocardiographic changes, yet each finding alone is relatively nonspecific. A combination of noninvasive prognostic parameters would be desirable for this tissue-based diagnosis. METHODS: We performed an analysis of 196 consecutive patients referred for endomyocardial biopsy because of clinical suspicion of cardiac amyloidosis. The diagnosis was confirmed in 58 patients (29%). The ECGs, echocardiograms, and right heart hemodynamic data were reviewed to determine which findings strongly correlate with the diagnosis. These findings were then used to build multivariate logistic regression models that predict the log-odds of having cardiac amyloidosis. RESULTS: The univariate analysis showed that low-voltage and pseudo-infarction patterns on the ECG and increased myocardial thickness and speckled-appearing myocardium on the echocardiogram were associated with biopsy-proven cardiac amyloidosis (each p < 0.01). In multivariate logistic regression models, a combination of a low voltage and measures of myocardial thickness produced the most statistically useful models. For instance, one model showed that if a low voltage was present and interventricular septal thickness is >1.98 cm, the diagnosis of cardiac amyloidosis could be made with a sensitivity of 72% and a specificity of 91%. In this model, the positive predictive and negative predictive values were 79% and 88%, respectively. CONCLUSIONS: In patients with suspected cardiac amyloidosis, a combination of noninvasive parameters-namely, a low voltage and increased intraventricular septal thickness-is a useful diagnostic tool.