Faecal leukocyte esterase activity is an alternative biomarker in inflammatory bowel disease

Background: Leukocyte cytosolic proteins (e.g., calprotectin) are emerging biomarkers for inflammatory bowel disease. Leukocyte aryl esterase activity has been commonly used for sensitive detection of leukocytes in human body fluids such as urine. Urine test strip results are generally reported in categories. As automated strip readers allow quantitative data to be reported, sensitive quantitative detection of leukocytes in body fluids has become possible. Here, we explored the use of leukocyte esterase as a potential alternative faecal biomarker for inflammatory bowel disease. Methods: We evaluated leukocyte esterase activity in faecal extracts and compared Cobas u 411 (Roche) quantitative reflectance data with calprotectin concentration for 107 routine samples. Stability of leukocyte esterase for trypsin digestion was carried out by adding trypsin to the extract. Incubation occurred at 37 ° C for 24 h or 48 h. Results: Reproducibility of the reflectance signal was good (within-run imprecision: 6.1%; between-run imprecision: 6.2%). Results were linear in the range 10 3 – 10 6 WBC/100 mg faeces. The lower limit of detection was 4 WBC/ μ L and the lower limit of quantification was 5 WBC/ μ L. Stability of LE activity in stool and faecal matrix was good. An adequate correlation was obtained between leukocyte esterase activity and the faecal calprotectin concentration: log(y)  =  4.28 + 0.29log(x). In vitro experiments monitored the digestion of leukocyte esterase and faecal calprotectin. Leukocyte esterase activity was significantly less affected by trypsin activity than calprotectin immunoreactivity. Conclusions: Quantitative leukocyte esterase activity of faecal extracts provides information about the leukocyte count in the gut lumen. Leukocyte esterase is a promising and affordable alternative biomarker for monitoring inflammatory bowel disease

Infliximab treatment in pediatric IBD patients: a single centre experience

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Faecal incontinence due to atrophy of the anal sphincter in myotonic dystrophy : a case report

Myotonic dystrophy or Steinert disease is an autosomal dominant multisystemic disorder with variable penetrance. The genetic defect is an amplified trinucleotide repeat in the 3-prime untranslated region of a proteinkinase gene on chromosome 19. Severity of symptoms increases with the number of repeats. Patients with myotonic dystrophy often present with gastrointestinal motility problems, such as intermittent diarrhoea, constipation, and also faecal incontinence. The underlying physiopathological mechanism of faecal incontinence differs from classic soiling due to faecal retention. We present a girl with congenital myotonic dystrophy and faecal incontinence due to anal sphincter atrophy; and give an overview of present knowledge on the pathophysiology of gastrointestinal problems associated with myotonic dystrophy. Abbreviations DM1: Myotonic Dystrophy type 1 DMPK: Dystrophia Myotonica Protein Kinas