Article

Diagnostic value of calprotectin in irritable bowel syndrome and in inflammatory bowel disease.

"Iuliu Haţieganu" University of Medicine and Pharmacy, 2nd Medical Clinic, Cluj-Napoca, Romania.
Romanian journal of internal medicine = Revue roumaine de médecine interne 01/2012; 50(1):3-6.
Source: PubMed

ABSTRACT The inflammation is an important component of the bowel wall structure. The amount of inflammation is gradually increased from normal state, to functional bowel disorders and to inflammatory bowel disease. Calprotectin is a recently established marker for intestinal inflammation. This paper surveys the present knowledge on fecal calprotectin testing as predictor of intestinal inflammation. We also show on a sample of patients that inflammation as tested with fecal calprotectin test may also be found, in lower degree, in irritable bowel syndrome. In inflammatory bowel disease, the calprotectin fecal test shows higher intensity values.

0 Followers
 · 
113 Views
  • [Show abstract] [Hide abstract]
    ABSTRACT: Chronic abdominal pain accompanying intestinal inflammation emerges from the hyperresponsiveness of neuronal, immune and endocrine signaling pathways within the intestines, the peripheral and the central nervous system. In this article we review how the sensory nerve information from the healthy and the hypersensitive bowel is encoded and conveyed to the brain. The gut milieu is continuously monitored by intrinsic enteric afferents, and an extrinsic nervous network comprising vagal, pelvic and splanchnic afferents. The extrinsic afferents convey gut stimuli to second order neurons within the superficial spinal cord layers. These neurons cross the white commissure and ascend in the anterolateral quadrant and in the ipsilateral dorsal column of the dorsal horn to higher brain centers, mostly subserving regulatory functions. Within the supraspinal regions and the brainstem, pathways descend to modulate the sensory input. Because of this multiple level control, only a small proportion of gut signals actually reaches the level of consciousness to induce sensation or pain. In inflammatory bowel disease (IBD) and irritable bowel syndrome (IBS) patients, however, long-term neuroplastic changes have occurred in the brain-gut axis which results in chronic abdominal pain. This sensitization may be driven on the one hand by peripheral mechanisms within the intestinal wall which encompasses an interplay between immunocytes, enterochromaffin cells, resident macrophages, neurons and smooth muscles. On the other hand, neuronal synaptic changes along with increased neurotransmitter release in the spinal cord and brain leads to a state of central wind-up. Also life factors such as but not limited to inflammation and stress contribute to hypersensitivity. All together, the degree to which each of these mechanisms contribute to hypersensitivity in IBD and IBS might be disease- and even patient-dependent. Mapping of sensitization throughout animal and human studies may significantly improve our understanding of sensitization in IBD and IBS. On the long run, this knowledge can be put forward in potential therapeutic targets for abdominal pain in these conditions.
    World Journal of Gastroenterology 01/2014; 20(4):1005-1020. DOI:10.3748/wjg.v20.i4.1005 · 2.43 Impact Factor
  • [Show abstract] [Hide abstract]
    ABSTRACT: Non-alcoholic fatty liver disease (NAFLD) and irritable bowel syndrome (IBS) are two very common diseases in the general population. To date, there are no studies that highlight a direct link between NAFLD and IBS, but some recent reports have found an interesting correlation between obesity and IBS. A systematic PubMed database search was conducted highlighting that common mechanisms are involved in many of the local and systemic manifestations of NAFLD, leading to an increased cardiovascular risk, and IBS, leading to microbial dysbiosis, impaired intestinal barrier and altered intestinal motility. It is not known when considering local and systemic inflammation/immune system activation, which one has greater importance in NAFLD and IBS pathogenesis. Also, the nervous system is implicated. In fact, inflammation participates in the development of mood disorders, such as anxiety and depression, characteristics of obesity and consequently of NAFLD and, on the other hand, in intestinal hypersensitivity and dysmotility.
    World Journal of Gastroenterology 09/2013; 19(33):5402-5420. DOI:10.3748/wjg.v19.i33.5402 · 2.43 Impact Factor
  • Source
    [Show abstract] [Hide abstract]
    ABSTRACT: We aimed to investigate the significance of faecal calprotectin (FC) levels in children diagnosed with Henoch-Schönlein purpura (HSP) and examine its relationships with gastrointestinal system (GIS), renal involvement and with clinical findings. In total, 66 children diagnosed with HSP for the first time and a control group of 25 healthy children were included. The cases were divided into mild and severe groups on the basis of GIS findings. FC was measured twice in all patients with HSP: within 3 days of onset of disease (FC1) and on day 15 (FC2). These results were compared with those of the control group. Faecal occult blood, gastric wall thickness and duodenal wall thickness were measured at the same time as FC1 in all patients, and the presence of renal involvement was recorded. Of the 66 patients, 37 (56%) were females (mean age, 7.5±2.9 years; range, 2.5-14.5 years) and were diagnosed with HSP. Renal involvement was detected in 19 (28%) cases and GIS involvement was found in 28 (43%) cases. GIS involvement was mild in 16 (53%) cases and severe in 12 (43%). A significant difference was detected in FC1 levels between the groups with and without GIS involvement (P=0.01). A marked difference was observed in FC1 levels between the groups with and without renal involvement (P=0.017). FC may be a reliable marker for HSP, particularly for identifying GIS and renal involvement as well as disease severity.

Full-text (2 Sources)

Download
189 Downloads
Available from
Dec 31, 2014