Role of MRI in Crohn's disease (original) (raw)
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Crohn's Disease – Disease for Immunologists, Proctologists, Gastroenterologists or Rheumatologists?
The Eurasia Proceedings of Health, Environment and Life Sciences
Crohn's Disease (CD) most commonly affects the terminal portion of the small intestine and the large intestine. CD can also affect any other part of the gastrointestinal tract, from mouth to anus. Inflammation of the intestines is usually not continuous, areas inflammation (foci of inflamed bowel) interspersed with normal areas intestines (segmental lesion). Depending on the severity of the inflammation the inner layer of the intestinal wall (mucosa) may turn red (erythematous) and swollen (edematous) with ulcers of different sizes and shapes (aphthae’s, superficial, deep, longitudinal), and the mucous membrane can have the appearance of a "cobblestone pavement". These lesions extend throughout the thickness intestinal wall and can lead to complications such as stenosis of the intestinal lumen and / or germination in other organs (penetration), resulting in abscesses (infiltration of intestinal contents into the abdominal cavity) or fistulas (channels that connect the ...
In the search of a cause of Crohn's disease
Indian Journal of Gastroenterology, 2009
While the exact cause of Crohn's disease (CD) is not known, it is thought that chronic inflammation in CD results from an inappropriate and chronic activation of the innate and adaptive mucosal immune systems in a genetically susceptible host, and that enteric microflorae play a pivotal role in the initiation and maintenance of the disease. 1 Organisms such as Pseudomonas maltophilia, Mycobacterium kansasii, Chlamydia trachomatis, Bacteroides fragilis, Listeria monocytogenes, Escherichia coli and Mycobacterium avium subspecies paratuberculosis (MAP) have been implicated and identified in the intestines of patients with CD; however, no other putative pathogenic organism except MAP causes a chronic granulomatous inflammation of the intestines in every other species in which it is present. 2 Moreover, because of remarkable clinical, morphological and epidemiological similarity between intestinal tuberculosis (caused by Mycobacterium tuberculosis) and CD in humans and Johne's disease (caused by Mycobacterium avium paratuberculosis) in cattle, a mycobacterial pathogen is thought to be a causative organism of CD. 3-7 An association and causality of Helicobacter pylori with peptic ulcer disease revolutionized the treatment of peptic ulcers; similar implication of MAP as a cause of CD has raised hopes amongst physicians, microbiologists and basic scientists for the cure of this disease. In the first report almost 25 years back, Chiodini and colleagues isolated cell-wall deficient cells, called sphero-plasts, from tissue samples after several months of incubation from patients with CD. These spheroplasts were sub-cultured and they later developed a cell wall that stained positively with Ziehl-Neelson staining; they were classified as mycobacterial like organisms. 9-11 These isolates were later confirmed as M. avium paratuberculosis by DNA hybridization. The unusual nature of the cell walldeficient MAP and the challenges in culture of MAP with its fastidious and slow growing requiring months to years to culture and multiple studies reporting failure to culture MAP from patients with CD dampened the initial zeal. 12 There was then a period of silence in the 1990s. With availability of better culture techniques and use of molecular techniques to identify MAP in 2000s, there was resurgence of interest of many laboratories in this field. There has been a flurry of publications since then relating CD and MAP. MAP infection in humans is difficult to detect. The organisms are intracellular and minimize their own immune recognition. They are therefore difficult to isolate and propagate in culture and are relatively resistant to chemical and enzymatic lysis. Reliable access to their DNA is only achieved during sample processing by combining exposure to stringent lysis buffers with an additional optimised mechanical disruption step. Freezing samples and tissue extracts especially at -20°C substantially reduces the PCR detection rate of their GC-rich DNA. The identification of MAP in patients with CD can be done by several different techniques such as culture of MAP from the intestines and blood; PCR amplification of blood or intestinal biopsies using IS900 DNA, a sequence specific for MAP; in-situ hybridization in tissues using IS900 sequence; serological tests using MAP specific antigens and direct visualization of MAP by light microscopy. 4,26 According to a meta-analysis, compared with individuals free of IBD, the pooled odds ratio (OR) of those with CD having MAP was 7.01 (95% CI 3.95-12.4) using PCR in tissue and 1.72 (1.02-2.90) in studies using ELISA in the serum. 27 According to another recent meta-analysis, MAP was detected more frequently from patients with CD compared with those with ulcerative colitis (risk difference 0.19, 95%
La radiologia medica, 2014
Purpose Few studies have correlated computed tomography enterography (CTE) findings with Crohn's disease (CD) clinical and biochemical activity. The aim of this study was to evaluate correlations between CTE findings with CD activity. Materials and methods The CTE datasets from 62 patients were retrospectively reviewed for different parameters: bowel wall thickening and hyperenhancement, mesenteric alterations, abdominal free fluid and complications related to the disease (fistulas, strictures, abscesses). Activity was assessed using the Crohn's Disease Activity Index (CDAI) and some biochemical markers (Creactive protein, erythrocyte sedimentation rate, alpha 2-globulins, fibrinogen, platelets, haemoglobin). Correlations between CTE parameters, clinical activity score and laboratory parameters were assessed by logistic regression. Results CDAI was significantly correlated with increased fat density (p = 0.03) and intestinal strictures (p = 0.04). Platelet counts were elevated in patients with enlarged mesenteric lymph nodes (p = 0.009) and the comb sign (p = 0.05). Serum alpha 2-globulins were higher in the presence of the comb sign (p = 0.03). Conclusion The CTE finding of perienteric inflammation (increased fat density) and vascular engorgement of the vasa recta in CD patients suggest that the disease is clinically active and that these patients may require more aggressive treatment than patients without these findings.
Tissue Studies in Screened First-degree Relatives Reveal a Distinct Crohnʼs Disease Phenotype
Inflammatory Bowel Diseases, 2014
Background: First-degree relatives of patients with Crohn's disease (CD) are at risk of developing the disease with 5% to 15% reported to be affected over time. Yet, a much greater proportion of them (.40%) shows features of "subclinical inflammation" with elevated intestinal inflammatory markers such as fecal calprotectin. The meaning of these findings is unclear in the absence of tissue data. Methods: Thirty-eight asymptomatic first-degree relatives of patients with CD underwent ileocolonoscopy and other tests including fecal calprotectin. All known causes of intestinal inflammation were carefully excluded. Age and gender-matched controls consisted of 10 individuals who underwent colonoscopy for other reasons. Histology was scored based on known methods. Results: Compared with controls, the relatives had significantly greater median values for fecal calprotectin and histological scores. In relatives, endoscopy identified 3 different phenotypes: (1) normal, (2) with minor lesions (aphthae or small superficial erosions), and (3) with typical CD inflammation. Based on the histological scores, the clustering analysis produced 3 corresponding highly separated clusters (61%, 26%, and 13% of the total, respectively) with divisive coefficient D ¼ 0.94. When followed up (on the average for 53 mo), individuals in the second cluster had histological scores similar to baseline values (P ¼ 0.12). Conclusions: Tissue studies in first-degree relatives of patients with CD reveal 3 distinct groups: normal, with minimal inflammation, and with frank disease. The second cluster represents a novel phenotype, which does not seem to develop the disease over time. These findings explain previous observations of "subclinical inflammation" in such population.
Differentiating Crohn’s Disease from Ulcerative Colitis - New Factors
Biomedical Journal of Scientific and Technical Research, 2019
Crohn's disease (CD) and ulcerative colitis (UC) have been known to physicians for decades. Unfortunately, so far there are many unknowns regarding CD and UC. There are numerous descriptions of clinical cases, different locations of disease symptoms, and descriptions of symptoms located both in the gastrointestinal tract and symptoms accompanying the disease. All this information sheds light on the etiology of inflammatory bowel disease (IBD) do not completely resolve their complexity. An analysis of the literature presented in the work indicates that the characteristics of diseases are often unambiguous. This contributes to the fact that IBD diagnostics are often difficult and create many problems [1-3]. Despite many years of research on inflammatory bowel diseases, they are still of interest to scientists today. Nonspecific inflammatory bowel disease is a term referring to chronic and recurrent gastrointestinal disease. A number of clinical symptoms distinguish between CD and UC, whose clinical picture is relatively diverse. However, in many cases the diagnosis is not straightforward, which contributes to the interest of researchers worldwide in the disorders under discussion. The inflammatory changes in the course of UC are continuous and limited to the mucous membrane of the large intestine. UC-related inflammation usually involves the mucosa and submucosa usually begins in the rectum and spread proximal to the colon. The affected tissue is swollen, with the presence of erosions and ulcers, which lead to spontaneous bleeding. In most cases, UC initially occurs smoothly, with worsening symptoms within a few weeks. It happens, however, that the disease begins suddenly and goes very quickly. In such cases, due to the lack of the effect of conservative treatment, surgical treatment is already implemented in the early stages of the disease. However, in most cases, after the first shot of the disease, it goes into remission, after which it becomes more severe again. Such continuous conditions of illness and remission may last even several dozen years [1,2]. In the case of CD, the condition most often includes the small intestine and caecum, which accounts for 40% of cases, only small intestine (30% of patients) and only large intestine (25% of cases). In situations where only the large intestine is covered, two forms of the disease are recognized. The first one concerns about two thirds of cases and consists in taking the entire length of the large intestine with the disease state, while the second involves the occurrence of staple
Natural history of Crohn's disease: Comparison between childhood‐and adult‐onset disease
Inflammatory Bowel …, 2010
Background: Childhood-onset Crohn's disease (CD) might reflect a more severe form of disease. To test this hypothesis we analyzed the long-term natural history of CD in an adult cohort of patients with childhood-onset compared to adult-onset CD. Methods: We selected 206 childhood-onset CD patients among 2992 adult patients with a diagnosis of CD established before December 31, 2000. Disease characteristics were prospectively assessed during follow-up until December 2007 and compared to adult-onset CD patients matched 2 to 1 on gender, year of CD diagnosis, and disease location. Results: Compared to adult-onset CD, patients with childhoodonset CD were more likely to have a severe disease, with an increased year-by-year disease activity index (37% of patient-years in childhood-onset group versus 31% in the adult-onset group, P < 0.001). Immunosuppressant requirement was also increased with a 10-year cumulative risk of 54 6 3% in childhood-onset CD group versus 45 6 2%, in the adult-onset CD group (P < 0.001). Cumulative risks of stricturing and penetrating complications and surgical resections were not statistically different between groups. Accordingly, these events occurred at a younger age in the childhood-onset CD group. At the age of 30 years the actuarial risk of having undergone an extensive intestinal resection was 48 6 5% in the childhoodonset group versus 14 6 2% in the adult-onset group (P < 0.001). Conclusions: Patients with childhood-onset CD exhibit a more active disease and require more immunosuppressive therapy. This feature is observed irrespective of the disease location, suggesting an intrinsic more severe phenotype.