| name | description | evidence |
|---|---|---|
| Ileal Crohn's Disease | Involves inflammation of the ileum, the latter part of the small intestine. | TRUNCATED |
| Colonic Crohn's Disease | Affects the colon (large intestine) with skip lesions. | TRUNCATED |
| Ileocolonic Crohn's Disease | Involves both the small intestine (ileum) and the colon. | TRUNCATED |
| reference | supports | snippet | explanation |
|---|---|---|---|
| PMID:37137806 | WRONG_STATEMENT | The crude prevalence of IBD increased by 47% in 2019 globally. | The available literature does not provide specific data on the percentage prevalence of Crohn's Disease alone globally; it talks about the prevalence of IBD as a whole. |
| PMID:35930087 | NO_EVIDENCE | This prospective, observational registry study was conducted at 19 tertiary centers in Japan. Patients newly diagnosed with Crohn''s disease after June 2016 (age >/= 16 years at informed consent) were enrolled between December 17, 2018 and June 30, 2020. | This study focuses on the prevalence and characteristics of Crohn's Disease specifically in Japan, not globally. |
| reference | supports | snippet | explanation |
|---|---|---|---|
| PMID:33587489 | SUPPORT | Patients were divided into a derivation (80%) cohort and a validation (20%) cohort. The primary outcome was progressive disease... In our final model, age at diagnosis older than 60 years was significantly associated with a lower risk of developing progressive disease... In patients with CD. | The study indicates that younger patients, particularly those aged less than 60 years, are at higher risk of developing progressive Crohn's disease. |
| PMID:37384664 | REFUTE | Logistic regression analysis of the initial characteristics showed that the age at diagnosis, gender, initial location and initial extra-intestinal manifestation are not associated with the progression of the disease. | This study states that the progression of Crohn's disease is not linked to the initial age of diagnosis among children and adolescents. |
| PMID:37266570 | PARTIAL | The best predictive model (PREDICT-EPIMAD) included the location at diagnosis, pANCA, and 6 single nucleotide polymorphisms. This model showed good discrimination... Decision curve analysis confirmed the clinical utility of the model. | Though the exact age range of 15-35 is not specifically discussed, the predictive model includes various factors that can affect disease progression, which might encompass age-related variations. |
| PMID:28051217 | NO_EVIDENCE | Our aim was to identify the phenotype evolution of Crohn's disease over time according to the Montreal Classification and to precise predictive factors of the need for immunosuppressant treatment or surgery... without association with age, sex or smoking habits. | This study did not find evidence associating age with the progression of Crohn's disease, focusing instead on phenotype and specific disease markers. |
| reference | supports | snippet | explanation |
|---|---|---|---|
| PMID:32242028 | SUPPORT | Several factors have been implicated in the cause of Crohn's disease, including a dysregulated immune system... The uncontrolled activation of the immune system toward antigens contained in the gut lumen in genetically predisposed subjects is believed to be the leading cause of inflammatory bowel disease. | The statement is supported as one of the major factors causing Crohn's Disease is the dysregulated immune system attacking the gastrointestinal tract. |
| PMID:36720220 | SUPPORT | Crohn's disease (CD) is a chronic gastrointestinal disease that is increasing in prevalence worldwide. CD is multifactorial, involving the complex interplay of genetic, immune, and environmental factors... we mapped markers of disease-associated myofibroblast activation and identified CHMP1A, TBX3, and RNF168 as regulators of fibrotic complications. | This study supports the mechanism involving the immune system leading to inflammation and chronic disease in the gastrointestinal tract. |
| PMID:21543977 | SUPPORT | The lymphatic system is re-emerging as a critical player in inflammatory and immune processes... Recent studies reporting lymphangitis, lymphangiogenesis, bacterial infiltration and lymph node infection, immune cell trafficking, and fat-wrapping in Crohn's disease suggest altered lymph drainage and lymphatic pumping, implicating the lymphatic system as a likely player in inflammatory disorders and IBDs. | The literature acknowledges the immune system's involvement in Crohn's Disease through various mechanisms, including lymphatic system dysfunction. |
| reference | supports | snippet | explanation |
|---|---|---|---|
| PMID:34313550 | SUPPORT | Crohn's disease (CD) is a major form of inflammatory bowel disease characterized by transmural inflammation along the alimentary tract. Changes in the microbial composition and reduction in species diversity are recognized as pivotal hallmarks in disease dynamics, challenging the gut barrier function and shaping a pathological immune response in genetically influenced subjects. | This study details changes in microbial composition and reduction in species diversity as key factors in the dynamics of Crohn's Disease, thereby supporting the statement. |
| PMID:18810765 | SUPPORT | The pathogenesis of both disease phenotypes is complex, the likely primary defect lies in the innate rather than adaptive immunity, particularly in the chemical antimicrobial barrier of the mucosa. This ileal and colonic defect in innate defense mediated by a deficiency of the protective alpha- and beta-defensins may enable the luminal microbes to invade the mucosa and trigger the inflammation. | This study indicates that defects in innate defense mechanisms allow microbial invasion, which triggers inflammation, supporting the involvement of microbiota alterations in Crohn's Disease. |
| PMID:23971750 | SUPPORT | Inflammatory bowel disease includes ulcerative colitis and Crohn's disease, which are both inflammatory disorders of the gastrointestinal tract. Both types of inflammatory bowel disease have a complex etiology, resulting from a genetically determined susceptibility interacting with environmental factors, including the diet and gut microbiota. | This article mentions the role of gut microbiota as an environmental factor in the etiology of Crohn's Disease, supporting the contribution of microbiome imbalance to disease mechanisms. |
| reference | supports | snippet | explanation |
|---|---|---|---|
| PMID:29246562 | SUPPORT | The most frequent symptoms are abdominal pain and diarrhoea, which can seriously affect patients' quality of life. | None |
| PMID:33946069 | SUPPORT | In Crohn's disease, inflammation causes pain. | None |
| PMID:35380673 | SUPPORT | The prevalence of pain [83.6% vs 59.1%; p < 0.001] and abdominal pain [68.7% vs 48.5%; p = 0.006] was higher in CD patients than in ulcerative colitis [UC] patients. | None |
| PMID:33836648 | SUPPORT | Using the patients'' self-reported information, we identified two subpopulations of Crohn's disease; these subpopulations differ in disease severity, associations with smoking, and genetic transmission patterns. | While this reference focuses on identifying subpopulations with varying disease severity, it underscores the heterogeneity of Crohn’s disease symptoms, indirectly supporting that abdominal pain is a frequent symptom. |
| reference | supports | snippet | explanation |
|---|---|---|---|
| PMID:22230271 | PARTIAL | Patients may experience diarrhea, abdominal pain, fever, weight loss, abdominal masses, and anemia. | This reference supports the presence of diarrhea and weight loss as frequent symptoms of Crohn's disease. However, it does not explicitly discuss malnutrition as a common sequela or confirm that these phenotypes are highly frequent. |
| PMID:38036713 | PARTIAL | Malnutrition might play a key role in the prognosis of patients with Crohn's disease (CD) ... Forty-one patients (24.8%) had body weight loss whereas 124 patients (75.2%) had no body weight loss. | This reference mentions weight loss and suggests a role for malnutrition in Crohn's disease prognosis, but does not confirm high frequency of gastrointestinal symptoms like diarrhea. |
| reference | supports | snippet | explanation |
|---|---|---|---|
| PMID:23111414 | SUPPORT | A high percentage of CD patients suffer from fatigue. | This reference confirms that fatigue is a common symptom among Crohn's disease patients. |
| PMID:37569413 | SUPPORT | Despite high prevalence and importance, the symptom is often underestimated in clinical practice. | The reference articulates the high prevalence of fatigue in inflammatory diseases, supporting the statement that fatigue is common among Crohn's disease patients. |
| name | presence | evidence | context |
|---|---|---|---|
| C-Reactive Protein (CRP) | Elevated | TRUNCATED | General inflammation |
| Fecal Calprotectin | Elevated | TRUNCATED | Intestinal inflammation |
| reference | supports | snippet | explanation |
|---|---|---|---|
| PMID:29358789 | SUPPORT | BACKGROUND AND OBJECTIVES: Crohn's disease is a multifactorial inflammatory disease affecting mainly the gastrointestinal tract. The genetic factors that are involved in the disease include mainly three mutations of the gene NOD2/CARD15 (R702W, G908R, 3020insC). | This reference states that NOD2 mutations are involved in Crohn's disease, supporting the association as a risk factor. |
| PMID:23352252 | SUPPORT | NOD2 gene mutations are associated with several diseases, and some of the mutations are of diagnostic value in Blau disease and NAID... The NOD2 variants located in the leucine-rich repeat (LRR) region are susceptible to Crohn disease. | This reference confirms the association of NOD2 gene mutations with Crohn's disease. |
| PMID:16773683 | SUPPORT | Investigations into the inheritance of the three risk alleles R702W, G908R and 1007fsInsC in NOD2 associated with susceptibility to Crohn's disease have demonstrated a remarkable amount of heterogeneity across ethnicities and populations. | This reference clearly establishes the association of specific NOD2 mutations with susceptibility to Crohn's disease. |
| PMID:12851870 | SUPPORT | The NOD2 gene, which is strongly associated with susceptibility to Crohn's disease (CD) of the terminal ileum, interacts with bacterial lipopolysaccharide (LPS), inducing cellular activation. | This study supports the role of NOD2 as a genetic risk factor for Crohn's disease. |
| PMID:32476786 | SUPPORT | While NOD2 mutations represent well established risk factors of CD, the role of other genes is incompletely understood. | This confirms that NOD2 is a well-established genetic risk factor for Crohn's disease. |
| PMID:11385577 | SUPPORT | Here we show, by using the transmission disequilibrium test and case-control analysis, that a frameshift mutation caused by a cytosine insertion, 3020insC, which is expected to encode a truncated NOD2 protein, is associated with Crohn's disease. | This study provides evidence of a specific NOD2 mutation associated with Crohn's disease. |
| PMID:17206682 | SUPPORT | The association of NOD2/CARD15 mutations with CD and BS, and possibly also early onset sarcoidosis, suggests a role for the gene in the development of granulomata and granulomatous diseases. | This statement supports the association of NOD2 with Crohn's disease (CD). |
| PMID:16987083 | SUPPORT | The mapping to CD of Nod2 variants that alter protein function represents one of the earliest, most well-established, associations in complex genetic disorders. | This reference emphasizes that the NOD2 association with Crohn's disease is well-established. |
| PMID:27076762 | SUPPORT | The highest accuracy, AUC of 0.78 was achieved with GRS combining 33 SNPs with optimal sensitivity and specificity of 75.0% and 72.7%, respectively... This includes variants in NOD2. | This study confirms the role of NOD2 variants as part of a genetic risk score for Crohn's disease. |
| reference | supports | snippet | explanation |
|---|---|---|---|
| PMID:27698206 | SUPPORT | Conclusion In this meta-analysis, the ATG16L1 genotype was significantly associated with the risk of developing Crohn''s disease. | None |
| PMID:25906181 | SUPPORT | Of interest, single-nucleotide polymorphisms in ATG16L1 (autophagy-related 16-like 1 [S. cerevisiae]), a key component in the autophagic response to invading pathogens, have been associated with an increased risk of developing Crohn disease. | None |
| PMID:12840668 | NO_EVIDENCE | CARD15 mutations are present in 30-50% of CD patients compared to 7-20% of healthy controls. Interestingly, CD patients often carry mutations on their two chromosomes suggesting a mutation dose effect. | The reference focuses on the association between CARD15 mutations and Crohn’s Disease, with no information regarding ATG16L1. |
| PMID:29795570 | NO_EVIDENCE | we find that ten rare genetic risk factors in NOD2 and LRRK2 are enriched in AJ (p < 0.005), including several novel contributing alleles, show evidence of association to CD. | The reference highlights genetic risk factors in NOD2 and LRRK2 for Crohn’s Disease, not ATG16L1. |
| PMID:27076762 | PARTIAL | We generated genetic risk scores (GRS) based on the number of risk alleles using weighted additive model. Discriminatory accuracy was measured by area under ROC curve (AUC)....The highest accuracy, AUC of 0.78 was achieved with GRS combining 33 SNPs with optimal sensitivity and specificity of 75.0% and 72.7%, respectively. | The study involves identification of SNPs for risk prediction, however ATG16L1 is not mentioned explicitly. Thus, it only partially supports the statement. |
| reference | supports | snippet | explanation |
|---|---|---|---|
| PMID:17068223 | SUPPORT | We found a highly significant association between Crohn's disease and the IL23R gene on chromosome 1p31, which encodes a subunit of the receptor for the proinflammatory cytokine interleukin-23. | This study identifies IL23R as a gene significantly associated with Crohn's disease, supporting the statement that IL23R is a genetic risk factor for the condition. |
| PMID:24989722 | SUPPORT | The study aimed to assess the contribution of the interleukin 23 receptor (IL23R) in determining disease susceptibility in two independent cohorts of CD. We demonstrate a strong increased CD risk for smokers and an additive interaction between IL23R SNPs and cigarette smoking. | This study supports the association between IL23R and Crohn's disease, while also highlighting the interaction between IL23R variants and environmental factors like smoking. |
| reference | supports | snippet | explanation |
|---|---|---|---|
| PMID:27016849 | SUPPORT | Smoking increases the risk of complications, recurrences and resort of surgery, corticosteroids or immunosuppressants. | The provided literature clearly states that smoking increases the risk and severity of Crohn's disease, aligning with the statement. |
| PMID:31014995 | SUPPORT | We identified 9 factors that increase risk of IBD: smoking (CD)... | The review identifies smoking as a significant environmental risk factor that increases the risk of Crohn's disease. |
| PMID:38238335 | SUPPORT | Compared to never smoking, current and previous smoking habits are associated with increased CD (P = 7.09 x 10(-10)) and UC (P < 2 x 10(-16)) risk, respectively. | This prospective cohort study finds that both current and previous smoking habits are associated with increased risk of CD, which supports the statement. |
| PMID:28838409 | SUPPORT | Understanding the potential environmental risk factors and natural history of CD in a given patient guides the physician when counseling the patient and selecting a treatment strategy. | The review discusses smoking as an important environmental risk factor, thereby supporting the statement. |
| reference | supports | snippet | explanation |
|---|---|---|---|
| PMID:33574618 | SUPPORT | Fiber-poor Western diets fuel inflammation. | This indicates that a Western diet, which is low in fiber, can contribute to inflammation, suggesting a potential exacerbation of symptoms in Crohn's Disease. |
| PMID:34010595 | SUPPORT | In mouse models, consumption of a Western diet for as little as 4 weeks led to Paneth cell dysfunction... Our findings provide a mechanistic link between poor diet and inhibition of gut innate immunity. | This study provides a direct mechanistic link between a Western diet and compromised gut immunity, which could exacerbate Crohn's disease symptoms. |
| PMID:33159156 | SUPPORT | Patients with IBD often believe certain foods influence their disease symptoms and consequently may alter their diet considerably... The association between diet and symptoms in patients with IBD and the mechanism(s) involved warrant further research. | This indicates that patients with inflammatory bowel disease, including Crohn's disease, often find that diet influences their symptoms, supporting the statement. |
| PMID:35595417 | PARTIAL | most patients report minimal nutritional education from their provider, and providers report few nutritional resources to help them educate patients. | While this indicates the importance of diet, it also highlights a lack of resources and education surrounding the dietary management of Crohn's disease, providing partial support. |
| reference | supports | snippet | explanation |
|---|---|---|---|
| PMID:15288007 | NO_EVIDENCE | Stress is also associated with IBD, but more as a modifier than an inducing factor, and its contribution is more obvious in IBD animal models than human IBD. | The literature suggests that stress is associated with IBD as a modifier and not necessarily as a direct trigger. |
| PMID:31574072 | SUPPORT | The unpredictable course of the disease, impaired function due to fatigue, and lack of bowel control were the most prominent causes of worry. The worries created feelings of stress, guilt, and frustration. The participants expressed a need to talk about their worries, to make them visible and recognized, and to be understood. | The study indicates that stress related to the disease itself is significant among Crohn's disease patients, which supports the claim that stress can worsen symptoms. |
| reference | supports | snippet | explanation |
|---|---|---|---|
| PMID:12786608 | SUPPORT | The mainstay of current medical treatment for mild to moderately active stages of Crohn's disease includes aminosalicylates, antibiotics, glucococorticosteroids and immunomodulators. | This reference states that aminosalicylates are included in the main treatments for mild to moderately active Crohn's disease. |
| PMID:34797442 | SUPPORT | 5-aminosalicylates (5-ASA) are frequently used in the management of Crohn's disease. | This reference supports the use of aminosalicylates for Crohn's disease treatment. |
| PMID:17339853 | REFUTE | Sulfasalazine and mesalazine are useful for the treatment of both active and quiescent ulcerative colitis, whereas they have no clinical effect on either active or inactive Crohn's disease. | This reference explicitly states that aminosalicylates have no clinical effect on Crohn's disease. |
| reference | supports | snippet | explanation |
|---|---|---|---|
| PMID:24532122 | SUPPORT | Corticosteroids have been used for decades to treat active Crohn's disease and remain the mainstay in the management of moderate-to-severe relapses in Crohn's disease. | This indicates that corticosteroids are indeed a primary treatment option for managing flare-ups in Crohn's disease. |
| PMID:32653651 | SUPPORT | corticosteroids are crucial for the induction of remission of moderate‑to‑severe flares in both UC and Crohn's disease. | This strengthens the claim that corticosteroids are used for short-term control during flare-ups to reduce inflammation in Crohn's disease. |
| PMID:18239408 | SUPPORT | The management of Crohn's disease usually consists of a succession of short-term acute phase treatments followed by a long-term maintenance therapy. [...] The drugs described in this article include [...] corticosteroids [...]. | This reinforces that corticosteroids are part of the short-term treatment strategy to control flare-ups in Crohn's disease. |
| reference | supports | snippet | explanation |
|---|---|---|---|
| PMID:17105689 | SUPPORT | The immunomodulatory drugs in the IBD arsenal include azathioprine, 6-mercaptopurine, methotrexate, cyclosporine, and tacrolimus. | The provided literature supports the statement that drugs like azathioprine and methotrexate are used as immunomodulators to manage Crohn's Disease. |
| PMID:35115294 | SUPPORT | Our results show that parenteral use of methotrexate is efficacious in inducing and maintaining remission as a step-up agent in azathioprine refractory Crohn's disease patients. | The study shows the use of methotrexate in patients who are refractory to azathioprine, supporting the statement that these drugs are used to treat Crohn's Disease by mitigating immune response. |
| PMID:16245637 | SUPPORT | First line immunosuppressants are Azathioprine and 6-Mercaptopurine while Methotrexate, Infliximab, Mycophenolatmofetil and other compounds represent alternative or rescue medications. | This reference confirms that Azathioprine and Methotrexate are used as immunosuppressants in the treatment of Crohn's Disease. |
| PMID:24913384 | SUPPORT | The only other long term disease-modifying options are the immunomodulators, methotrexate, azathioprine and mercaptopurine. | This review supports the use of methotrexate and azathioprine as immunomodulators for long-term management of Crohn's Disease. |
| reference | supports | snippet | explanation |
|---|---|---|---|
| PMID:18034589 | PARTIAL | Infliximab and adalimumab are currently the only biological agents approved for induction and maintenance treatment in adults (infliximab and adalimumab) and children (infliximab) with Crohn's disease. | This reference supports the use of anti-TNF agents (infliximab and adalimumab) for the treatment of moderate to severe Crohn's disease but does not mention vedolizumab directly. |
| PMID:26195652 | PARTIAL | Vedolizumab is an integrin-receptor antagonist for the treatment of CD and UC in adults with moderately to severely active disease. | This reference supports the use of vedolizumab (an integrin inhibitor) for the treatment of Crohn's disease but does not provide details on anti-TNF agents (infliximab and adalimumab). |
| PMID:26616476 | SUPPORT | Anti-TNF-alpha therapy is a novel approach that has transformed the way moderate-to-severe Crohn's disease (CD) is treated and has significantly improved clinical outcomes of patients. | This reference supports the use of anti-TNF agents for moderate to severe Crohn's disease. |
| reference | supports | snippet | explanation |
|---|---|---|---|
| PMID:19244154 | SUPPORT | Nutrition therapy of Crohn's disease is considered the first-line of treatment for Crohn's disease in children, especially in Europe. | This article supports the use of nutrition therapy as a treatment for managing symptoms and maintaining nutrition in Crohn’s disease. |
| PMID:38276922 | SUPPORT | New data in Crohn's disease supports the use of enteral liquid nutrition to help induce remission and correct malnutrition in patients heading for surgery. | This article supports the use of enteral nutrition as an effective therapy to induce remission and manage malnutrition in Crohn's disease. |
| PMID:36558412 | SUPPORT | Both under-and over-nutrition are prevalent in patients with Crohn's Disease (CD). | The study highlights the importance of dietary modifications to manage nutritional status in Crohn's disease patients. |
| PMID:35595414 | SUPPORT | The primary agents used in the treatment of Crohn's disease are aminosalicylates, corticosteroids, immunomodulators, and biologics. Each agent has different roles in the induction and maintenance of remission of disease. | While this primarily focuses on pharmacologic therapy, it does acknowledge the role of different agents in maintaining remission. |
| PMID:22410431 | SUPPORT | Although an elemental diet might lead to disease remission, reintroducing real foods and sustainable diets in patients with Crohn's disease is currently difficult, and would benefit from the sensitivity and rapid feedback provided by the field of nutrigenomics. | This reference suggests that dietary modifications can lead to remission and maintenance of Crohn's disease, validating the role of nutritional therapy. |
| reference | supports | snippet | explanation |
|---|---|---|---|
| PMID:21901520 | SUPPORT | The indications for surgery include the failure of medical management, especially the persistence or worsening of symptoms in spite of proper treatment and complications of the disease process. These complications include intestinal obstruction, intestinal perforation with fistula formation or abscess, free perforation, gastrointestinal bleeding, urologic complications, cancer, and perianal disease. | The excerpt indicates that surgery is reserved for complications such as strictures or fistulas among others, thus supporting the statement. |
| PMID:32279173 | SUPPORT | Therefore, current therapy of fibrotic strictures relies mainly on endoscopic and surgical procedures. | The statement mentions surgery for complications like strictures, which is supported by the snippet indicating that fibrotic strictures rely on surgical procedures for treatment. |
| PMID:21975159 | SUPPORT | Intestinal resection is almost always needed for the closure of symptomatic non-perianal fistulas. | The statement links surgery to the complication of fistulas, which is supported by the snippet explaining the need for intestinal resection to manage symptomatic non-perianal fistulas. |
| PMID:29462390 | SUPPORT | When isolated to the colon, and patients become medically refractory, there are several surgical options - segmental resection, subtotal colectomy with ileorectal anastomosis, or a total proctocolectomy and end ileostomy. Unfortunately, surgery does not cure CD, and, regardless of the extent of bowel removed, recurrence may be seen in the small bowel. | The snippet supports the statement by discussing various surgical options for patients who are medically refractory, involving the removal of affected bowel segments. |
| PMID:36926950 | SUPPORT | A partial resection of 3rd and 4th portion of the duodenum and the first loop of jejunum was performed, with duodenojejunal anastomosis. | The provided case demonstrates a scenario where surgery was performed due to refractory disease and complications, supporting the statement. |