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Colitis

Colitis is an inflammation of the mucosal lining of the colon, the large intestine responsible for absorbing water and forming stool, which can manifest as an acute or chronic condition affecting digestive function.^[1] This inflammation leads to swelling and irritation in the colon, often resulting in urgent, painful, or bloody bowel movements, and it represents a common gastrointestinal disorder with increasing global prevalence.^[2]^[1] Colitis encompasses several distinct types based on its underlying etiology, including infectious colitis caused by pathogens such as bacteria (e.g., Clostridium difficile, Campylobacter jejuni), viruses, or parasites; inflammatory bowel diseases like ulcerative colitis and Crohn's disease, which involve autoimmune responses; ischemic colitis due to reduced blood flow to the colon; microscopic colitis (collagenous or lymphocytic subtypes) characterized by inflammation visible only under a microscope; and other forms such as drug-induced, radiation-induced, or diversion colitis following surgical procedures.^[1]^[2] Each type varies in severity and chronicity, with infectious cases often resolving with treatment while autoimmune forms like ulcerative colitis may require lifelong management.^[1] The causes of colitis are diverse and depend on the specific type, ranging from microbial infections acquired through contaminated food or water to autoimmune dysregulation in inflammatory bowel diseases, vascular issues leading to tissue ischemia (particularly in older adults), adverse reactions to medications or radiation therapy, and immune deficiencies.^[2]^[1] Risk factors include age (ischemic colitis more common over 60), recent antibiotic use (predisposing to C. difficile infection), and genetic predispositions in inflammatory types, with epidemiological data indicating an incidence of approximately 20 cases per 100,000 for C. jejuni infections and a prevalence of up to 721 per 100,000 adults for inflammatory bowel disease in the United States (as of 2023).^[1]^[3]^[4] Common symptoms of colitis include abdominal pain or cramping, persistent diarrhea (often watery or bloody), urgency to defecate (tenesmus), fever, fatigue, and in severe cases, dehydration or weight loss, though presentations can vary by type and extent of inflammation.^[2]^[1] Diagnosis typically involves a combination of clinical evaluation, laboratory tests (such as stool analysis for pathogens or blood tests for inflammation markers like C-reactive protein), imaging studies (e.g., CT scans), and endoscopic procedures like colonoscopy with biopsy to confirm the type and rule out complications.^[2]^[1] Treatment for colitis is tailored to the underlying cause and may include antibiotics for infectious cases, anti-inflammatory medications such as 5-aminosalicylic acid (5-ASA) or corticosteroids for autoimmune types, dietary modifications to reduce irritation, and in refractory or complicated scenarios, immunomodulators, biologic therapies, or surgical intervention to remove affected colon segments.^[2]^[1] While many cases resolve with prompt care, chronic forms can lead to complications like colon perforation, toxic megacolon, or increased risk of colorectal cancer, underscoring the importance of early diagnosis and multidisciplinary management.^[2]^[1]

Overview

Definition

Colitis is defined as an inflammation of the colon, which is the large intestine, typically involving the mucosal lining and resulting in symptoms such as diarrhea and abdominal pain.^[1] This condition can manifest as acute or chronic inflammation, disrupting normal colonic function and potentially leading to ulceration or erosion of the affected tissue.^[5] Colitis is distinct from enteritis, which specifically refers to inflammation of the small intestine, and from gastroenteritis, an inflammatory process affecting both the stomach and intestines.^[6] While enteritis primarily impacts nutrient absorption in the small bowel, and gastroenteritis often involves upper gastrointestinal symptoms like vomiting, colitis is localized to the large intestine and focuses on water absorption and stool formation processes.^[7] The term "colitis" originates from the Greek "kolon," meaning colon, combined with the suffix "-itis," indicating inflammation, and entered medical usage around 1860 to describe colonic inflammatory conditions.^[8] It was first systematically described in 19th-century medical literature, with early accounts distinguishing it from other bowel disorders through postmortem examinations revealing mucosal changes in the colon.^[9] Anatomically, colitis primarily targets the colon but may extend to the rectum, resulting in proctocolitis, or penetrate beyond the mucosa into deeper layers of the bowel wall in severe instances.^[10] Common manifestations include ulcerative colitis, a chronic autoimmune variant confined to the colonic mucosa.^[11]

Epidemiology

Colitis encompasses a range of conditions, including inflammatory types such as ulcerative colitis (UC) and infectious forms, with varying global incidence and prevalence patterns. For inflammatory colitis, particularly UC, the global incidence is estimated at 5-10 cases per 100,000 person-years in high-prevalence regions like North America and Europe, though rates can reach up to 20 cases per 100,000 in certain populations.^[12] According to the Global Burden of Disease Study 2021, there were approximately 3.83 million prevalent cases of inflammatory bowel disease (IBD), which includes UC, worldwide, with age-standardized prevalence rates around 47 per 100,000; incidence continues to rise in East Asia, from about 64,000 new cases in 1990 to 164,000 in 2021, and projections indicate up to 1% prevalence in high-burden areas like Canada and Scotland by 2030.^[13]^[14] In contrast, infectious colitis, often manifesting as bacterial diarrhea, contributes to a substantial portion of global diarrheal burden; diarrheal diseases, which can include infectious colitis, cause nearly 1.7 billion episodes annually, predominantly in children under five in low- and middle-income countries.^[15] Bacterial pathogens like Campylobacter jejuni account for an estimated 25-30 cases per 100,000 population worldwide, underscoring the disproportionate impact in developing regions.^[1] Demographic trends in colitis reveal distinct patterns across age, gender, and ethnicity. UC typically exhibits bimodal age peaks, with onset most common between 15-30 years and a secondary peak at 50-70 years.^[12] Gender distribution shows a slight female predominance overall for UC, though males may have higher rates in pediatric cases.^[16] Ethnic variations are pronounced, with Ashkenazi Jewish populations facing a 2- to 4-fold increased risk of IBD compared to non-Jewish Europeans, attributed to founder mutations and genetic factors.^[17] Geographic variations highlight higher incidence and prevalence of inflammatory colitis in developed countries, where UC affects 200-300 individuals per 100,000 in North America and Europe, compared to lower rates in Asia and Africa historically.^[12] However, incidence is rising rapidly in newly industrialized regions, with East Asia reporting increases linked to urbanization and Westernized diets, potentially reaching 1 in 100 prevalence in high-burden areas by 2030.^[18] Post-2020 data indicate potential associations between COVID-19 and UC flares, driven by infection-related stress or direct viral effects on the gut, though no significant overall increase in adverse IBD outcomes has been observed.^[19] Certain risk correlations further shape colitis epidemiology. Smoking is inversely associated with UC development, conferring a reduced risk (odds ratio 0.58), while it nearly doubles the risk for Crohn's disease (odds ratio 1.76).^[20] Urban residence is linked to higher IBD incidence compared to rural areas, with meta-analyses showing urbanization as a key environmental risk factor.^[21]

Clinical Presentation

Signs and Symptoms

Colitis commonly manifests with abdominal cramping and pain, which is often localized to the left side of the abdomen in conditions such as ulcerative colitis due to involvement of the sigmoid colon and rectum.^[22] Chronic diarrhea is a hallmark feature, characterized by frequent and urgent bowel movements that may contain blood, mucus, or pus when the colonic mucosa is inflamed.^[22] Rectal bleeding is particularly prominent in cases with direct mucosal involvement, appearing as bright red blood in the stool or on toilet paper.^[22] In moderate to severe cases, systemic symptoms such as fever, unintended weight loss, and fatigue frequently accompany the gastrointestinal complaints, reflecting the inflammatory burden on the body.^[22] Tenesmus, a distressing sensation of incomplete evacuation and persistent urge to defecate despite an empty rectum, is another common rectal symptom arising from inflammation in the distal colon.^[22] The presentation can vary by etiology: acute infectious colitis often features a sudden onset of profuse watery diarrhea potentially leading to dehydration, while autoimmune forms like ulcerative colitis typically exhibit a relapsing-remitting pattern of symptoms. Ischemic colitis, common in older adults, presents with sudden severe abdominal pain (often left-sided) and bloody diarrhea but usually without fever. Microscopic colitis is characterized by chronic watery diarrhea without visible blood or significant pain.^[23]^[24]^[25]^[26] In pediatric patients with inflammatory bowel disease-related colitis, growth failure is a notable concern, often manifesting as delayed linear growth or pubertal development due to chronic inflammation and malnutrition.^[27] Extraintestinal manifestations occur in 10-20% of cases, particularly in autoimmune colitis, and may include peripheral joint pain (arthropathy), skin rashes such as erythema nodosum, and ocular inflammation like uveitis, which can parallel or precede intestinal symptoms.^[28]^[29]

Complications

Colitis can lead to several serious gastrointestinal complications, including toxic megacolon, characterized by acute dilation of the colon exceeding 6 cm in diameter, which carries a high risk of perforation and sepsis if untreated.^[30] Strictures, or narrowing of the intestinal lumen due to chronic inflammation and scarring, may obstruct bowel flow, particularly in cases of long-standing Crohn's colitis; these are less common in ulcerative colitis.^[12] Fistulas, abnormal tracts connecting the colon to adjacent organs such as the bladder or skin, arise from deep ulceration and transmural inflammation and are more characteristic of Crohn's colitis than ulcerative colitis, often resulting in recurrent infections or abscesses.^[12] Patients with long-standing ulcerative colitis face an elevated risk of colorectal cancer, estimated at 2 to 5 times higher than the general population, due to chronic mucosal inflammation promoting dysplasia.^[31] To mitigate this, clinical guidelines recommend initiating surveillance colonoscopies 8 to 10 years after diagnosis, with intervals of 1 to 3 years thereafter based on risk factors such as disease extent and family history.^[32] Systemic complications of colitis include anemia, primarily from chronic gastrointestinal blood loss and impaired iron absorption, affecting up to 30-60% of patients during flares.^[12] Malnutrition arises from reduced oral intake, malabsorption of nutrients, and increased metabolic demands from inflammation, leading to weight loss and deficiencies in vitamins and minerals.^[33] Osteoporosis is prevalent, impacting 10-30% of inflammatory bowel disease patients, driven by malabsorption of calcium and vitamin D, systemic inflammation, and long-term corticosteroid use, which accelerates bone density loss.^[34] Infectious superinfections, such as Clostridioides difficile, occur in approximately 5-10% of hospitalized patients with inflammatory bowel disease flares, exacerbated by disrupted gut microbiota, frequent antibiotic exposure, and immunosuppression, often precipitating severe flares or toxic megacolon.^[35] Mortality from colitis remains rare overall but rises significantly in fulminant cases; current rates for severe ulcerative colitis are approximately 2-5% at 3 years following admission with modern treatment, primarily due to perforation, sepsis, or multiorgan failure if intervention is delayed.^[36]

Pathophysiology

Underlying Mechanisms

Colitis encompasses a range of conditions characterized by inflammation of the colon, driven by complex interactions between genetic predispositions, environmental factors, and dysregulated immune responses that culminate in mucosal damage. At the core of this pathology is a dysregulated inflammatory cascade, where pro-inflammatory cytokines such as tumor necrosis factor-alpha (TNF-α), interleukin-6 (IL-6), and interleukin-1 (IL-1) are excessively released by activated immune cells, including macrophages and T cells, perpetuating chronic inflammation.^[37] This cytokine imbalance amplifies the recruitment and activation of neutrophils, which infiltrate the colonic mucosa, releasing reactive oxygen species and proteases that exacerbate tissue injury and ulcer formation.^[38] In severe cases, this cascade contributes to a self-sustaining cycle of inflammation, as seen in inflammatory bowel diseases (IBD) like ulcerative colitis and Crohn's disease.^[39] A key contributor to the initiation and progression of colonic inflammation is intestinal barrier dysfunction, often described as "leaky gut," where increased permeability of the epithelial tight junctions allows luminal antigens, bacteria, and toxins to translocate into the underlying lamina propria.^[40] This breach disrupts the mucosal barrier's integrity, primarily through downregulation of tight junction proteins such as zonula occludens-1 (ZO-1) and occludin, triggered by inflammatory cytokines and oxidative stress.^[41] Consequently, exposure of subepithelial immune cells to these foreign elements provokes an aberrant immune response, further amplifying cytokine production and neutrophil infiltration, which in turn worsens barrier permeability in a vicious cycle.^[42] Genetic factors play a pivotal role in predisposing individuals to colitis, particularly in IBD-associated forms, with genome-wide association studies (GWAS) identifying over 200 susceptibility loci that influence immune regulation and epithelial integrity.^[43] Among these, mutations in the NOD2 gene, such as the common R702W, G908R, and 1007fs variants, are strongly associated with Crohn's disease, impairing the recognition of bacterial peptidoglycans and leading to defective autophagy and unchecked microbial invasion in the intestinal mucosa.^[44] These genetic alterations, often involving innate immunity pathways, interact with environmental cues to lower the threshold for inflammatory responses in the colon. Environmental triggers, notably gut microbiota dysbiosis, significantly contribute to the underlying mechanisms of colitis by altering the microbial ecosystem in ways that promote inflammation. In affected individuals, there is a characteristic reduction in microbial diversity, with decreased abundance of beneficial Firmicutes and Bacteroidetes phyla, coupled with overgrowth of pathogenic species.^[45] A prominent example is the expansion of adherent-invasive Escherichia coli (AIEC) strains, which adhere to and invade epithelial cells, inducing chronic inflammation through secretion of virulence factors and disruption of the mucosal barrier.^[46] This dysbiosis not only facilitates antigen translocation but also modulates host immune responses, favoring pro-inflammatory Th17 cell differentiation and cytokine release.^[47] In vascular forms of colitis, such as ischemic colitis, the primary mechanism involves colonic hypoperfusion leading to tissue hypoxia, which impairs cellular metabolism and triggers ischemic injury.^[48] Upon restoration of blood flow, reperfusion exacerbates damage through the generation of reactive oxygen species, activation of neutrophils, and endothelial dysfunction, resulting in mucosal edema, hemorrhage, and potential necrosis.^[49] This biphasic process—hypoxia followed by reperfusion injury—underlies the acute presentation and highlights the role of hemodynamic instability in non-inflammatory colitis subtypes.^[50]

Risk Factors

Risk factors for colitis encompass both non-modifiable and modifiable elements that elevate susceptibility to colonic inflammation across its various forms. Genetic predisposition plays a significant role, particularly in inflammatory bowel disease (IBD)-associated colitis such as ulcerative colitis (UC), where individuals with a first-degree relative affected by the condition face an approximately 5-fold increased risk compared to the general population, with estimates ranging from 4- to 8-fold across studies.^[51]^[52] Age also influences vulnerability, with UC exhibiting a bimodal distribution of onset, featuring peaks typically in the 20-29 and 70-79 age groups for males, and 30-39 and 70-79 for females.^[53] Ethnicity further stratifies risk, as Caucasians, especially those of Ashkenazi Jewish descent, demonstrate higher incidence rates of UC than individuals of African or Asian ancestry.^[22] For ischemic colitis, key risk factors include advanced age (particularly over 60 years), cardiovascular diseases such as atherosclerosis or atrial fibrillation, and conditions causing low blood flow like hypotension or dehydration.^[48] Modifiable lifestyle factors contribute substantially to colitis development and exacerbation. Diets rich in processed foods, sugars, and ultra-processed items, while low in fiber, are associated with heightened IBD risk, potentially through promotion of gut dysbiosis—a microbial imbalance detailed in underlying pathophysiological mechanisms.^[54] Smoking presents a paradoxical effect: it appears protective against UC onset but increases the likelihood of Crohn's disease involvement of the colon and disease progression in those affected.^[55] Frequent use of nonsteroidal anti-inflammatory drugs (NSAIDs) elevates the risk of colitis flares by 2- to 4-fold, likely due to disruption of the intestinal mucosal barrier.^[56] Infectious and iatrogenic exposures represent additional modifiable risks, particularly for acute and opportunistic forms of colitis. Prior bacterial infections, such as those caused by Salmonella species, can trigger reactive colitis and are linked to a long-term elevated risk of developing UC.^[57] Antibiotic use disrupts the gut microbiota, substantially increasing susceptibility to pseudomembranous colitis from Clostridioides difficile overgrowth, with risk manifesting days to months post-exposure.^[58] For infectious colitis more broadly, risk factors include immunosuppression (e.g., from HIV or chemotherapy), travel to endemic areas, and consumption of contaminated food or water.^[1] Socioeconomic conditions, including poor sanitation in endemic regions, heighten exposure to pathogens like Salmonella and Shigella, thereby raising the incidence of infectious colitis through contaminated water and food sources.^[59]

Classification and Types

Inflammatory and Autoimmune Colitis

Inflammatory and autoimmune colitis encompasses chronic conditions characterized by immune dysregulation leading to persistent colonic inflammation, distinct from acute infectious or vascular etiologies. Ulcerative colitis (UC), the prototypical form, is an idiopathic inflammatory bowel disease (IBD) confined to the mucosa and submucosa of the colon, featuring continuous inflammation that invariably begins in the rectum and extends proximally in a contiguous manner.^[11] This pattern contrasts with the patchy, transmural involvement seen in Crohn's disease, limiting UC to the colorectum without small bowel or perianal disease.^[22] Subtypes of UC are defined by the extent of involvement: proctitis (E1), limited to the rectum; left-sided colitis (E2), extending to the splenic flexure; and pancolitis (E3), affecting the entire colon.^[60] These classifications guide prognosis and management, with pancolitis associated with higher risks of complications like toxic megacolon.^[61] Microscopic colitis represents another key autoimmune-mediated form, comprising lymphocytic colitis and collagenous colitis subtypes, both presenting with normal or near-normal endoscopic appearances but revealing inflammation on biopsy.^[62] In lymphocytic colitis, histology shows increased intraepithelial lymphocytes (>20 per 100 epithelial cells) and lamina propria inflammation without surface epithelial damage.^[63] Collagenous colitis, in contrast, features a thickened subepithelial collagen band (>10 μm) alongside similar lymphocytic infiltration, distinguishing it pathologically.^[64] This condition predominantly affects older adults, particularly females over 60, with a female-to-male ratio up to 9:1 for collagenous colitis, possibly linked to hormonal or autoimmune factors.^[65] Symptoms such as chronic watery diarrhea predominate, often without gross blood, underscoring the need for histological confirmation.^[66] The pathogenesis of these disorders involves dysregulated immune responses, primarily T-cell mediated, with aberrant activation of CD4+ T helper cells driving mucosal inflammation. In UC, an imbalance between pro-inflammatory Th17 cells (producing IL-17 and IL-23) and immunosuppressive regulatory T cells (Tregs) perpetuates chronic colitis, exacerbated by defects in epithelial barrier function and microbial dysbiosis.^[67] Autoantibodies further contribute, notably perinuclear antineutrophil cytoplasmic antibodies (pANCA) detected in 60-80% of UC patients, targeting antigens like myeloperoxidase and associating with more severe, treatment-refractory disease.^[68] These humoral responses likely arise from molecular mimicry between bacterial epitopes and host proteins, amplifying T-cell driven autoimmunity.^[69] Indeterminate colitis accounts for 5-10% of IBD cases, featuring overlapping histopathological and clinical traits of UC and Crohn's disease that preclude definitive classification at initial presentation.^[70] Such ambiguity often manifests as continuous colonic involvement with occasional granulomas or transmural elements suggestive of Crohn's, complicating surgical planning like ileal pouch-anal anastomosis.^[71] Over time, up to 70% of cases may resolve into UC or Crohn's based on longitudinal evolution, but persistent indeterminacy requires tailored monitoring.^[72] Diagnostic criteria for UC rely on the Montreal classification, which stratifies disease extent (E1-E3 as noted) and severity to standardize assessment and predict outcomes.^[73] Severity grading includes clinical remission (S0), mild disease (S1: ≤4 stools/day, no systemic signs), moderate (S2: >4 stools/day, minimal systemic toxicity), and severe (S3: ≥6 bloody stools/day with fever, tachycardia, or anemia).^[74] Endoscopic features like friable mucosa and loss of vascular pattern, combined with biopsy confirmation of crypt abscesses and basal plasmacytosis, solidify the diagnosis, often alongside symptoms such as bloody diarrhea.^[75] For microscopic colitis, random biopsies from normal-appearing colon are essential, as targeted sampling may miss diagnostic changes.^[76]

Infectious Colitis

Infectious colitis refers to inflammation of the colon resulting from invasion or toxin production by microbial pathogens, including bacteria, viruses, parasites, and fungi. This condition typically presents as an acute process, often accompanied by symptoms such as fever and bloody diarrhea, distinguishing it from chronic inflammatory forms. It is a significant cause of morbidity worldwide, particularly in settings with poor sanitation or immunocompromise, and can lead to severe complications like dehydration or toxic megacolon if untreated.^[1] Bacterial pathogens are the most common etiologic agents of infectious colitis. Clostridioides difficile (formerly Clostridium difficile) causes toxin-mediated colitis, often following antibiotic use, leading to pseudomembrane formation on the colonic mucosa—a hallmark visible on endoscopy or histology. This strain produces toxins A and B, which disrupt the cytoskeleton and cause cell death, resulting in watery or bloody diarrhea. Salmonella species, such as S. enterica serovar Typhi or non-typhoidal strains, and Shigella species induce dysentery-like symptoms through invasion of the colonic epithelium, producing bloody mucoid stools and tenesmus due to Shiga toxin effects in severe cases. Campylobacter jejuni, frequently waterborne from contaminated sources like undercooked poultry or unpasteurized milk, causes inflammatory colitis by adhering to and invading enterocytes, leading to similar bloody diarrhea. Enterohemorrhagic Escherichia coli (EHEC), particularly serotype O157:H7, is a key foodborne pathogen that produces Shiga-like toxins, causing hemorrhagic colitis and potentially progressing to hemolytic uremic syndrome.^[77]^[78]^[79]^[77] Viral pathogens contribute to infectious colitis, especially in outbreaks or vulnerable populations. Cytomegalovirus (CMV) primarily affects immunocompromised individuals, such as those with HIV/AIDS or post-transplant, causing ulcerations in the colonic mucosa through viral replication in endothelial cells and direct cytopathic effects. Norovirus, a leading cause of gastroenteritis outbreaks, can involve the colon in severe cases, particularly in closed settings like cruise ships or nursing homes, resulting in self-limited inflammation via norovirus-induced disruption of tight junctions.^[79]^[80]^[81] Parasitic causes are less common in developed countries but significant in endemic areas. Entamoeba histolytica leads to amebic colitis (amebiasis) by trophozoite invasion of the colonic mucosa, forming characteristic flask-shaped ulcers with undermining of the submucosa and surrounding necrosis, often presenting with chronic diarrhea or acute dysentery. Transmission occurs via fecal-oral route from contaminated water or food, and while rare in high-income settings due to improved hygiene, it remains a global health concern in tropical regions.^[82]^[83]^[84] Fungal pathogens rarely cause primary infectious colitis but can in severely immunocompromised hosts. Candida species, particularly C. albicans, may lead to colitis in patients with advanced HIV/AIDS, where overgrowth invades the mucosal barrier, exacerbated by CD4 counts below 200 cells/μL, resulting in ulcerative lesions similar to pseudomembranous candidiasis elsewhere in the gastrointestinal tract.^[85]^[86] Transmission of infectious colitis often occurs via the fecal-oral route, with foodborne outbreaks prominent for bacterial agents like Salmonella, Campylobacter, and E. coli O157:H7, linked to contaminated produce, undercooked meats, or unpasteurized dairy. Waterborne spread is common for Campylobacter and Entamoeba histolytica, while norovirus outbreaks thrive in crowded environments. Between 2018 and 2023, global surveillance has documented rising incidences of antibiotic-resistant strains, including multidrug-resistant Salmonella and C. difficile variants, driven by overuse in agriculture and healthcare, complicating treatment and increasing outbreak severity.^[87]^[77]

Vascular and Ischemic Colitis

Vascular and ischemic colitis, also known as ischemic colitis, arises from a sudden reduction in blood flow to the colon, leading to inflammation and potential injury of the colonic mucosa.^[88] This condition primarily affects older adults and results from hypoperfusion due to underlying vascular compromise, distinguishing it from immune-mediated or infectious forms of colitis.^[89] The pathophysiology involves acute hypoperfusion of the colonic vasculature, often triggered by atherosclerosis, systemic hypotension, or vasospasm, which impairs oxygen delivery to the bowel wall.^[90] Watershed areas, such as the splenic flexure (Griffith's point) and rectosigmoid junction (Sudeck's point), are particularly vulnerable due to their limited collateral blood supply from the superior and inferior mesenteric arteries.^[89] This hypoperfusion can lead to mucosal ischemia, followed by reperfusion injury upon restoration of blood flow, exacerbating tissue damage through oxidative stress and inflammation.^[90] In severe cases, prolonged ischemia progresses to full-thickness necrosis, necessitating urgent intervention.^[48] Risk factors strongly associate with cardiovascular comorbidities, including atherosclerosis, atrial fibrillation, heart failure, and peripheral arterial disease, which collectively impair mesenteric perfusion.^[91] Postoperative states, such as after aortic aneurysm repair, elevate risk due to potential embolization or clamping of mesenteric vessels, with reported incidences of 1-3% in elective cases.^[92] The condition predominantly affects individuals over 60 years, with a median age at diagnosis of approximately 71 years, and incidence rates ranging from 4.5 to 44 cases per 100,000 person-years, increasing with aging populations.^[93]^[94] Clinically, ischemic colitis manifests in subtypes ranging from transient, self-resolving forms that account for about 80-85% of cases and often resolve without intervention, to gangrenous variants involving transmural necrosis that require surgical resection in up to 20% of patients.^[90] Histological findings in affected tissue include mucosal sloughing, submucosal hemorrhage, edema, and hyalinized lamina propria, reflecting ischemic injury.^[95] On imaging, such as CT or plain radiographs, characteristic thumbprinting appears due to submucosal edema and hemorrhage, aiding early diagnosis.^[96]

Medication-Induced and Other Colitis

Medication-induced colitis encompasses inflammatory changes in the colon triggered by various pharmaceutical agents, distinct from infectious or ischemic etiologies. Nonsteroidal anti-inflammatory drugs (NSAIDs), including COX-2 inhibitors, are a common cause, leading to direct mucosal toxicity that manifests as erosions, ulcers, and diaphragm-like strictures, particularly in the right colon where drug concentrations are higher.^[97] Patients often present with bloody diarrhea, abdominal pain, weight loss, and iron deficiency anemia, with elderly individuals on long-term therapy at highest risk for severe complications.^[98] Chemotherapy agents induce intestinal mucositis, a broader gastrointestinal toxicity affecting up to 40-100% of patients, resulting in colitis-like symptoms such as diarrhea, ulceration, and barrier dysfunction due to epithelial cell death and inflammation.^[99] Immune checkpoint inhibitors, such as ipilimumab, provoke immune-mediated colitis in approximately 7-9% of patients on monotherapy and 10-18% all-grade (with ~7-10% severe) with combination therapy (e.g., ipilimumab plus nivolumab), characterized by lymphocytic or collagenous patterns mimicking inflammatory bowel disease.^[100] Radiation colitis arises as a complication of pelvic radiotherapy, typically for cancers like prostate or cervical, with acute forms occurring within three months due to mucosal edema, hyperemia, and friability from direct cellular damage.^[101] Chronic radiation colitis develops months to years later, featuring telangiectasias, fibrosis, and strictures from vascular endothelial injury and ischemia, often requiring endoscopic or surgical intervention for persistent bleeding or obstruction.^[102] Acute episodes are usually self-limited with supportive care, while chronic cases pose ongoing management challenges due to progressive tissue damage.^[103] Diversion colitis refers to nonspecific inflammation in the defunctionalized colonic segment proximal to an ostomy, resulting from the absence of the fecal stream and subsequent short-chain fatty acid deficiency, which impairs mucosal nutrition.^[104] Endoscopically, it appears as erythema, friability, and lymphoid hyperplasia, often asymptomatic but sometimes causing tenesmus or discharge; symptoms typically resolve upon reanastomosis or stoma reversal, restoring fecal flow.^[105] Treatment may involve short-chain fatty acid enemas or probiotics to mimic fecal stream benefits if reversal is delayed.^[106] Other forms of colitis include unclassifiable etiologies not fitting primary categories. Eosinophilic colitis, often allergic in origin, predominantly affects infants under six months, linked to cow's milk protein intolerance, presenting with bloody stools, eosinophilic infiltration, and resolution via dietary elimination.^[107] Factitious colitis involves self-induced mucosal injury, typically through surreptitious laxative abuse or enema use, simulating chronic diarrhea and inflammation; diagnosis requires exclusion of organic causes and psychiatric evaluation.^[108] Emerging reports highlight rare cases of colitis following mRNA COVID-19 vaccination (2021-2025), potentially linked to immune dysregulation akin to myocarditis, though causality remains unestablished and incidence is exceedingly low, warranting further surveillance in post-vaccination adverse event monitoring.^[109]

Diagnosis

History and Physical Examination

The history taking in suspected colitis begins with a detailed assessment of the patient's symptoms, including the onset and duration of diarrhea, which is often the presenting complaint. Characteristics of the stool, such as the presence of blood, mucus, or pus, are critical to elicit, as bloody diarrhea is a hallmark of inflammatory or infectious forms. Associated symptoms like abdominal cramping, urgency, tenesmus, fever, and recent weight loss should be explored, along with potential triggers such as recent travel to endemic areas, antibiotic use, or a family history of inflammatory bowel disease (IBD).^[11]^[1]^[110] Red flags in the history that warrant urgent evaluation include nocturnal diarrhea, unintentional weight loss exceeding 10% of body weight, persistent rectal bleeding, and onset after age 50, which may suggest ischemic colitis or underlying malignancy rather than benign causes. These features help prioritize patients for expedited diagnostic workup, as they indicate potential severity or complications like toxic megacolon.^[111]^[1]^[112] The physical examination focuses on vital signs to detect dehydration (e.g., tachycardia, hypotension) or systemic involvement (e.g., fever suggesting sepsis or infection). Abdominal palpation often reveals diffuse tenderness, particularly in the lower quadrants, with guarding or rebound tenderness signaling peritonitis in severe cases; distention may indicate ileus. A digital rectal examination is essential to assess for rectal tone, masses, or gross blood, providing immediate clues to mucosal involvement.^[110]^[12]^[1] For ulcerative colitis specifically, the Partial Mayo Score is a validated tool to gauge disease activity based on history and exam findings, incorporating stool frequency (0-3 points, where 0 is normal and 3 is ≥6 stools/day more than normal), rectal bleeding (0-3 points, where 0 is none and 3 is ≥50% of stools with blood), and physician's global assessment (0-3 points, based on overall clinical impression). A total score of 0-9 is calculated, with scores ≤2 indicating remission and ≥6 suggesting severe activity; this non-invasive index correlates well with endoscopic severity and guides initial management decisions.^[113]^[114] Building a differential diagnosis through history patterns is key: unlike irritable bowel syndrome (IBS), which features non-bloody, relapsing diarrhea often relieved by defecation without systemic symptoms like weight loss or fever, colitis typically presents with bloody stools and constitutional signs. Diverticulitis, in contrast, is suggested by acute, localized left lower quadrant pain in older patients with fever, differing from the more continuous or crampy pain in colitis.^[115]^[116]^[117]

Diagnostic Tests

Laboratory tests play a crucial role in the initial evaluation of suspected colitis by identifying signs of inflammation, infection, or anemia. A complete blood count (CBC) often reveals leukocytosis indicative of infection or inflammation and anemia due to chronic blood loss in the gastrointestinal tract.^[118] Inflammatory markers such as C-reactive protein (CRP) and erythrocyte sedimentation rate (ESR) are elevated in active disease, helping to assess severity and monitor response to therapy.^[119] Stool studies are essential to rule out infectious causes; for instance, detection of Clostridium difficile toxin confirms toxin-mediated colitis, while fecal calprotectin levels exceeding 50 μg/g suggest intestinal inflammation consistent with inflammatory bowel disease (IBD).^[120]^[121] Endoscopic procedures provide direct visualization and sampling of the colonic mucosa, serving as the cornerstone for confirming colitis. Colonoscopy with biopsy is considered the gold standard for diagnosis, allowing assessment of mucosal abnormalities such as friability, erythema, and ulcers, particularly continuous involvement from the rectum in ulcerative colitis (UC).^[122] In acute or severe cases where full colonoscopy poses risks like perforation, flexible sigmoidoscopy offers a safer alternative to evaluate the distal colon.^[123] Imaging modalities complement endoscopy by evaluating disease extent and complications beyond the reach of direct visualization. Computed tomography (CT) of the abdomen detects colonic wall thickening greater than 3 mm, fat stranding, and complications such as abscesses or perforation, aiding in the differentiation of colitis subtypes.^[124] Magnetic resonance imaging (MRI), particularly enterography or dedicated pelvic sequences, is preferred for assessing perianal disease in Crohn's colitis, revealing fistulas, abscesses, and inflammation with high soft-tissue resolution without ionizing radiation.^[125] Histopathological examination of biopsy specimens provides definitive characterization of colitis etiology. In UC, common findings include crypt abscesses, crypt distortion, and mucosal ulceration, reflecting chronic active inflammation limited to the mucosa.^[126] Crohn's disease features transmural inflammation with noncaseating granulomas in up to 30% of cases, patchy involvement, and fibrosis.^[127] Infectious colitis, such as cytomegalovirus (CMV) in immunocompromised patients, shows characteristic viral inclusions within endothelial or stromal cells on hematoxylin and eosin staining. Biopsy histopathology also helps distinguish infectious from autoimmune forms of colitis.^[128] Advanced diagnostic tools are employed for specific scenarios, such as evaluating small bowel involvement. Capsule endoscopy visualizes the small intestine to detect extension of Crohn's disease beyond the colon, identifying ulcers, strictures, and erythema with a sensitivity of approximately 80-90% for proximal lesions.^[129] In research settings, fecal microbiota analysis via sequencing techniques explores dysbiosis patterns associated with colitis, though it remains investigational for routine diagnosis.^[130]

Management

Pharmacological Treatments

Pharmacological treatments for colitis are tailored to the etiology, severity, and extent of disease, with the primary aims of inducing remission, maintaining symptom control, and minimizing complications. In inflammatory and autoimmune forms like ulcerative colitis (UC), agents target mucosal inflammation through anti-inflammatory, immunosuppressive, or cytokine-modulating mechanisms. For infectious colitis, therapies focus on eradicating pathogens while supportive care addresses dehydration and electrolyte imbalances. Drug selection depends on whether the colitis is autoimmune (favoring immunomodulators and biologics) or infectious (requiring antimicrobials), as detailed in prior classifications. Aminosalicylates (5-aminosalicylic acid or 5-ASA compounds), such as mesalamine, serve as first-line therapy for mild to moderate UC by delivering anti-inflammatory effects directly to the colonic mucosa, inhibiting prostaglandin synthesis and nuclear factor-kappa B pathways. Oral delayed-release formulations at doses of 2.4 to 4.8 g/day or rectal suppositories/enemas (1 g daily) are effective for both induction of remission (over 8 weeks) and long-term maintenance, with higher doses improving outcomes in extensive disease.^[131] Corticosteroids provide rapid control of acute flares in moderate to severe UC by broadly suppressing immune responses and reducing cytokine production, though they are reserved for short-term use due to risks like osteoporosis and infection. Oral prednisone at 40-60 mg/day for 1-2 weeks, followed by a gradual taper (e.g., 5-10 mg/week), is standard for systemic flares; budesonide (9 mg/day orally for 8 weeks) is preferred for ileal or right-sided colonic involvement owing to its site-specific activation and reduced systemic exposure compared to traditional steroids.^[132] Immunomodulators, including azathioprine and its active metabolite 6-mercaptopurine, are used for maintenance therapy in steroid-dependent moderate to severe UC, acting by inhibiting purine synthesis to impair T- and B-cell proliferation. Typical dosing is 2-2.5 mg/kg/day for azathioprine (or 1-1.5 mg/kg/day for 6-mercaptopurine), initiated after induction and monitored for myelosuppression via thiopurine methyltransferase testing.^[133] Biologic agents like anti-tumor necrosis factor (TNF) inhibitors, exemplified by infliximab, are indicated for moderate to severe UC refractory to conventional therapies, binding soluble and membrane-bound TNF-alpha to halt inflammatory cascades. The regimen involves intravenous infusions of 5 mg/kg at weeks 0, 2, and 6 for induction, followed by maintenance every 8 weeks, achieving clinical response in up to 70% of patients.^[134] Janus kinase (JAK) inhibitors, such as tofacitinib, represent targeted oral therapies for moderate to severe UC, selectively blocking JAK1 and JAK3 to disrupt intracellular signaling of pro-inflammatory cytokines like IL-6 and IL-23. Induction dosing is 10 mg twice daily for at least 8 weeks, transitioning to 5 mg twice daily for maintenance in responders, with efficacy comparable to biologics in clinical trials.^[135] In infectious colitis, antibiotics are selected based on the causative organism to restore microbial balance and resolve symptoms. For Clostridioides difficile-associated colitis, oral vancomycin at 125 mg four times daily for 10 days is the first-line treatment for non-severe initial episodes, superior to metronidazole in cure rates and recurrence prevention.^[136] For viral etiologies like cytomegalovirus (CMV) colitis in immunocompromised individuals, intravenous ganciclovir at 5 mg/kg twice daily for 2-3 weeks (or until viral clearance) inhibits viral DNA polymerase, achieving remission in most cases.^[137] For recurrent C. difficile colitis unresponsive to repeated antibiotics, fecal microbiota transplantation (FMT) via colonoscopy or capsules restores gut microbiome diversity, yielding cure rates of approximately 90% after a single procedure and serving as a guideline-recommended option.^[138]

Surgical Options

Surgical intervention is considered in colitis when medical therapies fail to control symptoms or when complications arise that threaten life or quality of life. In ulcerative colitis (UC), surgery offers a potential cure by removing the diseased colon and rectum, whereas in Crohn's colitis, operations are typically palliative, addressing localized complications without curing the underlying disease. Indications for surgery in UC include medically refractory disease, fulminant colitis unresponsive to intensive medical management, and the presence of dysplasia or colorectal cancer for prophylaxis. The lifetime risk of requiring colectomy in UC patients has historically been estimated at 25-30%, though contemporary rates show a decline to approximately 11% at 10 years due to advances in medical therapy. In Crohn's colitis, surgery is indicated for complications such as strictures, fistulas, or abscesses that do not respond to conservative treatment. The primary restorative procedure for UC is total proctocolectomy with ileal pouch-anal anastomosis (IPAA), which involves removal of the colon and rectum followed by creation of a J-shaped ileal pouch connected to the anus, allowing for continence without a permanent stoma in most cases. For emergent situations in UC, such as toxic megacolon or perforation, a subtotal colectomy with end ileostomy is performed initially, with IPAA potentially staged later once the patient stabilizes. In Crohn's colitis, management is tailored to disease distribution; segmental resection of affected colonic segments is preferred for localized disease to minimize bowel loss, while strictureplasty— a technique that widens narrowed areas without resection— is employed for fibrostenotic strictures, particularly in the small bowel or multiple sites, to preserve intestinal length. Common complications following IPAA in UC include pouchitis, an inflammation of the ileal pouch occurring in approximately 50% of patients within the first few years postoperatively. Pelvic surgery for colitis, such as IPAA, can also lead to infertility in females due to adhesions or tubal occlusion, with studies reporting approximately a threefold increased risk compared to non-surgical UC patients.^[139] Other risks encompass anastomotic leaks, pouch failure requiring excision in 5-10% of cases, and small bowel obstruction. Postoperative outcomes in UC patients undergoing IPAA demonstrate significant quality-of-life improvements, with most achieving good functional results and reduced disease-related symptoms, though bowel frequency and urgency may persist. Lifelong endoscopic surveillance of the pouch is recommended starting 1-2 years after IPAA to detect rare pouch neoplasia, which has a low cumulative incidence of about 0.5-3% at 20-25 years but is influenced by factors like prior dysplasia or primary sclerosing cholangitis. In Crohn's colitis, surgical recurrence rates remain high, with up to 50% requiring reoperation within 20 years, emphasizing the need for ongoing medical management postoperatively.

Supportive and Lifestyle Measures

Supportive and lifestyle measures play a crucial role in managing colitis by alleviating symptoms, preventing flares, and improving overall quality of life for patients with conditions such as ulcerative colitis (UC) and Crohn's disease (CD). These strategies emphasize patient empowerment through behavioral changes and environmental adjustments, complementing medical therapies without relying on pharmaceuticals. Evidence from clinical guidelines highlights their efficacy in reducing inflammation and supporting remission, particularly when tailored to individual triggers and disease activity.^[140] Dietary modifications are a cornerstone of supportive care, with recommendations varying by disease phase. During active flares, a low-residue diet—limiting high-fiber foods like nuts, seeds, beans, and raw vegetables—helps relieve abdominal pain and diarrhea by reducing bowel irritation and stool bulk.^[141] In remission, adopting a Mediterranean-style diet rich in fruits, vegetables, whole grains, lean proteins, and omega-3 fatty acids from fish and olive oil has shown promise in maintaining gut health and reducing inflammation, with studies indicating lower relapse rates compared to standard diets.^[142] Patients are advised to identify and avoid personal triggers, such as dairy products in those with lactose intolerance, which can exacerbate diarrhea and gas, though caffeine avoidance is less universally recommended and should be based on symptom tracking.^[143] These approaches prioritize nutrient-dense, anti-inflammatory foods while ensuring balanced intake to prevent malnutrition, a common concern in colitis.^[144] Hydration and nutritional support are essential to counteract dehydration from diarrhea and maintain electrolyte balance. Oral rehydration solutions, containing glucose and salts, are recommended to replace fluids lost during flares, with patients encouraged to consume 8-10 glasses of water daily alongside electrolyte-rich beverages.^[145] In pediatric CD, exclusive enteral nutrition—using liquid formulas as the sole source of nutrition for 6-8 weeks—induces remission in up to 80% of cases, promoting mucosal healing and growth without the side effects of corticosteroids.^[146] This therapy is particularly effective for mild-to-moderate disease, with guidelines endorsing it as a first-line option to control inflammation and support long-term nutritional status.^[147] Stress management techniques address the bidirectional link between psychological stress and colitis exacerbations, where heightened stress activates the hypothalamic-pituitary-adrenal (HPA) axis, potentially increasing gut inflammation.^[148] Practices such as mindfulness meditation, yoga, and cognitive behavioral therapy (CBT) have demonstrated benefits in reducing flare frequency and symptom severity, with randomized trials showing improved quality of life and lower disease activity scores after 8-12 weeks of intervention.^[149] These mind-body approaches help modulate stress responses, fostering resilience and better coping mechanisms for chronic illness management.^[150] Vaccination prophylaxis is vital for colitis patients, especially those on immunosuppressive therapies, to prevent opportunistic infections that could trigger flares. All adults with inflammatory bowel disease (IBD) should receive inactivated vaccines, including annual influenza (high-dose or adjuvanted preferred for immunosuppressed), tetanus-diphtheria-pertussis (Tdap) every 10 years, and pneumococcal vaccines (e.g., PCV20 or PCV15 followed by PPSV23 as of 2025 guidelines), with evidence showing reduced infection risk without compromising disease control.^[151] Live vaccines like measles-mumps-rubella (MMR) are contraindicated during immunosuppression but recommended prior to therapy initiation for non-immune patients.^[152] Routine screening and administration at initial diagnosis optimize protection.^[151] Patient education empowers individuals to recognize early flare signs, such as increased bowel frequency or abdominal pain, enabling timely intervention and better adherence to treatment plans. Structured programs focusing on symptom monitoring and self-management have been shown to decrease hospitalization rates by up to 30%.^[153] For CD patients, smoking cessation is a critical component, as continued smoking doubles the risk of flares and surgical needs, while quitting yields remission rates comparable to biologic therapies and reduces disease progression.^[154] Education combined with counseling achieves cessation rates of 20-40% in motivated patients, underscoring the need for tailored support.^[155]

Prognosis

Long-Term Outcomes

The prognosis of colitis varies significantly by type and severity. For infectious colitis, most cases are self-limited and resolve with supportive care or targeted antimicrobial therapy, with excellent outcomes unless complications like toxic megacolon occur.^[1] Ischemic colitis often improves within days with conservative management in mild cases, though severe forms requiring surgery carry higher mortality (up to 20% in complicated cases).^[1] Microscopic colitis typically responds well to treatments like budesonide, leading to symptom control and good quality of life in the majority of patients.^[1] In inflammatory bowel diseases (IBD) such as ulcerative colitis (UC) and Crohn's disease, outcomes depend on disease extent and response to therapy. Patients with mild UC typically experience near-normal life expectancy, with overall mortality rates below 1% and standardized mortality ratios close to 1 compared to the general population.^[156] In contrast, severe IBD is associated with a reduction of 5-8 years in life expectancy due to complications such as infections, colorectal cancer, and surgical interventions like colectomy.^[157] These outcomes highlight the importance of early disease control to mitigate long-term risks. Remission patterns in colitis vary by treatment and disease severity, with biologic therapies enabling 50-70% of patients with moderate-to-severe UC to achieve clinical remission during induction phases in clinical trials.^[158] Maintenance rates with biologics or small molecules sustain remission in over 40% of cases beyond one year, though relapse remains common without ongoing therapy.^[159] Approximately 10% of UC patients require colectomy within 10 years of diagnosis, a rate that has decreased over recent decades due to advances in medical management.^[160] Quality of life in colitis patients is significantly impacted, particularly in domains of work and education, where 20-30% report disability or reduced productivity attributable to disease flares and fatigue.^[161] Extraintestinal manifestations, such as peripheral arthritis, affect about 25% of IBD patients and contribute to ongoing functional limitations even in remission.^[162] Long-term monitoring is essential for detecting dysplasia and colorectal cancer risk, with guidelines recommending surveillance colonoscopies starting 8-10 years after diagnosis and performed annually or biennially for high-risk patients involving extensive colitis or family history.^[32] Post-2020 data indicate heightened mental health comorbidities in IBD patients, with approximately 30-35% experiencing anxiety or depression exacerbated by pandemic-related stressors and disruptions in care.^[163] In pediatric colitis, prognosis is generally favorable with treatment, though the disease is chronic in IBD forms; however, in some milder forms such as eosinophilic colitis, children may outgrow symptoms or develop tolerance to triggers after several years.^[1]

Prevention Strategies

Primary prevention strategies for colitis, particularly inflammatory bowel disease (IBD) forms like ulcerative colitis and Crohn's disease, focus on early-life and lifestyle interventions to mitigate risk factors. Breastfeeding in infancy has been associated with a reduced risk of developing IBD, with a meta-analysis indicating a pooled odds ratio of 0.69 for lower incidence rates.^[164] A balanced diet that promotes gut microbiota diversity, such as one rich in fiber and fermented foods, supports intestinal health and may help prevent dysbiosis linked to colitis onset.^[165] For ischemic colitis, prevention emphasizes cardiovascular health management, including control of hypertension, atherosclerosis, and avoidance of vasoactive drugs in at-risk older adults.^[1] To avoid infectious colitis, such as Clostridioides difficile-associated disease, rigorous hand hygiene with soap and water is essential, as it effectively removes spores that alcohol-based sanitizers cannot.^[166] Consuming safe water and food, along with practicing antibiotic stewardship to limit unnecessary prescriptions, further reduces the risk of C. difficile infection by preserving the gut microbiome.^[167] Secondary prevention targets individuals at elevated risk, including early screening for first-degree relatives of those with IBD, as familial history significantly increases disease likelihood and warrants proactive monitoring.^[168] Vaccination against hepatitis B is recommended for colitis patients, given the potential for impaired immune responses and links between liver complications and IBD progression, to prevent superimposed infections.^[169] For preventing flares in established colitis, adherence to prescribed maintenance medications is crucial to sustain remission and avoid exacerbations.^[170] Trigger avoidance, such as limiting nonsteroidal anti-inflammatory drugs (NSAIDs) like ibuprofen, helps prevent mucosal inflammation and flare-ups in IBD.^[171] In select cases, such as post-surgical pouchitis in ulcerative colitis patients, high-dose probiotics like VSL#3 have demonstrated efficacy in maintaining remission and preventing onset.^[172] Public health efforts in 2025 emphasize early intervention for at-risk populations through updated guidelines, promoting lifestyle modifications and timely screening to intercept IBD progression before symptoms manifest.^[173]

Research and Future Directions

Current Studies

Recent clinical trials investigating the microbiome's role in ulcerative colitis (UC) have focused on fecal microbiota transplantation (FMT) as a therapeutic intervention. Phase III randomized controlled trials have demonstrated FMT efficacy, with clinical remission rates ranging from 30% to 40% in active treatment arms compared to placebo groups, particularly when using multi-donor preparations delivered via colonoscopy.^[174] These trials, involving hundreds of participants, highlight sustained endoscopic improvements lasting up to 48 weeks in responders, underscoring FMT's potential to modulate dysbiotic microbial communities.^[175] Complementary studies on post-antibiotic dysbiosis in colitis models and patients reveal prolonged microbial imbalances, with reduced alpha diversity persisting for months after broad-spectrum antibiotic exposure, exacerbating inflammation in susceptible individuals.^[176] For instance, simulations of infection treatment with meropenem showed incomplete microbiota recovery even 30 days post-therapy, linking this dysbiosis to heightened colitis risk.^[177] Long-term follow-up genome-wide association studies (GWAS) have advanced the genetic understanding of colitis, identifying approximately 20 new susceptibility loci since 2020 through multi-ancestry analyses that integrate over 240 total IBD-associated variants, with about two-thirds shared between UC and Crohn's disease.^[178] These efforts, building on earlier cohorts, have pinpointed high-confidence risk genes like those involved in immune regulation, enhancing predictive models for disease onset. Recent AI analyses (as of November 2025) have further elucidated mechanisms of NOD2 mutations in Crohn's disease, potentially guiding targeted therapies.^[179]^[180] Epidemiological research incorporating COVID-19 cohorts has examined the impact of SARS-CoV-2 infection on IBD patients, with systematic reviews finding no significant increase in flare rates, though vigilant monitoring remains recommended during viral outbreaks.^[181] In pediatric IBD research, comparative studies have evaluated growth outcomes between early initiation of biologic therapies and conventional step-up approaches. Early biologic use, such as anti-TNF agents within the first year of diagnosis, has been associated with improved linear growth velocity and reduced risk of stunting, achieving higher rates of sustained remission and mucosal healing compared to delayed escalation from immunomodulators.^[182] Real-world data from cohorts indicate that children on early biologics experience fewer hospitalizations and better nutritional status, with reduced relapse rates and improved growth outcomes compared to step-up therapy.^[183] These findings, drawn from observational registries, suggest that proactive biologic intervention mitigates long-term developmental impacts in young patients.^[184] Global disparities in colitis incidence are evident from ongoing epidemiological studies in Asia, where rates have risen sharply due to urbanization and dietary shifts. Data from national registries, including those in China, report an incidence increase from approximately 1-2 per 100,000 in 2010 to over 5 per 100,000 by 2025 in urban centers, with prevalence doubling in East Asian populations between 1990 and 2021.^[185] For example, cohort analyses from 2022-2025 highlight a 4-5 fold surge in pediatric and adult cases in regions like Shanghai and Seoul, attributing this to environmental factors and improved diagnostics.^[186] These trends underscore the shifting global burden, with Asia now accounting for nearly half of new IBD cases annually.^[187] Large-scale registries such as the European Crohn's and Colitis Organisation (ECCO) and Groupe d'Etude Thérapeutique des Affections Inflammatoires du Tube Digestif (GETAID) databases continue to track real-world outcomes in colitis, providing insights into treatment persistence and complication rates. ECCO's multinational cohorts, encompassing over 10,000 patients, report steroid-free remission in 40-50% of UC cases on advanced therapies after one year, with lower hospitalization rates in early interveners.^[188] GETAID studies from France similarly demonstrate that real-world biologic efficacy aligns with trial data, with persistence rates exceeding 70% at 12 months and reduced surgery needs in monitored populations.^[189] These databases facilitate longitudinal analysis, revealing disparities in access and outcomes across demographics as of 2025.^[190]

Emerging Therapies

Recent advances in biologics for colitis include the development of IL-23 inhibitors, such as risankizumab, which is undergoing Phase III trials for ulcerative colitis (UC). In these trials, risankizumab has demonstrated endoscopic improvement in 36.5% of patients compared to 12.1% with placebo at week 12, highlighting its potential for achieving mucosal healing in moderate-to-severe UC.^[191] Additionally, extensions of anti-integrin therapies like vedolizumab involve subcutaneous formulations that maintain efficacy as maintenance therapy, with clinical remission rates sustained in responders transitioning from intravenous administration.^[192] Stem cell therapy represents another promising investigational approach, particularly mesenchymal stem cells (MSCs) for fistulizing Crohn's disease. Phase II studies have shown fistula closure rates of approximately 58% following MSC treatment, offering a targeted option for refractory perianal fistulas unresponsive to conventional therapies.^[193] Gene editing technologies, such as CRISPR, are in preclinical stages for addressing genetic factors in colitis, including trials targeting NOD2 mutations associated with Crohn's disease. These efforts, reported in 2024-2025 studies, aim to correct innate immune defects to prevent disease onset or progression in genetically susceptible individuals, though clinical translation remains early.^[194] Dietary interventions are also under investigation, with trials of the specific carbohydrate diet (SCD) in pediatric inflammatory bowel disease (IBD) showing symptomatic remission rates of 42.4% at 12 weeks, comparable to standard Mediterranean diets and suggesting a role in induction therapy.^[195] Nanotechnology offers novel targeted delivery systems for colitis treatment, exemplified by nanoparticle-encapsulated 5-aminosalicylic acid (5-ASA) in early Phase I evaluations. These formulations enable colon-specific release, enhancing drug efficacy at lower doses and reducing systemic side effects in UC models.^[196]

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Entamoeba histolytica is a protozoan that causes intestinal amebiasis as well as extra-intestinal manifestations.
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History and physical examination In patients with severe colitis, abdominal tenderness—along with fever and peritoneal signs—is an alarm signal for a poorer ...
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Follow a low residue diet to relieve abdominal pain and diarrhea. If you have strictures, it is especially important to avoid nuts, seeds, beans and kernels.
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