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Proctitis

Proctitis is an inflammatory condition affecting the lining of the rectum, the final section of the large intestine, which can manifest as either an acute or chronic disorder. It commonly presents with symptoms such as rectal pain, bleeding during bowel movements, diarrhea, a frequent urge to defecate (tenesmus), and discharge of mucus or pus from the rectum. Proctitis may arise from various underlying causes, including inflammatory bowel disease (IBD) such as ulcerative colitis and Crohn's disease (a common cause, affecting about 30% of people with IBD), sexually transmitted infections such as gonorrhea or herpes, gastrointestinal infections like Clostridioides difficile, radiation therapy for pelvic cancers, or surgical diversion of the fecal stream leading to diversion proctitis. Less commonly, it can stem from food protein allergies in infants, eosinophilic disorders, or idiopathic factors, with about 10% of idiopathic cases potentially progressing to ulcerative colitis. While not typically life-threatening, untreated proctitis can lead to complications such as anemia from chronic bleeding, ulcers, or fistulas, necessitating prompt diagnosis through physical examination, stool tests, and endoscopy procedures like sigmoidoscopy. Treatment is tailored to the etiology and may involve antibiotics or antivirals for infections, anti-inflammatory medications or steroids for IBD-related cases, or endoscopic interventions for radiation-induced proctitis, with most acute episodes resolving within 4 to 8 weeks under appropriate management.

Overview

Definition and classification

Proctitis is defined as the inflammation of the rectal mucosa distal to the rectosigmoid junction, limited to within 18 cm of the anal verge. This precise anatomical boundary distinguishes proctitis from more extensive forms of , focusing solely on the distal . Proctitis is classified by duration into acute and chronic forms. Acute proctitis represents short-term inflammation, typically resolving within weeks following treatment or resolution of the underlying trigger. In contrast, chronic proctitis is persistent or recurrent, enduring for months or years and often requiring long-term management. Classification by etiology encompasses several broad categories: infectious proctitis, caused by pathogens such as , viruses, or parasites; inflammatory proctitis, exemplified by involvement in inflammatory bowel diseases like ; radiation-induced proctitis, resulting from therapeutic radiation exposure to the pelvic region; ischemic proctitis, due to compromised blood supply to the rectal tissue; and idiopathic proctitis, where no specific cause is identified, often aligning with autoimmune or unexplained mucosal . The condition was first described in in the , particularly in the context of by figures such as Samuel Wilks in 1859. Modern classifications of proctitis evolved significantly in the 20th century through advancements in endoscopic techniques, such as , which enabled direct visualization and of rectal mucosa to refine diagnostic categories.

Epidemiology

Proctitis, encompassing various etiologies such as infectious, inflammatory, and radiation-induced forms, exhibits variable incidence and prevalence depending on the underlying cause and population studied. Overall incidence in the general population is not uniformly reported due to its multifactorial nature, but ulcerative proctitis, a common manifestation in (IBD), accounts for 25-55% of initial () diagnoses, with incidence ranging from 6.3 to 24.3 per 100,000 person-years globally, higher in and . Chronic proctitis affects approximately 20-30% of patients at presentation, contributing to its prevalence within the estimated 5 million global cases as of 2023. In high-risk groups, infectious proctitis shows markedly elevated rates, particularly among men who have sex with men (MSM), where rectal prevalence reaches 10-15% and contributes to proctitis in up to 20-30% of symptomatic cases linked to sexually transmitted infections (STIs) like and . Radiation proctitis occurs in 2-20% of patients receiving pelvic for malignancies, with forms affecting 2-8% long-term, influenced by radiation dose and technique. These patterns underscore higher burdens in specific cohorts, such as cancer survivors and sexually active MSM. Demographically, proctitis is more prevalent in adults aged 30-50 years, with a male predominance driven by infectious causes; gonococcal proctitis is notably common in those under 25. Incidence is elevated in MSM due to STI transmission via receptive anal intercourse and in regions with high IBD prevalence, such as and , where UC rates exceed those in . Post-radiation cases are prominent among pelvic cancer patients, predominantly in older adults. COVID-19 disruptions in screening and care led to rebounds through 2022, particularly and among MSM, potentially increasing infectious proctitis cases in high-risk populations; however, provisional CDC data as of 2024 indicates declining rates.

Inflammatory mechanisms

Proctitis involves the disruption of the rectal mucosal barrier, which initiates a cascade of inflammatory responses. This damage to the epithelial lining exposes underlying tissues to luminal contents, triggering the release of pro-inflammatory cytokines such as interleukin-1 (IL-1) and tumor necrosis factor-alpha (TNF-α) from resident immune cells. These cytokines amplify the inflammatory signal by recruiting and activating immune cells, leading to infiltration of neutrophils and lymphocytes into the rectal mucosa. Neutrophils, in particular, contribute to further tissue injury through the release of and proteases. Vascular changes play a central role in the progression of rectal , with cytokines inducing increased endothelial permeability in the rectal vasculature. This results in plasma extravasation, causing mucosal and contributing to friability and ulceration. The heightened vascular response exacerbates local and nutrient deprivation, perpetuating the inflammatory environment. Neural involvement in proctitis arises from the of visceral afferent pathways due to inflammatory mediators. of protease-activated receptors, particularly PAR-2, on enteric neurons enhances visceral , leading to sensations of tenesmus and urgency through amplified nociceptive signaling. The inflammatory process in proctitis typically progresses from acute epithelial damage to changes if unresolved, with persistent immune driving and extracellular matrix deposition, culminating in . Histologically, this is characterized by features such as crypt abscesses, formed by accumulation within glandular crypts, indicating active mucosal . These mechanisms underpin the in conditions like , where proctitis manifests as a localized form.

Cause-specific processes

In infectious proctitis, pathogens such as and directly invade the rectal mucosa, disrupting the epithelial barrier and triggering an acute inflammatory cascade that amplifies the general release observed in proctitis. Bacterial toxins produced by invaders like erode the mucosal surface, resulting in loss of vascular pattern, , and , which facilitates further microbial penetration and tissue damage. This invasion elicits a rapid neutrophil-dominated response, characterized by polymorphonuclear leukocytes infiltrating the site, leading to purulent and visible on or gram-stained smears of anorectal secretions. Diversion proctitis occurs after surgical diversion of the fecal stream, such as in or procedures, leading to a deficiency of (SCFAs) that normally nourish rectal epithelial cells. This nutrient deprivation impairs mucosal metabolism, promotes of colonocytes, and triggers chronic inflammation characterized by , mucosal friability, and ulceration, often without systemic symptoms. Radiation-induced proctitis arises from ionizing radiation's progressive injury to vascular during pelvic radiotherapy, altering inflammatory pathways through delayed vascular compromise rather than immediate or . This damage manifests 6-18 months post-exposure as obliterative , promoting , , and telangiectasias—fragile, dilated submucosal vessels that contribute to chronic and ischemia. The resulting hypoperfusion fosters tissue and mucosal , exacerbating ischemic changes in the rectal wall without the acute surge seen in infectious forms. In (IBD)-related proctitis, particularly limited to the , autoimmune dysregulation drives T-cell mediated inflammation targeting the mucosal layer, distinct from the vascular focus in radiation cases. Dysfunctional + and + T cells, influenced by genetic factors and microbial triggers, infiltrate the and attack rectal crypts, causing cryptitis, abscess formation, and superficial ulceration through proinflammatory cytokines like TNF and IFNγ. Chronic cycles of this T-cell driven damage lead to mucosal regeneration in isolated areas amid widespread erosion, forming pseudopolyps—polypoid islands of edematous, inflamed tissue that do not involve deeper layers as in . Ischemic proctitis develops from acute hypoperfusion of the rectal vasculature, often due to vascular or systemic , initiating through oxygen deprivation in a manner unrelated to immune dysregulation. This leads to mucosal , hemorrhage, and withering of crypts, as evidenced by dusky, necrotic appearances on extending proximally from the . Upon reperfusion, secondary injury amplifies via , recruiting neutrophils and worsening tissue damage in the rectal wall, though this process is typically self-limited if blood flow is restored promptly.

Etiology

Infectious causes

Infectious proctitis is primarily caused by sexually transmitted infections (STIs) and certain non-sexual microbial pathogens that invade the rectal mucosa. Among STIs, (gonorrhea) is a leading agent, often presenting as purulent rectal discharge and tenesmus following anal receptive intercourse. , particularly (LGV) serovars, causes ulcerative proctitis with in the rectal submucosa, predominantly affecting men who have sex with men (MSM). (syphilis) leads to chancres or in the anorectal region, while (HSV), typically HSV-2, results in painful vesicular lesions and ulceration. These STIs collectively account for the majority of acute proctitis cases in MSM, with gonorrhea and chlamydia being the most frequently identified. Non-sexual infections also contribute, particularly in vulnerable populations. Clostridium difficile (now ) causes pseudomembranous proctitis or following antibiotic disruption of the gut flora, with symptoms including bloody diarrhea and abdominal pain. (CMV) proctitis occurs mainly in immunocompromised individuals, such as those with advanced or post-transplant , manifesting as severe ulceration and bleeding due to viral replication in endothelial cells. Parasitic infections like (amebiasis) are seen in travelers to endemic areas, leading to flask-shaped ulcers in the rectal mucosa via invasion. Transmission of infectious proctitis typically occurs through anal intercourse for STIs, facilitating direct mucosal contact with infected secretions, or via the fecal-oral route for enteric pathogens and parasites, often linked to contaminated food or water. Key risk factors include multiple sexual partners, unprotected receptive , and ; for instance, infection substantially elevates the incidence of anorectal STIs due to impaired mucosal immunity. As of 2025, emerging concerns include the rise of antimicrobial-resistant N. gonorrhoeae strains, with showing decreased susceptibility to and , complicating of gonococcal proctitis and necessitating dual therapy or alternative regimens.

Noninfectious causes

Noninfectious causes of proctitis encompass a range of sterile inflammatory processes driven by autoimmune, ischemic, iatrogenic, or chemical mechanisms, distinct from microbial origins. These etiologies often result in chronic rectal mucosal inflammation, leading to symptoms such as and tenesmus, and are commonly associated with systemic conditions or therapeutic interventions. Allergic, , and idiopathic forms also contribute, particularly in pediatric or unexplained cases. Allergic proctitis, often food protein-induced allergic proctocolitis (FPIAP) in infants, is triggered by allergens like cow's milk or soy proteins passed through or formula, causing and infiltration; it typically resolves with avoidance and affects otherwise healthy infants. proctitis involves immune-mediated accumulation in the rectal mucosa, potentially linked to allergies or idiopathic factors, and is rare in adults but can mimic IBD. Idiopathic proctitis refers to cases without identifiable cause, with approximately 10% potentially progressing to . Inflammatory bowel disease (IBD) represents a primary noninfectious cause, with ulcerative proctitis serving as a limited form of (UC) that affects the exclusively or predominantly. Ulcerative proctitis accounts for 31-50% of UC cases at initial diagnosis, and up to 30% of all UC presentations begin as proctitis, potentially progressing to more extensive colonic involvement in 10-46% of cases over time. , another IBD variant, can involve the through transmural , often manifesting with perianal complications such as fistulae or abscesses, though rectal involvement is less common than in UC. Risk factors for IBD-related proctitis include , such as higher incidence in individuals of Jewish descent (3-5 times greater risk for UC), and younger age at onset, particularly in pediatric females for UC. Radiation proctitis arises as a complication of pelvic , commonly used in treating , , or rectal cancers, due to direct mucosal damage from leading to , , and . It occurs in 2-20% of patients receiving such therapy, with incidence varying based on dose (higher risk above 8 ) and delivery technique. The condition presents in two phases: acute proctitis, which develops during or shortly after treatment and is often self-limited within , and chronic proctitis, emerging 8-13 months post-therapy or even years later, characterized by persistent vascular changes and ulceration. Prior pelvic irradiation or concurrent increases susceptibility. Other noninfectious etiologies include ischemic proctitis, resulting from compromised rectal blood supply due to , , or procedural factors like aortoiliac , particularly in patients with vascular risk factors such as , , or prior abdominal operations. Diversion proctitis occurs in the defunctioned rectal segment following fecal diversion procedures (e.g., ), typically 3-36 months postoperatively, due to short-chain deficiency from lack of fecal stream; it affects fewer than 50% symptomatically and often resolves upon stoma reversal. Chemical proctitis stems from mucosal irritation by substances like enemas containing or other irritants, while autoimmune conditions such as can trigger proctitis through associated . General risk factors across these causes include prior pelvic , , and exposure to irritants, without any infectious transmission risk.

Clinical features

Symptoms

Proctitis commonly presents with , often described as tenesmus, which is a persistent sensation of needing to defecate despite an empty . Patients frequently report urgency to defecate, leading to frequent passages of small-volume stools that may contain blood, , or . is another hallmark symptom, sometimes alternating with , and can be noticeable on underwear or during wiping. In acute proctitis, symptoms develop suddenly and intensely, often including severe cramping and fever, particularly when caused by , with episodes lasting from days to weeks. Chronic proctitis, by contrast, features persistent or relapsing discomfort, such as ongoing tenesmus and , and may be accompanied by weight loss if associated with like ulcerative proctitis. Symptom severity can vary by ; for instance, sexually transmitted -related proctitis often involves burning pain during along with purulent discharge, while radiation-induced proctitis may manifest primarily as painless . These symptoms significantly impair , disrupting daily activities such as work, travel, and social interactions due to unpredictable urgency and the need for frequent bathroom access. Nocturnal urgency can lead to sleep disturbances, exacerbating and emotional distress in affected individuals.

Physical examination findings

Physical examination of patients with proctitis begins with visual inspection of the perianal region, which may reveal , fissures, external discharge, abscesses, ulcers, or other lesions such as chancres or in sexually transmitted infection-related cases. Perianal skin changes, including signs of fecal staining or soiling, can also be noted. The digital rectal examination typically elicits rectal tenderness, sphincter spasm, or the presence of masses, and may produce guaiac-positive stool indicating occult blood. This exam can be painful and may uncover purulent or bloody discharge. Endoscopic views, obtained via or , commonly demonstrate mucosal , friability, superficial erosions, ulcers, vesicles, or mucopurulent overlying the rectal mucosa, often limited to the distal 10-12 cm. In specific etiologies, such as infection, discrete vesicles or ulcers may appear, while Clostridioides difficile-associated proctitis can show pseudomembranous plaques on the mucosa. In severe acute cases, systemic signs including fever, , , or may be evident on general examination.

Diagnosis

Clinical evaluation

Clinical evaluation of proctitis begins with a detailed patient to identify potential etiologies and guide the . The onset of symptoms is crucial, with acute proctitis often linked to infectious causes such as sexually transmitted infections (STIs), while insidious onset may suggest noninfectious etiologies like (IBD) or . A thorough sexual is essential, particularly inquiring about receptive anal intercourse, as this increases risk for STIs including gonorrhea, chlamydia, herpes simplex virus, and syphilis, especially in men who have sex with men (MSM). of radiation therapy to the pelvis, typically for malignancies like prostate or cervical cancer, should be elicited, as symptoms may emerge 8 to 13 months post-exposure. Family of IBD, such as ulcerative colitis, is relevant, with individuals of Jewish descent facing a 3- to 5-fold higher risk. Recent travel to endemic areas can point to enteric pathogens like Salmonella or Shigella, while medication use, including enemas or antibiotics, may contribute to noninfectious or opportunistic causes. Differential diagnosis relies on historical patterns to distinguish proctitis from other anorectal conditions. For instance, bright red without systemic symptoms may suggest , whereas chronic or progressive bleeding with changes in bowel habits raises concern for . is considered if symptoms include left lower quadrant pain and fever, often in older patients with a history of , contrasting with the more isolated rectal involvement in proctitis. Red flags in the history warrant urgent evaluation to rule out malignancy or severe IBD. Unexplained , severe (e.g., ), or nocturnal symptoms such as or indicate possible or advanced inflammatory processes rather than benign causes. During the initial consultation, basic is provided to explain proctitis as of the rectal lining, often causing symptoms like or discomfort, and to emphasize the importance of safe sexual practices, such as use, to prevent infectious .

Diagnostic tests

Diagnosis of proctitis typically involves a combination of laboratory tests, endoscopic procedures, and imaging studies to confirm the presence of rectal and identify underlying etiologies such as or (IBD). These modalities help differentiate proctitis from other causes of rectal symptoms and guide targeted management. Stool studies are essential for evaluating infectious causes, particularly in patients with risk factors for sexually transmitted infections (STIs) or enteric pathogens. Routine stool culture can detect bacterial agents like Shigella or Campylobacter, which may present with proctitis-like symptoms. Polymerase chain reaction (PCR) assays, including multiplex STI panels, are recommended for detecting pathogens such as Chlamydia trachomatis, Neisseria gonorrhoeae, and herpes simplex virus from rectal swabs, offering higher sensitivity than culture for these organisms. Additionally, fecal calprotectin testing serves as a non-invasive marker of intestinal inflammation, with elevated levels (>50 μg/g) supporting diagnoses like IBD-associated proctitis by indicating neutrophil activity in the mucosa. Endoscopic evaluation is the cornerstone for direct visualization and confirmation of proctitis. or is often the first-line procedure, allowing assessment of the distal for , , ulceration, or , which are characteristic findings. Biopsies obtained during these procedures enable histopathological analysis; for instance, viral inclusions suggestive of (CMV) infection, such as enlarged cells with intranuclear inclusions, can be identified via or on tissue samples, particularly in immunocompromised patients. may be pursued if reveals extensive involvement or to evaluate for proximal disease in suspected IBD. Imaging studies are generally reserved for assessing complications rather than initial diagnosis, as endoscopy provides more direct evidence. Computed tomography (CT) or (MRI) of the can detect abscesses, fistulas, or perirectal inflammation in cases of severe or radiation-induced proctitis. enema, once common, is now rarely used due to the superiority of endoscopy and risks of but may show rectal strictures or ulceration in settings. Serologic and blood tests aid in identifying systemic associations or risk factors. HIV testing is recommended for all patients with acute proctitis, especially men who have sex with men (MSM) or those with STI risks, as immunosuppression increases susceptibility to opportunistic infections like CMV proctitis. Inflammatory markers such as (CRP) and (ESR) help differentiate IBD-related proctitis from infectious causes, with elevated levels (>5 mg/L for CRP) indicating active and prompting further IBD workup.

Management

Treatment approaches

Treatment of proctitis is etiology-specific, aiming to resolve inflammation, eradicate underlying pathogens or triggers, and prevent recurrence, with strategies guided by major clinical organizations such as the American Gastroenterological Association (AGA) and the Centers for Disease Control and Prevention (CDC). For infectious causes, targeted antimicrobial therapy is essential. For sexually transmitted infections (STIs), particularly gonococcal proctitis, the CDC recommends a single intramuscular dose of 500 mg (or 1 g for patients weighing ≥150 kg), often combined with 100 mg orally twice daily for 7 days to cover potential chlamydial co-infection. For non-STI gastrointestinal infections such as those caused by , treatment follows standard guidelines for C. difficile infection, with oral 125 mg four times daily for 10 days or 200 mg twice daily for 10 days as first-line options. In cases of (HSV)-associated proctitis, oral acyclovir 400 mg three times daily for 7-10 days is the standard regimen to reduce viral replication and symptom duration. Partner notification and treatment are critical components of STI management to curb transmission, as emphasized in CDC guidelines. For proctitis associated with (IBD), particularly ulcerative proctitis, first-line therapy involves topical 5-aminosalicylate (5-ASA) agents such as mesalamine suppositories at a dose of 1 g daily, which the recommends for mild-to-moderate cases to induce and maintain remission by reducing mucosal . If patients are refractory to or intolerant of mesalamine, rectal corticosteroids like enemas (100 mg nightly for 2-4 weeks) provide effective anti-inflammatory relief, though long-term use is avoided due to risks of systemic absorption. In refractory or severe IBD-related proctitis, biologic agents such as anti-tumor necrosis factor (TNF) therapies (e.g., 5 mg/kg intravenously at weeks 0, 2, and 6) are indicated to target cytokine-driven , per guidelines for moderate-to-severe . For diversion proctitis resulting from surgical diversion of the fecal stream, the preferred treatment is restoration of bowel continuity when feasible. If diversion is permanent, short-chain fatty acid (SCFA) enemas (e.g., 60 mL of 5% SCFA solution twice daily) or topical 5-ASA enemas can help alleviate symptoms by supporting mucosal nutrition and reducing inflammation. Radiation-induced proctitis, often chronic and manifesting as telangiectasias or bleeding, requires interventions focused on hemostasis and tissue repair; topical enemas (2 g nightly for 4-6 weeks) form a protective barrier over ulcerated mucosa, alleviating symptoms in acute phases as supported by clinical reviews. For persistent chronic bleeding, hyperbaric oxygen therapy (90 minutes daily at 2.0-2.5 atmospheres for 30-40 sessions) promotes angiogenesis and healing, while endoscopic effectively ablates telangiectasias with low complication rates, as outlined in American Society of Colon and Rectal Surgeons (ASCRS) guidelines. Overall management follows and CDC recommendations, escalating to surgical options like proctectomy in cases unresponsive to medical therapy, such as severe IBD flares with risk. Supportive measures, including , complement these targeted approaches but are addressed separately.

Supportive care

Supportive care for proctitis focuses on symptom relief and preventing exacerbation through non-pharmacologic and general measures applicable to various etiologies. Dietary modifications play a key role in managing bowel habits and reducing irritation. For chronic cases, a high-fiber or supplements can help normalize and promote regular bowel movements, potentially alleviating discomfort over time. During acute flares, a low-residue —limiting high-fiber foods such as whole grains, nuts, seeds, raw fruits, and —is recommended to minimize bulk and frequency, thereby reducing rectal straining and inflammation. Additionally, avoiding potential irritants like , products, high-fat foods, and spicy foods can help prevent worsening of symptoms by decreasing gastrointestinal irritation. Pain management strategies emphasize gentle, localized relief to avoid further mucosal damage. Sitz baths, involving soaking the perianal area in warm water for 10-15 minutes several times daily, provide effective symptomatic relief from , itching, and . Topical anesthetics, such as 2% lidocaine applied rectally, can numb the affected area and reduce hyperactive local reflexes, offering rapid improvement in discomfort for conditions like ulcerative proctitis. Nonsteroidal drugs (NSAIDs) may be used cautiously for control, but only under medical supervision due to the risk of exacerbating mucosal . softeners, such as or magnesium-based agents, are routinely advised to facilitate easier passage, thereby decreasing associated with . Hygiene practices and preventive measures are essential to support and reduce risks, particularly in infectious cases. Maintaining gentle perianal with unscented wipes or water cleansing after bowel movements helps prevent secondary irritation, while avoiding anal intercourse during active inflammation promotes mucosal recovery. Barrier protection, such as consistent use during sexual activity, is recommended to prevent sexually transmitted infections that could cause or worsen proctitis. Regular monitoring ensures timely adjustment of care and detection of complications. Patients should track symptoms such as , , and bowel changes, scheduling follow-up visits with a healthcare provider every 4-6 weeks initially or as symptoms evolve to assess response and overall progress. Increased fluid intake is encouraged to support and stool softening, with prompt medical consultation advised if symptoms persist or worsen despite supportive measures.

Prognosis and complications

Prognosis

The prognosis of proctitis varies significantly depending on its etiology, with acute infectious forms generally carrying an excellent outlook when treated promptly. In cases of acute infectious proctitis, often caused by sexually transmitted pathogens such as or , symptoms typically resolve within 1-2 weeks following appropriate antibiotic therapy, achieving resolution rates exceeding 90% in treated patients. However, without concurrent treatment of sexual partners, the risk of recurrence or reinfection can approach 20-30%, underscoring the importance of partner notification and therapy to prevent repeated episodes. For chronic forms associated with (IBD), such as ulcerative proctitis, outcomes are more variable but generally favorable with maintenance therapy. Studies indicate that approximately 87% of patients achieve long-term clinical remission with therapies including 5-aminosalicylates and biologics, though up to 28% may require escalation to advanced immunomodulators due to disease. Colectomy rates remain low at around 1% in limited proctitis cases, significantly better than in extensive . In radiation-induced proctitis, acute symptoms often self-limit within months post-treatment, but chronic manifestations affect 5-20% of patients, with 50-70% achieving symptom control through supportive measures like enemas or endoscopic interventions. Advanced radiation techniques, such as intensity-modulated radiation therapy, have reduced the incidence in high-resource settings. Key factors influencing include early and the patient's immune status. Timely identification and enhance rates across etiologies by preventing progression to complications such as strictures. In immunocompromised individuals, such as those with or undergoing immunosuppression, outcomes worsen; for instance, cytomegalovirus (CMV)-associated proctitis carries a mortality of up to 26%, primarily due to systemic complications.

Complications

Untreated or severe proctitis can lead to several local complications due to prolonged of the rectal mucosa. These include the formation of strictures, which narrow the rectal and may cause obstructive symptoms; fistulas, abnormal connections between the rectum and adjacent structures such as the skin or ; abscesses, localized collections of that can cause and require ; and, in rare cases, of the rectal wall, potentially leading to . In patients with (IBD)-associated proctitis, such as , the incidence of colorectal strictures is approximately 3.6%, with a cumulative probability of 2.3% at 10 years. Perianal complications like abscesses and fistulas occur with a cumulative incidence of approximately 16% at 10 years in ulcerative colitis cases. Systemic complications may arise from chronic or acute effects of proctitis, particularly in vulnerable populations. Chronic rectal bleeding can result in , characterized by fatigue and reduced oxygen-carrying capacity due to blood loss. In immunocompromised individuals, infectious proctitis—such as that caused by —can progress to and , a life-threatening systemic with high morbidity. Toxic megacolon, involving acute dilation and toxicity of the colon, is a rare but severe complication more commonly associated with extensive but possible in proctosigmoiditis extending from proctitis, with risks heightened by delayed treatment. Long-standing ulcerative proctitis elevates the of colorectal cancer, though to a lesser extent than more extensive disease involvement. Patients with face approximately a 2-fold increased of compared to the general overall, but this is lower (about 1.7-fold) for those limited to proctitis. Modern surveillance strategies have further reduced this risk. Psychological complications are common in proctitis, stemming from the chronic nature of the condition and associated discomfort. Up to 30% of patients with IBD-related proctitis experience anxiety or , influenced by ongoing pain, , and disease uncertainty. Effective management strategies, such as therapies, can mitigate these risks by reducing inflammation and improving .