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Clinical manifestations and diagnosis of arthritis associated with inflammatory bowel disease and other gastrointestinal diseases

Clinical manifestations and diagnosis of arthritis associated with inflammatory bowel disease and other gastrointestinal diseases
Literature review current through: May 2024.
This topic last updated: Feb 22, 2024.

INTRODUCTION — Arthritis is a recognized manifestation of several intestinal illnesses and conditions, including inflammatory bowel disease (IBD), bacterial and parasitic infections, gluten-sensitive enteropathy (celiac disease), pseudomembranous colitis, and Whipple's disease.

The clinical manifestations and diagnosis of arthritis associated with IBD are presented here. Other disorders associated with both gastrointestinal disease and joint involvement are discussed here briefly, particularly in the context of the differential diagnosis of patients with these symptoms and findings. The treatment of IBD-associated arthritis; and the pathogenesis, other clinical manifestations, diagnosis, and management of inflammatory bowel disease, including Crohn disease and ulcerative colitis, are reviewed in detail separately:

(See "Treatment of arthritis associated with inflammatory bowel disease".)

(See "Immune and microbial mechanisms in the pathogenesis of inflammatory bowel disease".)

(See "Clinical manifestations, diagnosis, and prognosis of Crohn disease in adults".)

(See "Overview of the medical management of mild (low risk) Crohn disease in adults".)

(See "Clinical manifestations, diagnosis, and prognosis of ulcerative colitis in adults".)

(See "Management of the hospitalized adult patient with severe ulcerative colitis".)

PATHOGENESIS — There are several mechanisms that may underlie concurrent inflammation in the gut and the joint, but the precise pathogenic pathways remain to be defined. A disturbance of the gut barrier is postulated as the first and primary process for most of these proposed mechanisms. An alternative suggestion is that shared genetic or environmental factors predispose individuals to various organ manifestations of these inflammatory conditions, such as gut or joint involvement [1,2]. In addition, there may be a role for translocation of pathogens, as occurs in parasitic rheumatism, in which case effective antihelminthic treatment resolves the arthritis. There may also be circulating microbial elements, as proposed for post-Yersinia reactive arthritis, in which case the pathogen cannot be cultured from the synovial fluid.

Both human leukocyte antigen (HLA) and non-HLA genes have been associated with different articular phenotypes, with an increase in HLA-B27 in patients with spondylitis/sacroiliitis (see 'Laboratory findings' below). Molecular mimicry, in which an immune response to a gut-derived antigen cross-reacts with normal host protein, has been invoked to explain the role of human leukocyte antigen (HLA)-B27 in post-dysenteric reactive arthritis, but this mechanism has proved difficult to confirm definitively in either the clinical setting or in experimental models of colitis. Circulating immune complexes, initiated by an immune response to gut microbes, have been implicated in the arthritis following intestinal bypass surgery.

The concept of distinctive trafficking of gut-derived immunocompetent cells has been supported by studies of the integrins which direct the homing patterns of circulating lymphocytes. Cells such as mucosa-associated invariant T cells (MAITS) can be recovered from the synovial fluid of patients with ankylosing spondylitis [3]. Integrins, such as alpha4-beta7 integrin, are thought to have a role in mediating trafficking of lymphocytes to gut and joint tissues, and integrin-expressing T cells are expanded in the joints of patients with ankylosing spondylitis [4].

Observations showing that a majority of patients with SpA exhibit subclinical gut inflammation indicate an even closer link between IBD and SpA than that suggested by the association between clinically manifest IBD and SpA manifestations [5,6] (see 'Prevalence' below). A detailed overview of the pathogenesis of SpA is presented separately. (See "Pathogenesis of spondyloarthritis".)

PREVALENCE — Ulcerative colitis and regional enteritis (Crohn disease) are the most frequently encountered types of idiopathic inflammatory bowel disease (IBD) associated with arthritis or spondylitis. In a 2016 systematic review and meta-analysis of the prevalence of axial and peripheral spondyloarthritis (SpA) in patients with IBD, peripheral arthritis, sacroiliitis, and ankylosing spondylitis were present in 13, 10, and 3 percent, respectively, with considerable heterogeneity of the results between studies [7]. Arthritis in general has been estimated to occur in 6 to 46 percent of patients with IBD [8-13], with spondylitis described in 1 to 26 percent [8,10,14-17]. As an example, in one cohort, 129 out of 350 patients with IBD reported at least one feature of spondyloarthritis (SpA); review of these patients' medical records showed 18 with axial SpA, 20 with peripheral SpA, and 14 with other rheumatic disorders [18]. Estimates vary for each form of joint involvement. (See 'Spondylitis and sacroiliitis' below and 'Type I arthropathy' below and 'Type II arthropathy' below.)

Arthritis is somewhat more likely in patients with large bowel disease and in those patients with other extraenteric features, such as erythema nodosum, stomatitis, uveitis, and pyoderma gangrenosum. Among patients with Crohn disease, those with colonic involvement are at higher risk of developing synovitis than those with isolated small bowel disease. Males and females are affected equally. Both children and adults are at risk for this complication of IBD.

Subclinical gut inflammation, documented by endoscopy, has been described in up to two-thirds of patients with spondyloarthritis (SpA) [5], a finding that was confirmed in a subsequent prospective cohort of patients classified with SpA according to the Assessment in SpondyloArthritis international Society (ASAS) criteria [6].

CLINICAL MANIFESTATIONS — The arthritis associated with inflammatory bowel disease (IBD) may manifest primarily with axial involvement, with features of spondylitis and sacroiliitis; with peripheral joint involvement; or with both axial and peripheral features. The peripheral arthritis is most commonly acute and remitting (Type I) or, less commonly, a chronic pattern with intermittent, more severe flares (Type II) [19]. Enthesitis, and less often, dactylitis, may also occur. (See 'Spondylitis and sacroiliitis' below and 'Type I arthropathy' below and 'Type II arthropathy' below and 'Enthesitis and dactylitis' below.)

The joints may be affected by conditions other than the characteristic forms of immune-mediated inflammatory arthritis associated with IBD reviewed here. An important example is infectious arthritis, which can occur in association with IBD and should be included in the differential diagnosis of IBD-related arthritis (see 'Differential diagnosis' below). The risk of septic arthritis of the sacroiliac or peripheral joints, which is a rare complication of IBD, is increased in patients with fistulization or bacteremia. Polymicrobial septic arthritis, although rare, may occur as the first sign of altered gastrointestinal (GI) mucosal integrity in a patient with underlying IBD.

Adverse effects of treatment for IBD may also affect joints. For example, glucocorticoid treatment is associated with increased risk of osteonecrosis (avascular necrosis of bone) and increased infections. (See "Treatment of nontraumatic hip osteonecrosis (avascular necrosis of the femoral head) in adults".)

Peripheral arthritis — A distinction has historically been made between two patterns of peripheral arthritis in patients with IBD-associated joint disease; however, this distinction between type 1 and type 2 arthropathy is no longer commonly used by most rheumatologists. Both subsets are considered to be peripheral SpA, without further differentiation.

Type I arthropathy — In type I arthropathy, the peripheral arthritis tends to be acute and pauciarticular (affecting six or fewer joints) [19,20]. It typically occurs early in the course of the bowel disease, is self-limiting (90 percent under six months), and is nonerosive. The knee is the joint most commonly affected.

Type I arthropathy affects about 5 percent of patients with IBD. Joint symptoms may occur prior to the onset of IBD symptoms, and this form of arthritis is often associated with flares of the bowel disease.

Type II arthropathy — In Type II arthropathy, patients have polyarticular disease, with metacarpophalangeal (MCP) joints being particularly involved [19]. Other joints (knees, ankles, elbows, shoulders, wrists, proximal interphalangeal [PIP], and metatarsophalangeal [MTP] joints) are less often affected. Approximately one-half of the patients with IBD have migratory arthritis. Active synovitis may persist for months and may recur repeatedly but is nonerosive. Episodes of exacerbations and remissions may continue for years.

Type II arthropathy affects 3 to 4 percent of patients with IBD. Articular involvement rarely precedes the diagnosis of IBD, and joint symptoms typically do not parallel the activity of bowel disease [19].

Spondylitis and sacroiliitis — Patients with spondylitis and/or sacroiliitis usually report symptoms with characteristic features of inflammatory back pain, which should alert the gastroenterologist or internist to the possibility of SpA; patients typically complain of prolonged stiffness in the back and/or buttocks in the morning or after rest. Stiffness and associated pain are often relieved by exercise. Back symptoms are generally unrelated to the activity of the IBD.

Physical examination may reveal limited spinal flexion and reduced chest expansion in patients with longstanding SpA. Spondylitis may be the only articular manifestation; or it may occur in association with any form of peripheral arthritis [19]. (See 'Type I arthropathy' above.)

Patients with IBD can exhibit imaging findings of axial SpA more frequently than is evident from the history and examination (see 'Radiographic findings' below). Asymptomatic sacroiliitis, detected by radiography, occurred in 4 to 18 percent of patients with IBD in one study [17], and a positive magnetic resonance imaging (MRI) suggestive of sacroiliitis may be present but without accompanying back pain [21], although MRI should be performed for the assessment of back pain only when clinically indicated.

Enthesitis and dactylitis — Enthesitis, inflammation of the tendon insertion to the bone; and dactylitis, inflammation of the digit, often termed "sausage-finger" or "sausage-toe," may occur in patients with IBD-associated arthritis, as in other forms of SpA. Plantar fasciitis, causing heel pain, and Achilles tendinitis are the most common forms of enthesitis observed. Estimates of the prevalence of enthesitis in a 2016 systematic review ranged widely, from 1 to 54 percent; most of the 14 estimates from the eight studies reported were in the lower part of this range [7]. The prevalence of dactylitis, based upon 10 estimates from six studies, was less common than enthesitis, and ranged from zero (in two studies) to 6 percent. (See "Clinical manifestations and diagnosis of peripheral spondyloarthritis in adults", section on 'Musculoskeletal features' and "Clinical manifestations of axial spondyloarthritis (ankylosing spondylitis and nonradiographic axial spondyloarthritis) in adults", section on 'Enthesitis' and "Clinical manifestations of axial spondyloarthritis (ankylosing spondylitis and nonradiographic axial spondyloarthritis) in adults", section on 'Dactylitis' and "Clinical manifestations and diagnosis of psoriatic arthritis", section on 'Periarticular disease'.)

Laboratory findings — The peripheral white blood cell count, hematocrit, erythrocyte sedimentation rate (ESR), and serum C-reactive protein (CRP) concentration usually reflect the activity of the intestinal disease and are therefore of little help in assessing arthritis or spondylitis. However, in patients with quiescent gut disease but persistent inflammatory back pain, an elevated CRP may be considered as an objective parameter of inflammation in the axial skeleton and may help to select patients for more intensive treatment. Serum levels of rheumatoid factor are not elevated. The anemia of chronic disease may accompany chronic inflammation of gut or joint and should initiate a search for subclinical inflammation in either site. An unexplained iron-deficiency anemia in an SpA patient may be the first clue to incipient IBD.

HLA-B27 is found in 50 to 75 percent of the patients with IBD-associated axial arthritis [16]. An increase in frequency in HLA-B27, B35, and DRB1*0103 has been described in those with a type I peripheral arthritis; type II arthropathy has been associated with HLA-B44 (and not B27) [19]. While the reported HLA associations are of interest in regard to pathogenesis, HLA typing has no role in management of individual patients (see "Treatment of arthritis associated with inflammatory bowel disease"). In one study, sacroiliitis in patients with Crohn disease was strongly associated with polymorphisms in the CARD15 gene [22].

Synovial fluids have typically yielded from 5000 to 12,000 white blood cells per microliter, predominantly polymorphonuclear leukocytes [16,17]. Synovial membrane biopsies reveal nonspecific abnormalities, including: proliferation of synovial lining cells, increased vascularity, and infiltration of mononuclear cells [16,17].

Radiographic findings — In patients with axial disease, radiographs of the spine and pelvis may show typical findings of ankylosing spondylitis and sacroiliitis (see "Clinical manifestations of axial spondyloarthritis (ankylosing spondylitis and nonradiographic axial spondyloarthritis) in adults", section on 'Musculoskeletal imaging'). Plain film radiographs of the peripheral joints may demonstrate soft-tissue swelling, juxta-articular osteoporosis, mild periostitis, and effusions, usually without erosions or destruction. Radiographs frequently have abnormal findings, even in asymptomatic patients with IBD.

As an example, in one study, plain film and computed tomography (CT) were used to evaluate the sacroiliac joints of 65 patients with IBD, none of whom had symptoms of sacroiliitis; 18 percent had findings of sacroiliitis by plain film and 32 percent had had abnormal sacroiliac joints noted by CT scanning [23]. However, as mentioned above, the evaluation of the sacroiliac joints by conventional radiographs is difficult to standardize. In another study, using CT scans in 233 Crohn disease, 83 ulcerative colitis, and 108 control patients, sacroiliitis was seen in 15, 17, and 6 percent of patients respectively [24].

Given that interpretation of radiographs of the sacroiliac joints is particularly difficult, especially in the early stages of the disease [25], the mere presence of an abnormal radiograph—in the absence of suggestive clinical signs and symptoms—does not necessarily indicate a higher risk for the development of spondylitis. MRI can also reveal changes (image 1), but such changes may be seen without accompanying back pain; the prognostic significance of inflammation in the sacroiliac joint by MRI is uncertain and is an area of active investigation. Thus, an MRI is indicated when evaluating back pain in these patients but not in asymptomatic individuals.

DIAGNOSIS — Inflammatory bowel disease (IBD)-associated arthritis should be suspected whenever an IBD patient develops joint pain, stiffness, or symptoms of inflammatory back pain. There may be accompanying joint swelling when peripheral joints, such as the hands or feet, are involved.

In patients whose arthritis affects a single joint (monoarthritis), or a few joints (oligoarthritis), it is particularly important to perform a joint aspiration to exclude septic arthritis, the presentation of which may be atypical in patients with IBD who are receiving antiinflammatory or immunosuppressive treatment. (See "Monoarthritis in adults: Etiology and evaluation".)

In IBD patients suspected of IBD-associated arthritis/spondyloarthritis (SpA), based upon the presence of joint pain or swelling, we perform a thorough general history and physical examination, with particular attention to the presence of tender or swollen joints. (See "Clinical manifestations and diagnosis of peripheral spondyloarthritis in adults" and "Diagnosis and differential diagnosis of axial spondyloarthritis (ankylosing spondylitis and nonradiographic axial spondyloarthritis) in adults".)

Other extraenteric features such as erythema nodosum should be explored and documented. Laboratory tests should include a complete blood count (CBC; with attention to leukocytosis and anemia) as well as erythrocyte sedimentation rate (ESR) and C-reactive protein (CRP). Other potential causes of similar symptoms should be excluded clinically. (See 'Differential diagnosis' below.)

Conversely, in SpA patients who develop abdominal pain, diarrhea, or weight loss, or who manifest an unexplained anemia, a referral to a gastroenterologist is indicated. This should address the possibility of IBD but also of gastrointestinal (GI) blood loss, which may accompany chronic nonsteroidal antiinflammatory drug (NSAID) therapy for the SpA.

DIFFERENTIAL DIAGNOSIS — The differential diagnosis of joint pain in a patient with IBD is broad. It includes both conditions that cause joint disease or joint-related symptoms in patients with IBD and conditions that can result in joint symptoms and findings that are associated with other causes of gastrointestinal symptoms (see 'Joint disease and IBD' below and 'Other diseases with bowel and joint involvement' below):

Joint disease and IBD — IBD may be associated with several different joint conditions other than IBD-associated inflammatory arthritis. These include:

Infectious arthritis – Infectious arthritis, either gonococcal or nongonococcal bacterial infection, or opportunistic infections due to fungi or mycobacteria are considerations, as they can cause an inflammatory monoarthritis or oligoarthritis. New-onset monoarthritis in an IBD patient should be considered septic until proven otherwise (with negative synovial fluid cultures). (See "Septic arthritis in adults" and "Disseminated gonococcal infection".)

Erythema nodosum – Erythema nodosum, which can occur in patients with IBD, may be difficult to distinguish from arthritis when lesions occur in a periarticular location. Inability to aspirate synovial fluid from a frankly swollen and painful joint, particularly the ankle, is one clue to the diagnosis (see "Erythema nodosum"). Cellulitis in the setting of an IBD-related bacteremia can mimic erythema nodosum and should be considered if redness and induration of skin is present. (See "Cellulitis and skin abscess: Epidemiology, microbiology, clinical manifestations, and diagnosis".)

Osteonecrosis – Osteonecrosis (avascular necrosis of bone) typically affects the hip, knee, and shoulder. Affected patients with IBD typically have been treated with glucocorticoids and experience pain that is out of proportion to the degree of joint stress pain or swelling. (See "Treatment of nontraumatic hip osteonecrosis (avascular necrosis of the femoral head) in adults".)

Hypertrophic osteoarthropathy – Hypertrophic osteoarthropathy with clubbing develops with varying frequency in patients with IBD, being most common in Crohn disease [17,26]. (See "Malignancy and rheumatic disorders", section on 'Hypertrophic osteoarthropathy'.)

Other diseases with bowel and joint involvement — In addition to ulcerative colitis and Crohn disease, several other illnesses and conditions have intestinal involvement and arthritis as prominent clinical features. These include, but are not limited to: reactive arthritis (formerly termed Reiter's syndrome), Whipple's disease, Behçet syndrome, celiac disease, parasitic infestation, pseudomembranous colitis, and arthritis occurring as a result of intestinal bypass surgery. These disorders are also considerations in the differential diagnosis of patients with suspected inflammatory bowel disease (IBD) and arthritis.

Reactive arthritis — Reactive arthritis, which can present as postdysenteric arthritis, may occur after enteric infection due to Salmonella, Shigella, Yersinia, or Campylobacter species; the incidence following bacterial dysentery has been reported to range from 2 to 33 percent [14] (see "Reactive arthritis"). An increased risk of arthritis is associated with Yersinia infection and presence of the human leukocyte antigen (HLA)-B27 genotype [8]. HLA-B27 is associated with a more chronic course of reactive arthritis. Joint pain following diarrheal illness due to pathogenic Escherichia coli infection has also been reported, but the risk of joint symptoms following E. coli infection is not affected by HLA-B27 status [27]. (See "Pathogenic Escherichia coli associated with diarrhea".)

A careful history and examination, along with stool cultures or serologies in selected patients, can help to distinguish reactive arthritis from arthritis with IBD. In patients with reactive arthritis, joint symptoms usually develop within two to three weeks of developing diarrhea. The knee, ankle, wrist, and sacroiliac joints are commonly involved. Demonstration of a pathogenic organism by stool culture and/or finding a rise in antibody titers to the putative organism is helpful in confirming the clinical suspicion of reactive arthritis. (See "Reactive arthritis".)

Whipple's disease — Whipple's disease is due to infection with Tropheryma whipplei. Infection can be wide spread and may mimic IBD, with diarrhea, malabsorption, and weight loss. Systemic infection is often associated with joint manifestations. The knee, ankle, and wrist are frequently affected. Uncommonly patients may develop spondylitis and or sacroiliac joint involvement. In some patients, the articular symptoms develop prior to symptomatic enteric involvement. Small bowel biopsy is usually diagnostic. (See "Whipple's disease".)

Behçet syndrome — Behçet syndrome is characterized by oral and genital ulceration, iritis, and occasionally central nervous system involvement. In addition, oligoarticular, asymmetric arthralgia, and/or arthritis may develop in approximately 50 percent of patients. The knee, ankle, wrist, and elbow are common sites of involvement. Mucosal ulceration of the small bowel is a frequent manifestation and may cause nausea, diarrhea, abdominal pain, and distension. Behçet syndrome may be particularly difficult to distinguish from IBD. The presence of prominent mucosal involvement (oral or genital), as well as pathergy, sterile neutrophilic infiltration of sites of injury, may be helpful diagnostically. (See "Clinical manifestations and diagnosis of Behçet syndrome".)

Celiac disease — Gluten sensitive enteropathy or celiac disease may be associated with arthritis in some patients [15]. Articular involvement was peripheral in 10 percent, axial in 8 percent, and combined in 9 percent. The arthritis is typically nonerosive and can be either oligo- or polyarticular. Joint symptoms may precede gastrointestinal manifestations of the disease. Joint symptoms respond to a gluten-free diet. However, arthritis is rarely a major feature of celiac disease. Previous studies to identify gliadin/anti-gliadin immune complexes proved not to be definitive. (See "Epidemiology, pathogenesis, and clinical manifestations of celiac disease in adults" and "Management of celiac disease in adults".)

Intestinal bypass arthritis — Intestinal bypass surgery was developed for the treatment of obesity in 1952; 11 years later, arthritis was recognized as a postoperative complication [8,14]. Polyarthralgia and sometimes arthritis has been reported to occur weeks or years following surgery in 8 to 36 percent of patients [8,14]. Because of an unacceptably high incidence of adverse effects, including arthritis, the jejunocolic and jejunoileal bypass operations have been abandoned [28]. (See "Bariatric surgery for management of obesity: Indications and preoperative preparation".)

Joint pain and tenderness exceed objective findings in most cases of intestinal bypass associated arthropathy, but episodes with abrupt onset of pain and inflammation may also develop. Tenosynovitis is common, with episodes possibly lasting for days and even months, affecting the knee, wrist, ankle, shoulder, and finger joints. It may also be responsible for pain in the neck and back. The risk of developing this syndrome is higher after jejunocolic than after jejunoileal surgery and higher in females than males. There is often an associated urticarial, vesicular, pustular, macular, or nodular skin eruption (see "Neutrophilic dermatoses", section on 'Bowel-associated dermatosis-arthritis syndrome'). The Raynaud phenomenon has been reported in one-third of patients.

Plain radiographs generally show no joint damage, although marginal erosions may develop in patients with persistent arthritis. Synovial fluids generally have white blood cell counts of 500 to 27,000 per microL with predominantly polymorphonuclear leukocytes. Tests for rheumatoid factor, antinuclear antibodies, and HLA-B27 are usually negative. Immune complexes (and cryoglobulins) containing bacterial antigens (eg, E. coli, B. fragilis), their antibodies, immunoglobulin A (IgA) secretory component, and various complement components (eg, C3, C4, C5) [14] have been detected but have no clinical utility.

Nonsteroidal antiinflammatory drugs (NSAIDs) and glucocorticoids are effective in controlling joint symptoms, but more lasting results can be achieved by use of antibiotic therapy to decrease bacterial overgrowth (see "Small intestinal bacterial overgrowth: Management"). Other treatment options that have been tried in refractory arthritis once an infectious arthritis is excluded have included methotrexate and other immunosuppressive drugs (see "Neutrophilic dermatoses", section on 'Bowel-associated dermatosis-arthritis syndrome'). Severe and refractory arthritis may require reanastomosis of the bowel.

Parasitic arthritis — Parasitic infections of the gut have been associated with arthritis and other rheumatic disease syndromes [14,29-32]. These include Strongyloides stercoralis, Taenia saginata, Endolimax nana, Dracunculus medinensis, Giardia lamblia, and Necator Americanus. Parasites may or may not be isolated from the joints, so this may represent a variant form of infectious arthritis or reactive arthritis, respectively. (See "Reactive arthritis".)

Pseudomembranous colitis — Arthritis associated with Clostridioides difficile has been described following antibiotic therapy in case series. In a report of four patients, arthritis developed 9 to 35 days after the onset of diarrhea [14]. The large joints of the lower extremity are most often affected. C. difficile was isolated from two patients. Generally, appropriate antibiotic treatment of C. difficile will resolve accompanying arthritis. The impact of fecal transplants on this arthritis has not been studied. (See "Clostridioides difficile infection in adults: Clinical manifestations and diagnosis".)

SOCIETY GUIDELINE LINKS — Links to society and government-sponsored guidelines from selected countries and regions around the world are provided separately. (See "Society guideline links: Spondyloarthritis".)

INFORMATION FOR PATIENTS — UpToDate offers two types of patient education materials, "The Basics" and "Beyond the Basics." The Basics patient education pieces are written in plain language, at the 5th to 6th grade reading level, and they answer the four or five key questions a patient might have about a given condition. These articles are best for patients who want a general overview and who prefer short, easy-to-read materials. Beyond the Basics patient education pieces are longer, more sophisticated, and more detailed. These articles are written at the 10th to 12th grade reading level and are best for patients who want in-depth information and are comfortable with some medical jargon.

Here are the patient education articles that are relevant to this topic. We encourage you to print or e-mail these topics to your patients. (You can also locate patient education articles on a variety of subjects by searching on "patient info" and the keyword(s) of interest.)

Basics topic (see "Patient education: Crohn disease in adults (The Basics)" and "Patient education: Ulcerative colitis in adults (The Basics)")

Beyond the Basics topic (see "Patient education: Crohn disease (Beyond the Basics)" and "Patient education: Ulcerative colitis (Beyond the Basics)")

SUMMARY AND RECOMMENDATIONS

Clinical manifestations – Arthritis, including peripheral arthritis, spondylitis, or sacroiliitis, occurs in a significant minority of patients with inflammatory bowel disease (IBD), including both ulcerative colitis and regional enteritis (Crohn disease); it is more likely in patients with large bowel disease and in those patients with gastrointestinal complications and other extraintestinal involvement. Enthesitis may occasionally occur, and dactylitis may infrequently be present. (See 'Prevalence' above and 'Clinical manifestations' above.)

Types of arthropathy – Type I peripheral arthritis in IBD may be acute, remitting, pauciarticular, and occur early in disease. It commonly involves the knee and is usually nondeforming. Type II peripheral arthritis may be more chronic with frequent relapses; it is frequently polyarticular and involves the metacarpophalangeal (MCP) joints. (See 'Clinical manifestations' above and 'Type I arthropathy' above and 'Type II arthropathy' above.)

Spondylitis and sacroiliitis – Spondylitis more frequently affects men with IBD. Typical symptoms are characteristic of inflammatory back pain, including prolonged stiffness and pain in the back and/or buttocks in the morning or after rest, which is often relieved by exercise. Back symptoms are unrelated to those of the gastrointestinal disease. Limited spinal flexion and reduced chest expansion may occur. Spondylitis may be the only articular manifestation or it may occur in association with type I peripheral arthropathy. (See 'Spondylitis and sacroiliitis' above.)

Laboratory findings – Acute phase reactants usually reflect the activity of the intestinal disease and are not useful in assessing peripheral arthritis or spondylitis; however, C-reactive protein (CRP) elevations may be an objective marker of inflammation in patients with axial arthritis and quiescent gut disease. Human leukocyte antigen B27 (HLA-B27) is found in 50 to 75 percent of the patients with axial arthritis and may be increased in type I peripheral arthritis, but HLA typing has no role in management of individual patients. Synovial fluids are moderately inflammatory. (See 'Laboratory findings' above.)

Radiographic findings – Radiographs of the spine and pelvis may show typical findings of ankylosing spondylitis and sacroiliitis. Radiographs, particularly of the sacroiliac joints, frequently have abnormal findings even in asymptomatic patients with IBD, but equivocal abnormalities should be interpreted with caution and always within the given clinical context. Plain radiographs of the peripheral joints may demonstrate soft-tissue swelling, juxta-articular osteoporosis, mild periostitis, and effusions, usually without erosions or destruction. (See 'Radiographic findings' above.)

Diagnosis – IBD-associated arthritis should be suspected in patients with IBD who develop joint pain, stiffness, or symptoms of inflammatory back pain. There is no pathognomonic finding to confirm that arthritis is due to IBD. It thus remains a diagnosis of exclusion, and septic arthritis should be excluded, particularly in patients with monoarthritis or oligoarthritis, given the risk of fistulization or bacteremia in patients with IBD. (See 'Diagnosis' above.)

Differential diagnosis – The differential diagnosis of arthritis associated with gastrointestinal disease also includes hypertrophic osteoarthropathy, osteonecrosis, erythema nodosum (particularly if periarticular), and other disorders in which both intestinal and joint or spine involvement may occur. (See 'Differential diagnosis' above.)

ACKNOWLEDGMENT — The editorial staff at UpToDate acknowledge Peter Schur, MD, and Filip van den Bosch, MD, PhD, who contributed to earlier versions of this topic review.

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Topic 7787 Version 39.0

References

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