Liz Fredrickson, PharmD, BCPS


Liz Fredrickson is an Associate Professor of Pharmacy Practice and Pharmaceutical Sciences at the Northeast Ohio Medical University (NEOMED) College of Pharmacy.


Topic Overview

Crohn’s disease (CD) is a chronic, inflammatory disease of the gastrointestinal (GI) tract and, along with ulcerative colitis (UC), is one of two GI disorders that comprise inflammatory bowel disease (IBD). This condition is relapsing and remitting in nature with inflammation that affects all layers of the bowel wall and can occur in any portion of the GI tract. Crohn’s disease has no clear etiology but is influenced by genetic, environmental, and immunological factors and has the potential to affect patients’ quality of life severely. Guidelines for managing CD include evidence-based recommendations for pharmacologic therapies alongside the suggestion to treat patients with CD using a shared decision-making model. Pharmacists play a vital role in the care of these patients and can share their medication expertise to guide treatment decisions and counsel patients.

Accreditation Statement


RxCe.com LLC is accredited by the Accreditation Council for Pharmacy Education (ACPE) as a provider of continuing pharmacy education.


Universal Activity Number (UAN): The ACPE Universal Activity Number assigned to this activity is 

Pharmacist 0669-0000-24-047-H01-P

Pharmacy Technician  0669-0000-24-048-H01-T

Credits: 2 contact hour(s) (0.2 CEU(s)) of continuing education credit


Type of Activity: Knowledge

Media: Internet/Home study Fee Information: $6.99

Estimated time to complete activity: 2 contact hour(s) (0.2 CEU(s)), including Course Test and course evaluation


Release Date: April 16, 2024 Expiration Date: April 16, 2027

Target Audience: This educational activity is for pharmacists and pharmacy technicians


How to Earn Credit: From April 16, 2024, through April 16, 2027, participants must:


Read the “learning objectives” and “author and planning team disclosures;”

Study the section entitled “Educational Activity;” and

Complete the Course Test and Evaluation form. The Course Test will be graded automatically. Following successful completion of the Course Test with a score of 70% or higher, a statement of participation will be made available immediately. (No partial credit will be given.)

Credit for this course will be uploaded to CPE Monitor®.

Learning Objectives: Upon completion of this educational activity, participants should be able to:

Describe the etiology and pathophysiology of Crohn's disease

Compare and contrast pharmacologic therapies for Crohn’s disease

Identify mechanisms of action and side effect profiles of medications used to treat Crohn’s disease

Recall medication counseling points for patients with Crohn’s disease


The following individuals were involved in developing this activity: Liz Fredrickson, PharmD, BPCS, and Pamela Sardo, PharmD, BS. Pamela Sardo and Liz Fredrickson have no conflicts of interest or financial relationships regarding the subject matter discussed. There are no financial relationships or commercial or financial support relevant to this activity to report or disclose by RxCe.com or any of the individuals involved in the development of this activity.

© RxCe.com LLC 2024: All rights reserved. No reproduction of all or part of any content herein is allowed without the prior, written permission of RxCe.com LLC.

Educational Activity


A Guide for the Management of Crohn’s Disease Introduction

Crohn’s disease is a chronic inflammatory bowel disease that affects the gastrointestinal tract. This continuing education activity will review the etiology, pathophysiology, and classification of Crohn’s disease. The appropriate diagnosis and treatment of Crohn’s disease is critical to maintaining a patient’s quality of life and avoiding complications from the disease. This includes the ability to differentiate between Crohn’s disease and ulcerative colitis. This activity will also discuss available pharmacologic treatments, including mechanisms of action, side effect profiles, and recommended placement in therapy. Finally, it will highlight the role of pharmacists and pharmacy technicians as members of interdisciplinary care teams.


Overview of Crohn’s Disease


Crohn’s disease (CD) is a chronic disease of the gastrointestinal (GI) tract and, along with ulcerative colitis (UC), is one of two GI disorders that comprise inflammatory bowel disease (IBD).1 This condition is relapsing and remitting in nature with inflammation that affects all layers of the bowel wall.1 It can be difficult for clinicians to differentiate between CD and UC: up to 15% of patients with CD have features so similar to UC that misdiagnosis may result.2,3 Crohn’s disease is notable for affecting any part of the digestive tract from mouth to rectum,4 whereas UC tends to affect the rectum and colon. Crohn’s disease has no clear etiology but is influenced by genetic, environmental, and immunological factors and has the potential to affect patients’ quality of life severely.1 Evidence-based management of CD involves various pharmacologic therapies in conjunction with treating patients using a shared decision-making model.1 Pharmacists play a vital role in the care of these patients and can share their medication expertise to guide treatment decisions and counsel patients.

Etiology and Epidemiology


Crohn’s disease is an idiopathic disease with no clear etiology, but genetic, environmental, and immunological factors influence its development.1 From a global perspective, CD is more common in North America and Western Europe and has an incidence of between 3 and 20 cases per 100,000 person- years.5 The age of initial presentation is bimodal, with a peak incidence around age 15 to 20 years followed by a second peak between age 60 and 70.6-8 However, individuals of any age may be diagnosed.1 Females are slightly more predisposed to CD compared to males.5


Risk Factors


As with UC, the precise etiology of CD is unknown; however, there are numerous factors that, in combination, are believed to put patients at risk of developing this disease. These encompass genetic, infectious, immunologic, and environmental causes.1,9


The Microbiome


Microorganisms are believed to play an important role in triggering inflammation and, ultimately, the development of IBD.10 This may begin with dysbiosis (an imbalance in gut microbes) or increased proinflammatory bacteria within the GI tract.10 Compared to healthy individuals, patients with IBD have fewer numbers and less diversity of microbiota in addition to the presence of more aggressive bacterial groups.10 Various microorganisms, including viruses, protozoans, and mycobacteria, have been thought to play a role in developing IBD.10 An estimated one-third of patients with CD have increased amounts of adherent-invasive E. coli in their ileal tissue.11




A family history of IBD is also a significant risk factor for its development.10,12 A patient with a first-degree relative with IBD has a 20-fold increased risk of the disease.7,10 An individual’s genetic predisposition to IBD

varies by population, with individuals of African-American and Asian descent having lower risks.13 Over one hundred genetic markers are associated with CD, and immunoreactivity to gut bacteria may be key in the development of the disease.6 Nucleotide-binding oligomerization domain protein 2 (NOD2) is involved in the recognition of pathogens in the innate immune system, and also mutations in NOD2 predispose patients to CD.7,10


Immune-Mediated Risks


Both autoimmune and nonautoimmune mechanisms may contribute to the development of IBD.10 The mucosal immune system encompasses 75% of all lymphocytes within healthy individuals, making it the largest component of the immune system.14 After the loss of effective intestinal barrier function, lymphocytes, plasma cells, mast cells, macrophages, and neutrophils are able to infiltrate the bowel wall and form granulomas.7 In CD specifically, Th1 cytokine activity is excessive, and increased expression of interferon-y and production of interleukin (IL) 2, IL-17A, and IL-22 are seen within CD.10


Environment and Lifestyle


An individual’s environment and lifestyle, including their diet and medication use, may play important roles in the development of IBD.7,12 Various environmental risk factors have been noted for IBD, including cigarette smoking, antibiotic use during childhood, breastfeeding, use of oral contraceptives, low vitamin D levels, and tea and coffee consumption.4 These risk factors are compared between CD and UC in Table 1.7 It is thought that a Western diet, which includes a high intake of fat and sugar and a low intake of fiber, heightens the risk of IBD.7 In addition, the hygiene hypothesis may explain the increased incidence of IBD in industrialized countries. This theory suggests that exposure to various microorganisms in early childhood through things such as family pets and living on a farm can protect against the development of autoimmune and allergic diseases.7

Table 1

Comparison of Environmental and Lifestyle Risk Factors for IBD Development12

Risk FactorCrohn’s DiseaseUlcerative Colitis
SmokingIncreased risk in CaucasiansProtective effect in Caucasians and Asians
Antibiotic use in ChildhoodIncreased risk for Caucasians; Protective effect in AsiansIncreased risk in Caucasians
BreastfeedingProtective effect in Asians and Caucasians in most studiesProtective effect in Asians and Caucasians in most studies
Oral Contraceptive useRisk in CaucasiansInconclusive
Low Vitamin D LevelsRisk in CaucasiansRisk in Caucasians
Tea or Coffee ConsumptionRisk in CaucasiansProtective in Asians


Pathophysiologic Features of Crohn’s Disease


The pathophysiologic features of CD and UC can overlap, adding complexity in diagnosing one disease over the other. The main distinguishing features are the extent and distribution of inflammation and the depth of bowel wall involvement.7 These features are compared in Table 2.10


Table 2

Comparison of the Pathologic Features of CD and UC10

Rectal involvementRareCommon
Ileal involvementVery commonRare
Transmural involvementCommonRare
Crypt abscessesRareVery common
Linear cleftsCommonRare
Cobblestone appearanceCommonAbsent

Manifestations of IBD in the GI Tract


Crohn’s disease is transmural, extending the full thickness of the bowel wall.10 Unlike UC, which tends to be confined to the rectum and colon, CD can occur at any point in the GI tract.10 It is common for patients with CD to have segments of a diseased bowel separated by segments of a healthy bowel, resulting in a “cobblestone” appearance.10


Complications of CD include small bowel strictures, fistulas, and bleeding.7 The risk of cancer for patients with CD is present but not as high as that associated with UC.10 Crohn’s disease can be progressive in nature, and the following risk factors put patients at greater risk of progressive disease:1


Young age at diagnosis

Having initial extensive bowel involvement, ileal involvement, perianal or severe rectal disease

Presenting with a penetrating or stenosis disease phenotype


Extraintestinal Manifestations of IBD


Crohn’s disease and UC are associated with organ involvement that occurs outside the GI tract or extraintestinal manifestations.10 These complications are summarized in Table 3.10


Table 3

Extraintestinal Manifestations of IBD10


Fatty infiltration resulting in malabsorption

Includes nonalcoholic fatty liver disease, pericholangitis, autoimmune hepatitis, liver abscess, cirrhosis


Includes peripheral and axial arthropathies

Symptoms can occur prior to the development of IBD symptoms

OcularIncludes dry eye, blepharitis, iritis, uveitis, episcleritis, conjunctivitis
 Occurs in ~29% of IBD patients
Dermatologic and Mucocutaneous

Includes erythema nodosum, pyoderma gangrenosum, aphthous ulceration, Sweet’s


Hematologic, Coagulation, Pulmonary, Metabolic Abnormalities

Includes anemia (prevalence of 74%), iron deficiency, chronic blood loss, inflammation, malnutrition, hemolysis, or bone marrow suppression due to medications

Increased risk of venothromboembolism

Osteopenia in 32-36% of patients

Osteoporosis in 2-15% of patients

Includes pneumonia, bronchiectasis, bronchiolitis obliterans


Clinical Presentation of Crohn’s Disease


Crohn’s disease has notable cardinal symptoms, including abdominal pain (which is worse after eating and often localized to the right quadrant), diarrhea, and fatigue.6 While chronic diarrhea is the most common symptom of CD, some patients may not experience this symptom.6 Fatigue is also commonly present and may be due to a combination of inflammation, anemia, and deficiencies in vitamins and minerals.6 Patients can also present with weight loss, fever, growth failure, anemia, and/or recurrent fistulas.3 In one systematic review, patients with CD were found to have an increased risk of bone fractures (up to 30-40% increased risk) and a 3-fold higher risk of thromboembolism.15 For most patients, symptoms occur intermittently, and a few patients will experience continuous symptoms or long periods of remission from symptoms.1 Patients may experience symptoms for years before being diagnosed and sometimes are misdiagnosed with irritable bowel syndrome.6 Importantly, a patient’s symptoms do not correlate precisely with the presence of active inflammation; thus, clinicians should obtain objective data from endoscopic or other imaging techniques to ensure proper treatment.1


Diagnosing Crohn’s Disease


The journey through symptoms, diagnosis, and treatment to quell the fiery inflammation can be long and difficult. In one study, one in four

individuals with IBD reported GI symptoms to their primary care physician more than six months before receiving a diagnosis.16 No single test can be utilized to diagnose CD.1 Instead, the diagnosis is made clinically, using a combination of laboratory, endoscopic, radiographic, and physical examination findings.1 Laboratory findings are commonly used to confirm the degree of disease severity.1 For many patients, CD will be confirmed upon uncovering the presence of chronic intestinal inflammation.1 When inflammation is limited to the colon, it can be challenging to differentiate CD from UC. Crohn’s disease is likely when colonic involvement is discontinuous with skip areas. The rectum is spared; deep, linear colon ulcers, strictures or fistulas, or granulomatous inflammation are present.1 The degree of bowel damage that occurs can be quantified using the Lemann index scoring system.1,17 Using this system, average scores increase as the disease duration increases.17 Differentiating clinical features are detailed in Table 4.


Table 4

Clinical Features of Crohn’s Disease and Ulcerative Colitis10

FeatureCrohn’s DiseaseUlcerative Colitis
Malaise, feverCommonUncommon
Rectal bleedingCommonCommon
Abdominal tendernessCommonMay be present
Abdominal massCommonAbsent
Abdominal painCommonUnusual
Abdominal wall and internal fistulasCommonAbsent
Aphthous or linear ulcersCommonRare


Laboratory Testing


Laboratory testing can be used to assess inflammation, anemia, dehydration, and malnutrition.1 Common laboratory findings are summarized in Table 5.1

Table 5

Common Laboratory Findings in CD1

Fecal calprotectin (fCal)Increased; most sensitive screening test
Fecal lactoferrin (FL)Increased
Platelet countIncreased
Serum C-reactive protein (CRP)Increased in the subset of CD patients; useful to measure elevated inflammation
Erythrocyte sedimentation rate (ESR)Increased; does not differentiate IBD from IBS


An estimated 40% of patients with mild inflammation may have normal ESR and CRP levels, making these labs less useful in this case.1 Fecal markers, including fCal and FL, are helpful to monitor disease and a patient’s response to treatment.1 The ACG guidelines note that both genetic testing and serologic markers of IBD are not indicated to establish a diagnosis of CD.1




As part of the initial patient evaluation, the ACG guidelines recommend all patients undergo a colonoscopy with intubation of the terminal ileum.1 Additionally, a biopsy is recommended in patients with suspected IBD.1 Mucosal changes that indicate CD include nodularity, edema, ulcerations, friability, and stenosis.18,19 Approximately 80% of patients with IBD will have mucosal involvement that can be viewed by colonoscopy.1 Documenting the distribution and severity of the disease at the time of diagnosis is critical. These findings ultimately impact further screenings, the disease prognosis, and treatment decisions.1 Various scoring systems are available to quantify mucosal involvement, including the Crohn’s Disease Endoscopic Index of Severity (CDEIS) and the Simple Endoscopic Score for Crohn’s Disease (SES- CD), with the latter considered easier to utilize.1,20,21

Determining Disease Activity


A patient’s features at the time of diagnosis, including the age of onset, disease distribution, location, disease phenotype, and disease activity, guide initial and future medical management and thus should be documented within the patient’s medical record.1 There are four types of clinical disease activity related to CD: remission, mild, moderate, and severe.1 Disease activity depends on numerous factors, including clinical measures, the impact on the patient’s quality of life, and complications of the disease and therapies.1 In general, patients with mild disease are ambulatory and can eat and drink normally.22 A CD activity score for mild disease is between 150 and 220, indicating minimal impact on quality of life (QOL).1


Patients with moderate or severe CD have activity scores of 220-450 and >450, respectively. Patients with moderate CD have chronic diarrhea and abdominal pain. They can experience weight loss and fever because of inflammation. Patients with severe CD often have significant weight loss, fever, and complications that may include obstruction or intra-abdominal abscesses. These symptoms may continue even with aggressive medical therapies.1 Patients with a severe CD have a significantly decreased QOL.1


The Montreal classification system is employed for the disease phenotype.23,24 This is presented in Table 6 below.23,24 The letter “p” is added to the B subtypes if perianal disease is present.24 While the location of the disease usually remains stable, the behavior of the disease typically progresses from B1 to B2 or B3.1


Monitoring disease activity involves using objective inflammatory measures to achieve tight control of the disease process.1 This includes fecal markers, serum markers, imaging studies, and endoscopic assessments. Clinicians can treat their patients “to target,” which involves using clinical and inflammatory parameters to determine when remission occurs.1,10 As adjuncts to monitoring disease therapy, fCal and FL can be sensitive markers of CD activity and correlate with endoscopic indices.25,26 Serial CRPs may also be valuable in monitoring disease activity and patient response to therapy.1

Table 6

Montreal Classification System1,23

Age at diagnosis

A1, </ 16 years

A2, 17-40 years

A3, >40 years


L1, ileal

L2, colonic

L3, ileocolonic

L4, isolated upper gastrointestinal


B1, nonstricturing nonpenetrating

B2, stricturing

B3, penetrating


Management of Crohn’s Disease


Given the complexity and aggressive nature, Managing CD is often more challenging than managing UC.10 Treatment goals endeavor to increase the patient’s quality of life, decrease disease complications, promote mucosal healing, control inflammation, control symptoms resulting from active inflammation, and minimize adverse effects of drug therapies.1,10 Per the ACG guidelines, mucosal healing is a key target in assessing the efficacy of treatments for CD.1 Mucosal healing is defined as the absence of ulceration, and various scoring systems may be used to quantify the degree of ulceration and inflammation for patients with CD.1


Nonpharmacologic and Lifestyle Approaches


Smoking cessation should be promoted among patients with CD, given cigarette smoking has been shown to worsen disease activity and accelerate the recurrence of CD.1 Studies have found smoking is associated with increased rates of surgical intervention, IBD hospitalizations, and peripheral arthritis.27,28 By ceasing smoking, patients can decrease CD flares and the need for steroids and immunomodulatory therapy.29

Clinicians should also work closely with patients to assess and manage stress, depression, and anxiety.1 Numerous studies have found these psychological issues have the potential to increase symptoms of IBD.1 Perceived stress can derive from issues around disease management and the impact of CD on a patient’s life.1,30 Additionally, patients with anxiety or major depression also have a greater risk of surgery and use of healthcare resources.1,31


Dietary therapies may be utilized adjunctively to medical therapies in patients with mild-moderate or low-risk disease.1 Various suggestions include using elemental, semi-elemental, or other defined diets.1 Additionally, iron, vitamin D, and B12 levels can be checked, and supplements can be started as needed.6


Finally, the ACG guidelines recommend avoidance of nonsteroidal anti- inflammatory drugs (NSAID) usage in CD as this can exacerbate disease activity.1 Conversely, they conditionally recommend antibiotic use not be restricted in CD patients to prevent disease flares.1


Pharmacologic Approaches


In selecting medications for CD, clinicians need to consider the location and severity of the disease, any present disease-associated complications, and the future prognosis.1 Employment of therapeutic modalities must be individualized to the patient, considering their symptom response and tolerance to the therapies.1 A step-down or target-to-treat approach is utilized for patients with CD.13 Clinicians should first seek to treat any acute disease and induce remission and then work to maintain this remission in addition.1 This also reduces the risk of future complications and relapse.32 For active disease, treatments should be continued until remission or failure to improve occurs.1 To confirm remission, endoscopy or imaging should be utilized to confirm findings.1 Generally, patients should improve within 2-4 weeks of starting treatment and achieve maximal improvement by 12-16 weeks.1 However, adverse effects can occur much more quickly.1

If a patient achieves a symptomatic response, they can then be considered for maintenance therapy.1 Patients with mild-to-moderate disease who do not improve are candidates for alternative therapies or dose adjustments of their current medications.1 Clinicians could also consider escalating to treatment of moderate-severe disease, depending on the patient’s status.1


Pharmacists play a key role in the management of CD by reviewing medication lists to avoid drug-drug interactions, monitoring for and mitigating adverse effects of CD therapies, and assisting with therapeutic drug monitoring. ACG guidelines recommend assessing drug levels of biologics and antidrug antibody levels for patients with active CD.1 When medications fail, this can result from three different causes: mechanistic failure, immune- mediated drug failure, or non-immune-mediated drug failure. Possible scenarios are considered in Table 7.1 Pharmacists can also assist in providing critical patient education to optimize adherence to therapies.


Table 7

Scenarios for Drug Failure in Patients with CD1

Mechanistic failure

The patient has therapeutic levels but no antibodies, and the presence of active

mucosal ulceration

Consider utilizing a different class of medication
Non-immune mediated failure

The patient has subtherapeutic trough concentrations and no

anti-drug antibodies

Result of rapid drug clearance; consider dose increases
Immune-mediated drug failure

The patient has low or undetectable trough concentrations and high

antidrug antibody titers

Obtain minimal therapeutic target trough levels

Medications used in treating CD work to suppress the overly active immune system.6 The pharmacologic management of CD is split into induction therapy (achieving control of inflammation within three months) and maintenance therapy (sustaining control beyond three months). Induction involves high doses of steroid-sparing medications to cause rapid clinical remission. Maintenance therapy entails lower doses of medications that typically are used for the entirety of the patient’s life to ensure remission.6 When selecting therapies, a patient’s risk profile, disease severity, and risk of disease progression should be considered.


Mild-to-Moderately Severe Disease and Low-Risk Disease


Treatment of patients with mild disease can be challenging. The benefits of utilizing effective agents should be balanced with the risks of adverse effects of these agents, as well as the cost to the patient.1




Aminosalicylates have shown efficacy in treating UC, but their role in managing CD is more limited.10 Mesalamine (5-aminosalicylic acid (5-ASA) is a topical anti-inflammatory agent shown to be effective within the lumen of the intestine.1 This medication is the active component of sulfasalazine, with an unclear mechanism of action.33,34 It may exert benefits via scavenging free radicals, inhibiting leukocyte motility, and interfering with TNF-alpha.10,35 Studies have found oral mesalamine is not consistently effective in causing remission and mucosal healing for active CD.36,37 The recommended dose is 1 gram 3-4 times a day.34 Significant side effects include delayed hypersensitivity reactions with potential fever, myocarditis/pericarditis, interstitial nephritis, liver injury, pancreatitis, and interstitial pulmonary disease.34 Intolerance syndrome (diarrhea, fever, and abdominal pain) may occur in 7-14% of patients, and renal effects (interstitial nephritis, renal failure syndrome) are also a risk.34

Sulfasalazine is a combination of mesalamine with sulfapyridine, which is a carrier that delivers 5-ASA to the colon.38 Sulfasalazine has shown efficacy for mild-moderate disease in patients with active colonic CD or ileocolonic CD; however, it is not better than placebo with regard to mucosal healing in patients with CD.39-41 It is available in immediate and delayed-release formulations, with a recommended dose of 3-6 grams per day in divided doses for up to 16 weeks.42 Significant side effects include blood dyscrasias, GI effects (nausea, vomiting, diarrhea), and delayed hypersensitivity reactions.38 Topical preparations (enemas and suppositories) may have limited utility in the treatment of CD.1




Corticosteroids are the primary treatment for CD flares.1 They modulate the immune system and inhibit the production of cytokines and mediators and can be given via oral, parenteral, or rectal routes.10 Corticosteroids are able to reduce signs and symptoms of active CD and also induce remission in patients with moderate-severe active CD.1 Oral formulations can be utilized in mild-moderate disease, but systemic agents are needed for moderate-severe CD.1 These agents do not consistently result in mucosal healing. Controlled ileal release (CIR) budesonide can be used short-term for relief of mild- moderate CD symptoms when the disease is in the terminal ileum or right colon.1 Because it is a topical agent with a large first-pass effect, this minimizes a patient’s systemic exposure and lessens side effects.1 The dose is 9 mg once daily in the morning for a duration of up to 8 weeks.41


Antimicrobial therapy


Broad-spectrum antibiotics can be helpful in treating a subset of CD patients.1 This may be due to their immunosuppressive effects and ability to eliminate bacterial overgrowth.1 Metronidazole may be useful in preventing post-operative CD recurrence but has not been shown better than placebo with regard to inducing remission.1,42,43 Similarly, ciprofloxacin is not more effective than placebo when inducing remission but has similar efficacy to mesalamine for active CD.1,42,44,45

Moderate-to-Severe Disease/Moderate-to-High-Risk Disease


Systemic Corticosteroids


Corticosteroids may be useful in alleviating flare signs and symptoms for moderate-severe disease.1 However, the ACG guidelines note they are ineffective for maintenance therapy for CD.1 These agents do not promote mucosal healing and induce a wide array of harmful side effects, including bone loss, mood disorders, insomnia, hyperglycemia, hypertension, acne, and weight gain, among others.1 If they are used for flares, use should be short- term. Recommended prednisone-equivalent doses range from 40-60 mg/day.1 The dose can be given for 1-2 weeks and then tapered off at weekly intervals, with tapers not exceeding three months.1 An estimated 20% of patients are steroid refractory, and up to 33% may become steroid dependent.1 Corticosteroid use is contraindicated in patients with perforating complications, such as fistulas and abscesses.1




The immunomodulators are untargeted therapies that include azathioprine, 6-mercaptopurine, and methotrexate. The ACG guidelines recommend the use of these agents in the treatment of active CD in patients with moderate-severe disease who are symptomatic despite corticosteroid use and as adjunctive therapies to reduce immunogenicity against biologic therapies.1 These agents do have a slow onset of action (8-12 weeks) and thus are not effective for induction in active, symptomatic disease.1




Azathioprine is the prodrug of mercaptopurine, and both are useful as steroid-sparing agents.1 TMPT testing is important to consider before starting azathioprine or 6-mercaptopurine.1 For induction or maintenance of remission, the initial dose of azathioprine is 50 mg once daily.46 This can be titrated up to 2.5 mg/kg once daily over the course of 12 or more weeks.46 Lean body weight dosing is preferred. Azathioprine is given for 1-2 years in general.46

Adverse effects include allergic reactions, pancreatitis, myelosuppression, nausea, infections, hepatotoxicity, and malignancies that include nonmelanoma skin cancer, and lymphoma.46 6-mercaptopurine is dosed at

0.75 to 1.5 mg/kg/day, and adverse effects include rash, diarrhea, nausea, vomiting, and bone marrow depression that is dose-related.47




Methotrexate is also an effective steroid-sparing agent and can be given either orally, intramuscularly (IM), or subcutaneously (SUBQ).5 It can be used with steroids to treat moderately active steroid-dependent or resistant CD.1 Dosing is 15-25 mg IM or SUBQ once weekly (given with folic acid as methotrexate blocks folate).42 The maximum recommended dose is 25 mg/week.48 The dose can be reduced to 15 mg/week if remission is sustained after four months.48 Side effects include nausea, vomiting, hepatotoxicity, bone marrow suppression, pancreatitis, pulmonary toxicity, skin cancer, and lymphoma.48


Anti-TNF Agents


Anti-TNF agents include infliximab, adalimumab, and certolizumab, and all three have similar efficacy rates.1,10 Choice often depends on the patient’s preference, cost of medication, and preferred route of administration.1,10 This group of biologics works via neutralizing cytokines that promote inflammation and is useful in the treatment of CD that is resistant to corticosteroids and for CD refractory to thiopurines or methotrexate.1 Infliximab can be combined with thiopurines and is more effective in combination than either agent alone for patients naïve to these medications.1 Combination is preferred, provided the patient does not have risk factors to preclude this strategy.1


The anti-TNF agents have been found more effective than placebo for inducing response, remission, and partial and complete healing of mucosa in patients with CD.49,50 Benefits of this class of medications include their rapid onset of effect, which usually occurs within two weeks of starting therapy.1

Treatment is generally more effective when started earlier, preferably within two years of disease onset.1 These agents are summarized in Table 8.51-53


Table 8

Anti-TNF Medications51-53

Generic (Brand)DescriptionIndicationDose
Infliximab (Remicade)

Chimeric mouse-human IgG1

monoclonal antibody

Moderate-severe CD and fistulizing CD that has failed conventional therapy

IV: 5 mg/kg at 0,2,6 weeks,

then 5 mg/kg

every 8 weeks. Can increase the dose to 10

mg/kg every 8 weeks

Adalimumab (Humira)

Fully human IgG1

monoclonal antibody directed against TNF-α

Moderate-to-severe CD that has failed to respond to conventional therapy

SUBQ: 160 mg

over 1-2 days, then 80 mg two weeks later. 40 mg every other

week for maintenance

Certolizumab pegol (CimziaPEGylated Fab fragment to TNF-αModerate-to-severe CD that has failed to respond to conventional therapy

SUBQ: 400 mg.

Repeat doses 2

and 4 weeks later.


dose of 400 mg every 4 weeks


Patients at risk of serious side effects include those with prior demyelinating disorders, congestive heart failure, and prior lymphoma or malignancies.8 Clinicians should assess patients for active or latent tuberculosis before starting anti-TNF therapies.1 They should also be screened for opportunistic infections, including histoplasmosis and blastomycosis.1 For patients at high risk of TB, this testing should also be considered before starting corticosteroids or other immunomodulators. If TB is discovered, the patient will require chemoprophylaxis for weeks to months prior to starting

anti-TNF medications.1 Patients should also be assessed for viral hepatitis before starting therapy, and carriers should receive treatment to avoid a hepatitis B flare and liver failure.1


Pharmacists can assist the care team in ensuring patients are up to date on vaccinations, including pneumococcal pneumonia, varicella, human papillomavirus, inactivated influenza, hepatitis A, and herpes zoster.1 These should be given before starting therapy. Live attenuated vaccines should be avoided.1


Biosimilar Anti-TNF Agents


Biosimilar anti-TNF agents include biosimilar infliximab and biosimilar adalimumab.1 These may be used in moderate-severe CD and for de novo induction and maintenance therapy.1 A biosimilar is a product highly similar to the reference product with minor differences in clinically inactive components and no clinically meaningful differences between the products regarding safety, potency, or purity.1 Biosimilars for infliximab include infliximab dyyb, CT-P13, and infliximab-abda, infliximab-qbtx.1 Adalimumab has adalimumab-atto and adalimumab-adbm.1 Every biosimilar has a structural complexity and different glycosylation patterns, though the amino acid sequence remains the same. Biosimilars are not the same as generic medications because they differ in solubility, stability, clearance, and immunogenicity from one another.1 There has been some concern that small differences in the safety and efficacy of these medications compared to their reference products may be worsened in IBD.1


Agents Targeting Leukocyte Trafficking


Agents targeting leukocyte trafficking include anti-integrin therapy (vedolizumab) and natalizumab (an anti-alpha 4 integrin antibody).1 Vedolizumab is recommended with or without an immunomodulator for patients with moderate-severe active CD and for induction of symptom remission.1 Natalizumab can be considered for induction of symptom remission in active CD as well.1 It can also be used for maintenance of

natalizumab-induced remission if serum antibody to John Cunningham (JC) virus is negative.1


Natalizumab interferes with leukocyte trafficking and inhibits binding to vascular cell adhesion molecule-1 and mucosal addressin cell adhesion molecule-1.54 The recommended dose is 300 mg infused over 1 hour every four weeks, and it should be discontinued if no effect is seen within 12 weeks.54 This agent is useful in patients who have failed other therapies but come with a serious risk of progressive multifocal leukoencephalopathy (PML) caused by the JC virus.1 In patients with JC virus-positive antibodies or prior use of immunosuppressive agents, this risk is as high as 1 in 100.1 The anti- JC virus antibody should be checked prior to starting therapy and minimally every 6 months after.1


Vedolizumab selectively inhibits α4β7 integrin interaction with mucosal addressin cell adhesion molecule-1.55 This makes it relatively specific for leukocyte trafficking to the gut.1 This agent has found utility in patients with moderate-severe CD who had a poor response to or were intolerant to a TNF blocker or immunomodulator or those with inadequate response or intolerance to corticosteroids.1 Dosing is 300 mg at 0, 2, and 6 weeks and then every 8 weeks thereafter.55 Unlike natalizumab, no cases of PML have been reported with vedolizumab.1 This agent has been found to be more effective than placebo for inducing response, remission, and achieving mucosal healing.1 The onset of effect is slower than with anti-TNF agents, however—up to 10 weeks.1


Agents Targeting IL-12/23 (Anti-p40 Antibodies)


Agents targeting IL-12/23 (anti-p40 antibodies) include ustekinumab. ACG guidelines recommend for moderate-severe CD in patients who failed previous corticosteroid, thiopurine, methotrexate, and anti-TNF therapies or patients with no prior use of anti-TNF agents.1 Ustekinumab is an anti-p40 antibody that inhibits IL-12 and 23.1 Overall, it has a good safety profile. Studies are needed to compare this agent with vedolizumab, and other anti- TNF agents.1 Induction dosing is weight-based.56 Patients weighing ≤55 kg receive 260 mg IV as a single dose, patients weighing >55 kg to 85 kg receive

390 mg IV as a single dose, and patients weighing >85 kg receive 520 mg IV as a single dose.56 For maintenance dosing, patients receive 90 mg every eight weeks starting eight weeks after the induction dose.56


Other Medications


The ACG guidelines do not recommend the use of cyclosporine, mycophenolate mofetil, or tacrolimus for use in CD.1


Treating Severe/Fulminant Disease


As mentioned above, severe disease has a CD activity score >450.1 Fulminant CD is a severe form of CD marked by a sudden onset in symptoms.57

Anti-TNF agents can be used in patients with severe or fulminant CD.1 Intravenous corticosteroids can also be used per the ACG guidelines.1 Methylprednisolone is recommended for acute treatment at a dose of 40-60 mg/day.1 A bolus of corticosteroids can be used prior to infliximab treatment to prevent anti-drug antibodies.1


Novel Agents


Some agents in various stages of development for treating patients with CD include anti-integrins like etrolizumab and ozanimod, as well as anti-IL-23 agents such as risankizumab and brazikumab, along with selective Janus kinase-1 inhibitors like filgotinib and upadacitinib.1


Drug Monitoring


Drug monitoring is an important part of a CD treatment plan. As discussed above, clinicians must monitor a drug’s efficacy and adverse events, and consider alternative treatment options. This includes a consideration of the interplay between IBD therapies and the gut microbiome.58 The gut microbiome can alter IBD therapeutics making them more effective or diminishing their effects. Therapies can also change the gut microbiome’s

composition and functionality.58 This is discussed in detail by O'Reilly C, Mills S, Rea MC, et al. (2023).58 Drug monitoring is summarized in Table 9.13


Table 9

Drug Therapy Monitoring13

Drug(s)Adverse Drug ReactionMonitoring ParametersComments

Nausea, vomiting, headache

Rash, anemia, pneumonitis

Hepatotoxicity, nephritis

Thrombocytopenia, lymphoma

Folate, complete blood count

Liver function tests, Scr, BUN

Increase the dose slowly over 1-2 weeks
MesalamineNausea, vomiting, headacheGI disturbances 
CorticosteroidsHyperglycemia, dyslipidemiaBlood pressure, fasting lipid panelAvoid long-term use if possible, or consider budesonide
Osteoporosis, hypertension, acneGlucose, vitamin D, bone density 
Edema, infection, myopathy, psychosis  
Azathioprine/ mercaptopurine

Bone marrow

suppression, pancreatitis, lymphoma

Complete blood countCheck TPMT activity or NUDT15 phenotype
Liver dysfunction, rash, arthralgia

Scr, BUN, liver function tests,

genotype/ phenotype

May monitor TGN
MethotrexateBone marrow suppression, pancreatitisComplete blood count, Scr, BUNCheck baseline pregnancy test
Pneumonitis, pulmonary fibrosis, hepatitisLiver function testsChest x-ray
Infliximab Adalimumab Certolizumab pegol

Infusion-related reactions (infliximab), infection

Heart failure, optic neuritis,

Blood pressure/heart rate (infliximab)Need negative PPD and viral serologies
Drug(s)Adverse Drug ReactionMonitoring ParametersComments
 demyelination, injection site reaction, signs of infection

Neurologic exam, mental status

Trough concentrations (infliximab)

Antidrug antibodies (all agents)

Natalizumab VedolizumabInfusion-related reactions

Brain MRI, mental status, progressive multifocal leukoencephalopath


Vedolizumab is not associated with PML
UstekinumabInfections, skin cancersSigns/symptoms of infection, annual skin exam

Rare instances of reversible posterior leukoencephalopathy

syndrome (RPLS)

Avoid live vaccines


Surgical Options


Surgery may be required for some patients with IBD. Surgeries can include resection of affected intestine segments or draining or abscesses.1 Colectomy may also be needed for patients with uncontrolled disease despite maximized therapies or if complications occur, such as toxic megacolon or colonic strictures.1 In CD, surgery is generally reserved for patients with intractable hemorrhage, perforation, persistent or recurrent obstruction, abscess, cancer, dysplasia, or medically refractory disease.1


Maintaining Remission


Maintaining patients in remission can be extremely challenging. Many patients will wish to stop medications once remission is achieved due to the side effect profiles of these agents.6 Pharmacists can assist patients with maintaining medication adherence; patients should be counseled that

stopping medications can lead to the risk of relapse and increase the risk of surgery and other complications.6 This can be continued for patients with low- risk disease who initially respond to sulfasalazine.1 Systemic corticosteroids should not be used for maintenance, as they cannot alter the disease course but elicit numerous untoward effects.1 Methotrexate and thiopurines may be options for maintenance therapy but typically are not as effective as biologic therapies or when used in combination with biologic therapies. The anti-TNF agents are options for maintenance therapy, and combination with a thiopurine should be considered. If patients achieve success with vedolizumab, natalizumab, or ustekinumab, these can also be considered for use as maintenance agents.1


The Role of the Pharmacy Technician


Pharmacy technicians are important members of the health care team. Oftentimes, patients may come to the pharmacy seeking treatment for GI- related symptoms, and pharmacy technicians can assist pharmacists in identifying patients who may have IBD or be candidates for referral. Pharmacy technicians can also recognize when patients may not adhere to IBD therapies and assist pharmacists in recognizing and helping these patients. Additionally, pharmacy technicians have served on clinical care teams, where they assist with submitting prior authorizations to insurance companies, following up on appeals, and determining if patients are eligible for financial assistance.59




Crohn’s disease is one of two gastrointestinal disorders that encompass IBD. A chronic and complex gastrointestinal disorder, CD has the potential to impact a patient’s quality of life severely and negatively. Treatment of the disease has seen a significant increase in available pharmacologic therapies in recent years. These agents should be selected based on disease activity and risk of disease progression, with consideration of adverse effects and costs to patients.

Drug monitoring is an important part of a CD treatment plan. Clinicians must monitor a drug’s efficacy and adverse events and consider alternative treatment options. This includes considering the interplay between IBD therapies and the gut microbiome.


Pharmacy technicians are important members of the health care team. Oftentimes, patients may come to the pharmacy seeking treatment for GI- related symptoms, and pharmacy technicians can assist pharmacists in identifying patients who may have IBD or be candidates for referral.

Course Test

Which of the following factors increases the risk of developing Crohn’s disease (CD) in Caucasians?



Smoking cessation


High vitamin D levels

Which of the following pathologic features indicate CD more than ulcerative colitis?



Rectal bleeding

Continuous disease distribution

Abdominal tenderness


Which of the following is true regarding the pathophysiology of CD?


Crohn’s disease is normally confined to the colon and rectum

Crohn’s disease commonly has a “cobblestone” appearance in which the diseased bowel is separated by segments of healthy bowel

Crohn’s disease is often mild and not progressive in nature

Unlike ulcerative colitis, Crohn’s disease is not associated with extraintestinal complications

Which of the following classes of medications are used primarily to treat CD flares but should not be used long-term?



Anti-TNF agents



Which of the following agents has a slow onset of action and is ineffective for induction in active, symptomatic CD?






A patient who may receive azathioprine therapy should have which of the following tests completed prior to initiating therapy?

PML test





A patient who develops pancreatitis from a CD medication is most likely taking which of the following?






Which anti-TNF agent is a chimeric mouse-human IgG1 monoclonal antibody that is given intravenously to treat CD?





Patients should be counseled to do which of the following prior to starting anti-TNF therapy?

Receive the live, attenuated influenza vaccine

Be treated for tuberculosis

Receive the pneumococcal pneumonia vaccine

Receive treatment for viral hepatitis

Which of the following is an appropriate counseling point pharmacists can provide to patients with CD?


The majority of medications used to treat Crohn’s disease have an onset of action of 16-20 weeks

Numerous vaccinations are required prior to starting mesalamine therapy

Stopping medications during the maintenance phase of treatment can lead to the risk of relapse and increase the risk of surgery and other complications

Crohn’s disease is limited in nature, and medications are often only needed for 2-4 weeks


Lichtenstein GR, Loftus EV, Isaacs KL, Regueiro MD, Gerson LB, Sands BE. ACG Clinical Guideline: Management of Crohn's Disease in Adults [published correction appears in Am J Gastroenterol. 2018 Jul;113(7):1101]. Am J Gastroenterol. 2018;113(4):481-517.


Yu YR, Rodriguez JR. Clinical presentation of Crohn's, ulcerative colitis, and indeterminate colitis: Symptoms, extraintestinal manifestations, and disease phenotypes. Semin Pediatr Surg. 2017;26(6):349-355. doi:10.1053/j.sempedsurg.2017.10.003

Guindi M, Riddell RH. Indeterminate colitis. J Clin Pathol.

2004;57(12):1233-1244. doi:10.1136/jcp.2003.015214

Wilkins T, Jarvis K, Patel J. Diagnosis and management of Crohn's disease. Am Fam Physician. 2011;84(12):1365-1375.

Feuerstein JD, Cheifetz AS. Crohn Disease: Epidemiology, Diagnosis, and Management. Mayo Clin Proc. 2017;92(7):1088-1103. doi:10.1016/j.mayocp.2017.04.010

Cushing K, Higgins PDR. Management of Crohn Disease: A

Review. JAMA. 2021;325(1):69-80. doi:10.1001/jama.2020.18936

Kaplan GG, Ng SC. Understanding and Preventing the Global Increase of Inflammatory Bowel Disease [published correction appears in Gastroenterology. 2017 Jun;152(8):2084]. Gastroenterology. 2017;152(2):313-321.e2. doi:10.1053/j.gastro.2016.10.020

Gajendra M, Priyadarshini L, Catinella, AP, et al. A comprehensive review and update on Crohn’s disease. Dis Mon. 2018 Feb;64(2):20–57. doi: 10.1016/j.disamonth.2017.07.001

Salgado VCL, Luiz RR, Boéchat NLF, et al. Risk factors associated with inflammatory bowel disease: A multicenter case-control study in Brazil. World J Gastroenterol. 2020;26(25):3611-3624. doi:10.3748/wjg.v26.i25.3611

Hemstreet BA. Inflammatory Bowel Disease. In: DiPiro JT, Yee GC, Haines ST, Nolin TD, Ellingrod VL, Posey L. eds. DiPiro’s Pharmacotherapy: A Pathophysiologic Approach, 12th Edition. McGraw Hill; 2023.

Darfeuille-Michaud A, Boudeau J, Bulois P, et al. High prevalence of adherent-invasive Escherichia coli associated with ileal mucosa in Crohn's disease. Gastroenterology. 2004;127(2):412-421. doi:10.1053/j.gastro.2004.04.061

Vedamurthy A, Ananthakrishnan AN. Influence of Environmental Factors in the Development and Outcomes of Inflammatory Bowel

Disease. Gastroenterol Hepatol (N Y). 2019;15(2):72-82.

Huang C, Haritunians T, Okou DT, et al. Characterization of genetic loci that affect susceptibility to inflammatory bowel diseases in African

Americans. Gastroenterology. 2015;149(6):1575-1586. doi:10.1053/j.gastro.2015.07.065

Chang JT. Pathophysiology of Inflammatory Bowel Diseases. N Engl J Med. 2020;383(27):2652-2664. doi:10.1056/NEJMra2002697

Peyrin-Biroulet L, Loftus EV Jr, Colombel JF, Sandborn WJ. Long-term complications, extraintestinal manifestations, and mortality in adult Crohn's disease in population-based cohorts. Inflamm Bowel Dis. 2011;17(1):471-478. doi:10.1002/ibd.21417

Blackwell J, Saxena S, Jayasooriya N, et al. Prevalence and duration of gastrointestinal symptoms before diagnosis of Inflammatory Bowel Disease and predictors of timely specialist review: a population-based study. J Crohns Colitis. Published online July 15, 2020. doi:10.1093/ecco-jcc/jjaa146

Pariente B, Cosnes J, Danese S, et al. Development of the Crohn's disease digestive damage score, the Lémann score. Inflamm Bowel Dis. 2011;17(6):1415-1422. doi:10.1002/ibd.21506

Coremans G, Rutgeerts P, Geboes K, Van den Oord J, Ponette E, Vantrappen G. The value of ileoscopy with biopsy in the diagnosis of intestinal Crohn's disease. Gastrointest Endosc. 1984;30(3):167-172. doi:10.1016/s0016-5107(84)72358-3

Geboes K, Ectors N, D'Haens G, Rutgeerts P. Is ileoscopy with biopsy worthwhile in patients presenting with symptoms of inflammatory bowel disease?. Am J Gastroenterol. 1998;93(2):201-206. doi:10.1111/j.1572-0241.1998.00201.x

Mary JY, Modigliani R. Development and validation of an endoscopic index of the severity for Crohn's disease: a prospective multicentre study. Groupe d'Etudes Thérapeutiques des Affections Inflammatoires du Tube Digestif (GETAID). Gut. 1989;30(7):983-989. doi:10.1136/gut.30.7.983

Daperno M, D'Haens G, Van Assche G, et al. Development and validation of a new, simplified endoscopic activity score for Crohn's disease: the SES-CD. Gastrointest Endosc. 2004;60(4):505-512. doi:10.1016/s0016-5107(04)01878-4

Van Assche G, Dignass A, Panes J, et al. The second European evidence-based Consensus on the diagnosis and management of Crohn's disease: Definitions and diagnosis. J Crohns Colitis. 2010;4(1):7-27. doi:10.1016/j.crohns.2009.12.003

Silverberg MS, Satsangi J, Ahmad T, et al. Toward an integrated clinical, molecular and serological classification of inflammatory bowel disease: report of a Working Party of the 2005 Montreal World Congress of Gastroenterology. Can J Gastroenterol. 2005;19 Suppl A:5A-36A. doi:10.1155/2005/269076

Gasche C, Scholmerich J, Brynskov J, et al. A simple classification of Crohn's disease: report of the Working Party for the World Congresses

of Gastroenterology, Vienna 1998. Inflamm Bowel Dis. 2000;6(1):8-15. doi:10.1097/00054725-200002000-00002

Klimczak K, Lykowska-Szuber L, Eder P, et al. The diagnostic usefulness of fecal lactoferrin in the assessment of Crohn's disease activity. Eur J Intern Med. 2015;26(8):623-627. doi:10.1016/j.ejim.2015.06.015

Schoepfer AM, Beglinger C, Straumann A, et al. Fecal calprotectin correlates more closely with the Simple Endoscopic Score for Crohn's disease (SES-CD) than CRP, blood leukocytes, and the CDAI. Am J Gastroenterol. 2010;105(1):162-169. doi:10.1038/ajg.2009.545

Lunney PC, Kariyawasam VC, Wang RR, et al. Smoking prevalence and its influence on disease course and surgery in Crohn's disease and ulcerative colitis. Aliment Pharmacol Ther. 2015;42(1):61-70. doi:10.1111/apt.13239

Kuenzig ME, Lee SM, Eksteen B, et al. Smoking influences the need for surgery in patients with the inflammatory bowel diseases: a systematic review and meta-analysis incorporating disease duration. BMC Gastroenterol. 2016;16(1):143. Published 2016 Dec 21. doi:10.1186/s12876-016-0555-8

Cosnes J, Beaugerie L, Carbonnel F, Gendre JP. Smoking cessation and the course of Crohn's disease: an intervention study. Gastroenterology. 2001;120(5):1093-1099. doi:10.1053/gast.2001.23231

Goodhand JR, Wahed M, Mawdsley JE, Farmer AD, Aziz Q, Rampton DS. Mood disorders in inflammatory bowel disease: relation to diagnosis, disease activity, perceived stress, and other factors. Inflamm Bowel Dis. 2012;18(12):2301-2309. doi:10.1002/ibd.22916

Ananthakrishnan AN, Gainer VS, Perez RG, et al. Psychiatric co- morbidity is associated with increased risk of surgery in Crohn's disease. Aliment Pharmacol Ther. 2013;37(4):445-454. doi:10.1111/apt.12195

Peyrin-BirouletPeyrin-Biroulet L, Sandborn W, Sands BE, et al. Selecting Therapeutic Targets in Inflammatory Bowel Disease (STRIDE): Determining Therapeutic Goals for Treat-to-Target. Am J Gastroenterol. 2015;110(9):1324-1338. doi:10.1038/ajg.2015.233

Brogden RN, Sorkin EM. Mesalazine. A review of its pharmacodynamic and pharmacokinetic properties, and therapeutic potential in chronic inflammatory bowel disease. Drugs. 1989;38(4):500-523. doi:10.2165/00003495-198938040-00003

Lialda (Mesalamine). Package Insert. Shire US, Inc. 2007.

Teruel AH, Gonzalez-Alvarez I, Bermejo M, et al. New Insights of Oral Colonic Drug Delivery Systems for Inflammatory Bowel Disease Therapy. Int J Mol Sci. 2020;21(18):6502. Published 2020 Sep 5. doi:10.3390/ijms21186502

Ford AC, Kane SV, Khan KJ, et al. Efficacy of 5-aminosalicylates in Crohn's disease: systematic review and meta-analysis. Am J Gastroenterol. 2011;106(4):617-629. doi:10.1038/ajg.2011.71

Hanauer SB, Strömberg U. Oral Pentasa in the treatment of active Crohn's disease: A meta-analysis of double-blind, placebo-controlled trials. Clin Gastroenterol Hepatol. 2004;2(5):379-388. doi:10.1016/s1542-3565(04)00122-3

Azulfadine. (Sulfasalazine). Package Insert. Pfizer. 2009.

Malchow H, Ewe K, Brandes JW, et al. European Cooperative Crohn's Disease Study (ECCDS): results of drug treatment. Gastroenterology. 1984;86(2):249-266.

Summers RW, Switz DM, Sessions JT Jr, et al. National Cooperative Crohn's Disease Study: results of drug treatment. Gastroenterology. 1979;77(4 Pt 2):847-869.

Entocort (Budesonide). Package Insert. Perrigo. 2016.

Khan KJ, Ullman TA, Ford AC, et al. Antibiotic therapy in inflammatory bowel disease: a systematic review and meta-analysis [published correction appears in Am J Gastroenterol. 2011 May;106(5):1014. Abadir, A [corrected to Abadir, Amir]]. Am J Gastroenterol. 2011;106(4):661-673. doi:10.1038/ajg.2011.72

Sutherland L, Singleton J, Sessions J, et al. Double blind, placebo controlled trial of metronidazole in Crohn's disease. Gut. 1991;32(9):1071-1075. doi:10.1136/gut.32.9.1071

Colombel JF, Lémann M, Cassagnou M, et al. A controlled trial comparing ciprofloxacin with mesalazine for the treatment of active Crohn's disease. Groupe d'Etudes Thérapeutiques des Affections Inflammatoires Digestives (GETAID). Am J Gastroenterol. 1999;94(3):674-678. doi:10.1111/j.1572-0241.1999.935_q.x

Steinhart AH, Feagan BG, Wong CJ, et al. Combined budesonide and antibiotic therapy for active Crohn's disease: a randomized controlled trial. Gastroenterology. 2002;123(1):33-40. doi:10.1053/gast.2002.34225

Imuran (Azathioprine). Package Insert. Pharmaceuticals International. 2011.

Mercaptopurine. Package Insert. Stasson Pharmaceuticals. 2020.

Methotrexate. Package Insert. West-Ward Pharmaceuticals Corp. 2020.

Kawalec P, Mikrut A, Wiśniewska N, Pilc A. Tumor necrosis factor-α antibodies (infliximab, adalimumab and certolizumab) in Crohn's disease: systematic review and meta-analysis. Arch Med Sci. 2013;9(5):765-779. doi:10.5114/aoms.2013.38670

Ford AC, Sandborn WJ, Khan KJ, Hanauer SB, Talley NJ, Moayyedi P. Efficacy of biological therapies in inflammatory bowel disease: systematic review and meta-analysis. Am J Gastroenterol. 2011;106(4):644-660. doi:10.1038/ajg.2011.73

Remicade (Infliximab). Package Insert. Janssen Biotech. 2013..

Humira (Adalimumab). Package Insert. Abbott Laboratories. 2011.

Cimzia (Certolizumab pegol). Package Insert. UCG Inc. 2016.

Tysabri (Natalizumab). Package Insert. Elan Pharmaceuticals. 2012.

Entyvio (Vedolizumab). Package insert. 2022.

Stelara (Ustekinumab). Package Insert. Janssen. 2012.

Parray FQ, Wani ML, Malik AA, et al. Ulcerative colitis: a challenge to surgeons. Int J Prev Med. 2012;3(11):749-763.

O'Reilly C, Mills S, Rea MC, et al. Interplay between inflammatory bowel disease therapeutics and the gut microbiome reveals opportunities for novel treatment approaches. Microbiome Res Rep. 2023;2(4):35. doi:10.20517/mrr.2023.41

Choi DK, Rubin DT, Puangampai A, Lach M. Role and Impact of a Clinical Pharmacy Team at an Inflammatory Bowel Disease Center. Crohns Colitis 360. 2023;5(2):otad018. Published 2023 Apr 15. doi:10.1093/crocol/otad018



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