IBD nursing: Crohn's disease and ulcerative colitis care guide

LS
By Lindsay Smith, AGPCNP
Updated March 22, 2026

Inflammatory bowel disease (IBD) affects approximately 3 million adults in the United States. The two primary forms — Crohn’s disease and ulcerative colitis — share features of chronic intestinal inflammation but differ in location, depth of involvement, complications, and surgical management. For nursing students, knowing how to distinguish these conditions, anticipate complications, and deliver evidence-based care is essential for clinical practice and NCLEX success. This reference covers the pathophysiology, clinical presentation, diagnostics, pharmacology, nursing interventions, and exam-focused review points for both diseases.

Use this alongside the GI bleed nursing reference, the cirrhosis nursing reference, and the electrolyte imbalances guide for a complete GI and hepatic knowledge base.


Crohn’s disease vs ulcerative colitis: key differences

The comparison table below is the single most tested concept in IBD nursing. Before memorizing interventions or medications, commit these distinctions to memory.

FeatureCrohn's diseaseUlcerative colitis
GI tract locationAnywhere from mouth to anus (most common: terminal ileum)Colon and rectum only
Distribution patternSkip lesions — diseased segments separated by normal bowelContinuous inflammation starting at the rectum and extending proximally
Depth of inflammationTransmural (full thickness — all bowel wall layers)Mucosal and submucosal layers only
Rectal involvementVariable — often sparedAlmost always involved (disease starts here)
Gross appearanceCobblestone mucosa, aphthous ulcersErythematous, friable mucosa with pseudopolyps
HistologyNon-caseating granulomas (pathognomonic)Crypt abscesses, goblet cell depletion
Fistulas and abscessesCommon (transmural inflammation creates abnormal tracts)Rare
StricturesCommon — fibrotic narrowing of bowel lumenUncommon
Stool characteristicsNon-bloody diarrhea, steatorrhea if ileal involvementBloody diarrhea with mucus and pus
Weight loss and malnutritionCommon (impaired absorption across affected segments)Less common unless severe pancolitis
Colorectal cancer riskIncreased (lower than UC)Significantly increased after 8–10 years of disease
Smoking effectWorsens disease — increases flares and surgical riskParadoxical mild protective effect (but cessation still recommended for overall health)
Surgery curative?No — disease can recur at anastomotic sitesYes — total proctocolectomy removes all diseased tissue

Memory tip: Think of Crohn’s as Cobblestone, Creeping fat, Can occur anywhere, and has Complicated fistulas. Ulcerative colitis is Uniform (continuous), Ulcerative (bloody), and limited to the Upper layers (mucosa/submucosa).


Pathophysiology overview

Both Crohn’s disease and ulcerative colitis result from a dysregulated immune response in genetically susceptible individuals. Environmental triggers — infections, stress, diet, and in the case of Crohn’s, smoking — activate mucosal T cells that produce excess pro-inflammatory cytokines (TNF-alpha, interleukins IL-12, IL-23, and IL-6). The resulting chronic inflammation damages the intestinal lining, but the pattern of damage differs between the two diseases.

Crohn’s disease

Crohn’s inflammation is transmural, meaning it penetrates through the mucosa, submucosa, muscularis, and serosa. This full-thickness involvement explains why Crohn’s produces fistulas (abnormal connections between the bowel and adjacent structures), abscesses, and strictures. The disease can affect any segment of the GI tract, though the terminal ileum and proximal colon are most common. Skip lesions — areas of diseased bowel separated by normal tissue — are a hallmark finding. Histologically, non-caseating granulomas are present in approximately 30% of biopsies and are considered pathognomonic.

The transmural inflammation also leads to “creeping fat,” where mesenteric adipose tissue wraps around the serosal surface of the affected bowel. This is visible on imaging and at surgery.

Ulcerative colitis

UC inflammation is confined to the mucosal and submucosal layers. It begins in the rectum and extends proximally in a continuous, uninterrupted pattern. Four subtypes describe the extent of involvement:

  • Ulcerative proctitis — rectum only (mildest form)
  • Proctosigmoiditis — rectum and sigmoid colon
  • Left-sided colitis — descending colon, sigmoid, and rectum
  • Pancolitis — entire colon involved (most severe, highest cancer risk)

Repeated cycles of ulceration and healing produce pseudopolyps (islands of regenerating mucosa) and scar tissue. Over time, the colon loses its haustra (normal folds), producing the classic “lead pipe” appearance on barium enema. The loss of haustral folds impairs water absorption, contributing to the profuse, bloody diarrhea characteristic of UC.


Clinical presentation and assessment

Nursing assessment of IBD requires systematic evaluation of GI symptoms, nutritional status, hydration, and extraintestinal findings.

Crohn’s disease presentation

  • Abdominal pain — typically right lower quadrant (terminal ileum); cramping, often postprandial
  • Diarrhea — non-bloody, watery to semi-formed; 4–6 stools per day during flares
  • Weight loss — progressive, from malabsorption and decreased oral intake due to pain
  • Perianal disease — fistulas, fissures, abscesses, skin tags (present in up to 30% of patients)
  • Fever and fatigue — systemic inflammatory response
  • Oral ulcers — aphthous stomatitis, particularly during flares
  • Palpable mass — right lower quadrant fullness may indicate thickened bowel loops or abscess

Ulcerative colitis presentation

  • Bloody diarrhea — hallmark symptom; stool contains blood, mucus, and pus
  • Stool frequency — 10–20 episodes per day during severe flares
  • Tenesmus — persistent urge to defecate despite an empty rectum (due to rectal inflammation)
  • Left-sided abdominal cramping — reflecting colonic involvement
  • Urgency — sudden, compelling need to evacuate; can cause incontinence
  • Weight loss — less pronounced than Crohn’s unless pancolitis is present

Key nursing assessments

  • Stool monitoring: document frequency, consistency, color, and presence of blood or mucus each shift
  • Abdominal assessment: auscultate bowel sounds (hyperactive during flares; absent or hypoactive may signal toxic megacolon), palpate for tenderness, distention, or masses
  • Nutritional status: daily weights, albumin levels, prealbumin, BMI tracking, dietary intake recording
  • Hydration status: monitor intake and output, skin turgor, mucous membrane moisture, urine specific gravity
  • Perianal skin assessment: inspect for fistula openings, excoriation, fissures (especially in Crohn’s)
  • Pain assessment: use a validated pain scale; note relationship to meals and bowel movements
  • Psychosocial assessment: screen for anxiety, depression, and social withdrawal — chronic IBD has high rates of mood disorders

Diagnosis and lab values

Endoscopy and imaging

Colonoscopy with biopsy is the gold standard for diagnosing and differentiating Crohn’s disease from ulcerative colitis. Key endoscopic findings include:

  • Crohn’s: aphthous ulcers, cobblestone mucosa, skip lesions, strictures; biopsy shows non-caseating granulomas
  • UC: continuous erythema, friability, pseudopolyps, loss of vascular pattern; biopsy shows crypt abscesses, goblet cell depletion

CT enterography or MR enterography is used for Crohn’s to evaluate small bowel involvement, strictures, fistulas, and abscesses. Barium studies may show the “lead pipe” sign in UC or “string sign” (narrowed ileum) in Crohn’s.

Laboratory values

Lab testExpected finding in active IBDClinical significance
CRP (C-reactive protein)Elevated (>10 mg/L)Acute-phase inflammatory marker; correlates with disease activity
ESR (erythrocyte sedimentation rate)Elevated (>20 mm/hr)Non-specific inflammation marker; slower to change than CRP
Fecal calprotectinElevated (>250 μg/g)Neutrophil-derived protein specific to intestinal inflammation; used to distinguish IBD from IBS and monitor disease activity
CBCLow hemoglobin/hematocrit (anemia); elevated WBC; elevated plateletsAnemia from chronic blood loss (UC) or malabsorption of iron, B12, folate (Crohn's); thrombocytosis increases DVT/PE risk
CMPLow albumin, electrolyte abnormalities (low K+, low Mg2+)Hypoalbuminemia indicates malnutrition; diarrhea depletes potassium and magnesium
Vitamin levelsLow B12 (ileal Crohn's), low folate, low vitamin D, low ironTerminal ileum absorbs B12; widespread malabsorption in Crohn's affects multiple nutrients
pANCA / ASCApANCA positive in ~70% UC; ASCA positive in ~60% Crohn'sSerologic markers that can support differentiation when endoscopy is inconclusive

Disease activity scoring

Clinicians use validated scoring tools to classify disease severity and guide treatment decisions. Two commonly referenced indices:

Harvey-Bradshaw Index (HBI) — Crohn’s disease

A simplified clinical scoring tool that does not require laboratory data. It assesses five parameters: general well-being, abdominal pain, number of liquid stools per day, abdominal mass, and complications (arthralgia, uveitis, erythema nodosum, aphthous ulcers, fistula, abscess, anal fissure).

HBI scoreDisease severity
<5Clinical remission
5–7Mild disease
8–16Moderate disease
>16Severe disease

Mayo Score — ulcerative colitis

A composite index scored from 0 to 12 that evaluates four components: stool frequency, rectal bleeding, endoscopic findings, and physician global assessment. Each component is scored 0–3.

Mayo scoreDisease severity
0–2Remission
3–5Mild disease
6–10Moderate disease
11–12Severe disease

Nurses should understand these indices because provider notes and treatment plans frequently reference them, and changes in score guide medication adjustments.


Medications used in IBD

IBD pharmacotherapy follows a stepwise approach: milder agents first, escalating to biologics for refractory disease. Some clinicians use a “top-down” approach for severe presentations, starting with biologics and de-escalating once remission is achieved.

Drug classExamplesMechanismNursing considerations
5-aminosalicylates (5-ASA)Mesalamine (Asacol, Lialda, Pentasa), sulfasalazineTopical anti-inflammatory; inhibits prostaglandin and leukotriene synthesis in intestinal mucosaFirst-line for mild-moderate UC. Sulfasalazine is contraindicated in sulfa allergy. Monitor renal function (rare interstitial nephritis). Available as oral, rectal suppository, or enema formulations. Advise patients to swallow delayed-release tablets whole.
CorticosteroidsPrednisone, prednisolone, budesonide (Entocort), methylprednisolone IVBroad anti-inflammatory and immunosuppressive; reduce cytokine productionUsed for acute flares, not maintenance (taper over weeks). Monitor blood glucose (steroid-induced hyperglycemia). Assess for adrenal suppression if used long-term. Watch for infection masking. Long-term risks: osteoporosis, cataracts, myopathy, cushingoid features. Budesonide has fewer systemic side effects due to high first-pass metabolism.
Immunomodulators (thiopurines)Azathioprine (Imuran), 6-mercaptopurine (6-MP)Inhibit purine synthesis to suppress T-cell proliferationSlow onset (3–6 months for full effect). Monitor CBC regularly — risk of bone marrow suppression (leukopenia, thrombocytopenia). Check TPMT/NUDT15 enzyme levels before starting (poor metabolizers at high risk of myelosuppression). Increased risk of lymphoma with long-term use. Avoid live vaccines. Report signs of infection immediately.
Immunomodulators (other)Methotrexate (Crohn's only)Folate antagonist; suppresses immune-mediated inflammationGiven IM or SubQ weekly. Supplement with folic acid 1 mg daily (reduces side effects). Teratogenic — requires reliable contraception. Monitor LFTs and CBC. Avoid alcohol.
Biologic — anti-TNF agentsInfliximab (Remicade), adalimumab (Humira), certolizumab pegol (Cimzia)Monoclonal antibodies that neutralize tumor necrosis factor-alphaScreen for latent TB (tuberculin skin test or QuantiFERON-Gold) and hepatitis B before starting — risk of reactivation. Monitor for infusion reactions (infliximab: fever, chills, dyspnea, chest tightness during IV administration). Increased risk of serious infections and malignancy. No live vaccines during treatment. Teach patients to report fever, persistent cough, or unusual fatigue.
Biologic — anti-integrinVedolizumab (Entyvio)Blocks alpha-4-beta-7 integrin, preventing lymphocyte migration to gut mucosaGut-selective — lower systemic immunosuppression than anti-TNF agents. Given IV every 8 weeks after induction. Still screen for TB before initiation. Monitor for nasopharyngitis, headache, arthralgia. Progressive multifocal leukoencephalopathy (PML) is a theoretical risk — report new neurological symptoms.
Biologic — anti-interleukinUstekinumab (Stelara)Blocks IL-12 and IL-23, reducing T-cell activationApproved for both Crohn's and UC. IV induction dose followed by SubQ maintenance every 8 weeks. Screen for TB. Monitor for infections, injection site reactions. Lower malignancy risk profile than anti-TNF agents in available data.
JAK inhibitorsTofacitinib (Xeljanz)Inhibits Janus kinase pathway to reduce cytokine signalingApproved for UC. Oral administration (advantage over IV biologics). Increased risk of herpes zoster — consider vaccination before starting. Monitor lipid panel (may increase cholesterol). Risk of thromboembolic events — assess VTE risk factors. Monitor CBC.
AntibioticsMetronidazole, ciprofloxacinReduce bacterial overgrowth in strictured or fistulizing bowelMetronidazole used for Crohn's perianal fistulas. Avoid alcohol with metronidazole (disulfiram-like reaction). Long-term metronidazole can cause peripheral neuropathy — report tingling or numbness. Monitor for C. difficile.
AntidiarrhealsLoperamide (Imodium), diphenoxylate-atropine (Lomotil)Decrease intestinal motilityUse with caution — contraindicated in severe colitis (risk of precipitating toxic megacolon). Short-term use for symptom relief in mild disease only. Never give during acute flare without provider approval.

Nursing interventions

Priority nursing interventions for IBD patients are organized by clinical need. During acute flares, fluid and electrolyte management takes precedence; during remission, the focus shifts to medication adherence and patient education.

Fluid and electrolyte management

Frequent diarrhea (10–20 episodes daily in severe UC) depletes fluid volume and electrolytes rapidly. Nursing actions include:

  • Maintain accurate intake and output records every shift
  • Administer IV fluid replacement as ordered (normal saline or lactated Ringer’s)
  • Monitor electrolytes — potassium, magnesium, calcium, and sodium are commonly depleted
  • Assess for signs of dehydration: dry mucous membranes, decreased skin turgor, concentrated urine, orthostatic hypotension
  • Weigh the patient daily at the same time, same scale, same clothing
  • Replace electrolytes per protocol (IV potassium never exceeds 10 mEq/hr via peripheral line)

See the electrolyte imbalances reference for detailed management of hypokalemia and hypomagnesemia.

Nutritional support

Malnutrition is common in IBD — especially in Crohn’s, where any segment of the absorptive tract can be affected.

  • During flares: Bowel rest (NPO) with IV fluids or total parenteral nutrition (TPN) may be ordered for severe cases. When oral intake resumes, advance diet gradually: clear liquids, then low-residue, then regular diet as tolerated.
  • Low-residue diet during flares: Avoid raw fruits and vegetables, whole grains, nuts, seeds, and high-fiber foods that increase stool bulk and can worsen obstruction risk in Crohn’s.
  • Foods to avoid: Dairy (many IBD patients have concurrent lactose intolerance), caffeine, alcohol, spicy foods, and gas-producing foods (beans, broccoli, carbonated beverages).
  • High-protein, high-calorie diet: Recommended during remission to rebuild lean body mass and promote mucosal healing.
  • Enteral nutrition: Exclusive enteral nutrition (EEN) using polymeric formulas is a first-line therapy for inducing remission in pediatric Crohn’s and an adjunct in adult Crohn’s. It provides complete nutrition while reducing antigenic stimulation of the gut.
  • Vitamin and mineral supplementation: Supplement B12 (if terminal ileum is diseased or resected), folate, iron, vitamin D, and calcium as indicated by lab values.
  • Consult a registered dietitian for individualized nutrition plans.

Pain management

  • Assess pain using a validated scale; document location, character, timing, and aggravating factors
  • Administer prescribed analgesics — acetaminophen is preferred
  • Avoid NSAIDs (ibuprofen, naproxen, ketorolac) — they can trigger or worsen IBD flares by disrupting mucosal prostaglandin protection
  • Opioids should be used cautiously and briefly; chronic opioid use in IBD is associated with narcotic bowel syndrome and increased mortality
  • Non-pharmacologic approaches: heat application, positioning, relaxation techniques

Bowel output monitoring

  • Document stool frequency, volume, consistency, color, and presence of blood, mucus, or pus
  • Test stool for occult blood when gross bleeding is absent but anemia progresses
  • Monitor for signs of worsening: increasing frequency, new blood in previously non-bloody stools (Crohn’s), progressive abdominal distention
  • Report sudden cessation of diarrhea with increasing abdominal distention — may indicate toxic megacolon

Skin care

  • Perianal care: Frequent liquid stools cause perianal excoriation. Clean gently with warm water (no harsh soaps) after each bowel movement. Apply barrier cream (zinc oxide, dimethicone) to protect intact skin. Use sitz baths for comfort.
  • Perianal fistula care: Assess fistula openings for drainage amount, color, and odor. Keep the area clean and dry. Report increased purulent drainage or fever. Seton drains may be in place — secure and monitor.
  • Ostomy care (if applicable): Patients with total proctocolectomy for UC will have an ileostomy. Monitor stoma color (should be beefy red — report dusky or black discoloration), measure output, maintain peristomal skin integrity, and educate the patient on appliance changes. Ileostomy output is liquid and high-volume, increasing dehydration risk. Refer to a wound/ostomy care nurse (WOCN) for individualized teaching.

Psychosocial support

IBD is a chronic, relapsing condition that significantly impacts quality of life. Rates of anxiety and depression are 2–3 times higher in IBD patients compared to the general population.

  • Screen for depression and anxiety using validated tools (PHQ-9, GAD-7)
  • Acknowledge the impact of chronic illness on body image, relationships, and daily functioning
  • Refer to mental health services, support groups, and the Crohn’s and Colitis Foundation
  • Discuss strategies for managing unpredictable symptoms in school, work, and social settings

Complications to monitor

Toxic megacolon

Toxic megacolon is a life-threatening complication primarily associated with ulcerative colitis (though it can occur in Crohn’s colitis). The colon dilates to greater than 6 cm on abdominal X-ray, with systemic toxicity.

Warning signs:

  • Sudden decrease in stool frequency (paralyzed colon stops evacuating)
  • Rapidly increasing abdominal distention and tympany
  • Fever greater than 38.6°C (101.5°F)
  • Tachycardia greater than 120 bpm
  • Absent or hypoactive bowel sounds (previously hyperactive)
  • Peritoneal signs: rebound tenderness, guarding, rigidity

Nursing response: Withhold antidiarrheal medications (they worsen dilation). Maintain NPO status. Continuous abdominal assessment. Prepare for emergent decompression or surgery. This is a surgical emergency if perforation occurs.

Perforation

Transmural inflammation (Crohn’s) or severe dilation (toxic megacolon in UC) can lead to bowel perforation. Assess for acute abdomen: sudden severe pain, rigid abdomen, absent bowel sounds, fever, tachycardia. Perforation causes peritonitis — notify the provider immediately and prepare for surgical intervention.

Fistulas (primarily Crohn’s)

Fistulas are abnormal communications between the bowel and adjacent structures:

  • Enteroenteric — bowel to bowel
  • Enterocutaneous — bowel to skin surface
  • Enterovesical — bowel to bladder (presents as pneumaturia, recurrent UTIs)
  • Enterovaginal — bowel to vagina (passage of stool or gas vaginally)
  • Perianal — bowel to perianal skin (most common)

Nursing care: monitor drainage, maintain skin integrity around fistula openings, track output for fluid balance, and support nutritional status. Perianal fistulas are treated with antibiotics (metronidazole), setons, and anti-TNF biologics.

Strictures and bowel obstruction (primarily Crohn’s)

Chronic inflammation leads to fibrotic narrowing. Assess for obstructive symptoms: colicky abdominal pain, nausea, vomiting, abdominal distention, high-pitched or absent bowel sounds. Strictures may require endoscopic dilation or surgical resection.

Colorectal cancer

UC patients with pancolitis for 8–10 years or longer have a significantly elevated risk. Surveillance colonoscopy is recommended every 1–2 years starting 8 years after diagnosis. Crohn’s colitis also carries elevated risk, though lower than UC. Ensure patients understand the importance of adherence to surveillance schedules.

Extraintestinal manifestations

IBD can affect organ systems beyond the GI tract. These complications occur in up to 25% of patients:

  • Musculoskeletal: peripheral arthritis (most common extraintestinal manifestation), ankylosing spondylitis, sacroiliitis
  • Dermatologic: erythema nodosum (tender red nodules on shins), pyoderma gangrenosum (deep, painful skin ulcers)
  • Ocular: uveitis, episcleritis — report eye pain, redness, or vision changes immediately
  • Hepatobiliary: primary sclerosing cholangitis (PSC) — strongly associated with UC; presents with elevated alkaline phosphatase and bile duct strictures on MRCP
  • Hematologic: venous thromboembolism risk is 2–3 times higher in IBD patients (elevated platelets and inflammatory state create a hypercoagulable state); assess for DVT/PE symptoms
  • Oral: aphthous ulcers (common in Crohn’s)

Patient education

Effective patient education improves medication adherence, reduces preventable flares, and empowers patients to recognize warning signs that need medical attention.

Medication adherence

Many IBD patients stop maintenance medications during remission because they feel well. Emphasize that 5-ASA agents and immunomodulators are designed to maintain remission, and stopping them increases relapse risk. Teach patients to never discontinue medications without consulting their gastroenterologist.

Smoking cessation

Smoking has a direct and divergent effect on IBD: it worsens Crohn’s disease (doubles the risk of flares and surgical recurrence) while showing a paradoxical mild protective effect in ulcerative colitis. Despite this UC-specific finding, smoking cessation is recommended for all IBD patients because the cardiovascular, pulmonary, and cancer risks far outweigh any intestinal benefit. After quitting, UC patients may experience a temporary flare — providers should anticipate this and adjust therapy proactively.

Diet and nutrition

  • Follow a low-residue diet during flares; transition to a balanced, high-protein diet during remission
  • Keep a food diary to identify personal trigger foods
  • Stay hydrated — aim for at least 2 liters of fluid daily, more if diarrhea is active
  • Avoid NSAIDs, as they can trigger flares
  • Limit alcohol, which irritates the intestinal lining

Stress management

Psychological stress does not cause IBD, but it can trigger flares in established disease. Encourage stress-reduction strategies: regular exercise (as tolerated), mindfulness, adequate sleep, and professional counseling when needed.

Cancer surveillance

Patients with UC (especially pancolitis) or Crohn’s colitis should begin surveillance colonoscopies 8 years after diagnosis, then every 1–2 years. Those with concurrent PSC should start annual colonoscopy at the time of PSC diagnosis, regardless of IBD duration.

When to seek emergency care

Teach patients to go to the emergency department for: sudden severe abdominal pain with distention, high fever with abdominal rigidity, large-volume rectal bleeding, signs of dehydration unresponsive to oral fluids, or symptoms of bowel obstruction (vomiting, inability to pass stool or gas).


NCLEX tips

  • Crohn’s = skip lesions, transmural, terminal ileum, fistulas, cobblestone mucosa. UC = continuous, mucosal, colon only, bloody diarrhea, pseudopolyps.
  • Toxic megacolon is primarily a UC complication. Warning signs: sudden decrease in diarrhea, increasing abdominal distention, absent bowel sounds, fever, tachycardia. Withhold antidiarrheals. This is a surgical emergency.
  • TB screening is required before starting any biologic therapy (infliximab, adalimumab, vedolizumab, ustekinumab). A positive tuberculin skin test or QuantiFERON-Gold requires treatment for latent TB before the biologic can begin.
  • No live vaccines while on immunosuppressive therapy (azathioprine, 6-MP, methotrexate, biologics). This includes MMR, varicella, live influenza (nasal spray), and oral polio.
  • NSAIDs are contraindicated in IBD — they can precipitate flares. Acetaminophen is the preferred analgesic.
  • Sulfasalazine is contraindicated in sulfa allergy. Use mesalamine (non-sulfa 5-ASA) as an alternative.
  • Fecal calprotectin is the best non-invasive test to distinguish IBD from IBS. Elevated calprotectin indicates intestinal inflammation; normal levels suggest functional (non-inflammatory) disease.
  • Smoking worsens Crohn’s, has a paradoxical protective effect in UC — but cessation is still recommended for overall health. Expect this as a test question asking you to identify correct patient teaching.
  • Metronidazole is used for Crohn’s perianal fistulas. Teach patients to avoid alcohol (disulfiram-like reaction) and report peripheral neuropathy symptoms (tingling, numbness).
  • Total proctocolectomy cures UC because the disease is confined to the colon. Crohn’s cannot be cured surgically — it recurs at anastomotic sites.
  • B12 deficiency occurs in Crohn’s when the terminal ileum is diseased or resected (the terminal ileum is the exclusive absorption site for B12). UC does not cause B12 deficiency because the colon does not absorb B12.
  • Azathioprine and 6-MP require TPMT enzyme testing before initiation. Patients with low TPMT activity are at high risk for life-threatening myelosuppression.