Faculty
Gary R. Lichtenstein, MD Louis Kuritzky, MD
Director, Inflammatory Bowel Assistant Professor
Disease Center Emeritus
Professor of Medicine Family Medicine
Hospital of the University of Residency Program
Pennsylvania University of Florida
Philadelphia, PA Community Health &
Family Medicine
Gainesville, FL
Disclosures
Gary R. Lichtenstein, MD
Consulting for: Abbvie, Actavis, Alaven, Celgene, Ferring, Hospira,
Ironwood Pharmaceuticals, Janssen Orthobiotech, Luitpold
Pharmaceuticals, Merck, Pfizer, Prometheus Laboratories, Inc.,
Romark, Valeant, Shire Pharmaceuticals, Takeda, UCB
Louis Kuritzky, MD
Has no relevant financial relationships to disclose.
Learning Objectives
Apply evidence-based testing and tools to
diagnose IBD in primary care practice
Discuss efficacy and safety of conventional
and biologic therapies for IBD
Develop a health maintenance plan for a
patient with IBD
IBD, inflammatory bowel disease.
WHY SHOULD PRIMARY CARE CLINICIANS
BE CONCERNED ABOUT IBD?
Louis Kuritzky, MD
Scope of IBD in USA
Estimated prevalence1
• UC: 37-346:100,000
• CD: 26-199:100,000
Physician visits: >700,000/year2
Hospitalizations: 100,000/year2
Annual direct costs: ~$4 billion3
1. Lichtenstein G. 2012. Goldman's Cecil Medicine. 24th ed. . Philadelphia, PA: Elsevier Saunders; 2012:913-921.
2. CDC. http://www.cdc.gov/ibd/. 2015.
3. Lichtenstein GR. Am J Gastroenterol. 2016.[Abstract 682]
Clinical Consequences
of Delayed IBD Diagnosis
Poor quality of life
Early referral to GI is
Relapse rates important for
effective treatment
Increased cancer risk
Infection risk Delayed diagnosis
Anemia ↓
Delayed treatment
CD: Progressive disease w/strictures
↓
CD: penetrating disease Worse outcomes
GI, gastrointestinal.
Anderson NN, et al. JAMA. 2014;311:2406-2413.
Kotlyar D, et al. Gastroenterol. 2015; 13:847-858.
Lichtenstein GR, et al. Am J Gastroenterol. 2012;107:1409-1422.
What is the Role of
Primary Care Clinicians in IBD?
• IBD patients do not receive preventive services at the same rate as general
medical patients
• Immunosuppressive and biological agents are being used earlier and for
longer in the course of disease
– Potential to increase the risk of opportunistic and serious infections in
IBD patients
IBD-Related Health Issues Addressed by Primary Care Clinicians
Monitoring IBD-related complications Pap smears
Osteoporosis Smoking cessation
Iron deficiency Dermatological evaluation
Cardiovascular disease Psychosocial factors
Cancer Sexual/reproductive health
Vaccination Medication adherence
Monitoring laboratory studies Recognition of IBD relapse and/or acute severe colitis
Sinclair JA, et al. Gastroentergology. 2012;41(2):325-337.
Bennett A, et al. World J Gastroenterol. 2015;21(15):4457-4465.
Gikas A. Int J Gen med. 2014;7:159-173
The Role of
Primary Care Clinicians in IBD
Initial recognition of signs +
symptoms that warrant specialist
investigation and diagnostic
evaluation
Ongoing health maintenance for
the IBD patient
IDENTIFYING IBD IN PRIMARY CARE
Louis Kuritzky, MD
Etiologic Theories in Inflammatory Bowel
Disease
Mucosal Immune System
Genetic (Immuno-Regulatory
predisposition Defect)
IBD
Environmental Triggers
(luminal bacteria,
infection, NSAIDs,
smoking)
Clinical Features
of Ulcerative
Colitis
Colon only
Rectal involvement
Mucosal disease
Diffuse ulceration, granularity,
friability, bleeding, exudate
No fistulas or granulomas
Non-smokers
No prior appendectomy
Symptomatology of Ulcerative Colitis
Altered bowel movements
- Increased stool frequency
- Decreased stool consistency
Abdominal pain
- LLQ cramping, relieved with
defecation
- Tenesmus
Blood in stool
Clinical Features of Crohn’s Disease
Any segment
Rectal sparing
Skip lesions
Transmural
Aphthous ulcers, serpiginous
ulcers, cobblestoning
Fistulae
Granulomas
Smokers
Crohn’s Disease Symptomatology
Chronic or nocturnal diarrhea and abdominal pain
Postprandial RLQ abdominal pain, distension
Weight loss
Fever
Rectal bleeding
RLQ, right lower quadrant
Lichtenstein GR et al. Am J Gastroenterol 2009;104:465-83; quiz 464, 484.
Extraintestinal Manifestations of IBD
Peripheral arthritis
Joints Ankylosing spondylitis and
sacroiliitis
Kidney stones
Pyoderma gangrenosum
Interstitial Renal Skin Erythema nodosum
nephritis
Venous Episcleritis
Hypercoagula
thrombosi ble state
Eyes Uveitis
s Cataracts
Hepatobili
ary Sclerosing
cholangitis
Gallstones
Levine JS, et al. Gastroenterol Hepatol (N Y). 2011;7(4):235-241.
Components of IBD Diagnosis
• History
• Physical Examination
• Labs
– CBC, CMP, ESR, CRP, iron studies,
Endoscopy vitamin B12
• Fecal calprotectin or lactoferrin
Histology • Stool
– C difficile toxin, culture, ova &
parasites
• Colonoscopy
Radiography • EGD if CD suspected
– Wireless capsule endoscopy of small
intestine
Clinical course of symptoms – CT and MRI enterography
– Barium small bowel follow through
– Device assisted balloon enteroscopy
CBC, complete blood count; CMP, comprehensive metabolic panel; CRP, C-reactive protein;
EGD = esophagogastroduodenoscopy; ESR, erythrocyte sedimentation rate; CT, computed tomography; MRI, magnetic
resonance imaging.
Mill J, Lawrence IC. WJG. 2014;20(29):9691-9698.
Kornbluth A, et al. Am J Gastroenterology. 2010;105(3):501-523.
CURRENT TREATMENT OVERVIEW
Gary R. Lichtenstein, MD
Treatment Goals
Induce clinical remission (absence of symptoms)
Avoid short- and long-term toxicity of treatment
Enhance quality of life
Maintain steroid-free remission
• Avoid repeated courses of steroids!
Induce “deep” remission
• Biologic remission (normalization of biomarkers)
• Mucosal healing
Prevent complications (hospitalizations, surgery, etc)
Reduce cancer risk
Reenaers C, et al. World J Gastroenterol. 2012;18(29):3823-3827
Hommes D, et al. J Crohns Colitis. 2012;6(Suppl 2):S224-S234.
Progression of Digestive Disease Damage
and Inflammatory Activity
Stricture
Inflammatory Activity
Surgery
(CDAI, CDEIS, CRP)
Digestive Damage
Fistula/abscess
Stricture
Disease Diagnosis Early
onset disease
Pre-clinical Clinical
Pariente B et al. Inflamm Bowel Dis 2011;17(6):1415-22
CDAI: Crohn's Disease Activity Index; CDEIS : Crohn’s Disease Endoscopic
Index of Severity; CRP: C-Reactive Protein
Risk Factors for a More Severe
Disease Course
Crohn’s Disease Ulcerative Colitis
Early age at diagnosis (<40) Early age at diagnosis (<40)
Perianal involvement Early steroid treatment
Severe deep ulcerations on Extensive colitis
endoscopy Hospitalization @ diagnosis
Multiple areas of bowel
involvement Elevated inflammatory
Current tobacco use markers
- CRP, ESR
Other
- Prior resections
Low serum albumin
- Stricturing or penetrating
disease
- Early steroid treatment
Peyrin-Biroulet L, et al. Clin Gastroenterol Hepatol. 2016;14(3):348-354.
Treatment Paradigm Shift:
Decision-Making in IBD
OLD = treat based on NEW = treat based on
symptoms objective markers of
• But symptoms are insensitive and inflammation
nonspecific for bowel • Serologic (CRP reduction)
inflammation • Endoscopic (mucosal healing)
• Radiographic (CTE/MRI
improvement)
Conventional Approach to Induction Therapy:
Step Up
Disease Severity
at Presentation Investigational agent/
Surgery
Anti-TNF +/-IS Anti-TNF/Anti-Integrin
Severe Anti-Integrin +/- IS
Systemic Thiopurine/
Moderate Corticosteroid MTX
Budesonide Budesonide
Mild Induction
Maintenance
Therapy is stepped up according to severity at presentation or failure at prior step
Clinical approach to use “mildest” form of drug therapy to treat patients first
Move to next step in non-responders
Step Up Management
Advantages Disadvantages
Patients attain remission with
Patients have to ‘earn’ most
less toxic therapy
Potentially more toxic effective treatments
↓ QoL before patients
therapies reserved for severe
obtain optimal therapy
or refractory disease High likelihood of surgery
Minimizes risk of adverse
Disease is not modified
events
Cost-sparing (short-term?)
New Paradigm: Treating Beyond Symptoms
Early
“Top-Down Approach”
IMs + TNF
Severe antagonist
Anti-TNF Agents UC CD
Infliximab + +
Adalimumab + +
TNF antagonist
+/- IMs Golimumab +
Certolizumab +
Corticosteroids
Moderate +/- IMs Pegol +
Anti-integin Agents
Corticosteroids
Vedolizumab + +
Conventional Natalizumab +
”Bottom-Up Approach”
IMs, immunosuppressant; UC, ulcerative colitis; CD, Crohn’s disease.
D'Haens GR. Nat Rev Gastroenterol Hepatol. 2010 Feb;7(2):86-92.
Terdiman JP, et al. Gastroenterology. 2013 Dec;145(6):1459-63.
Sandborn WJ, et al. J Crohns Colitis. 2014;8(9):927-935. Amezaga AJ, et al. Curr Gastroenterol Rep. 2016 Jul. 18 (7):35.
Evolving Treatment Approach in UC
Current Approach Emerging Approach
Newer therapies w/favorable
Assessment of prognosis
safety + side-effect profiles
Optimization of AZA/6-MP
Individualized therapy based
dose or metabolites
on genetics + physiology
Earlier adoption of biologic
Treatment to hard endpoints
therapy when appropriate e.g. mucosal healing or
Appreciation for the its surrogates)
implications of mucosal Disease monitoring to
healing
prevent relapse
Current Medications for Active Disease
5-Aminosalicylic acid Immunomodulator agents
- azathioprine, 6-mercaptopurine,
derivatives
methotrexate, cyclosporine
- sulfasalazine, mesalamine,
Tumor necrosis factor inhibitors
balsalazide, olsalazine
- Infliximab
Antibiotics - Adalimumab
- metronidazole, ciprofloxacin, - certolizumab pegol
rifaximin - golimumab
Corticosteroid agents Anti-integrin agents
- hydrocortisone, prednisone, - natalizumab
- vedolizumab
methylprednisolone,
Anti-IL-12/23 agents
prednisolone, budesonide,
- Ustekinumab
dexamethasone
Current Medical Therapies for
Symptomatic Relief
Antidiarrheal agents
• diphenoxylate and atropine, loperamide,
cholestyramine
Anticholinergic antispasmodic agents
• dicyclomine, hyoscyamine
Serious Side Effects of Prolonged GCS
Therapy
Hypertension <20%
Diabetes 2.33 relative risk for beginning insulin
Infection 13-20%
Osteoporosis <50%
Myopathy 7%
Cataracts 22% (dose-dependent)
Psychosis (3-5%)
*Overall GCS therapy (not only therapy for CD).
Sandborn W. Can J Gastroenterol. 2000;14(suppl C):17C-22C.
Predictors of Serious Infection &
Death in CD
6273 patients in the TREAT registry; average follow-up: 5.2 years
Predictors of
Serious Infection HR Predictors of Death HR
Moderate to severe CD 2.24 Use of prednisone 2.14
Use of narcotic pain 1.98 Use of narcotic pain 1.79
relievers relievers
Use of prednisone 1.57
Use of IFX 1.43
Abbreviations: IFX, infliximab; HR, hazard ratio. P < .05 for all.
Lichtenstein GR, et al. Am J Gastroenterol. 2012;107(9):1409-1422.
Safety and Toxicity
Mesalamine Considerations
5-ASA
1
AZA/6-MP 4
MTX5-6
Low incidence of Incidence of kidney Pancreatitis (4%) Nausea/vomiting
adverse effects impairment occurs in Allergy (2%) Bone marrow
Diarrhea, less than 1 in 200 Bone marrow suppression
headache, nausea (<0.5%) patients suppression (4%) Liver scarring
most common treated with 5-ASA2 Liver toxicity (9%)
Serious infection (2%)
Abdominal pain
Dyspepsia
Acute tolerance
syndrome Clinically important Increased risk of Contraindicated if
interstitial nephritis lymphoma attempting pregnancy
Nephrotoxicity occurs in 1 in 500 Nonmelanoma skin
patients―50% of cases cancer
Pancreatitis occur in the first year, Abnormal Pap smears
and others may occur
many years later3
1. Feagan BG, et al. Cochrane Database Syst Rev. 2012;10:CD000544. 2. Gisbert JP, et al. Inflamm Bowel Dis.
2007;13(5):629-638. 3. World MJ, et al. Nephrol Dial Transplant. 1996;11(4):614-621. 4. Kotlyar D, et al, Clinical
Gastroenterology and Hepatology. 2015;13:847–858. 5. Lichtenstein GR, et al. Am J Gastroenterol.
2009;104(2):465-483. 6. Methotrexate injection USP [package insert]. Lake Forest, IL: Hospira, Inc.; 2011.
Anti-TNF Drug Safety
Infection and malignancy
• Black-box warning for serious infection and malignancy for all anti-TNF therapies 1-3
Black-box warning for HSTCL (ADA and IFX)1,2
Reactivation of hepatitis B4
Skin cancer4
Psoriasis4
Autoimmunity (lupus-like syndrome <1%)4
Immunogenicity―antibodies to anti-TNF4
Demyelinating disorders, CHF, liver toxicity4
CHF, congestive heart failure; 1. Remicade [package insert]. Horsham, PA: Janssen Biotech, Inc.; 2013.
2. Humira [package insert]. North Chicago, IL: AbbVie, Inc.; 2013.
HSTCL, hepatosplenic T-cell lymphoma
3. Simponi [package insert]. Horsham, PA: Janssen Biotech, Inc; 2013.
4. Bongartz T, et al. JAMA. 2006;295(19):2275-2285.
Anti-Integrin Drug Safety
Should not be used in patients:
• With impaired immunity
• Taking immunosuppressants (i.e Natalizumab)
• Taking TNF inhibitors
Increased risk for progressive multifocal
leukoencephalopathy (PML)
Headache, fatigue, depression, rash, nausea, abdominal
discomfort, UTI, arthralgia, respiratory infection
Ongoing Therapeutic Monitoring
Mesalamines
• Periodic kidney function w/urine + blood tests
Corticosteroids
• Bone health issues
Thiopurines
• TPMT, CBC, LFT during therapy
Methotrexate
• CBC, LFT, renal function during therapy, alcohol avoidance, pregnancy prevention
Anti-TNF
• Consider annual TB test
• Coccidiomycosis + histoplasmosis testing for patients living or who have lived in high
prevalence regions
Anti-Integrin
• Monitor for PML, LFTs, TB screening according to local practice, infection,
neurological symptoms
TPMT, thiopurine methyltransferase; CBC, complete blood count; LFT, liver function tests;
TB, tuberculosis; TNF, tumor necrosis factor.
EXTRAINTESTINAL MANIFESTATIONS
AND COMORBIDITIES
Louis Kuritzky, MD
Immune-Mediated Inflammatory Disorders
Bacteria Environmental factors
Genetics Others
Immunological alterations of
acquired + innate immunity
INFLAMMATION
Axial skeleton Kidney
Gut Eye
Peripheral joints Liver
Skin
Levine JS, Burakoff R. Gastroenterol Hepatol (N Y). 2011;7(4):235-241.
Dermatological Manifestations
• Erythema nodosum:
• Most common skin
manifestation
• Crohn’s disease >ulcerative colitis
• Up to 5% of patients
• Usually parallels disease activity
• Extensor surfaces of the
extremities
Skin Cancer
→ Sun protection
→ Dermatology screening
Levine JS, Burakoff R. Gastroenterol Hepatol. 2011;7(4):235-241
Dermatological Manifestations
• Pyoderma gangrenosum:
• Ulcerative colitis ~2%,
Crohn’s disease ~5 % of
patients
• Destructive cutaneous lesion
• Most common site is the legs
• Independent of disease
activity in 50% of patients
• Other skin lesions:
• Psoriasis ~10% in Crohn’s
disease
• Sweet’s syndrome
• Metastatic Crohn’s disease
Levine JS, Burakoff R. Gastroenterol Hepatol. 2011;7(4):235-241
Musculoskeletal Manifestations
• Peripheral arthritis:
• Occurs in 15% of patients
• Female:male ratio = 1:1
• Large joints,
nondeforming, nonerosive
• Spondylitis in 1-26%
• Male>female
• Sacroilitis:
• Frequency varies with
diagnostic modality:
• MRI pelvis Early diagnosis is key
• X-ray: 4-18% Back pain + morning stiffness
Symptoms unrelated to IBD activity
• Nuclear scan: up to 52%
Levine JS, Burakoff R. Gastroenterol Hepatol. 2011;7(4):235-241
Assess Bone Mineral Density
BMD decreased by • e.g. steroids, methotrexate,
some medications cyclosporine
Osteoporosis/
osteopenia
• Repeat in 1 year if abnormal
Measure BMD/DEXA • 2 years if normal + no change in status
• 1 year if normal + change in status
Bisphosphonates,
calcium, vitamin D
www.ccfa.org
Bernstein CD, et al. Clin Gastro Hepo. 2006
Ocular Manifestations
• Affects 43% of IBD patients
• Most commonly involve anterior chamber:
• Episcleritis: 2-5%
• Posterior chamber:
• Uveitis 0.5-3%
• Female:male ratio = 4:1
• Bilateral
• 75% have associated arthritis
• Requires immediate evaluation/emergency
• From steroid treatment:
• Cataracts
Annual screening
Felekis T, et al. Inflamm Bowel Dis. 2009. Levine JS, Burakoff R. Gastroenterol Hepatol. 2011;7(4):235-241
Hypercoagulable State
• Thrombosis in IBD: 1.3-6.4%
• Mostly follows disease activity
• Multifactorial:
• Factor V Leiden deficiency
• Thrombocytosis
• Hyperhomocysteinemia
• Catheters
Owczarek D, et al. World J Gastroenterol. 2014;20(1):53-63.
Hepatobiliary Complications
Primary sclerosing cholangitis:
• Occurs in 2% of ulcerative colitis patients
• 90% of primary sclerosing cholangitis patients have
ulcerative colitis
• Cholangiocarcinoma
Fatty liver
Effects of medications
Gallstones:
• ~33% of patients with ileal disease
Levine JS, Burakoff R. Gastroenterol Hepatol. 2011;7(4):235-241
Aphthous Stomatitis
Most common oral lesion in IBD
Highly variable response to steroids and
antibiotics
Need to consider nutritional deficiencies
- Folate
- Zinc
- Vitamin B12
- Iron
Levine J. In: Kirsner JB, ed. Inflammatory Bowel Disease. 5th ed. 2000:397.
Su CG et al. Gastroenterol Clin North Am. 2002;31:307.
Renal Manifestations in IBD
Occur in 4% to 23% of Obstructive uropathy
patients - Especially in CD, may occur
from intestinal inflammation
Nephrolithiasis most pressing on ureter
common - Treatment is surgery
- Prevalence of 7% to 10% Urinary tract fistulization
- Multifactorial causes - May present as
- Usually calcium oxalate stones pneumaturia, fecaluria,
From hyperoxaluria or recurrent infection
Treatment includes calcium - Successfully treated with
- Also uric acid stones immunomodulators,
Treat as any other anti-TNF therapy
kidney stone
Su CG et al. Gastroenterol Clin North Am. 2002;31:307.
Vaccinations, Cancer screening
HEALTH MAINTENANCE IN IBD
Louis Kuritzky, MD
Recommended Immunization Schedule for Adults
Aged 19 Years or Older, by Vaccine and Age Group
• Consider vaccinating ALL susceptible IBD patients at diagnosis before
immunosuppressed
• ”High-dose" flu vaccine available for people ≥65 years
Caution for
patients on anti-
TNF
Check Varicella UNLESS
on prednisone > 20 mg/day or
on immunosuppressives
(currently or recently Give to ALL patients
discontinued within 3 months (high, low or planned
immune suppression)
and once 5 years later
If non immune, then vaccinate.
If infected, treat prior to starting
anti-TNF medications
Kim DK, et al. Ann Intern Med. 2016;164(3):184-194.
Will the Vaccinations Work in
Immunosuppressed IBD Patients?
IBD patients receiving pneumovax, tetanus, influenza and HIB on
azathioprine/6MP monotherapy had a normal response to
vaccinations
Adult
- IBD patients receiving pneumococcal vaccine had poor response if on
combination anti-TNF + immunomodulator therapy
Pediatric
- IBD patients receiving influenza vaccine had a poor response if on
combination anti-TNF + immunomodulator therapy
In patients with juvenile systemic lupus, main predictor of LACK
of response was a higher disease activity (not immune
suppression)
Lu Y, et al. Am J Gastroenterol 2009;104:444-53.
Melmed GY. Gastroenterol Hepatol. 2008;4(12):859-861
Campos LM, et al. Arthritis Care Res 2013;65:1121-1127
Colorectal Cancer Risk in IBD
• Duration of disease >8 years
• Family history of colorectal
cancer increases risk
• Primary sclerosing cholangitis
(PSC)
Farraye FA, et al. Gastroenterology. 2010;138:746-774.e4.
Cancer Surveillance
Screening colonoscopy 8-10
years after symptom onset to
detect dysplasia
Surveillance colonoscopy
every 1-3 years to detect
dysplasia with colectomy if
positive
CRC, colorectal.
Farraye FA, et al. Gastroenterology. 2010;138:746-774.e4.
American Society for Gastrointestinal Endoscopy and American Gastroenterological Association. GIE. 2015;81(3):489-
501
Smoking Cessation
HEALTH MAINTENANCE IN IBD
Gary R Lichtenstein, MD
Cigarette Smoking and IBD: Meta-Analysis
Ulcerative Colitis Crohn’s Disease
• 13 studies, >11,000 patients • 9 studies, >10,000 patients
for UC for CD
• Current smoking is • Current smoking is
protective of development associated with CD
of UC – OR, 1.76 (95% CI, 1.40-2.22)
– OR, 0.58 (95% CI, 0.45-0.75) • Former smoking is weakly
• Quitting smoking is associated with CD
associated with UC – OR, 1.30 (0.97-1.76)
– OR, 1.79 (1.37-2.34)
Effects of cessation: 65%
lower risk of flare up vs
continuing Lower needs for
steroids + medications
Mahid SS, et al. Mayo Clin Proc. 2006;81(11):1462-1471.
Abbreviations: OR, odds ratio; CI, confidence interval.
Effective Medications
for Smoking Cessation
Nicotine replacement products
Over-the-counter (nicotine patch [which is
also available by prescription], gum,
lozenge)
Prescription (nicotine patch, inhaler, nasal
spray)
Prescription non-nicotine medications:
bupropion SR,2 varenicline tartrate
Counseling and medication are both
effective for treating tobacco dependence,
and using them together is more effective
than using either one alone
SR, sustained release.
http://www.cdc.gov/tobacco/data_statistics/fact_sheets/cessation/quitting/index.htm#methods
Depression Screening
• Affects 15%-35% of IBD patients
– Relapsing nature of disease
– Chronic pain
– Steroids
• American College of Preventive Medicine/USPSTF
recommend screening
SCREENING QUESTIONS
1. Over the past month, have you felt down, depressed, or hopeless?
2. Over the past month, have you felt little interest or pleasure in doing things?
Siu AL, et al. JAMA. 2016;315(4):380-7
Self-Management in IBD
Self-management is • Entails clear goals, understanding
critical to patient of the disease, plan of action to
improvement reduce symptoms or prevent
disease activity
Psychological issues,
shared decision • Depends on a good
making, and individual patient/clinician relationship
patient characteristics
should be discussed
Kennedy A, et al. Health Educ Res. 2005;20(5):567-578.
Bennett AL, et al. World J Gastroenterol. 2015;21(15):4457-4465.
SUMMARY
Health Maintenance Summary
Vaccinations: influenza, pneumococcal pneumonia, zoster, Hep A, Hep B
DEXA Scan
• All CD and UC patients with conventional risk factor for abnormal BMD
Refer to GI to attempt corticosteroid withdrawal
• 6-MP / AZA, MTX, anti-TNF , Anti-integrin therapy Anti- IL – 12/23
A multivitamin daily; folate, calcium
Colon cancer surveillance
• After 8-10 years colonoscopy with biopsies [1-3 years] to assess for dysplasia
Annual Pap smears if immunocompromised
DEXA, dual-energy X-ray absorptiometry; GI, gastrointestinal; AZA, MTX, TNF
Health Maintenance Summary
Frequent dermatological evaluation: melanoma/NMSC
Beware of NSAIDs in IBD
• Disease may flare, bleeding may occur
Beware of other steroid side effects
•Cataracts, hypogonadism, osteonecrosis, etc.
Pregnancy
•Ensure that medications are safe + disease is in remission
Diagnosis
•In those with symptoms/signs, remember genetics
•When EIM present, think of disease
NMSC, non-melanoma skin cancer
NSAIDs, non-steroidal anti-inflammatory drugs; EIM, extraintestinal manifestations.