In the United States, gastrointestinal disorders in geriatric patients account for a significant portion of clinician visits, inpatient hospitalizations, and healthcare expenditures.1 Inflammatory bowel disease (IBD), a group of debilitating conditions of which the vast majority of cases are composed of ulcerative colitis (UC) and Crohn’s disease (CD), is found with increasing frequency in the elderly. This may be partially attributed to an increasing number of IBD patients currently living into old age.2 This article will review treatment issues and briefly discuss the relevance of vitamin D in IBD.
IBD affects up to 0.5% of the population in developed countries and an increasing proportion in developing nations.3-5 These conditions are most prevalent in Western countries and in areas of northern latitude.6,7 For example, the incidence and prevalence of IBD are higher in northern Europe, North America, Australia, and New Zealand than in Asia.3,4,8,9 Along those lines, the incidence of IBD in the Indian subcontinent is low; however, migrants to developed countries located at northern latitudes have a greatly increased risk of IBD.10 Furthermore, the onset of UC and exacerbations of CD are noted to peak in winter months in the Northern Hemisphere.11,12 The highest reported prevalence rates of IBD are in Scandinavia, Great Britain, and North America.6,7 The physiological activity of vitamin D is thought to be related to these observations. (See below, Vitamin D Deficiency in IBD.)
Although IBD affects both genders equally, some studies indicate that more women suffer from CD, whereas more males suffer from UC.7 While onset of IBD is more common in early adulthood, epidemiologic evidence suggests a bimodal distribution of the age of onset of both UC and CD; peak incidence occurs in the second and third decades and a late-onset minor peak between 60 and 80 years.1,13-15 Notably in the elderly population, there are challenges in diagnosis of gastrointestinal (GI) disorders that go beyond those of other patients. These include 1) comorbid illnesses such as dementia and depression that may impair communication between the patient and the caregiver; 2) medications, such that therapeutic and adverse effects may cloud the clinical picture in seniors, in whom polypharmacy is common; and 3) intestinal symptoms in the elderly that may be manifestations of other diseases.1
Etiology, Underlying Pathogenesis, and Complications
While the exact etiology of UC and CD is not known, both conditions are believed to be caused by similar factors. Infectious factors such as viruses (e.g., in measles), protozoans, mycobacteria (e.g., Mycobacterium paratuberculosis), and other bacteria (e.g., Chlamydia trachomatis, Escherichia coli) are all suspect agents.16,17 Genetic factors also predispose patients to IBD, especially to CD. Characterized by a tendency for immune activation—both autoimmune and nonautoimmune—and inflammation, IBD is associated with a dysregulated mucosal immune response to intestinal microorganisms in a genetically susceptible host.18
In addition to intestinal complications, the IBD patient is at increased risk of systemic immune-related phenomena such as arthritis, nutritional deficiencies related to malabsorption of vitamin B12 and folic acid, anemia secondary to blood loss from the GI tract, and bone disease, of which osteoporosis and fractures are of particular concern.18 While psychological factors (e.g., stress, emotional or physical trauma) are thought overall not to be an etiological factor, changes in mental health appear to potentially correlate with remissions and exacerbations, particularly with regard to UC.15
Ongoing Inflammation: Risk of Colon Cancer
In patients with long-standing IBD, the risk of colon cancer is a significant complication that appears to be related to the degree of ongoing inflammation.1 Risk increases substantially after 8 to 10 years of disease; when appropriate, surveillance for colon cancer includes annual colonoscopy with random mucosal biopsies for observation of early or advanced dysplasia.1
The goals of treatment of IBD are 1)
resolution of acute inflammation and complications, such as fistulas or
abscesses; 2) alleviation of systemic manifestations like arthritis; 3)
maintenance of remission; and 4) in certain cases, palliation or cure
with surgery.15 Although the evaluation of IBD severity is
difficult due to the largely subjective nature of the assessment, more
objective measures, disease rating scales, and indices have been
developed, including those that assess quality of life (see Reference
15). Selected agents used in treating IBD can be found in TABLE 1.
Of note, there is a considerable difference between the goals of, and
approach to treatment for, UC and CD; for detailed discussions of IBD
medication therapy, including algorithm treatment approaches and
specific dosing guidelines, consult References 15 and 19. In order to
treat these diseases properly, realistic therapeutic goals for each
individual must be conceptualized by the clinician and ideally should
include collaboration with the patient to address issues including
quality of life and medication (TABLE 1) risks versus benefits.
Selected Tips Regarding Drug Therapy in the Elderly
Intolerance of drug therapy often limits the usefulness of drugs that treat IBD. Adverse effects may be significant in some cases, thus requiring discontinuation of the therapy. Some of the nuances of IBD therapy are discussed below, focusing on the elderly, to encourage the tailoring of the medication regimen to the individual in conjunction with ongoing assessment (e.g., history and physical), close monitoring (e.g., selected laboratory tests), and evaluation of therapeutic outcomes.
Avoiding NSAIDs: Reports have indicated that NSAIDs may trigger IBD occurrence or trigger exacerbation of underlying IBD; if possible, their use should be avoided.15,20,21 The mechanism by which this occurs is thought to be inhibition of prostaglandin production via cyclooxygenase inhibition that may impair mucosal barrier protection. If the benefit of treatment (e.g., of patients with symptomatic arthritis) outweighs the potential risk of IBD flare, the use of NSAIDs may be warranted in some patients.21 Of note, the elderly are a high-risk population for adverse effects from NSAIDs; up to 60% of elderly people can develop peptic ulceration and/or hemorrhage asymptomatically.19
Sulfasalazine: Unlike other sulfonamides, sulfasalazine is not absorbed when administered orally or as a suppository and is, therefore, reserved for the treatment of chronic IBD. Of note, it is intestinal flora that split sulfasalazine into two components: 5-aminosalicylate, which exerts an anti-inflammatory effect, and sulfapyridine, which can lead to toxicity in patients who are slow acetylators, whereby it precipitates at neutral or acidic pH, causing crystaluria (stone formation).22 Nephrotoxicity may develop secondary to crystaluria; preventing this adverse effect requires adequate hydration and alkalinization of urine.22 Patients receiving sulfasalazine should receive oral folic acid supplementation to prevent anemia secondary to malabsorption.15
Transient warfarin potentiation occurs with concomitant sulfasalazine use owing to displacement of warfarin from binding sites on serum albumin; free methotrexate levels may be increased because of displacement as well.22 Other potential problems associated with sulfasalazine are hypersensitivity reactions such as rashes, angioedema, and Stevens-Johnson syndrome; in order to direct appropriate therapy, it is of paramount importance to investigate a report of a previous sulfa allergy with regard to a description of the reaction.22,23 Granulocytopenia, thrombocytopenia, and hemolytic anemia (i.e., in patients with glucose 6-phosphate dehydrogenase deficiency) can occur.22 Since sulfonamides condense with formaldehyde, sulfasalazine is contraindicated in patients who receive methenamine for urinary tract infections.22
Mesalamine: Approximately 80% to 90% of patients who are intolerant to sulfasalazine’s adverse effects will tolerate oral mesalamine derivatives.24 With regard to rectal suppositories, the elderly may have difficulty administering and retaining this dosage form.19 In light of age-related renal function decline, serum creatinine should be monitored often during therapy.19
systemic corticosteroids are effective in moderate-to-severe active UC
and CD, high doses must often be used for extended periods; thus, their
use confers a higher risk of complications in the elderly, including
accelerated bone loss and fractures, hypertension, and glucose
intolerance.1,15 Use of systemic corticosteroids in geriatric
patients should involve the lowest possible dosage, and for the
shortest possible time. For long-term use, bone mineral density should
be monitored and fracture prevention strategies should be instituted (TABLE 2).19,25 Corticosteroids are not effective as maintenance treatment in either UC or CD.15
Immunomodulator and Immunosuppressive Agents: These drugs are associated with an increased risk for toxicity in the elderly. Recommended dosages should be reduced when initiating therapy in geriatric patients because of possible decreased metabolism, reduced renal function, and presence of comorbidity-drug interactions and drug-drug interactions.19
Biological Agents: All tumor necrosis factor alpha (TNF-α) inhibitors predispose patients to development of serious infections; studies indicated that the elderly have an increased incidence of infection and malignancy compared to younger adults under 65 years of age.19 The use of natalizumab, a novel biological agent, is associated with the development of progressive multifocal leukoencephalopathy.26 In light of the higher incidence of infections and malignancies in the geriatric population, caution and close monitoring are advised when these agents are used in the elderly.19 In addition, elderly patients with a history of heart failure may be at risk for exacerbation. Infliximab is contraindicated for individuals with New York Heart Association (NYHA) Class III-IV heart failure; caution is advised in those with congestive hear failure or NYHA Class I-II.19,26
Vitamin D Deficiency in IBD
Vitamin D deficiency is more common in adults and children with IBD (especially CD), as compared with healthy controls, and correlates with a poorer health-related quality of life.27-32
Factors such as malabsorption (i.e., secondary to mucosal disease or
surgical resection) and reduced sunlight exposure, physical activity,
and dietary intake are likely to contribute to this finding.18
not specifically studied in patients with IBD, it is thought that an
active inflammatory state may cause a reduction in total 25(OH)D3 levels, owing to reduced hepatic
production of vitamin D–binding protein.33
Garg and colleagues point out that the relationship between IBD and the
vitamin D axis appears to be a multi-faceted one involving the ongoing
maintenance of musculoskeletal health (TABLE 2) and possibly the
control of disease-related activity via immunomodulation, and
modification of the risk of IBD-associated malignancy.18 A
review of the role of vitamin D in bone health, immune regulation, and
cancer prevention in IBD is available at
While onset of IBD is common in young adults, it also is found with increasing frequency in the elderly. Currently, there is a greater and better variety of agents to treat patients with IBD for both acute conditions and remission maintenance. Medication regimens for senior IBD patients, based on the nuances of these therapies, require careful and appropriate geriatric dosing, monitoring, and ongoing assessment.
1. Maratchi LS, Greenwald DA. Common large intestinal disorders. In: Halter JB, Ouslander JG, Tinetti ME, et al, eds. Hazzard’s Geriatric Medicine and Gerontology. 6th ed. New York, NY: McGraw-Hill; 2009:1091-1102.
2. Wald A. The large bowel. In: Fillit HM, Rockwood K, Woodhouse K, eds. Brocklehurst’s Textbook of Geriatric Medicine and Gerontology. 7th ed. Philadelphia, PA: Saunders Elsevier; 2010: 661-677.
3. Wilson J, Hair C, Knight R, et al. High incidence of inflammatory bowel disease in Australia: a prospective population-based Australian incidence study. Inflamm Bowel Dis. 2010;16:1550-1556.
4. Cosnes J, Gower-Rousseau C, Seksik P, Cortot A. Epidemiology and natural history of inflammatory bowel diseases. Gastroenterology. 2011;140:1785-1794.
5. Loftus EV Jr. Clinical epidemiology of inflammatory bowel disease: incidence, prevalence, and environmental influences. Gastroenterology. 2004;126:1504-1517.
6. Langmead L, Rampton D. A GP guide to inflammatory bowel disease. Practitioner. 2001;245:224-229.
7. Sandler RS, Eisen GM. Epidemiology of inflammatory bowel disease. In: Kirsner JB, ed. Inflammatory Bowel Diseases. Philadelphia, PA: WB Saunders; 2000:89-112.
8. Baumgart DC, Bernstein CN, Abbas Z, et al. IBD around the world: comparing the epidemiology, diagnosis, and treatment: proceedings of the World Digestive Health Day 2010 – Inflammatory bowel disease task force meeting. Inflamm Bowel Dis. 2011;17:639-644.
9. Gearry RB, Richardson A, Frampton CM, et al. High incidence of Crohn’s disease in Canterbury, New Zealand: results of an epidemiologic study. Inflamm Bowel Dis. 2006;12:936-943.
10. Carr I, Mayberry JF. The effects of migration on ulcerative colitis: a three-year prospective study among Europeans and first-and second-generation South Asians in Leicester (1991-1994). Am J Gastroenterol. 1999;94:2918-2922.
11. Moum B, Aadland E, Ekbom A, Vatn MH. Seasonal variations in the onset of ulcerative colitis. Gut. 1996;38:376-378.
12. Zeng L, Anderson FH. Seasonal change in the exacerbations of Crohn’s disease. Scand J Gastroenterol. 1996;31:79-82.
13. Ekbom A. The epidemiology of IBD. Inflamm Bowel Dis. 2004;10(suppl.1):S32-S34.
14. Loftus EV Jr. Clinical epidemiology of inflammatory bowel disease: incidence, prevalence and environmental influences. Gastroenterology. 2004;126:1504-1517.
15. Hemstreet BA. Inflammatory bowel disease. In: DiPiro JT, Talbert RL, Yee GC, et al, eds. Pharmacotherapy: A Pathophysiologic Approach. 8th ed. New York, NY: McGraw-Hill Inc; 2011:587-605.
16. Shanahan F, Bernstein CN. The evolving epidemiology of inflammatory bowel disease. Curr Opin Gastroenterol. 2009;25:301-305.
17. Lakaos PL, Fischer S, Lakatos L, et al. Current concept of the pathogenesis of inflammatory bowel disease-crosstalk between genetic and microbial factors: pathogenic bacteria and altered bacterial sensing or changes in mucosal integrity take “toll.” World J Gastroenterol. 2006;12:1829-1841.
18. Garg M, Lubel JS, Sparrow MP, et al. Vitamin D and inflammatory bowel disease: established concepts and future directions. Aliment Pharmacol Ther. 2012;36(4):324-344.
19. Semla TP, Beizer JL, Higbee MD. Geriatric Dosage Handbook. 17th ed. Hudson, OH: Lexi-Comp, Inc; 2012.
20. Podolsky DK. Inflammatory bowel disease. N Engl J Med. 2002;347:417-429.
21. Singh F, Graff LA, Bernstein CN. Do NSAIDs, antibiotics, infections, or stress trigger flares in IBD? Am J Gastroenterol. 2009;104:1298-1313.
22. Clark MA, Finkel R, Rey JA. eds. Pharmacology. 5th ed. Baltimore, MD: Lippincott Williams & Wilkins; 2012:409,414-416.
23. Zagaria ME. Cutaneous adverse reactions: Stevens-Johnson syndrome. US Pharm. 2008;33(4):20-26.
24. Navarro F, Hanauer SB. Treatment of inflammatory bowel disease: safety and tolerability issues. Am J Gastroenteol. 2003;98(suppl):S18-S23.
25. Rodrigues CA. The small bowel. In: Fillit HM, Rockwood K, Woodhouse K, eds. Brocklehurst’s Textbook of Geriatric Medicine and Gerontology. 7th ed. Philadelphia, PA: Saunders Elsevier; 2010:652-660.
26. Epocrates Essentials Version 13.10.1 www.epocrates.com. Accessed November 11, 2013.
27. Ulitsky A, Ananthakrishnan AN, Naik A, et al. Vitamin D deficiency in patients with inflammatory bowel disease: association with disease activity and quality of life. JPEN J Parenter Enteral Nutr. 2011;35:308-316.
28. Silvennoinen J. Relationships between vitamin D, parathyroid hormone and bone mineral density in inflammatory bowel disease. J Intern Med. 1996;239:131-137.
29. Tajika M, Matsuura A, Nakamura T, et al. Risk factors for vitamin D deficiency in patients with Crohn’s disease. J Gastroenterol. 2004;39:527-533.
30. McCarthy D, Duggan P, O’Brien M, et al. Seasonality of vitamin D status and bone turnover in patients with Crohn’s disease. Aliment Pharmacol Ther. 2005;21:1073-1083.
31. Siffledeen JS, Siminoski K, Steinhart H, et al. The frequency of vitamin D deficiency in adults with Crohn’s disease. Can J Gastroenterol. 2003;17:473-478.
32. Levin AD, Wadhera V, Leach ST, et al. Vitamin D deficiency in children with inflammatory bowel disease. Dig Dis Sci. 2011;56:830-836.
33. Bouillon R, ed. The Vitamin D Binding Protein (DBP). 3rd ed. London, England: Elsevier; 2011.
34. Lewis NR. Guidelines for osteoporosis in inflammatory bowel disease and coeliac disease. 2007. www.bsg.org.uk/images/stories/clinical/ost_coe_ibd.pdf. Accessed November 11, 2013.
35. Clinical Practice Committee. American Gastroenterological Association medical position statement: guidelines on osteoporosis in gastrointestinal diseases. Gastroenterology. 2003;124:791-794.
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