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Kevin W. Olden, M.D., Series Editor
Hormonal Influences on the Gastrointestinal Tract and Irritable Bowel Syndrome
by Sharmela Thevarajah, Margaret Polaneczky, Ellen J. Scherl and Christine L. Frissora
Irritable bowel syndrome (IBS) is a common disorder of gastrointestinal (GI) function that affects more women than men in most Western countries. Often among women, symptoms of IBS appear to be related to hormone status (e.g., menstruating, pregnant, menopausal, taking oral contraceptives or hormone replacement therapy). In some women, symptoms wax and wane in concert with their menstrual cycle. One potential explanation for the observed variability in IBS symptoms is that sex hormones affect GI motility and function. The purpose of this review is to describe the growing body of evidence that supports a role for sex hormones in the pathophysiology and/or symptom presentation of IBS.
IBS: CLINICAL SYMPTOMS
Reported prevalence rates range from 3% to 20%, with most estimates concentrated between 10% and 15% (2). Although IBS affects individuals of all races and both sexes, women are more commonly affected than men in Western nations at a ratio of approximately 2:1, a phenomenon that has yet to be completely explained (3–6). In North American studies, the female predominance is greater among individuals who seek medical attention (3–4:1) as compared with those who do not (<2:1) (7); however, it is unclear if this reflects underreporting in men or a true predominance in women. Sex differences in presentation of symptoms have been described, including more IBS with diarrhea among men and more IBS with constipation and bloating among women (8). IBS is one of the most common disorders seen in the primary care setting. Women often present to their gynecologist first, as this may be
BS is a disorder in which abdominal pain or discomfort is a primary symptom. It is accompanied by a change in bowel habit and abnormal stool frequency (defined as >3 bowel movements per day [diarrhea] or <3 bowel movements per week [constipation]) (1). IBS patients also commonly report hard or loose/watery stools, a feeling of incomplete evacuation after bowel movement, bloating and/or abdominal distension, and the passage of mucus.
Sharmela Thevarajah, M.D., Resident; Margaret Polaneczky, M.D., Associate Professor of Clinical Medicine, Ellen J. Scherl, M.D., Associate Professor of Clinical Medicine; and Christine L. Frissora, M.D., FACP, FACG, Associate Professor of Medicine; The Weill Medical College of Cornell University, New York, NY. 62
PRACTICAL GASTROENTEROLOGY • MAY 2005
primarily among women who are not receiving hormone replacement therapy (HRT) (34). Studies have shown that more than 40% to 57% of Crohn’s disease patients and one third of ulcerative colitis patients who were in remission had comorbid IBS (11. Responding to follicle-stimulating hormone (FSH) secretion from the pituitary gland. Many women with IBS report that symptoms fluctuate with 63 . This results in IBD overtreatment and IBS undertreatment.. GI symptoms increase and intestinal transit decreases (28). which is increased during the follicular phase compared with the luteal phase (28.g. Coexistence of IBS and Other GI Disorders IBS often coexists with other GI disorders. During pregnancy. Reports of abdominal bloating increase after menopause.g. and prostacyclin.33). suggesting a potential protective effect of this hormone (23). primarily prostaglandin F2α (PGF2α).12). especially in quiescent disease. may have an impact on IBS. The direct costs associated with IBS are estimated to be as high as $10 billion per year. or immediate postmenstrual phase. Cycling Female Sex Hormones During the reproductive years in women. IBS can contribute to symptoms of IBD.31). Several studies have reported negative effects on quality of life (14–16). the normal menstrual cycle is characterized by predictable and cyclic changes in estrogen and progesterone levels (Figure 1) that may influence bowel activity. inflammatory bowel disease [IBD]) (10).g. SERIES #7 the only physician they ever see. which peak around day 13. There also exists the question as to whether hormone differences are associated with specific symptoms (e. Alterations in rectal sensitivity (27) (increased during menses) and GI transit. The intraovarian events leading to ovulation involve estrogeninduced production of prostaglandins. gastroesophageal reflux disease. also have been reported. However.13). for differences in prevalence and symptom presentation among women and between women and men (23. at least in part. Other studies showed that menses (a time of declining/minimal ovarian hormone levels) was associated with looser stools compared with the follicular and luteal phases (30. many patients with IBD are diagnosed initially with IBS (11. It also has been proposed that hormonal disparities and fluctuations may be responsible. PGE2. IBS accounts for 12% of diagnoses in the primary care setting (5) and is responsible for 30% to 50% of referrals to gastroenterologists (9). if the symptoms of IBS are mistaken for an IBD flare. Furthermore. a time during which estrogen and progesterone levels are high. Men with IBS have lower serum luteinizing hormone (LH) than men without IBS. their menstrual cycles and that flares occur in the perimenstrual and perimenopausal phases (24–26).. comorbid IBS tends to be underdiagnosed and undertreated. bloating) or with the wider spectrum of IBS symptoms.. the granulose cells of the ovarian follicles secrete gradually increasing levels of estradiol.22). including the simple fact that more women than men experience IBS. IBS: IMPACT IBS symptoms affect the lives of patients and their families. celiac disease. dyspepsia. estrogen predominates and progesterone levels are low. and indirect costs as high as $20 billion annually (excluding prescription and over-the-counter drug costs) (21. IBS is diagnosed more often in women with dysmenorrhea than in those who cycle normally (32). Furthermore. The PRACTICAL GASTROENTEROLOGY • MAY 2005 IBS: A ROLE FOR HORMONES? A variety of observations support the hypothesis that female sex hormones.Hormonal Influences on the Gastrointestinal Tract and IBS TREATMENT OF IRRITABLE BOWEL SYNDROME. both functional (e. once a diagnosis of IBD is established. In the follicular phase. These thoughts are all intriguing. Additional evidence comes from reports of menstrual cycle-related symptom fluctuations. as well as on work-related and social activities (17–20). Changes in hormone status associated with pregnancy or menopause also may influence symptoms. inducing the pituitary LH surge that heralds ovulation.29). but exactly how hormonal factors influence IBS remains unclear. and fluctuations thereof. chronic constipation) and organic (e. all of which are measurable in follicular fluid.
triggering the events in the uterine endometrium that lead to menstruation. et al. and sensitization of nerve endings. 2001:2154-2172. eds.Hormonal Influences on the Gastrointestinal Tract and IBS TREATMENT OF IRRITABLE BOWEL SYNDROME. ovarian. Endometrial prostaglandin levels are three times higher in the luteal than in the follicular phase. 15th ed. Disorders of the ovary and female reproductive tract. ischemia. Other molecules produced include endothelin-1. LH = luteinizing hormone. Kasper DL. with lower levels of PGE2 also produced. PGF2α release leads to smooth muscle contraction. Harrison’s Principles of Internal Medicine. (Reprinted with permission from Carr BR. Rising luteal phase estrogen levels are thought to induce luteolysis. the corpus luteum secretes both estrogen and progesterone. These events involve complex interplay of 64 PRACTICAL GASTROENTEROLOGY • MAY 2005 prostaglandins. With the decline of the corpus luteum. FSH = follicle-stimulating hormone. Levels are highest (continued on page 67) . In: Braunwald E. mediated by PGF2α via endoethelin-1 and tumor necrosis factor-alpha (TNF-α) in the corpus luteum. estrogen and progesterone levels drop. metalloproteinases. NY: McGraw-Hill. Bradshaw KD. and other lytic enzymes. E2 = estrogen. and basal body temperature changes and relationships throughout the normal menstrual cycle. New York. The endometrium also produces prostaglandins. and cytokines. After ovulation. SERIES #7 Figure 1. cytokines. Progesterone levels peak 8 to 9 days after ovulation. the predominant one being PGF2α. endometrial. Fauci AS.) P = progesterone. PGE2 is a smooth muscle relaxant. Hormonal. release of this prostaglandin-rich fluid is thought to cause the pain that sometimes occurs with ovulation. TNF-α.
and bloating. Clinical Evidence Linking Female Hormones to Bowel Function It has been postulated that cycling female sex hormones are related to changes in bowel habits. data on file). which is the likely explanation for the increased pain associated with their menstruation. TNF-α. In contrast. breast tenderness. Endothelin has potent effects on GI smooth muscle. misoprostol also invokes prostaglandin effects in the uterus (uterine muscle contractions) that can lead to complications in pregnancy. and prostaglandins also exert effects on the GI tract. Altered prostaglandin levels can result in abdominal pain. alterations in GI transit (increased during the follicular phase compared with the luteal phase) (28. Estrogen receptors are found throughout the GI tract (36) in components of the pelvic floor (37) and in sensory neurons of the dorsal root ganglia (38). delays gastric emptying. high levels of estradiol and progesterone during PRACTICAL GASTROENTEROLOGY • MAY 2005 67 . Alternatively. and intestines. Prostaglandin production has been thought to influence diarrhea associated with menses by inhibiting transepithelial ion transport in the small intestine. In the 1980s. medications that inhibit production of gastric acid or coat the lining of the GI tract can provide protection to patients on long-term NSAID therapy. Medications to reduce acid production. neutralize the acid. there is a significant increase in the uterine expression of PGF2α (41). It also is a potent stimulator of gallbladder motility. TNF-α induces inflammation. leading to contraction of the esophagus. The perimenopausal transition is characterized by its unpredictability and by wide fluctuations in estrogen levels throughout the cycle. Nonsteroidal anti-inflammatory drugs (NSAIDs) are the most common treatment modality. and decreases trans-sphincteric flow (39). and leads to irritability. place. prostaglandins provide a protective effect for patients taking medications that inhibit GI COX enzymes. In the gut.Hormonal Influences on the Gastrointestinal Tract and IBS TREATMENT OF IRRITABLE BOWEL SYNDROME. Heitkemper and colleagues (1988) reported that menses (a time of declining/minimal ovarian hormone levels) was associated with looser stools compared with the follicular and luteal phases (30). Therefore. endothelin. Prostaglandins are a diverse set of molecules derived from the modification of essential fatty acids. stimulation of GI motility. these local chemical messengers play a vital role in numerous functions. use of these agents can lead to GI depletion of prostaglandins (42). When present at the proper time. maintaining homeostasis. suggesting that female sex hormones may play a role in IBS symptomatology. or coat the lining of the GI tract often are used as adjunctive therapies in patients taking NSAIDs for chronic conditions. prostaglandins. and amount. colonic contractions. There may be a relative progesterone deficiency due to lack of ovulation or luteal phase deficiencies as the quality of the ovarian follicles diminish. and has a modulatory effect on GI motility (39). are implicated in the proper maintenance of mucosal blood flow. which relaxes the smooth muscle in the gut. SERIES #7 (continued from page 64) during menstruation. misoprostol should not be used in women known or thought to be pregnant. and secretion of bicarbonate to help neutralize acids (40). increases colonic transit time. particularly those of the E type. However. This estrogen-dominant environment can occur even in the presence of hot flushes. however. This nitrogen oxide synthetase induced smooth muscle relaxation clinically results in bloating. Bloating can occur when estrogen induces nitric oxide synthetase. In women who experience dysmenorrhea. including premature labor and abortion (Pfizer. Potential Hormonal Influences on the GI Tract Estrogen. and diarrhea. Misoprostol (Cytotec®) is a synthetic PGE1 analog that stimulates secretion of gastric mucus and production of bicarbonate. These hormones have a relaxing effect on the lower esophageal sphincter and decrease colonic transit. Studies have shown that estrogen and progesterone exert many effects on the GI tract (36). stimulation of the mucous secretion lining the gut surface. and they have higher levels of PGF2α in their menstrual fluid (35). Women who experience dysmenorrhea have greater endometrial prostaglandin levels than do asymptomatic women. stomach. when most PGF2α release from the endometrium occurs.29) were reported. stimulates sphincter of Oddi motility. Levels of estradiol may be markedly increased because of ovarian follicular response to elevated FSH levels. and induces flow of fluid into GI tissues.
They also reported firmer consistency of the stool during the luteal phase. as expected.Hormonal Influences on the Gastrointestinal Tract and IBS TREATMENT OF IRRITABLE BOWEL SYNDROME. Triadafilopoulos and colleagues (1998) prospectively studied 228 women (170 postmenopausal and 58 premenopausal) who presented for evaluation at a primary care practice facility. Because the GI system of IBS patients may already be sensitive. this may be an explanation for the increased rectal sensitivity noted in IBS patients at menses. selfreported bowel frequency and stool consistency were not significantly different during the menstrual. Kamm and colleagues (1989) reported that. in their later study of 29 female patients with IBS. They measured serum estradiol and progesterone levels and GI transit times at 2 points during the menstrual cycle. it did not appear to affect rectal motility or sensitivity in 20 healthy women (31). Houghton and colleagues concluded that women with IBS are predisposed to fluctuations in visceral sensitivity associated with the menstrual cycle. under normal physiologic conditions. SERIES #7 the luteal phase were reported to be associated with delayed GI transit (28). However. women with IBS had increasing levels of rectal sensitivity at the time of menses compared with all other phases of the menstrual cycle (27). because acute episodes of diarrhea are associated with increases in rectal sensitivity in women (but not men) and IBS patients are more susceptible to sensitizing events. follicular.45). et al (2002) reported a significant worsening of abdominal pain and bloating and more frequent bowel movements during menses (27). in contrast to healthy women. This increase in rectal sensitivity was not related to changes in rectal compliance or wall tension. (At the time of their participation in the study. Similar to past studies. they concluded that the menstrual cycle plays a role in determining GI transit time in normally menstruating women. Healthy women describe changes in bowel habits during their menstrual cycle. The authors also posed a second explanation—that prostaglandin release during menses may play a role in rectal sensitivity. or luteal phase. the release of prostaglandins.) The authors (continued on page 70) . which may account for firmer stools during this phase of the menstrual cycle. A suggestive physiologic mechanism may be the increased intestinal prostaglandin production that causes contraction of colonic smooth muscle or the increased intestinal secretions related to variation in progesterone levels (43). may be enough to trigger a further increase in this sensitivity. known to induce afferent nerve sensitization.01) prolonged during this phase as compared with the follicular phase. The authors also noted that anxiety and depression remained unaltered throughout the menstrual cycle—a finding that was consistent with past studies demonstrating that psychological traits are not associated with perimenstrual bowel-related symptoms (25. they found that. Wald and colleagues (1981) described different findings in a more recent report of their study of hormone levels and GI transit times in 15 normally menstruating women (28). They based this conclusion on their observation that mean transit times (whole gut transit) and stool weights were not significantly different during the follicular versus the luteal phase of the menstrual cycle in 18 healthy women. Further evidence for a role of female hormones in bowel function comes from studies conducted in women in the perimenopausal and postmenopausal states. once in the follicular phase (days 8–10) when progesterone levels are low. none of these women presented for evaluation of abdominal or genitourinary symptoms. Whereas other early clinical studies failed to show a relationship between female hormones and bowel function. The authors reported that progesterone levels did increase during the luteal phase. and once in the luteal phase (days 18–20) when progesterone levels are elevated. and women with IBD experience an even higher prevalence of GI symptom–related fluctuations. and that GI transit time was significantly (P < 0. sex hormones have no major effect on bowel function (44). Furthermore. Jackson and colleagues (1994) reported that. although the phase of the menstrual cycle may affect 68 PRACTICAL GASTROENTEROLOGY • MAY 2005 transit. However. Houghton. investigators used a previously validated GI symptom questionnaire designed to evaluate symptoms consistent with IBS (46). Based on these findings. The authors considered the possibility that. GI transit was determined via monitoring of breath hydrogen levels at 10-minute intervals after the ingestion of lactulose (to determine time from ingestion until delivery to the cecum). a growing body of evidence suggests that such a relationship exists.
This is in agreement with what is known about premenstrual syndrome—those who suffer from this condition do not exhibit differences in ovarian hormone levels compared with healthy individuals. 48% vs 27%. Dysmenorrhea..4%.to 49-year-old age group.Hormonal Influences on the Gastrointestinal Tract and IBS TREATMENT OF IRRITABLE BOWEL SYNDROME. The authors concluded that there is a high prevalence of altered bowel function and IBS-like GI complaints among women in the perimenopausal and postmenopausal periods. neuroticism.8% of patients. Data from an earlier study conducted by Heitkemper and colleagues (1992) also suggested a relationship between symptoms and the menstrual cycle in women with FBD. and 34% vs 18%. nausea. Estrogen receptor (ER) expression in the levator ani fascia was increased significantly (P < 0. The study looked at 55 women undergoing surgery for asymptomatic gynecological (n = 10) or symptomatic urogynecological (n = 45) conditions. perimenstrual. and other symptoms and recorded stool frequency and consistency. Functional bowel disorder. was diagnosed in 61% of patients with dysmenorrhea compared with 20% of patients without dysmenorrhea (P < 0.e. as 70 PRACTICAL GASTROENTEROLOGY • MAY 2005 identified via history and physical examination. and constipation. which are symptoms suggestive of IBS. defined as abdominal pain with altered bowel function. rather. Copas and colleagues (2001) attempted to explain various pelvic floor disorders. were receiving HRT. Crowell and colleagues (1994) noted an overlap in diagnoses of dysmenorrhea and functional bowel disorders (FBDs) in their 12-month evaluation of 383 women (aged 20 to 40 years) who presented to a single Planned Parenthood clinic (32). Interestingly. However.001). This may explain why longterm HRT does not appear to favorably impact pelvic floor disorders and suggests that down-regulation of receptors or relative tissue dominance of the progestin component of therapy is the cause. the authors reported no significant group differences in ovarian hormone levels or stool consistency/frequency scores. estrogen use did not affect GI symptoms in either group. and diarrhea higher at menses than did the group without FBD.01). Prostaglandin levels were measured in vaginal dialysate on the first day of menses in a subset of subjects (n = 44) and were elevated in women with dysmenorrhea regardless of bowel symptoms. Serum estrogen and progesterone concentrations were measured during menses and during the follicular and luteal phases. respectively. The group with FBD also reported higher levels of perimenstrual symptoms on six of the eight Menstrual Distress Questionnaire-T subscales (P < 0. Twenty-four of the women. and heartburn/acid regurgitation were also more common among postmenopausal women than premenopausal women. as opposed to 14% of premenopausal women (P < 0. as measured using the NEO Personality Inventory ). Laxative usage.05). patterns of GI symptoms and select mood and somatic symptoms were evaluated across two menstrual cycles in a group of 19 women with and 39 women without FBD (45). In this study. with prevalence rates of 9. gaseousness/excessive flatulence.4% vs 3. by evaluating hormone receptor expression in the levator ani muscle and fascia. The authors concluded that the observed relationship between menstrual and bowel symptoms and the overlap in diagnoses of dysmenorrhea and functional bowel disease were evidence of a common physiologic basis for many of the symptoms characteristic of these disorders.001) in symptomatic women receiving long-term HRT when compared with age-matched women without HRT. which make up the pelvic floor (37). was present in 19. all of whom were symptomatic. Stomach pain was higher during the remaining days as well. The authors concluded that ER expression is significantly higher in symptomatic women when compared with asymptomatic women of the same age. diarrhea. the two groups did not differ in occurrence of abdominal pain. they differ in their (continued on page 72) . SERIES #7 (continued from page 68) found that 38% of postmenopausal women reported altered bowel function. including fecal incontinence. but that long-term use of estrogen leads to a significant decrease in ER expression. women rated their GI. Interestingly. The prevalence of IBS-type complaints peaked at a high of 36% among the 40. Each day. age-matched women. The group with FBD rated stomach pain.03) in symptomatic women not receiving HRT when compared with asymptomatic. A relationship between bowel symptoms (bowel symptom inventory ) and menstrual symptoms (Moos’ Menstrual Distress Questionnaire ) was evident throughout the study and was independent of psychological differences (i. but was significantly lower (P < 0.
In a study of 477 female patients with IBS. bloating. including abdominal pain. diarrhea.Hormonal Influences on the Gastrointestinal Tract and IBS TREATMENT OF IRRITABLE BOWEL SYNDROME. Hormonal Influences on Serotonin Activity? Serotonin (5-hydroxtryptamine [5-HT]). Collectively. et al (1990) assessed differences in GI complaints between female patients at a family planning clinic and women with IBS or FBD who were referred to a gastroenterology clinic (25). Heitkemper. The authors noted also that reports of bowel symptoms during menstruation were not associated with psychological traits or with menses-related changes in mood. is vital to normal gut function. as well as serotonin polymorphisms. oral contraceptive users reported fewer symptoms of abdominal pain than did nonusers. In a subsequent study of women with IBS. in this case. constipation. the same difference as in the total male and female samples was observed. in terms of somatic. in predicting response to treatment is an area of interest. Heitkemper and colleagues (2004) described a specific relationship between bloating and menses-associated symptoms such as uterine cramping and breast tenderness (50). One third of patients who denied symptoms of IBS or FBD reported that menstruation was associated with one or more bowel symptoms.) All patients were asked whether gas. However. especially increased bowel gas. with complaints worse during menses. but restrictive criteria for IBS were not satisfied. SERIES #7 (continued from page 70) responses to normal hormonal fluctuations. GI symptoms also appear to be influenced by the menstrual cycle in women with IBS. (Criteria for diagnosis of IBS were abdominal pain plus altered bowel habits. Compared with controls.. A recent study has shown that estrogen and progesterone influence the level of 5-HT type 3 (5-HT3) receptor mRNA (54). Of women younger than age 45. which is a target of pharmacologic intervention in patients with diarrhea-predominant IBS. and also reported a higher percentage of days with hard and with loose stools. GI symptoms were significantly affected by the menstrual cycle phase. women with IBS had significantly more severe GI symptoms. 50. In ovariectomized rats. . psychological. 5-HT3 receptor transcript levels returned to normal. et al (2003) reported in another study that women with IBS had higher symptom severity. gas. these results suggest that 5-HT3 receptor activity. or alternating constipation and diarrhea). when postmenopausal women were compared with a group of age-matched men. however. The potential effect of sex hormones such as estrogen and progesterone on serotonin remains to be elucidated. also is regulated by female sex hormones. however. diarrhea. than did women in a control group (49). Lee. however. et al (2001) reported that 40% of all female patients with IBS reported menstrual cycle-related worsening of symptoms (8). Among women with IBS. in the central nervous system and other target organs.e. Similarly. a 5-HT3 receptor antagonist that is used to treat diarrhea-predominant IBS (55. The authors did report. and GI symptoms.52). the authors 72 PRACTICAL GASTROENTEROLOGY • MAY 2005 argued against a significant role for menstrual cyclerelated hormone fluctuations in causing symptom differences. It is responsible for initiating and maintaining peristalsis. lower levels of PGE2 and progesterone resulted in significantly higher amounts of 5-HT3 receptor mRNA. that premenstrual women were two times more likely to complain of nausea than were postmenopausal women with IBS. mediating secretion in the GI tract. and diarrhea. However. there were no significant differences between the two groups with respect to gas.8% reported experiencing menstrual cycle-related worsening of symptoms. when premenopausal women with IBS were compared with postmenopausal women. which is produced mainly by and stored in enterochromaffin cells in the GI tract. and bloating. Furthermore. there was no significant difference in bowel habit predominance (i. When ovariectomized animals were treated with estradiol and progesterone. Whitehead. the importance of serotonin and its receptors.56). patients with IBS were significantly more likely to experience exacerbations of each of these bowel symptoms. Additional studies highlight the importance of the serotonin reuptake transporter in IBS as polymorphisms in this gene resulted in a differential response to alosetron. Recent research has uncovered a potential role for abnormal serotonin expression and/or signaling in IBS and other GI disorders (53). and modulating the sensation of pain (51. based on two findings. First. or constipation occurred during menstruation. constipation. highlighting the concept that menstrual status does not affect bowel habit predominance.
Lee O. 122(4):1140-1156. Defining and diagnosing irritable bowel syndrome. 5. Muller-Lissner SA. Scherl EJ. Gastroenterology. Dig Dis Sci. 24(4):675-689. categorization and selection of patients for clinical trial participation should not focus solely on IBS subtypes. Quality of life in inflammatory bowel disease in remission: the impact of IBS-like symptoms and associated psychological factors. After switching to low-estrogen formulations. Fennerty MB. Minderhoud IM. Drossman DA. Munakata J. 8. Hays RD. 1999. Keefer L. 2002. Brandt LJ. Heaton KW. et al. Frank L. Gastroenterology. Naliboff B. 2001. in preparation of this manuscript. Blanchard EB. PhD. Clin Cornerstone. Naliboff B. Am J Manag Care. Oldenburg B. 2002. Gralnek IM. Silk DB. Svedlund J. constipation. 112(6):2120-2137. References 1. 4(4):22-33. 2001. Wismeijer JA. 12.. Furthermore. Whitehead WE. Systematic review of the comorbidity of irritable bowel syndrome with other disorders: what are the causes and implications? Gastroenterology. Mayer EA. Sex differences in prevalence and symptom presentation. Am J Gastroenterol. To this end. Camilleri M. Lackner J. Koloski NA. 2002. is the primary component of the recently introduced oral contraceptive Yasmin®. Irritable bowel syndrome: a technical review for practice guideline development. Am J Gastroenterol. Ciesla G. and alternators). Evidence-based position statement on the management of irritable bowel syndrome in North America. such as chronic daily NSAIDs or angiotensin-converting enzyme inhibitors. 49(3):469474. or Alesse®). 96(7):2184-2193. 13 Suppl 2:65-69. 2002.g. SERIES #7 IBS SYMPTOMS IN PATIENTS USING ORAL CONTRACEPTIVES Oral contraceptive use should be investigated among patients seeking relief from GI symptoms. 2. Impact of irritable bowel syndrome on personal relationships and working practices. 120(3):652-668. Longstreth GF. as well as differences and fluctuations based on hormone status. 2003. Jones KR. Irritable bowel syndrome. 15. The impact of functional gastrointestinal disorders on quality of life. 8(5):373-374. Patients taking Yasmin® should avoid potassium supplementation or other medications that affect potassium levels. 11. Chang L. Chang L. Krasner S. PRACTICAL GASTROENTEROLOGY • MAY 2005 SUMMARY There now exists a considerable body of evidence supporting a role for sex hormones in the development of IBS symptoms. patients experience less bloating and less weight gain. HRT) in the management of patients with IBS symptoms remains to be defined. 6. 2004. Zaman A.Hormonal Influences on the Gastrointestinal Tract and IBS TREATMENT OF IRRITABLE BOWEL SYNDROME. 3. Irvine EJ. Recipients typically lose weight initially (3–4 pounds) but return to baseline weight after 6 months. Eur J Gastroenterol Hepatol.g. van Berge Henegouwen GP.. Naliboff B. American College of Gastroenterology Functional Gastrointestinal Disorders Task Force. Because estrogen excess can cause nausea. Thompson WG. patients taking preparations high in estrogen may benefit from switching to low-estrogen formulations (i. Preparations with increased progestin content (e. 4. a C21 progestin derivative of spironolactone that has both progestational and mineralocorticoid effects. Palsson O. Talley NJ. especially in patients with functional nausea who are also thin. Abrahamsson H. Camilleri M. Schuster MM. Mircette®. Am J Gastroenterol. Lee OY. 18. Mayer EA. Whitehead WE. 2002. 26(4):361-372. Gillberg R.. 45 Suppl 2:II43-II47. 97(11 Suppl):S1-S5. 2000. diarrhea.e. and cyclic weight gain. Am J Gastroenterol. Smout AJ. 9. Systematic review on the management of irritable bowel syndrome in North America. 13. Acknowledgment The authors would like to acknowledge the editorial assistance of Maribeth Bogush. Am J Gastroenterol. 10. An important next step is to determine whether sex or hormone status affects the efficacy of standard management approaches. 13(11):1327-1332. Clin Ther. 7(8 Suppl):S246-S251. Bjornsson ES. The effects of various types of HRT on the GI tract are not yet understood. 2002. 97(2):389-396. as they currently do (i. 2000. Kleinman L. Irritable-inflammatory bowel disease: recognizing a new overlap syndrome and an enigma wrapped inside a puzzle. 2001. 97(11 Suppl):S7-S26. Sykes MA. The impact of irritable bowel syndrome on health-related quality of life. the role of sex hormones (e. IBS-like symptoms in patients with inflammatory bowel disease in remission: relationships with quality of life and coping behavior. Axelsson J. 95(1):67-71. Gut. Simren M. 16. Functional bowel disorders and functional abdominal pain. Rentz A. Kim JJ. Kilbourne A. Bjorkman D.e. 2001. bloating. Psychopathology in irritable bowel syndrome: support for a psychophysiological model. they should also focus on sex and hormone status. Drossman DA. Gastroenterology. have been described. 14. 2002. Management of the irritable bowel syndrome. Demulin 1/35®) also may be beneficial. Drospirenone. Health-related quality of life associated with irritable bowel syndrome: comparison with other chronic diseases. 1999. 7. Inflamm Bowel Dis. oral contraceptives. Review article: gender-related differences in functional gastrointestinal disorders. 17. Mayer EA. Schmulson M. Aliment Pharmacol Ther. Whether “natural” progestins will offer any advantage is not known. Boyce PM. those containing only 20 µg of estrogen such as Loestrin 1/20®. J Behav Med. It produces mild diuresis (similar to spironolactone 25 mg). 119(3):654-660. I 73 . Gender-related differences in IBS symptoms. Zacker C.. 1997.
Cheng L. 30(1):30-34. 2002:227-242. 41. Eliakim R. Chang L. 2002. Bethesda. The role of serotonin in the pathophysiology of irritable bowel syndrome.gastro. 39(12):2607-2611. Accessed November 16. Heitkemper MM. 25. Burr RL. Hunt RH. et al. 20. The development of a menstrual distress questionnaire. 1990. IBS in the Real World Survey: Summary Findings. Houghton LA. The NEO Personality Inventory Manual. 2003. 55(1):1-46. Coco AS. 2001. 50. Heller BR. et al. Sable K.Hormonal Influences on the Gastrointestinal Tract and IBS TREATMENT OF IRRITABLE BOWEL SYNDROME. 18(9):1443-1450. 30(5):605608. 25(5):192-200. Yu BP. Pharmacogenomics J. gastrointestinal and urogenital tracts. Gut. Shetzline MA. Scarpignato C. eds. et al. Houghton LA. Gastroenterology. 95(9):2296-2300. Jackson NA. Gastroenterology. 37. Kane SV. Gastrointestinal symptoms and bowel patterns across the menstrual cycle in dysmenorrhea. 2001. Gut. Effects and mechanisms of action of endothelins on non-vascular smooth muscle of the respiratory. Am J Gastroenterol. 31. Shaver JF. Cheskin LJ. Kamm MA. Connors LG. Kane S. 2001:1-86. 53. et al. J Adv Nurs. Gut. 45(10):781-788. Martin R. Heitkemper MM. Estrogen receptor-alpha and -beta coexist in a subpopulation of sensory neurons of female rat dorsal root ganglia. 23.. Pattern of gastrointestinal and somatic symptoms across the menstrual cycle. Am J Manag Care. The Burden of Gastrointestinal Diseases. Coates MD. Carlson PJ. 2002. Whorwell PJ. Symptoms across the menstrual cycle in women with irritable bowel syndrome. Functional bowel disorders in women with dysmenorrhea. Dancey CP. Gastroenterology. II. D’Orleans-Juste P. Wald A. 1980. 1993. Van Thiel DH. 2002. Lennard-Jones JE. 1988. Finlayson M. 2004. 80(6):1497-1500. Jarrett M. Li TJ. 8:1443-1447. Jackson N. Scherl E. Carter E. Womens Health. 98(6):1485-1489. Caudle MR. Estrogen. 2002. Basel. org/clinicalRes/pdf/burden-report. 30(6):853-867. 2000. Backhouse S. 1968. Estrogen. 46. 1981. Irritable bowel syndrome: toward a cost-effective management approach. 2002.pdf. 7(8 Suppl):S268-S275. Int J Fertil Womens Med. progesterone. Adv Prostaglandin Thromboxane Res. Psychosom Med. 36. 32. The menstrual cycle affects rectal sensitivity in patients with irritable bowel syndrome but not healthy volunteers. Milwaukee. Prostaglandin levels in menstrual fluid of nondysmenorrheic and of dysmenorrheic subjects with and without oral contraceptive or ibuprofen therapy. 2003. Tanaka A. Ameen V. Jarrett ME. Gastrointestinal transit: the effect of the menstrual cycle. Woods NF. SERIES #7 19. Walker E. Towards a better understanding of patients with irritable bowel syndrome. 51. Relationship of bloating to other GI and menstrual symptoms in women with irritable bowel syndrome. 3(2):64-66. Triadafilopoulos G. 47(3):136-142. Am J Gastroenterol. 55. Gut. 21. eds. Md: American Gastroenterological Association. Cain KC. Lea R. Li MQ. 126(7):1657-1664. 1994. Farthing MJ. Gender issues in the management of inflammatory bowel disease and irritable bowel syndrome. 60(2):489-496. 56. 38. Serotonin-transporter polymorphism pharmacogenetics in diarrhea-predominant irritable bowel syndrome. Evidence for exacerbation of irritable bowel syndrome during menses. Dawood MY. Abulafia O. Linden DR. Zacker C. Currer B. Olden K. Neurosci Lett. Whorwell PJ. Day S. Irritable bowel syndrome genophenomics: correlation of serotonin-transporter polymorphisms and alosetron response. Dong WG. and androgen receptor expression in levator ani muscle and fascia. 54. 34. McCrae RR. Whorwell PJ. Mawe GM. 1995. 2004. Serious lower gastrointestinal clinical events with nonselective NSAID or coxib use. Ovarian hormone modulates 5-hydroxytryptamine 3 receptors mRNA expression in rat colon with restraint stress-induced bowel dysfunction. Frissora CL. Does the menstrual cycle affect anorectal physiology? Dig Dis Sci. Heitkemper MM. Takeuchi K. World J Gastroenterol. 5(1):55-60. 2001. Heitkemper M. 37(2):108-113. 39. Burr RL. Turnbull GK. 2004. Rae GA. Gastroenterol Nurs. 35. Bowel function and transit rate during the menstrual cycle. Moses PL. Primary dysmenorrhea. 93(10):1867-1872. 89(11):1973-1977. Lewis MJV. 123(5):1686-1701. Kato S. 10(18):2723-2726. [Abstract #168]. et al. Chan WY. Houghton LA. J Reprod Med. Relationships between symptoms. Available at: http://www. Wang J-Y. Laine L. Costa PT. progesterone and the gastrointestinal tract. Heitkemper MM. Crowell MD. American Gastroenterological Association. 74 PRACTICAL GASTROENTEROLOGY • MAY 2005 . Frontiers of Gastrointestinal Research Series. Heitkemper MM. 7(8 Suppl): S252-S260. The menstrual cycle and its effect on inflammatory bowel disease and irritable bowel syndrome: a prevalence study. 24. 52. Sherer DM. Mahoney CR. Crowell MD. Martin J. Atanasova E. Bukovsky A. Whorwell PJ. 47. Md: Clinical Psychometric Research. Crowell MD. Grellet C. 2002. Am J Gastroenterol. Gender differences and irritable bowel syndrome. Hanauer SB. 33. Wis: International Foundation for Functional Gastrointestinal Disorders. Abdominal distension in females with irritable bowel syndrome (IBS): the effect of the menopause and hormone replacement therapy. Nurs Res. Luo HS. Enterochromaffin cells and 5-HT signaling in the pathophysiology of disorders of gastrointestinal function. Reicin A. Am J Manag Care. Whitehead WE.48(3 Suppl 1):A-43. Regul Pept. Morris J. 10(8):785-795. Am Fam Physician. Gastroenterology. 1994. 50(4):471-474. 319(2):71-74. 1998. 1999. 44. Hertig V. 26. 29. Copas P. 1989. Bond EF. Crowell MD. 2004. In: Cho C-H. Vol 25. Dubin NH. J Womens Health Gend Based Med. 45. 42. Curr Opin Investig Drugs. 123(2):425432. Jackson NA. Hoechstetter L. 43. 27(4): 55-66. 2001. Mitchell ES. Gastroenterology. et al. Cain KC. Dig Dis Sci. 98(2):420430. Asbury B. Papka RE. Towson. Switzerland: Karger. Barron JJ. Molecular defects in mucosal serotonin content and decreased serotonin reuptake transporter in ulcerative colitis and irritable bowel syndrome. Storey-Workley M. Do male sex hormones protect from irritable bowel syndrome? Am J Gastroenterol. 2002. Gastroenterology. Bowel dysfunction in postmenopausal women. Lennard-Jones JE. 1992. 2003. menstrual cycle and orocaecal transit in normal and constipated women. Calixto JB. 28. Talley NJ. 22. Robinson JC. Gastroenterology. Jarrett ME. 102(2):505-513. 49. 2000. Jr. Gastrointestinal Mucosal Repair and Experimental Therapeutics. Houghton LA. Moos RH. 40. Elder RF. Thompson DG. 2004. 1983. 124(2):288-292. 30. 27. 48. 1998. Camilleri M. 1989. 49(1):88-95. Xu L. Women with irritable bowel syndrome: differences in patients’ and physicians’ perceptions. International Foundation for Functional Gastrointestinal Disorders. Gastrointestinal protective action of prostaglandin E2 and EP receptor subtypes.
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