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CLINICAL REVIEW
Gastrointestinal symptoms and disorders in patients with eating
disorders
Yasuhiro Sato
1
•Shin Fukudo
1,2
Received: 13 August 2015 / Accepted: 7 October 2015
ÓJapanese Society of Gastroenterology 2015
Abstract The two most clinically serious eating disorders
are anorexia nervosa and bulimia nervosa. A drive for
thinness and fear of fatness lead patients with anorexia
nervosa either to restrict their food intake or binge-eat then
purge (through self-induced vomiting and/or laxative
abuse) to reduce their body weight to much less than the
normal range. A drive for thinness leads patients with
bulimia nervosa to binge-eat then purge but fail to reduce
their body weight. Patients with eating disorders present
with various gastrointestinal disturbances such as post-
prandial fullness, abdominal distention, abdominal pain,
gastric distension, and early satiety, with altered esopha-
geal motility sometimes seen in patients with anorexia
nervosa. Other common conditions noted in patients with
eating disorders are postprandial distress syndrome, supe-
rior mesenteric artery syndrome, irritable bowel syndrome,
and functional constipation. Binge eating may cause acute
gastric dilatation and gastric perforation, while self-in-
duced vomiting can lead to dental caries, salivary gland
enlargement, gastroesophageal reflux disease, and elec-
trolyte imbalance. Laxative abuse can cause dehydration
and electrolyte imbalance. Vomiting and/or laxative abuse
can cause hypokalemia, which carries a risk of fatal
arrhythmia. Careful assessment and intensive treatment of
patients with eating disorders is needed because gastroin-
testinal symptoms/disorders can progress to a critical
condition.
Keywords Eating disorder Anorexia nervosa Bulimia
nervosa Gastrointestinal symptom Gastrointestinal
disorder
Eating Disorders and Gastrointestinal (GI)
Symptoms/Disorders
The Diagnostic Statistical Manual of Mental Disorders 5
th
Edition lists several disorders related to eating behaviors
[1]. The two most clinically serious eating disorders are
anorexia nervosa (AN) and bulimia nervosa (BN). Among
patients with AN, a drive for thinness and intense fear of
fatness leads them to engage in two types of energy-re-
stricting activities—restricting food intake, which is
referred to as AN of the restrictive type (ANR), and binge
eating followed by purging behavior, i.e., self-induced
vomiting and/or laxative abuse, which is referred to as AN
of the binge-purge type (ANBP). In addition, AN patients
perform excessive physical exercise. Together, these
activities result in bodyweight loss. Despite the loss of
weight, however, AN patients still consider themselves fat
(due to body image distortion) and refuse to acknowledge
their illness. AN commonly develops in young women,
with a prevalence rate in this population of 0.3 % [2]. The
mortality rate of AN is 5.1 % per decade [3], which is the
highest among mortality rates for stress-related disorders.
AN patients frequently present with associated psychiatric
disorders such as depression, obsessive–compulsive disor-
der, and personality disorder [4]. They also show several
types of cognitive dysfunction, including cognitive inflex-
ibility [5–7], impaired decision making [8,9], reward-
processing disturbance, and altered interoceptive aware-
ness [10]. In many cases, AN patients are resistant to
treatment.
&Yasuhiro Sato
yassat@hosp.tohoku.ac.jp
1
Department of Psychosomatic Medicine, Tohoku University
Hospital, Sendai, Japan
2
Department of Behavioral Medicine, Tohoku University
Graduate School of Medicine, Sendai, Japan
123
Clin J Gastroenterol
DOI 10.1007/s12328-015-0611-x
BN patients are also preoccupied with a drive for thin-
ness and engage in binge eating, purging, and exercise.
However, they cannot achieve a reduction in body weight
and remain at normal weight. As with AN, BN tends to
develop in adolescence and is prevalent in young women.
The prevalence rates for BN are 1 % in young women and
0.1 % in young men [2]. BN patients also show psychiatric
disorders and cognitive dysfunctions. A shift from AN to
BN or from BN to AN has been reported in some cases.
Complaints of GI symptoms are frequent among patient
with eating disorders. In a study by Salvioli et al. of
patients with eating disorders (39 with AN and 9 with BN),
96 % reported postprandial fullness, 90 % reported
abdominal distention, and more than half complained of
abdominal pain, gastric distension, early satiety, and nau-
sea [11]. In addition, Salvioli et al. found a significant
correlation between GI symptoms and hypochondriasis. In
other studies, AN patients tended to complain of early
satiety, post-prandial discomfort or recurrent vomiting
[12], severe constipation, and bowel obstruction [13], while
BN patients tended to experience bloating (74.4 %) and
flatulence (74.4 %), followed by constipation (62.8 %),
decreased appetite (51.2 %), abdominal pain (48.8 %),
borborygmi (48.8 %), and nausea (46.5 %) [14].
Common GI Symptoms/Disorders in Patients
with Eating Disorders
Esophageal symptoms and disorders
Although patients with eating disorders may report distur-
bances in swallowing, there is little evidence of esophagus
malfunction in AN [15]. Such esophageal symptoms without
evidence of structural abnormalities, referred to as functi onal
GI disorders (FGID) of the esophagus, include functional
dysphagia, globus, and functional heartburn, as defined by
the Rome III criteria [16] and co-occur with eating disorders
at rates of 6, 1, and 22 %, respectively (Fig. 1)[17].
To date, only a few studies have focused on esophageal
motor function in patients with eating disorders, despite the
clinical importance of evaluating such motor activity.
Stacher et al. found that 7 of 30 patients initially diagnosed
with AN had esophageal achalasia; one patient had diffuse
esophageal spasm, another had severe gastroesophageal
reflux disease with upper esophageal sphincter hyper-
tonicity, and 6 had nonpropulsive, repetitive, high-ampli-
tude, prolonged contractions of the lower segment of the
esophagus [18]. However, the very high prevalence of
esophageal motility disorders among the patients in that
study suggests referral bias [15]. Another study showed
that the basal pressure of the lower esophageal sphincter
was higher in ANR patients than in ANBP patients and
healthy controls, but still within the normal range [19] and
this difference disappeared after treatment. Another study
evaluating esophageal motility in 26 BN patients [20]
found normal motility in 18 patients, incomplete lower
esophageal sphincter relaxation in 4, vigorous achalasia in
2, and achalasia and diffuse esophageal spasm in one
patient each. In contrast, another study on patients with
bulimic eating disorders (8 with BN and 4 with mixed
features of AN and BN) revealed normal esophageal
motility in all 12 patients [21].
Slow gastric motility and functional dyspepsia
As mentioned earlier, patients with eating disorders fre-
quently report postprandial fullness, abdominal distention,
gastric distension, early satiety, and nausea [11]. Both AN
and BN patients have reported more severe postprandial
distress than healthy controls [22]. These symptoms may
be attributed to postprandial distress syndrome, a subtype
of functional dyspepsia. Functional dyspepsia, itself a type
of FGID, manifests as postprandial fullness, early satiation,
epigastric pain, or epigastric burning without any structural
disease [16]. In patients with eating disorders, one study
Fig. 1 Gastrointestinal disorders of patients with eating disorders
Clin J Gastroenterol
123
reported a prevalence rate of 45 % for postprandial distress
syndrome [17], and another study reported a prevelance
rate of 23 % for functional dyspepsia (Fig. 1)[23].
Slow gastric motility contributes to these gastric symp-
toms. AN patients have shown slow gastric emptying [12,
24–28] in addition to gastric dysrhythmia, impaired antral
contractility, delayed emptying of solids, decreased post-
cibal blood levels of norepinephrine and neurotensin, and
impaired autonomic function [26]. Slow gastric emptying in
these patients was found to correlate with nausea, vomiting,
and gastric fullness [27], and has the potential to lead to
difficulties during re-feeding and weight restoration [29].
In BN patients, gastric relaxation after food intake was
significantly diminished [30], although gastric emptying
was normal [28,31]. Gastric compliance in BN showed no
difference from that in controls [32].
Several prokinetic agents have been tested for their
effects on delayed gastric emptying. Domperidone, a dopa-
mine D2-receptor selective antagonist used as a prokinetic
agent for the stomach, improved delayed gastric emptying in
AN patients [18,33]. Domperidone is available in Japan, but
not in the United States. Another prokinetic agent, cisapride,
a serotonin 5-HT4 agonist with weak 5-HT3 antagonistic
action, effectively enhanced gastric emptying in AN patients
[34–36]. However, cisapride is not available in most coun-
tries because of the critical cardiac adverse effects of QT
prolongation and ventricular tachycardia. Metoclopramide is
another dopamine antagonist that proved useful for
improving gastric motility [25,37]. In contrast, the proki-
netic agent erythromycin, which is popularly used as an
antibiotic, was tested in BN patients but failed to achieve a
significant clinical response [31]. Other prokinetics such as
mosapride, itopride, and acotiamide are used in Japan, but
these drugs have not been specifically tested in patients with
eating disorders.
Superior mesenteric artery syndrome
Superior mesenteric artery (SMA) syndrome is the result of
compression of the third portion of the duodenum, which
lies between the aorta and the vertebral column posteriorly
and the superior mesenteric artery anteriorly (Fig. 1)[38].
In healthy individuals, the arch of the SMA is held away
from the aorta by the mesenteric pad of fat. Considerable
loss of mesenteric fat in conditions such as burns, pro-
longed bedrest, rapid growth in children without corre-
sponding weight gain, and AN, serves to reduce the
aortomesenteric angle [39]. Weight loss is regarded to be a
risk factor for SMA syndrome [40]. The symptoms of the
syndrome are appetite loss, abdominal pain, postprandial
distension, abdominal fullness, nausea, and vomiting [41].
Radiological methods are useful for diagnosing SMA
syndrome. Barium swallow radiography demonstrates an
extremely dilated stomach and restriction of contrast flow
past the third portion of the duodenum [42]. Computed
tomography (CT) reveals dilation of the stomach and
proximal duodenum in addition to severe narrowing of the
third portion of the duodenum (Fig. 1). Contrast-enhanced
CT reveals compression of the duodenum between the
SMA and aorta [42].
SMA syndrome has frequently been reported in AN
patients [39,42–51]. Elbadaway presented four possible
explanations for the relationship between SMA syndrome
and AN [39]. First, acute or subacute SMA syndrome may
develop as a complication in AN patients. Second, chronic
SMA syndrome may simulate AN [52]. Third, chronic SMA
syndrome may complicate AN, in which case either syn-
drome may be diagnosed but probably not both. The fourth
possibility is that chronic SMA syndrome precipitates AN.
In a case report, Jordaan et al. pointed out that ‘Not
diagnosing SMA syndrome in a timely fashion may lead to
a delay in treatment, prolonged bowel obstruction, and an
increased risk of developing fear and avoidance of food’
[45]. In their female patient, although they noted interplay
between psychological and physical factors and arrived at a
diagnosis of ‘eating disorder not otherwise specified’, the
diagnosis according to DSM-5 criteria would be ‘restric-
tive/avoidant food intake disorder’.
In cases of total intestinal obstruction due to SMA
syndrome, decompression with nasogastric tube placement
and surgical consultation will probably be necessary [42].
Conservative treatments have been used with some
patients, including oral hypercaloric liquid feeding [52],
nasojejunal tube feeding [42,49], and total parenteral
nutrition [49], whereas other patients have been treated
surgically with duodenojejunostomy [39,43,45]. These
treatments sometime failed because the patients refused to
restore their body weight due to a psychopathological
desire for thinness.
BN patients rarely develop SMA syndrome because of
their normal body weight. Ikegaya et al. reported a fatal
case of BN in a woman who consumed enormous amounts
of solid food, where her distended stomach compressed the
SMA and pinched the duodenum, eventually leading to
fatal total intestinal obstruction [48].
Irritable bowel syndrome
Irritable bowel syndrome (IBS) is one of the most frequent
FGIDs. IBS patients have abdominal pain or discomfort
that is relieved with defecation, altered frequency of bowel
movement, and altered stool consistency [16]. Four sub-
types of IBS have been defined—with diarrhea (IBS-D),
with constipation (IBS-C), mixed (IBS-M), and unsubtyped
(IBS-U). Approximately 41–52 % of patients with eating
disorders have IBS [17,23,53], with 68.8 % of BN
Clin J Gastroenterol
123
patients diagnosed with IBS (Fig. 1)[54]. Although none
of these studies reported on the subtypes of IBS, IBS-C is
probably predominant given that IBS was weakly predicted
by laxative use (not abuse) in one study [17].
Constipation
Constipation is one of the most common GI symptoms
among patients with eating disorders. Functional constipation
is an FGID with difficult, infrequent, and incomplete defe-
cation that does not fulfill the criteria for IBS [16], i.e.,
without abdominal pain or discomfort. On the basis of the
Rome II or Rome III criteria, 11–24 % of patients with eating
disorder are diagnosed with functional constipation [17,23,
53]. Constipation has been reported in 67–83 % of AN
patients [55,56] and 62.8 % of BN patients (Fig. 1)[14].
Constipation in AN is thought to be caused by reflex
hypofunctioning of the colon due to lack of food intake
[57] or by poor nutrition and hypokalemia due to purging
[29]. The possibility of constipation being caused by
antidepressant medication, particularly tricyclic antide-
pressants, should also be considered in such patients [29].
Low triiodothyronine (T3) syndrome, which is character-
ized by a markedly decreased T3 level, normal or sub-
normal thyroxine (T4) level, and normal basal thyrotropin
(TSH) level, is a persistent finding in AN [58]. It is thought
to be a beneficial response designed to ‘spare calories’ [59].
This hypothyroidism-like condition may also cause con-
stipation, in addition to dry skin, hypothermia, bradycardia,
hypotension, sluggish tendon reflexes, and pleural or
pericardial or peritoneal effusions [60].
An investigation using a radiopaque marker revealed
that whole-gut transit time was significantly longer in both
AN and BN patients than in controls [61]. In a study using
a radiopaque marker and anorectal manometry, 8 of 12 AN
patients (66.7 %) showed slow colonic transit times, while
5 (41.7 %) had significantly lower resting anal canal
pressures than healthy controls [56]. Colonic transit time
normalized in the 8 patients who completed a 4-week re-
feeding program. However, anorectal manometry did not
normalize in these patients. Therefore, pelvic floor dys-
function might be a characteristic trait of AN patients.
Although increased food intake and weight gain appear
to relieve constipation to some extent in AN patients, the
specific physiologic factors that bring about the improve-
ment in constipation have yet to be determined [62].
Rectal prolapse
Several case reports have documented the complication of
rectal prolapse in patients with eating disorders (Fig. 1)
[63–67]. Predisposing risk factors for rectal prolapse
include history of pelvic surgery, obstetric trauma, elevated
intra-abdominal pressure, advanced age, and chronic con-
stipation [68]. Approximately 80–90 % of patients with
rectal prolapse are women [69]. Patients with rectal pro-
lapse exhibit a diminished anal canal pressure [70].
Therefore, patients with eating disorders are predisposed to
rectal prolapse.
Hepatic injury
Many AN patients show liver dysfunction (Fig. 1).
Although the liver dysfunction is mild and restores to
normalcy with nutritional recovery, some patients can
progress to severe hepatic failure that may eventually be
fatal [71–73]. Excess accumulation of fat in the liver
causes elevation of liver enzymes in AN patients [74]. One
report suggests that oxidative stresses in hepatocytes could
be related to the pathogenesis of liver injury in AN patients
[75].
GI Symptoms Specific to Binge2Purge Behavior
Both ANBP patients and BN patients consume large
amounts of food and then discharge the food with self-
induced vomiting and/or laxative/diuretic abuse. These
behaviors can result in serious health problems.
Binge eating
In the United States, 2.0–3.8 % of female college students
have been reported to be bulimic [76]. In a study of 456
female nursing school and junior college students in Japan,
35 students (7.7 %) admitted to binge eating more than
once a week, 38 (8.3 %) to self-induced vomiting, and 21
(4.5 %) to using laxatives. The reported prevalence of
binge-eating behavior among women varies widely
depending on the sample population, ranging from 24 %
among adults from family practice clinics to 90 % among
college students [77].
Several case reports have been published on patients who
developed acute gastric dilatation due to excessive food
consumption (Fig. 2)[78–80]. Acute gastric dilatation may
sometimes be life-threatening, as food compaction in the
stomach may obstruct gastric blood circulation, leading to
necrosis and perforation of the stomach wall (Fig. 2)[81–84].
Self-induced vomiting
Many ANBP and BN patients vomit voluntarily after binge
eating. In fact, 8.06 % of ANBP patients and 29.50 % of
BN patients show Russell’s sign—the presence of lesions
such as calluses on the dorsal aspect of the hand as a
consequence of self-induced vomiting [85]. As the illness
Clin J Gastroenterol
123
progresses, many patients can vomit reflexively without
mechanical stimulation [86]. Patients with bulimic behav-
ior present with dysphagia and odynophagia, although their
esophageal motility is within normal range [21]. This may
be due to continuous acid exposure. Vomited acidic gastric
juice causes a number of problems such as dental caries,
salivary gland enlargement and inflammation, and gas-
troesophageal reflux disease (GERD) (Fig. 2).
Mallory–Weiss syndrome is a mucosal and submucosal
tear of the esophagus or stomach at or near the gastroe-
sophageal junction [87], and is typically indicated by non-
bloody vomiting followed by hematemesis. Although
ANBP and BN patients are considered susceptible to this
syndrome because they frequently vomit, there is no clear
data on the prevalence of the syndrome in eating disorder
patients in the English-language literature. Similarly, the
prevalence of another severe esophageal complication,
esophageal rupture (Boerhaave syndrome), is also
unknown.
Kiss et al. performed esophagogastroduodenoscopy in
37 patients with long-standing BN and found the endo-
scopic appearance of the esophageal and gastric mucosa
was normal in 23 patients [88]. However, 8 patients
showed signs of mild esophagitis, which were not related to
the duration or severity of bulimic behavior or to symptoms
of gastroesophageal reflux. Two of these 8 patients had
sliding hiatal hernias. The remaining 6 patients had
superficial mucosal erythema in the stomach or duodenum
but did not exhibit actual erosions, ulcers, or bleeding. Kiss
et al. concluded that mucosal injury consequent to chronic,
self-induced vomiting in patients with BN is relatively
infrequent and limited. There is no similar report of
endoscopy findings in AN patients.
Esophageal achalasia is a dysmotility disorder of
unknown etiology, manifesting as dysphagia and vomiting.
In this condition, the vomitus is not acidic because the
swallowed food stops just above the esophagocardiac
junction. Achalasia has been mistaken for eating disorders,
particularly in young female AN patients [89–95].
Electrolyte imbalance
Bulimic patients frequently present with electrolyte abnor-
malities, with hypokalemia occurring in 0–23.5 % of
patients, hypochloremia in 8.8–26.2 %, and elevated bicar-
bonate levels in 8.2–23.5 % [96]. Hypokalemia is the most
serious of these abnormalities since it can cause cardiac
arrhythmias, rhabdomyolysis, muscle weakness, hypoka-
lemic cardiomyopathy, and tetany [97]. As well as direct loss
of potassium from vomiting, the concomitant loss of chloride
ions and gastric acid leads to hypokalemic hypochloremic
metabolic alkalosis [97]. The treatment of marked hypoka-
lemic metabolic alkalosis requires volume repletion (with
intravenous normal saline) [86], and oral potassium chloride
is generally preferred for potassium repletion [86].
Oral symptoms
Oral lesions such as dental erosion, parotid gland swelling,
dental caries, and periodontal disease are frequently noted
in eating disorder patients with binge-purge behavior
(Fig. 2)[98]. In a university dental clinic, 9 of 400 patients
were females with BN [99]. Bulimic patients often report
increased sensitivity of the teeth to hot, cold, and acidic
substances, suggestive of damage to dental enamel [100].
Gentle brushing and use of a fluoride mouth rinse imme-
diately after purging may prevent caries [86]. Parotid gland
swelling is effectively treated with oral administration of
pilocarpine hydrochloride [101].
Hyperamylasemia
In one study, hyperamylasemia was found in 61 % of BN
patients and in 20 % of ANR patients (Fig. 2), with more
than three-quarters of BN patients showing a close positive
Fig. 2 Gastrointestinal-related binge-purge behavior by patients
with eating disorders. aDisorders induced by binge eating, bdisorders
induced by self-induced vomiting, cdisorders induced by laxative
abuse
Clin J Gastroenterol
123
correlation between the frequency of vomiting and total
serum amylase levels, and both frequency and type of
vomiting appearing to be associated with the extent of
salivary gland enlargement [102]. The hyperamylasemia in
patients with AN or BN is often caused by increased
salivary-type amylase activity [103]. In a study on the
amylase and isoamylase activity in 17 patients with eating
disorders, 6 showed elevated amylase activity, with 5 of the
6 having isolated increases in salivary isoamylase activity
[103]. Hyperamylasemia does not require any treatment.
Gastroesophageal reflux disease
GERD is a condition characterized by the reverse flow of
gastric contents through the esophagus and, in some cases,
into the pharynx [100]. In bulimic patients, spontaneous
reflux of acidic gastric contents into the lower esophagus
may occur due to laxity of the lower esophageal sphincter
after repeated vomiting [86]. Endoscopic investigations
revealed that 8 of 37 patients with bulimic behavior had
mild esophagitis (Fig. 2)[88]. Acid reflux has been
observed in BN patients evaluated by 24-h pH monitoring
and esophagography [104]. Proton-pump inhibitors are the
first-line therapy for GERD because of their efficacy,
safety, and cost-effectiveness [86].
Esophageal cancer
Long-term exposure to acidic gastric juice causes Barrett’s
esophagus, characterized by metaplasia from squamous to
columnar epithelium. Barrett’s esophagus is a precursor to
esophageal adenocarcinoma and increases carcinogenic
risk by 11-fold [105]. There have been several case reports
of patients with purging behavior who developed Barrett’s
esophagus [106], which then progressed to esophageal
cancer [107,108]. Other reports have described BN
patients who developed esophageal cancer in the absence
of Barrett esophagus [109,110]. In a large cohort study of
3,617 patients with a history of hospitalization for eating
disorder, 7 were found to have esophageal cancer [111].
The standardized incidence ratio of patients with eating
disorders to the general population was 6.1 in that study.
Thus, patients hospitalized previously with eating disorders
are thought to be at increased risk of developing esopha-
geal cancer. All the patients with esophageal cancer in the
abovementioned study had squamous cell carcinomas
although adenocarcinoma would be more in line with
expectations. Therefore, the involvement of confounding
factors, including alcohol, smoking, and nutritional defi-
ciency, appears to be a more plausible explanation than
acidic damage. Further extensive research is needed to
elucidate the relationship between self-induced vomiting,
Barrett esophagus, and esophageal cancer.
Laxative abuse
Laxative abuse is another common purging behavior in
patients with eating disorders. One study indicated that
36.5 % and 7.9 % of patients with eating disorders reported
laxative abuse and enema abuse, respectively [112].
Patients believe that laxatives help to remove the calories
in food and keep them thin. However, in fact, only
10–12 % of ingested calories are lost as a result of laxative
use because laxatives have little effect on the small intes-
tine where caloric absorption primarily occurs [86].
Chronic watery diarrhea (Fig. 2) caused by laxative
abuse leads to dehydration and electrolyte imbalance.
Laxative abuse results in the loss of potassium and bicar-
bonate via the stool, resulting in hypokalemia and non-
anion gap metabolic acidosis [97]. The development of
hypokalemia may be marked by generalized muscle
weakness, lassitude, skeletal muscle paralysis, rhabdomy-
olysis with renal impairment, and nerve palsies [113].
More severe hypokalemia can result in cardiac arrhyth-
mias, with an increased risk of sudden death. Expulsion of
water via stool causes dehydration, leading to hypotension,
tachycardia, postural dizziness, and syncope [113].
Melanosis coli, or pseudomelanosis coli, refers to dark-
ening of the colonic mucosa as a result of chronic use of
laxatives, especially anthraquinone derivatives (Fig. 2)
[114]. No correlation between colorectal cancer and mela-
nosis coli or laxative use has been noted [115]. The condi-
tion can resolve gradually after laxative withdrawal [114].
So-called ‘cathartic colon’ is a loss of normal colonic
peristalsis because of long-term habituation to stimulant
laxatives. However, the cathartic colon is not induced by
currently available laxatives even when used over long
periods or in excessive doses [116]. Cathartic colon must
not be mistaken for laxative abuse.
Patients’ erroneous beliefs about the normal number and
frequency of bowel movements are usually obstacles in the
treatment of laxative abuse, so educating them on normal
bowel physiology is an essential first step in treatment
[113]. Patients with eating disorders have been reported to
have increased anxiety levels with laxative withdrawal
[117]. Body weight gain due to constipation and edema due
to fluid retention may contribute to their increasing anxiety,
and close supervision is required during this time to ensure
that withdrawal is successful [113].
Conclusion
Patients with eating disorders present with various GI
symptoms/disorders, some of which are critical. Therefore,
careful assessment and intensive treatment is needed. Data
on the prevalence of GI symptoms/disorders in patients
Clin J Gastroenterol
123
with eating disorders have been mainly obtained from
small-scale studies. As such, comprehensive and extensive
surveys on GI symptoms/disorders are necessary among
patients with eating disorders to elucidate the actual nature
of these intractable disorders and facilitate the development
of innovative treatment strategies. Few clinical trials have
been conducted on therapeutic measures for GI symptoms/
disorders in patients with eating disorder patients, and to
achieve better treatment outcomes, large randomized con-
trol trials are warranted.
Compliance with ethical standards
Conflict of Interest: Yasuhiro Sato and Shin Fukudo declare that
they have no conflict of interest.
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