Accepted Manuscript

Medical Complications of Anorexia Nervosa and Bulimia

Patricia Westmoreland, MD, Mori J. Krantz, MD, Philip S. Mehler, MD, FAED, FACP
PII:

S0002-9343(15)00582-3

DOI:

10.1016/j.amjmed.2015.06.031

Reference:

AJM 13081

To appear in:

The American Journal of Medicine

Received Date: 22 May 2015

Revised Date:

19 June 2015

Accepted Date: 19 June 2015

Please cite this article as: Westmoreland P, Krantz MJ, Mehler PS, Medical
Complications of Anorexia
Nervosa and Bulimia, The American Journal of Medicine (2015), doi:
10.1016/j.amjmed.2015.06.031.
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ACCEPTED MANUSCRIPT

Medical Complications of Anorexia Nervosa and Bulimia

Mori J. Krantz, MD2,4

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Patricia Westmoreland, MD1

Philip S. Mehler, MD, FAED, FACP1,3,4

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Eating Recovery Center of Denver, 7351 E Lowry Blvd, Suite 200, Denver, CO 80230
– Pwestmoreland@eatingrecoverycenter.com
2

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Cardiology Division, Denver Health Medical Center, Denver, CO, 777 Bannock St.,
MC0960, Denver, CO 80204 – Mkrantz@dhha.org
3

ACUTE at Denver Health, Denver Health Medical Center, 777 Bannock Street,
MC4000, Denver, CO 80204 – PMehler@dhha.org
4

Corresponding Author:

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Department of Medicine, University of Colorado Health Sciences Center

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Philip S. Mehler, MD, FAED, FACP

777 Bannock Street, MC 4000

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Denver, CO 80204
303-602-4972

Email: PMehler@dhha.org
Funding Source – None

Conflict of Interest – None

Word Count: 3,888
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ABSTRACT
Anorexia nervosa and bulimia nervosa are serious psychiatric illnesses related to

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disordered eating and distorted body images. They both have significant medical

complications associated with the weight loss and malnutrition of anorexia nervosa
as
well as from the purging behaviors which characterize bulimia nervosa. No body

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system is spared from the adverse sequela of these illnesses, especially as

anorexia
nervosa and bulimia nervosa become more severe and chronic. Here we review the

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medical complications which are associated with anorexia nervosa and bulimia
nervosa
as well as the treatment for said complications. We also discuss the epidemiology
and

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psychiatric comorbidities of these eating disorders.

Keywords: Anorexia Nervosa, Bulimia, Medical Complications, Hypokalemia,

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Osteoporosis
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INTRODUCTION
Anorexia nervosa and bulimia nervosa are serious psychiatric illnesses with
substantial morbidity and mortality. It is the psychiatric illness with the highest
mortality

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rate.1-7 Mortality is also increased in patients with bulimia nervosa.8 In both

anorexia
nervosa and bulimia nervosa, much of the increased mortality rate is attributable
to the
medical complications inherent to these two illnesses.

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Although anorexia nervosa and bulimia nervosa are defined as separate

disorders in the psychiatric Diagnostic and Statistical Manual 5th Edition (DSM-
5),9 they

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both fall into the category of disordered eating, driven by an irrational fear of
normal
body weight, a desire for thinness, and leading to body image distortion.10
Cultural
ideals of beauty and thinness may incite the development of disordered eating in
vulnerable individuals, who have a genetic predisposition towards anxiety and

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perfectionism.11 Both starvation and purging may initially calm these feelings of
anxiety
and reduce obsessions and compulsions via a serotonergic neuronal pathway.12, 13
During the course of anorexia nervosa and bulimia nervosa, comorbid mental

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disorders also emerge as a result of altered neurotransmitter metabolism and/ or

endocrine changes that result from caloric deprivation.14-17 Almost 50% of
adolescent

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patients with anorexia nervosa meet criteria for at least one comorbid psychiatric
illness.18 Eating disorders are strongly associated with mood and anxiety
disorders, and
the type and severity of these comorbidities is increased in patients who have the
most
severe eating disorders.19-23
In addition, patients with bulimia nervosa who have comorbid borderline
personality disorder have poorer outcomes than those without borderline personality
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disorder when both groups are treated with psychotherapy and pharmacotherapy.24,25
Psychiatric comorbidity, as well as a history of suicidal or self-harm ideation,
and
comorbid mental illnesses all confer an increased risk of death in patients with
eating

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disorders.25-28 Problems socializing, and difficulties with being assertive, are

factors that
contribute to maintaining an eating disorder. 29 Temperament traits of harm
avoidance,

patients who recover from eating disorders.30

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combined with high reward dependence, are protective factors seen more commonly in

Treatment of anorexia nervosa and bulimia nervosa is multi-dimensional. In

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addition to nutritional rehabilitation, cognitive-behavioral psychotherapy, along

with
family therapy, have been shown to be effective in treating patients with anorexia
nervosa,31 although the benefit of these therapies have been mostly noted in the
weight
maintenance phase of treatment.32

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There is only minimal to moderate evidence that psychiatric medications are

efficacious in treating patients with anorexia nervosa. Despite the prevalence of
mood
and anxiety symptoms in patients with anorexia nervosa, medications used to treat

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these conditions are not necessarily useful treatment adjuncts for reducing the
symptoms of anorexia nervosa. In one study, fluoxetine assisted in preventing
relapse

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in weight-restored patients with anorexia nervosa.33 However this finding was not
replicated in a subsequent study.34 While there may be evidence for using
antidepressants in the weight maintenance phase, antidepressants do not ameliorate
eating disorder pathology in patients who are acutely underweight.35 The poor
response to antidepressants is believed to result from starvation-induced
abnormalities
in serotonin receptors.36
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In addition to concerns regarding the efficacy of antidepressants in patients with

anorexia nervosa, there is also considerable debate as to the efficacy of
antipsychotics
in treating their symptoms. Low-dose antipsychotic medications may be useful in

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treating delusional beliefs regarding body image, intense ruminations about food,
and
the hyper-arousal and as well as anxiety induced by having to face weight

restoration.37,38 Although atypical antipsychotic medications promote weight gain

in

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normal weight individuals, they do not have this effect in patients with anorexia

nervosa.35,39 However, patients with eating disorders may not accept reassurance in

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this regard. Despite the paucity of associated weight gain, there remains concern
that
the risk of using these medications outweighs their potential benefit.40 First
generation
antipsychotics (typical antipsychotics) lower the seizure threshold. Side effects
of
second-generation antipsychotics (atypical antipsychotics), such as orthostasis,

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prolonged QTc, and hepatotoxicity are of concern.

Despite continued debate regarding the usefulness of pharmacotherapy in

patients with anorexia nervosa, pharmacotherapy for bulimia is well established.

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Fluoxetine (at doses of 60 mg or higher) is FDA-approved for bulimia nervosa, and

other selective serotonin reuptake inhibitors (as well as other classes of

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antidepressants) have been found to be useful in treating patients with bulimia

nervosa.32,37 The effect of fluoxetine in treating the symptoms of bulimia nervosa
appears to be independent of its effects on mood, and is reportedly related to the
effects
of the medication on satiety, thereby reducing binge eating.41,42 Cognitive
behavioral
therapy is a well-established psychotherapeutic treatment for bulimia nervosa.32,43
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MEDICAL COMPLICATIONS - ANOREXIA NERVOSA

Anorexia nervosa can adversely affect almost every body system. The
complications arise as a direct result of weight loss and malnutrition. However,
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are no studies which define which body mass index (BMI) is associated with a
particular
medical complication. The eyes may be affected by lagophthalmos, wherein the
eyelids
do not totally cover the eye during sleep, resulting in irritation to the cornea
and mild

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ocular discomfort.44 Treatment involves taping the eyes shut at night after first
applying

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a sterile lubricant.

GASTROINTESTINAL

Dysphagia can frustrate the ingestion of oral calories during the early stages of
refeeding. It is due to weakened and uncoordinated pharyngeal muscles. As a result,

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patients may complain of coughing with eating or may have a history of aspiration
pneumonia. The diagnosis is made by a modified barium swallow test and the
treatment depends on weight restoration and input from a speech therapist to define

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proper food consistencies.45 Patients with anorexia nervosa have significantly

slowed
gastric emptying at their nadir weights which is accompanied by complaints of early

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satiety, nausea and bloating.46 This gastroparesis ultimately resolves with weight
gain,
but symptoms may respond early on to low dose, short-term usage of metoclopramide
before meals. Acute gastric dilatation is a serious condition which can lead to
gastric
perforation if not recognized early.47 It can occur independently as an isolated
finding in
the early phases of refeeding or, it can occur as a result of the superior
mesenteric
artery syndrome.48 Superior mesenteric artery syndrome is defined by the extrinsic
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compression of the third portion of the duodenum by the superior mesenteric artery,
due
to loss of a fatty tissue pad which normally maintains the angle between the
superior
mesenteric artery and the aorta. Significant left upper quadrant abdominal pain
with

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eating, emesis during the meal and early satiety should prompt an evaluation for
gastric
dilatation or superior mesenteric artery syndrome, via an abdominal radiograph or
CT
scan. Treatment of superior mesenteric artery syndrome is aimed at weight
restoration

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to reconstitute the fat pad. This can be achieved by a soft or liquid oral diet or
by enteral
feeds via a nasojejunal tube or a percutaneously placed one.49 Acute gastric
dilation is

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first treated by gastric decompression with a nasogastric tube, followed by similar

treatments to those used in superior mesenteric artery syndrome. Just as there is
slowing of the proximal gastrointestinal tract, there is also slowing of colonic
function,
resulting in constipation as an accompanying symptom in anorexia nervosa.50 Osmotic

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laxatives are useful along with reassurance that the patient’s prior bowel pattern
should
return over a few weeks with ongoing progressive nutritional rehabilitation.
Elevated liver transaminases occur frequently at patient’s nadir weights.51 This

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generally represents apoptosis, a programmed hepatocyte death as a result of

malnutrition. Aspartate aminotransferase (AST) and alanine aminotransferase (ALT)

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are the most frequently affected in a range of 2-4 times elevated, but severe
elevations
have also been reported to occur.52 ALT is more elevated than AST. The prevalence
of
liver enzyme abnormalities correlates with lower BMI’s, hypoglycemia and the
development of refeeding hypophosphatemia.53 Progressive nutritional support will
resolve these elevations over the first few weeks of refeeding. Alkaline
phosphatase
and bilirubin are not commonly affected. Less frequently, elevations of the AST and
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ALT may be due to steatosis as a result of actual refeeding. A liver ultrasound can
help
elucidate the cause since in steatosis, a fatty enlarged liver will be noted.54

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CARDIAC

As noted above, anorexia nervosa has the highest mortality of any psychiatric
disorder. Sudden cardiac death along with other medical complications and suicide

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account for about 60% of the deaths. The exact cause of sudden death in anorexia
nervosa remains unknown. Autopsy studies do not reveal evidence of obstructive

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coronary artery disease.55 It has been postulated that alterations in cardiac

conduction
and repolarization contribute to heightened mortality though a single unifying
mechanism. Bradycardia is commonly noted in patients and reflects heightened vagal
tone in the setting of substantial weight loss. This often recovers with
restoration of body

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weight. A resting heart rate of less than 60 beats per minute, for example, was
seen in
95% of patients in a consecutive series.56 Sinus bradycardia in and of itself does
not
require specific therapy, but current guidelines recommend hospitalization for a
heart

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rate less than 40 beats per minute. High-grade atrioventricular block is

exceedingly rare
and suggests underlying structural heart disease that may be unrelated to anorexia

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nervosa itself. Temporary pacemakers are rarely required. Persistent junctional

rhythm
has been described among patients with severe anorexia nervosa, which may be
extinguished with exercise.57,58
Patients may present with prolongation of the rate-corrected QT (QTc) interval on

surface electrocardiography and a commonly held belief was that this is the primary
cause of sudden cardiac death. However, this relationship is confounded by
concurrent
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QTc-prolonging medications and depletion of serum potassium and magnesium levels.

In a series of patients with severe anorexia nervosa, marked QTc interval
prolongation
(>500 ms) was actually uncommon in the absence of contributing factors.59
Similarly,

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Facchini and colleagues observed 29 patients with anorexia and found marked
QTcprolongation in only 2 individuals.60 Both had profound hypokalemia, and after

potassium repletion, the QTc interval normalized. Therefore, to date, an

independent

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causal pathway between anorexia nervosa, QTc-prolongation, torsade de pointes, and

sudden cardiac death have not been demonstrated. Expectant management of delayed

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repolarization is generally adequate and includes electrolyte repletion,

discontinuation of
QTc-prolonging medications, and serial 12-lead electrocardiography.
Severe anorexia nervosa is also known to change cardiac structure. Many
patients develop left ventricular atrophy and subsequent annular changes that lead
to

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mitral valve prolapse. Patients occasionally develop pericardial effusions, which

are
generally self-limited and resolve with weight restoration. Among the most
prominent
cardiovascular structural abnormalities is a substantial reduction in left
ventricular

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myocardial mass with preserved left ventricular systolic function. This is

generally
reversible with refeeding. One study demonstrated myocardial fibrosis/scar
manifested

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by late gadolinium enhancement on magnetic resonance imaging (MRI) in nearly a

quarter of patients.61 Although echocardiographic atrophy and fibrosis by MRI have
been demonstrated, histologic abnormalities in the heart have been poorly
characterized until very recently: a published autopsy report showed left
ventricular
atrophy with endocardial and interstitial fibrosis, focal myxoid material
deposition with
mast cells, and increased cytoplasmic lipofuscin.62 Although most cardiac
structural
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abnormalities are reversible in this condition, the presence of myocardial scar

suggests
that malignant arrhythmias remain a possible mechanism of increased mortality in
this

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disease.

PULMONARY

As opposed to the cardiac system, the lungs are not adversely affected for the

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most part. There appear to be some pulmonary function test abnormalities associated
with anorexia nervosa which are similar to those seen with emphysemia.63 It is not
clear

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if this impairment recedes with refeeding. Spontaneous pneumothorax has been

reported in anorexia nervosa along with prolonged air leaks.64

HEMATOLOGY

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As anorexia nervosa becomes worse, there is trilinear hypoplasia causing

anemia, leukopenia and thrombocytopenia. Anemia occurs in 40% of these patients,
with leukopenia noted in 30% and thrombocytopenia in about 10%.65 The cytopenia are

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due to gelatinous marrow transformation with atrophy of the normal fat content in
the
marrow and replacement by a mucopolysacharide.66 Iron deficiency is not typically

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found and red cell indices are normal. Although often neutropenic, surprisingly,
these
patients do not appear to be more susceptible to infectious complications.67
However,
they also do not manifest a typical febrile response to infections and inflammatory
markers are suppressed, which can cause a delay in the diagnosis of an infection.68
The cytopenias resolve with weight restoration; growth factors are not indicated in
anorexia nervosa.69 Very recently, plasma levels of vitamin B12 and folate have
been
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found to be increased. The increase is artificial as it was found to be due to

hepatocyte
dysfunction with leakage of the vitamins from these cells.70

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MUSCULOSKELETAL

Osteoporosis is common in anorexia nervosa and occurs early in the disease.71

Decreased bone density is evident after just one year of anorexia nervosa,

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notwithstanding the relatively young age of these patients. The risk of subsequent

fragility fractures is markedly elevated, both in adults and adolescents with

anorexia

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nervosa.72,73 Fracture incidence increases soon after diagnosis of anorexia nervosa

and remains so many years later. This is one of the rare complications of anorexia
nervosa which may leave irreversible damage even after recovery. Thus, the need for
obtaining bone density testing in all patients with a disease duration of more than
one

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year. In contrast to postmenopausal osteoporosis, in anorexia nervosa the loss of

bone
mineral density is due to both decreased bone formation along with increased bone
resorption. Also, trabecular bone is more affected than cortical bone. Yet, the
exact

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etiological factors involved in their loss of bone density is not clear. Putative
factors
include the overlap between the normal accrual of peak bone mass and the age of

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onset of anorexia nervosa, along with the typical hypogonadal state, elevated
cortisol
levels and growth hormone resistance found in anorexia nervosa as will be described
below.

There are currently no treatments specifically approved for the osteoporosis of

anorexia nervosa. Weight gain and resumption of menses are key and are associated
with significant increases in spine and hip bone mineral density.74 However
estrogen
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therapy does not appear to be of much value in anorexia nervosa. Many randomized
controlled trials have found it to be ineffective, a fact which is underappreciated
in the
medical community.75-77 Also, the withdrawal bleeding associated with their usage
can

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mislead patients into believing they are getting better. Transdermal estrogen
patches
have shown promising results in adolescents.78 Calcium and vitamin D by themselves
do not restore bone density.79 Bisphosphonates have been shown to be effective in

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anorexia nervosa with an increase of 3-4% in spine bone mineral density after
twelve
months of treatment.80 Teriparatide, a recombinant parathyroid hormone, has
recently

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demonstrated very favorable effects in this population.81 There are no data as yet
with
denosumab.82 Testosterone therapy may be effective in male patients with anorexia
nervosa who also have low serum testosterone levels. Males with anorexia nervosa

ENDOCRINE

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actually have more severe degrees of osteoporosis then their female counterparts.83

There are multiple endocrine abnormalities associated with anorexia nervosa.

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Most patients, both female and male, are hypogonadal, due to reversion to a
prepubertal state wherein pulsatile hypothalamic gonadotropin releasing hormone

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(GNRH) secretion is reduced, causing low levels of follicle stimulating hormone

(FSH)
and leutinizing hormone (LH).84 Thus, amenorrhea is commonly noted in most, but not
all females with anorexia nervosa. Leptin may have a causal role in the
amenorrhea.85
Resumption of menses generally occurs at the weight where the periods ceased or at
more than 90% of ideal body weight.86 Some patients, however, have prolonged
amenorrhea even after weight restoration, and fertility may be permanently
adversely
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affected.87 In males with anorexia nervosa, the low testosterone levels affect
potency,
libido and muscle strength.
Cortisol levels have been noted to be elevated due to both increased adrenal

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production and decreased renal clearance.88 Growth hormone levels are also noted to
be elevated, but insulin growth factor-1 (IGF-1) levels are low, indicating a state
of

growth hormone resistance.89 Most patients have thyroid function abnormalities

which

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closely mimic sick euthyroid syndrome. These resolve with weight gain.90

Hypoglycemia occurs as anorexia nervosa becomes more severe, as a result of

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depleted hepatic glycogen stores. It is a poor prognostic sign which requires close
monitoring.91 There is also evidence that Type 1 diabetes may be related to the
development of anorexia nervosa, although the specifics are inconclusive.92
However,
what is very clear is that some of these insulin-dependent diabetic patients
realize that

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they can induce weight loss via reducing their use of insulin, thereby causing
hyperglycemia and a resultant osmotic diuresis. This accelerates microvascular

NEUROLOGIC

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complications.93

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Brain atrophy changes occur as a result of the malnutrition of anorexia nervosa.

Neurocognitive functioning may be permanently impaired even though brain atrophy

improves with weight restoration.94 Both gray and white matter are affected.

DERMATOLOGIC
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There are multiple skin changes that occur in anorexia nervosa. These include
xerosis, lanugo hair growth on the spine and sides of the face, thinning of the
hair,
acrocyanosis and perinosis. Increased acne and carotenoderma have also been

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described.95 None of these are signs of virilization, but rather are either related
to

prevent heat loss. They all resolve with weight gain.

MEDICAL COMPLICATIONS OF BULIMIA

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Self-Induced Vomiting

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reduced subcutaneous tissue or to the body’s attempt to maintain core temperature

and

While the mortality rate associated with bulimia is much less than in anorexia
nervosa, it is also elevated due to the severe electrolyte and acid base
alterations which
can be associated with purging behaviors. Ninety percent of the purging behaviors

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found in bulimia are either self-induced vomiting or the abuse of stimulant

laxatives.
With self-induced vomiting, the complications can be divided into the local adverse
effects of vomiting and the electrolyte-acid base abnormalities which can ensue as
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behavior becomes more extreme. Excessive vomiting can lead to persistent gastric
acid reflux leading to dysphagia and dyspepsia. Treatment is cessation of this
behavior

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and the administration of proton pump inhibitors. Whether patients with bulimia
should
be screened for Barrett’s esophagus is not clear.96 There have been reports of
esophageal malignancy in bulimia.97 But, even screening for Barrett’s esophagus is
the
general population with reflux has recently been questioned due to lack of proof of
efficicacy.98 Hematemesis is usually due to the limited Mallory-Weiss tears.
Epistaxis
and subconjunctival hemorrhages are self-limited, but recurrent epistaxis in a
young
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female should raise the question of covert bulimia. Perimolysis refers to erosion
of the
dentin and enamel on the lingual service of the teeth due to repeated exposure to
stomach acid.99 Similarly, oral mucositis and cheilitis are found in these patients
from

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the recurrent vomiting. Recommended therapies include oral hygiene such as gentle
brushing and use of a fluoride mouthwash.100 Acid exposure also causes damage to
the larynx with inflammatory changes to the vocal cords and a hoarse voice.101

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Parotid gland enlargement, or sialadenosis, is a common feature of self-induced

vomiting, although the precise mechanism remains elusive.102 Tissue examination of

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these parotid glands reveals large acini with prominent zymogen granules without
other
pathology. Of note, sialadenosis develops 3-4 days after the cessation of chronic
excessive self-induced vomiting and can be very distressing to a patient with
bulimia
whose focus on body image is exaggerated. The swelling is bilateral, with minimal

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tenderness. There may be elevation of the salivary isonmylase enzyme serum

level.103
Treatment should ideally be preemptive and comprised of use of sialagogues such as
tart candies, along with an anti-inflammatory medication and the frequent
application of

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hot packs. Usually this will help prevent, or if started late, said treatment
usually
resolves the issue within 1-2 weeks. Rarely, oral pilocarpine may be judiciously
used to

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help resolve the sialadenosis.104

The most dangerous medical complications of self-induced vomiting relate to the

acid-base and electrolyte changes which ensue as a result thereof. These

aberrations
are the same which occur with abuse of diuretics as the preferred mode of purging,
but
in general those encountered with self-induced vomiting are more profoundly
abnormal.
The most common electrolyte abnormalities are a metabolic alkalosis and
hypokalemia.
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With vomiting this is due both to loss of acid and potassium in the vomitus, as
well as
from the volume depleted state causing increased aldosterone secretion to sustain
their
blood pressure. This course of compensatory events is referred to as pseudo-
Bartter’s

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syndrome.105 It predisposes these patients to a distressing propensity towards

edema
formation with the cessation of purging behaviors as well as if intravenous saline
repletion is required and infused too quickly.106 These patients must be treated

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differently than, for example, a patient with acute gastroenteritis in need of

intravenous
saline, in whom it can be safely infused rather quickly.107 While the protective
elevated

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aldosterone levels will self-normalize after a few weeks of no ongoing purging

behaviors, it is often purposeful to initiate spironolactone in a starting dose of
25-50 mg
daily, to both prevent and treat edema formation. The finding of hypokalemia, in an
otherwise healthy young adult, is highly specific for the diagnosis of covert
bulimia.108

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The potentially severe degrees of hypokalemia and metabolic-alkalosis and resulting

cardiac arrhythmias which can develop in those who excessively purge, is the likely
reason for the elevated mortality rate associated with bulimia nervosa.109
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hypokalemia was reported to be especially dangerous in females, which is the gender

mostly identified to have bulimia.110

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Most patients with bulimia nervosa use their fingers to provoke vomiting.

However, some abuse syrup of ipecac to accomplish this. This is even more dangerous
because, emetine, the alkaloid in ipecac which induces vomiting, is a direct
cardiac
toxin.111 This toxicity is cumulative. Each bottle of ipecac contains 30 mg of
ementine
and with a dose of just 1,250 mg, there can be the development of an irreversible
cardiomyopathy and severe congestive health failure.112
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Laxative Abuse
Excessive laxative abuse is the other main mode of purging.113 Hypokalemia is

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again a potential risk of this behavior. However in contrast to diuretics and self-
induced
vomiting, laxative abuse is initially associated with a hyperchloremic metabolic
acidosis
which eventually reverts to a state of metabolic alkalosis after a chronic volume

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depleted state evolves. In addition to the electrolyte abnormalities, laxative

abuse
causes expected local gastrointestinal adverse effects including rectal prolapse,

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diarrhea, hemorrhoids and hematochezia.114,115 There has long been a debate whether
stimulant initiative cause colorectal cancer.116

One final and major complication of laxative abuse is the cathartic colon
syndrome.117 For many years it has been known that stimulant laxatives, whose

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mechanism of action is based on stimulation of peristalsis via a direct effect on

Auerbach’s plexus in the colon, can cause permanent harm to these nerve plexi.118
As a
result of chronic usage, the colon is converted into an inert tube incapable of the

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propagation of fecal material and severe constipation ensues,119 which may

necessitate
a colectomy. The exact amount of time or quantity of abuse needed to cause the

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cathartic colon syndrome is unknown. Therefore it is important to exhort these

patient
to cease abuse of laxatives which either contain senna, cascara, phenothalcin or
bisocodyl. The aforementioned edema formation which can develop can also be
treated with spironolactone and patient concerns about resultant constipation can
be
allayed with substitution of a judicious amount of an osmotic laxative.120,121 Much
less
commonly patients with bulimia purge via the usage of enema type products.122 The
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main dangers from them are attributable to the electrolyte abnormalities previously
mentioned, but also from the potential for fatal hyperphosphatemia from the sodium-

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phosphate active ingredients.123

CONCLUSION

In summary, both anorexia nervosa and bulimia nervosa inherently have a litany

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of medical complications associated with them. While most of them are treatable
after
effective medical interventions and psychotherapy. To halt the disease process,
these

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are a notable few which are associated with permanent harm. Therefore, given the
relatively young age of onset of these illnesses, there is an impelling need for
informed

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medical treatment to help achieve a successful treatment outcome.

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REFERENCES
1. Sullivan PF. Mortality in anorexia nervosa. Am J Psychiatry. 1995;152:1073-1074.

1999;173:11-53.

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Clinical Significance

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•
•

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Anorexia nervosa and bulimia have many medical complications associated with
them
In anorexia nervosa the medical complications are due to weight loss and
malnutrition
In bulimia the medical complications are due to the mode and frequency of purging
Most complications are reversible with early effective treatment

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