eating disorders, bulimia, anorexia.doc

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Eating disorders: Epidemiology, pathogenesis, clinical features, and course of illness Author Sara F Forman, MDSection Editor Joel Yager, MDDeputy Editor David Solomon, MDDisclosures

All topics are updated as new evidence becomes available and our peer review process iscomplete.Literature review current through: Dec !" . # This topic last updated: Sep $, !" .INTROD !TION % Many aspects o& the 'nited States culture display an obsession with weight

loss. (omen)s maga*ines typically have a cover highlighting a story about weight management,

dieting hints, or how to tighten speci&ic muscle groups. Models and actors display an unattainable

level o& thinness. Some athletes relentlessly pursue a leaner body &or per&ormance enhancement.

+ur culture)s obsession to achieve lower weight conveys an unavoidable message to maturing

adolescents. According to the !! Youth -is /ehavior Survey, 0$ percent o& adolescent girls

believed that they were overweight and 1! percent were attempting to lose weight. 2n the 0! days

be&ore 3uestioning, 4 percent o& adolescent girls reported that they had tried vomiting or had

ta en la5atives to help control their weight.

6he epidemiology, pathogenesis, and clinical &eatures o& eating disorders are reviewed here.

6reatment and outcomes o& eating disorders7 medical complications o& eating disorders and their

management7 evaluation &or medical complications and criteria &or hospitali*ation7 and the

re&eeding syndrome in anore5ia nervosa are discussed separately.

8See 9Eating disorders: 6reatment and outcome9 .;

8See 9Anore5ia nervosa in adults and adolescents: Medical complications and theirmanagement9 .;

8See 9/ulimia nervosa and binge eating disorder in adults: Medical complications and

their management9 .;

8See 9Anore5ia nervosa in adults: Evaluation &or medical complications and criteria &or

hospitali*ation to manage these complications9 .;

8See 9Anore5ia nervosa in adults and adolescents: 6he re&eeding syndrome9 .;

DE"INITION# % According to the American =6-;, eating disorders include ? " @:

Anore5ia nervosa

/ulimia nervosa

Eating disorders not otherwise speci&ied

$nore%ia nervosa % 6he DSM=2>=6- criteria &or anore5ia nervosa include re&usal to maintain

body weight at or above a minimally normal weight &or age and height, intense &ear o& gaining
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weight or becoming &at despite being underweight, distorted perception o& body weight and

shape, and amenorrhea 8 table " ; ?" @. 6he diagnosis is discussed separately. 8See 9Anore5ia

nervosa in adults: Diagnosis, associated clinical &eatures, and assessment9, section on

)Diagnostic criteria) and 9Anore5ia nervosa in adults: Diagnosis, associated clinical &eatures, and

assessment9, section on )Di&&erential diagnosis) .;

&ulimia nervosa % 6he DSM=2>=6- criteria &or bulimia nervosa include recurrent episodes o&

binge eating and inappropriate compensatory behavior to prevent weight gain, occurring on

average at least two times per wee &or three months 8 table ; ?" @. 6he diagnosis is discussed

separately. 8See 9/ulimia nervosa in adults: linical &eatures, diagnosis, and assessment9,

section on )Diagnosis) and 9/ulimia nervosa in adults: linical &eatures, diagnosis, and

assessment9, section on )Di&&erential diagnosis) .;

Eating disorder not otherwise specified % DSM=2>=6- also includes a de&inition &or Eating

Disorder Bot +therwise Speci&ied 8ED=B+S; ? " @. 6his category includes patients with clearly

aberrant eating patterns and weight management habits who do not meet the criteria &or anore5ianervosa or bulimia nervosa. 6he most notable prototypes are binge eating disorder, night eating

syndrome, sleep related eating disorder, and purging disorder.

&inge'eating disorder % According to research criteria, binge=eating disorder is de&ined as

eating an amount o& &ood in a discrete period o& time that is de&initely larger than most people

would eat in a similar period o& time under similar circumstances ? " @. 6hese episodes occur at

least twice a wee &or at least si5 months. Episodes o& binge eating are associated with a lac o&

control and with distress over the eating. Additional in&ormation about the de&inition o& binge=

eating disorder, as well as the epidemiology, treatment planning, and use o& cognitive=behavior

therapy are discussed separately. 8See 9/inge=eating disorder: +verview o& treatment inadults9 and 9/inge=eating disorder: ognitive=behavioral therapy 8 /6;9 .;

E(IDE)IOLO*+ % 6rends in the epidemiology o& eating disorders are di&&icult to assess

because o& changes in the diagnostic criteria over time, and because detection by sel&=report may

not be reliable in an illness characteri*ed by secrecy and denial ? @. Most studies report increased

prevalence over the past $! years ? 0@, although trends over the past "! years are debated. +ne

study among college students in ali&ornia noted a decrease in bingeCpurge behaviors &rom the

" 4!s to the " !s ? @. owever, most clinicians believe that increased numbers o& eating

disordered patients are presenting to their practices.

6he li&etime prevalence o& anore5ia nervosa in women is estimated to be !.0 to " percent ? $@.

-ates &or men are signi&icantly lower. Data &rom the Bational omorbidity -eplication survey

indicate a li&etime prevalence o& !. and !.0 percent &or women and men respectively ? 1@. Data

&rom a Finnish birth cohort study suggest a higher li&etime prevalence 8 . percent;, with inclusion

o& untreated cases identi&ied by screening ? @.
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/ulimia nervosa is now diagnosed using more stringent criteria in the DSM=2> than in earlier

editions o& the DSM. 6his, combined with the shorter length o& time that this illness has been

recogni*ed, clouds interpretation o& epidemiologic data.


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signi&icantly increased compared with controls a&ter weight recovery ? 0 @. 2n comparison, white

matter did not signi&icantly di&&er &rom controls a&ter weight recovery. 6he signi&icance o& these

&indings is unclear.

(RE#ENT$TION $ND #!REENIN*

$nore%ia nervosa % 6he core &eatures o& anore5ia nervosa are an abnormally low body weight,

intense &ear o& gaining weight, distorted perception o& body weight and shape, and amenorrhea

?" @. 6he clinical &eatures o& anore5ia nervosa are discussed separately. 8See 9Anore5ia nervosa in

adults: Diagnosis, associated clinical &eatures, and assessment9, section on )Associated clinical

&eatures) and 9Anore5ia nervosa in adults: Diagnosis, associated clinical &eatures, and

assessment9, section on )Diagnostic criteria) .;

&ulimia nervosa % 6he core &eatures o& bulimia nervosa are binge eating 8ie, eating an amount

o& &ood that is de&initely larger than most people would eat under similar circumstances; and

inappropriate compensatory behavior to prevent weight gain ? " @. 6he prototypic se3uence o&

behavior in bulimia nervosa consists o& caloric restriction, binge eating, and sel&=induced vomiting

?0$ @. 6he clinical &eatures o& bulimia nervosa are discussed separately. 8See 9/ulimia nervosa in

adults: linical &eatures, diagnosis, and assessment9, section on ) linical &eatures) and 9/ulimia

nervosa in adults: linical &eatures, diagnosis, and assessment9, section on ) omorbid

psychopathology) .;

#creening tools % A number o& other instruments have been developed to identi&y patients with

eating disorders. Some are long and not ideally suited &or screening in a primary care setting. At

least two shorter instruments have been developed and, although neither has been e5tensively

validated, may help identi&y patients who need &urther evaluation ? 01,0 @.

(e suggest the S +FF 3uestionnaire, which consists o& &ive 3uestions ? 01,04 @:

Do you ma e yoursel& # ic because you &eel uncom&ortably &ullK

Do you worry you have lost ! ontrol over how much you eatK

ave you recently lost more than One stone 8" pounds or 1.0$ g; in a three month

periodK

Do you believe yoursel& to be " at when others say you are too thinK

(ould you say that " ood dominates your li&eK

A second short tool, the Eating disorder Screen &or


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Do you currently su&&er with or have you ever su&&ered in the past with an eating disorderK

8Yes is abnormal;

6he original study describing the S +FF reported that a 9yes9 to two or more 3uestions was

associated with a sensitivity and speci&icity o& "!! and 4 .$ percent &or the diagnosis o& an eating

disorder ? 01 @. A subse3uent report that proposed and evaluated the ES< &ound that two abnormal

responses to the ES< had a sensitivity and speci&icity o& "!! and " percent, and that the

sensitivity and speci&icity o& S +FF was lower 8 4 and 44 percent, respectively; ? 0 @. Further

validation o& both o& these instruments is needed in broader populations.

6he Eating Attitudes 6est 8EA6; is one o& the most widely used sel&=report eating disorder

instruments. 6he 1=item version has an accuracy rate o& at least ! percent when screening

patients &or the presence o& a DSM=2> eating disorder, using a cuto&& score o& ! 8 table 0 ; ?0 @.

6he


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)EDI!$L !O)(LI!$TION# % Many medical complications can occur during starvation or

persistent purging ? "!, "= 0 @.

$nore%ia nervosa % omplications o& anore5ia nervosa include myocardial atrophy, mitral valve

prolapse, pericardial e&&usion, bradycardia, &unctional hypothalamic amenorrhea, antenatal and

postpartum problems, osteoporosis, gastroparesis, and constipation 8 table $ ;. 2n addition, growthdisturbance can occur in adolescents. Medical complications o& anore5ia nervosa and their

management are discussed separately. 8See 9Anore5ia nervosa in adults and adolescents:

Medical complications and their management9 .;

&ulimia nervosa and .inge eating disorder % omplications o& bulimia nervosa include

dehydration, hypo alemia, menstrual irregularities, Mallory=(eiss syndrome, ipecac=induced

myopathy, and erosion o& dental enamel. Electrocardiogram changes can occur in both disorders.

Medical complications o& bulimia nervosa and binge eating disorder, and their management are

discussed separately. 8See 9/ulimia nervosa and binge eating disorder in adults: Medical

complications and their management9 .;

!O R#E O" ILLNE##

$nore%ia nervosa % +utcome studies have &ocused upon anore5ia nervosa ? , $@. +ne review

&ound that appro5imately $! percent o& patients have good outcomes 8de&ined by return o&

menses and weight gain;, $ percent have intermediate outcomes, and $ percent have a poor

outcome ? $@.

A number o& patients with anore5ia nervosa have a bulimic phase during their recoveries.


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&ulimia nervosa % +ne study that &ollowed " 0 women with bulimia nervosa &ound that the

number o& patients who continued to meet the &ull criteria &or bulimia nervosa declined as the

duration o& &ollow=up increased ? $ @. owever, recurrent binging and purging behaviors persisted

over appro5imately "! years o& &ollow=up in 0! percent. Substance abuse and long duration o& the

disorder were associated with poor outcome.

)ORT$LIT+ % Several studies suggest that all cause mortality is elevated in patients with eating

disorders ? $0 @.

$nore%ia nervosa % Anore5ia nervosa appears to be associated with increased mortality:

A meta=analysis o& studies conducted between " ! and " 4! 80,!!1 patients

&ollowed &or a median o& 4 years; &ound that all cause mortality was !.$1 percent per year

?$ @. Medical complications o& anore5ia nervosa accounted &or appro5imately $! percent

o& the deaths and suicide accounted &or $ percent. eterogeneity was not reported.

A review o& &our studies 811! patients; &ound that all cause mortality was $ times the

e5pected value 8based upon general population mortality statistics;, and suicide deaths

were 0 times greater ? $0 @.

A subse3uent prospective study o& "01 patients &ollowed &or a median o& nine years &ound

that all cause mortality was " times greater compared with the general population

8standardi*ed mortality ratio "".1, $ 2 $.$= ".0;, and that completed suicide was $

times greater in patients with anore5ia nervosa 8standardi*ed mortality ratio $1. , $ 2

"$.0=" $. ; ? $$ @. Duration o& anore5ia nervosa and severity o& alcohol use disorder were

associated with an increased ris o& all cause mortality.

owever, most mortality studies &or anore5ia nervosa were per&ormed at re&erral centers thatspeciali*ed in treatment resistant patients who were o&ten hospitali*ed, and mortality rates may

be lower outside o& these centers. A retrospective community study e5amined mortality in !4

patients with relatively mild anore5ia nervosa 8most had never seen a psychiatrist and &ew had

been hospitali*ed &or the disorder; over a median &ollow=up o& years7 all cause mortality &or

patients and &or the general population were comparable 8standardi*ed mortality ratio !. , $ 2

!. ="."; ? $1 @.

&ulimia nervosa % /ulimia nervosa may possibly be associated with increased mortality:

A retrospective study o& !1 patients who were &ollowed &or a mean o& " years through

the 'nited States Bational Death 2nde5 &ound that all cause mortality was appro5imately

twice as high, compared with the general population 8standardi*ed mortality ratio ".1,

$ 2 "."= . ;, and that the rate o& suicide was appro5imately seven times greater

8standardi*ed mortality ratio 1.$, $ 2 .4=" .4; ? $ @

A retrospective study o& 1 patients &ollowed &or to "$ years &ound that all cause

mortality was nine times the e5pected value ? $0,$4 @
http://www.uptodate.com/contents/eating-disorders-epidemiology-pathogenesis-clinical-features-and-course-of-illness/abstract/52http://www.uptodate.com/contents/eating-disorders-epidemiology-pathogenesis-clinical-features-and-course-of-illness/abstract/53http://www.uptodate.com/contents/eating-disorders-epidemiology-pathogenesis-clinical-features-and-course-of-illness/abstract/54http://www.uptodate.com/contents/eating-disorders-epidemiology-pathogenesis-clinical-features-and-course-of-illness/abstract/53http://www.uptodate.com/contents/eating-disorders-epidemiology-pathogenesis-clinical-features-and-course-of-illness/abstract/53http://www.uptodate.com/contents/eating-disorders-epidemiology-pathogenesis-clinical-features-and-course-of-illness/abstract/55http://www.uptodate.com/contents/eating-disorders-epidemiology-pathogenesis-clinical-features-and-course-of-illness/abstract/56http://www.uptodate.com/contents/eating-disorders-epidemiology-pathogenesis-clinical-features-and-course-of-illness/abstract/57http://www.uptodate.com/contents/eating-disorders-epidemiology-pathogenesis-clinical-features-and-course-of-illness/abstract/53,58http://www.uptodate.com/contents/eating-disorders-epidemiology-pathogenesis-clinical-features-and-course-of-illness/abstract/52http://www.uptodate.com/contents/eating-disorders-epidemiology-pathogenesis-clinical-features-and-course-of-illness/abstract/53http://www.uptodate.com/contents/eating-disorders-epidemiology-pathogenesis-clinical-features-and-course-of-illness/abstract/54http://www.uptodate.com/contents/eating-disorders-epidemiology-pathogenesis-clinical-features-and-course-of-illness/abstract/53http://www.uptodate.com/contents/eating-disorders-epidemiology-pathogenesis-clinical-features-and-course-of-illness/abstract/55http://www.uptodate.com/contents/eating-disorders-epidemiology-pathogenesis-clinical-features-and-course-of-illness/abstract/56http://www.uptodate.com/contents/eating-disorders-epidemiology-pathogenesis-clinical-features-and-course-of-illness/abstract/57http://www.uptodate.com/contents/eating-disorders-epidemiology-pathogenesis-clinical-features-and-course-of-illness/abstract/53,58


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owever, in a prospective study o& ""! patients with bulimia nervosa, mortality &or patients and

mortality &or the general population were comparable 8standardi*ed mortality ratio ".0, $ 2

!.!= . ; ? $$ @.

Eating disorder not otherwise specified % Eating disorders not otherwise speci&ied may be

associated with increased mortality. A retrospective study o& 4! patients with an eating disordernot otherwise speci&ied, who were &ollowed &or a mean o& " years through the 'nited States

Bational Death 2nde5, &ound that all cause mortality was nearly twice as high compared with the

general population 8standardi*ed mortality ratio ".4, $ 2 ".0= .$;, and that the rate o& suicide

was nearly &our times greater 8standardi*ed mortality ratio 0. , $ 2 "."="!.!; ? $ @

IN"OR)$TION "OR ($TIENT# % 'p6oDate o&&ers two types o& patient education materials,

I6he /asics and I/eyond the /asics. 6he /asics patient education pieces are written in plain

language, at the $ th to 1 th grade reading level, and they answer the &our or &ive ey 3uestions a

patient might have about a given condition. 6hese articles are best &or patients who want a

general overview and who pre&er short, easy=to=read materials. /eyond the /asics patienteducation pieces are longer, more sophisticated, and more detailed. 6hese articles are written at

the "! th to " th grade reading level and are best &or patients who want in=depth in&ormation and

are com&ortable with some medical Gargon.

ere are the patient education articles that are relevant to this topic. (e encourage you to print or

e=mail these topics to your patients. 8You can also locate patient education articles on a variety o&

subGects by searching on Ipatient in&o and the eyword8s; o& interest.;

/asics topics 8see 9


10/49

control and with distress over the eating. 8See )/inge=eating disorder) above and 9/inge=

eating disorder: +verview o& treatment in adults9 .;

6he estimated li&etime prevalence o& anore5ia nervosa in women is !. and in men !.0

percent. 6he estimated li&etime prevalence o& bulimia nervosa in women is " to ".$

percent. 6he estimated li&etime prevalence o& binge=eating disorder in women is 0.$ and

men .! percent. 8See )Epidemiology) above and 9/inge=eating disorder: +verview o&

treatment in adults9, section on )Epidemiology) .;

6here is no consensus regarding the causes o& eating disorders. A combination o&

genetic, biological, psychological, &amily, environmental, and social &actors probably

contribute to developing an eating disorder. 8See )


11/49

. (a eling A. Epidemiology o& anore5ia nervosa.


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.


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$ . Neel


14/49

About 's # Bews &rom 'p6oDate # ontact 's # elp Log in

Bew Search


15/49

8See 9Eating disorders: Epidemiology, pathogenesis, clinical &eatures, and course o&

illness9 .;

8See 9Eating disorders: 6reatment and outcome9 .;

8See 9/inge=eating disorder: +verview o& treatment in adults9 .;

8See 9Anore5ia nervosa in adults and adolescents: Medical complications and their

management9 .;

DE"INITION#

&ulimia nervosa % /B is mar ed by episodes o& binge eating. 2n addition, there are

inappropriate compensatory behaviors to prevent weight gain, including sel&=induced vomiting7

misuse o& la5atives, diuretics, or enemas7 e5cessive e5ercise7 &asting7 or strict diets 8 table " ; ?0@.

6he de&inition o& /B is discussed separately. 8See 9Eating disorders: Epidemiology,

pathogenesis, clinical &eatures, and course o& illness9, section on )/ulimia nervosa) .;

&inge eating disorder % /ED is characteri*ed by episodes o& binge eating, without theinappropriate compensatory behaviors that are seen in bulimia nervosa. 6he de&inition o& /ED is

discussed separately. 8See 9/inge=eating disorder: +verview o& treatment in adults9, section on

)De&inition o& binge=eating disorder 8/ED;) .;

)EDI!$L E-$L $TION % 6he medical evaluation should pursue symptoms and signs o& the

medical complications described below. 2n addition, all patients with /B should receive a basic

panel o& laboratory tests, and additional tests as indicated by &indings &rom the history and

physical e5amination.


16/49

+ther signs that are o&ten present include hair loss, edema, and scarring or calluses on the

dorsum o& the hand.

La.oratory assessment % 6ests should be guided by the symptoms and physical &indings.

Haboratory tests indicated &or all patients with /B include ? @:

Serum electrolytes

/lood urea nitrogen

Serum creatinine

omplete blood count including di&&erential

Hiver &unction tests

'rinalysis

Severely ill patients with /B warrant additional tests ? @:

Serum calcium, magnesium, and phosphorous

Electrocardiogram 8E O;

For patients with suspected pancreatitis, clinicians should chec serum amylase, &ractionated &or

salivary gland isoen*yme ? @.


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Diarrhea and malabsorption

Steatorrhea


18/49

Acute pancreatitis may develop in patients who abuse alcohol ? @. A review o& $ studies &ound

that among patients with /B, 0 percent met criteria &or alcohol abuse andCor dependence ? "" @. 2n

addition, pancreatitis can occur in patients with /B who do not abuse alcohol or who have been

abstinent &rom alcohol &or many years7 the etiology is unclear and not necessarily related to

vomiting ? " @. 6reatment o& pancreatitis is discussed separately. 8See 96reatment o& acute

pancreatitis9 .;

)allory'/eiss syndrome % Force&ul vomiting may cause longitudinal mucosal lacerations in

the distal esophagus and pro5imal stomach.


19/49

venous Gugular pressure, and eliminate postural changes in pulse and blood pressure. Additional

in&ormation about rehydration is discussed separately. 8See 9Maintenance and replacement &luid

therapy in adults9, section on )-eplacement &luid therapy) .;

!ardiac % ardiac complications are rare in patients with /B ? @. omplications include ? @:

ypotension and orthostasis

Sinus tachycardia


20/49

Small, chronic doses have caused cumulative, &atal to5icity in a &ew patients. 6he lethal chronic

dose is not nown. Absorption o& emetine is enhanced in patients who become re&ractory to the

emetic e&&ects o& the drug during chronic misuse.


21/49

6hyroid &unction is usually normal in /B ? @. A study compared $ bulimic women with 1 healthy

control women and &ound similar values &or &ree 6 and &ree 60 ? " @.

Dental % Oastric acid in vomitus so&tens and erodes dental enamel, which may cause sensitivity

to hot and cold temperatures in &ood and drin s ? @. Some patients e5hibit decalci&ication o& the

teeth 8perimylolysis;, particularly on the lingual, palatal, and posterior occlusal sur&aces ? @. 6eethmay also become discolored, and caries and gum disease may occur.

Enamel loss can be reduced by instructing patients to wash out their mouth a&ter vomiting, gargle

with ba ing soda in water to al alini*e their mouth, wait at least 0! minutes be&ore brushing their

teeth, and use al aline toothpaste ? @. ot and cold &oods and li3uids should be limited as needed

to avoid pain. Acidic &oods 8eg, &ruit and yogurt; should also be limited ? $@. hewing sugarless

gum is recommended to increase salivary &low. 2n addition, a dentist should be consulted &or

restorative procedures a&ter purging is controlled.

#0in % A nearly pathognomonic dermatologic complication is scarring or calluses on the dorsum

o& the hand 8-ussellTs sign7 due to pressure o& the teeth against the s in while stimulating the gag

re&le5 to induce vomiting; 8 picture " ; ? , @. A study o& " patients with /B detected this sign in 0!

percent ? ! @. erosis, poor s in turgor, petechia, telogen e&&luvium, and acne may also be seen

? " @.

Sel&=inGurious behavior is common in /B, and patients may show acute or chronic signs o& trauma

&rom cuts or burns ? $@.

Other % +ther medical complications include &luctuation o& body weight, vitamin de&iciencies,

aspiration pneumonitis, and conGunctival hemorrhage ? , , @.

)EDI!$L !O)(LI!$TION# O" &IN*E E$TIN* DI#ORDER %


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&ree o& psychiatric disorders 8 versus " percent;, but the association o& /ED with poor health was

not signi&icant when the analyses controlled &or comorbid mood disorders.

O.esity % Many patients with /ED are obese and su&&er the medical complications associated

with obesity ? ,4@. 6he complications o& obesity are discussed separately. 8See 9 ealth ha*ards

associated with obesity in adults9 .;

2t is not clear i& /ED is associated with medical complications beyond those observed in obese

patients ? , , 0 @. Several studies show higher rates o& gastrointestinal, cardiovascular,

pulmonary, and rheumatologic disorders or symptoms in obese patients with /ED compared to

obese patients without /ED, but the di&&erences are generally not statistically signi&icant.

Dia.etes % /ED does not appear to be associated with diabetes. 2n an observational study, "0

patients with /ED were matched &or age, se5, and body mass inde5 with "0 individuals with no

history o& an eating disorder. +ver &ive years o& &ollow=up, the incidence o& new=onset type

diabetes was similar &or subGects with and without /ED 8"! versus 4 percent; ? @. Although an

epidemiologic study o& patients treated in primary care and obstetric gynecology settings &ound

that diabetes was present in signi&icantly more patients with /ED compared with patients who

had no eating disorder 81 versus 0 percent;, the comparison did not control &or body mass inde5

?" @.

Most studies indicate that /ED or binge eating do not signi&icantly a&&ect glycemic control in type

diabetes ? @.

Diagnosis and treatment o& diabetes are discussed separately. 8See 9+verview o& medical care in

adults with diabetes mellitus9 .;

ypercholesterolemia % An observational study o& patients with /ED matched &or body massinde5 with individuals with no eating disorder &ound that hypercholesterolemia occurred in

signi&icantly more patients with /ED 80! versus " percent; ? @.

O#(IT$LI1$TION % ertain medical complications re3uire inpatient treatment on an internal

medicine, psychiatric, or combined ward. 6he choice depends upon the patientTs medical and

psychiatric status, and available resources. riteria &or inpatient treatment and principles o&

management in this setting are discussed separately. 8See 9Eating disorders: 6reatment and

outcome9, section on ) ospitali*ation) .;

IN"OR)$TION "OR ($TIENT# % 'p6oDate o&&ers two types o& patient education materials,

I6he /asics and I/eyond the /asics. 6he /asics patient education pieces are written in plain

language, at the $ th to 1 th grade reading level, and they answer the &our or &ive ey 3uestions a

patient might have about a given condition. 6hese articles are best &or patients who want a

general overview and who pre&er short, easy=to=read materials. /eyond the /asics patient

education pieces are longer, more sophisticated, and more detailed. 6hese articles are written at
http://www.uptodate.com/contents/bulimia-nervosa-and-binge-eating-disorder-in-adults-medical-complications-and-their-management/abstract/4,8http://www.uptodate.com/contents/health-hazards-associated-with-obesity-in-adults?source=see_linkhttp://www.uptodate.com/contents/health-hazards-associated-with-obesity-in-adults?source=see_linkhttp://www.uptodate.com/contents/health-hazards-associated-with-obesity-in-adults?source=see_linkhttp://www.uptodate.com/contents/bulimia-nervosa-and-binge-eating-disorder-in-adults-medical-complications-and-their-management/abstract/2,4,23http://www.uptodate.com/contents/bulimia-nervosa-and-binge-eating-disorder-in-adults-medical-complications-and-their-management/abstract/2,4,23http://www.uptodate.com/contents/bulimia-nervosa-and-binge-eating-disorder-in-adults-medical-complications-and-their-management/abstract/2,4,23http://www.uptodate.com/contents/bulimia-nervosa-and-binge-eating-disorder-in-adults-medical-complications-and-their-management/abstract/22http://www.uptodate.com/contents/bulimia-nervosa-and-binge-eating-disorder-in-adults-medical-complications-and-their-management/abstract/17http://www.uptodate.com/contents/bulimia-nervosa-and-binge-eating-disorder-in-adults-medical-complications-and-their-management/abstract/2http://www.uptodate.com/contents/bulimia-nervosa-and-binge-eating-disorder-in-adults-medical-complications-and-their-management/abstract/2http://www.uptodate.com/contents/overview-of-medical-care-in-adults-with-diabetes-mellitus?source=see_linkhttp://www.uptodate.com/contents/overview-of-medical-care-in-adults-with-diabetes-mellitus?source=see_linkhttp://www.uptodate.com/contents/bulimia-nervosa-and-binge-eating-disorder-in-adults-medical-complications-and-their-management/abstract/22http://www.uptodate.com/contents/bulimia-nervosa-and-binge-eating-disorder-in-adults-medical-complications-and-their-management/abstract/22http://www.uptodate.com/contents/eating-disorders-treatment-and-outcome?source=see_link&anchor=H17#H17http://www.uptodate.com/contents/eating-disorders-treatment-and-outcome?source=see_link&anchor=H17#H17http://www.uptodate.com/contents/bulimia-nervosa-and-binge-eating-disorder-in-adults-medical-complications-and-their-management/abstract/4,8http://www.uptodate.com/contents/health-hazards-associated-with-obesity-in-adults?source=see_linkhttp://www.uptodate.com/contents/health-hazards-associated-with-obesity-in-adults?source=see_linkhttp://www.uptodate.com/contents/bulimia-nervosa-and-binge-eating-disorder-in-adults-medical-complications-and-their-management/abstract/2,4,23http://www.uptodate.com/contents/bulimia-nervosa-and-binge-eating-disorder-in-adults-medical-complications-and-their-management/abstract/22http://www.uptodate.com/contents/bulimia-nervosa-and-binge-eating-disorder-in-adults-medical-complications-and-their-management/abstract/17http://www.uptodate.com/contents/bulimia-nervosa-and-binge-eating-disorder-in-adults-medical-complications-and-their-management/abstract/2http://www.uptodate.com/contents/overview-of-medical-care-in-adults-with-diabetes-mellitus?source=see_linkhttp://www.uptodate.com/contents/overview-of-medical-care-in-adults-with-diabetes-mellitus?source=see_linkhttp://www.uptodate.com/contents/bulimia-nervosa-and-binge-eating-disorder-in-adults-medical-complications-and-their-management/abstract/22http://www.uptodate.com/contents/eating-disorders-treatment-and-outcome?source=see_link&anchor=H17#H17http://www.uptodate.com/contents/eating-disorders-treatment-and-outcome?source=see_link&anchor=H17#H17


23/49

the "! th to " th grade reading level and are best &or patients who want in=depth in&ormation and

are com&ortable with some medical Gargon.

ere are the patient education articles that are relevant to this topic. (e encourage you to print or

e=mail these topics to your patients. 8You can also locate patient education articles on a variety o&

subGects by searching on Ipatient in&o and the eyword8s; o& interest.;

/asics topic 8see 9


24/49

Dental complications o& /B include erosion o& dental enamel, decalci&ication and

discoloration o& the teeth, caries, and gum disease. 8See )Dental) above.;

Dermatologic complications include scarring or calluses on the dorsum o& the hand

8-ussellTs sign; 8 picture " ;, 5erosis, poor s in turgor, petechia, telogen e&&luvium, and

acne. 2n addition, patients with sel&=inGurious behavior will show acute or chronic signs o&

trauma &rom cuts or burns. 8See )S in) above.;


25/49

"4. Mannucci E, -otella F, -icca >, et al. Eating disorders in patients with type " diabetes: ameta=analysis. J Endocrinol 2nvest !!$7 4: " .

" . Monteleone


26/49

complications and their managementFind


27/49

/inge eating and purging V mar ed by episodes o& binge eating and inappropriate

compensatory behaviors to prevent weight gain, including sel&=induced vomiting and

misuse o& la5atives, diuretics, or enemas

6he clinical &eatures and diagnosis o& AB are discussed separately. 8See 9Eating disorders:

Epidemiology, pathogenesis, clinical &eatures, and course o& illness9, section on )Anore5ia

nervosa) .;

6his topic reviews the medical complications o& the restricting type o& AB. omplications due to

the binging and purging behaviors are discussed separately within the conte5t o& the medical

complications that occur in patients with bulimia nervosa and binge eating disorder. 8See 9/ulimia

nervosa and binge eating disorder in adults: Medical complications and their management9 .;

)EDI!$L E-$L $TION %


28/49

Substantial weight loss in AB is accompanied by atrophy o& cardiac muscle, decreased cardiac

mass, and reduced cardiac chamber volumes 8 picture " ; ?"$ @. 6his leads to decreased cardiac

output, reduced e5ercise capacity, an attenuated blood pressure response to e5ercise, and

subGective &atigue ? " @. Some individuals may also display decreased contractility. Most cardiac

changes become clinically signi&icant only when the patient is below 4! percent o& ideal body

weight. 6he wea ened heart muscle generally improves with weight gain, and heart si*e

normali*es with clinical recovery over wee s to months ? "4 @.


29/49

ventricular arrhythmia, particularly in patients with hypo alemia or hypomagnesemia ? =0"@. An

E O at baseline will screen &or these potential abnormalities. E O abnormalities should dissipate

with weight restoration and correction o& any underlying electrolyte abnormality. An overview o&

management o& arrhythmias is discussed separately. 8See 9Arrhythmia management &or the

primary care clinician9 .;

2ncreased L6 dispersion is another mar er o& increased arrhythmic ris in patients with AB,

particularly in patients who weigh less than 4! percent o& ideal body weight ? 0 =0 @. Bormally, the

length o& the L6 interval is similar between each o& the E O leads. L6 dispersion re&ers to the

di&&erence between the ma5imum L6 interval and the minimum L6 interval occurring in any o& the

leads on a routine " =lead E O, and re&lects heterogeneous ventricular depolari*ation. 6he

etiology o& increased L6 dispersion in AB is un nown but may be due to direct inGury o& the

myocardium during starvation.


30/49

wea ness, and cognitive impairment. +rthostasis may also indicate the need &or hospitali*ation,

depending upon the severity ? "! @. Evaluation and treatment o& orthostatic hypotension are

discussed separately. 8See 9Mechanisms, causes, and evaluation o& orthostatic and postprandial

hypotension9 and 96reatment o& orthostatic and postprandial hypotension9 .;

&radycardia % /radycardia 8R1! beats per minute; is o&ten &ound in patients with AB, with heartrates as low as $ beats per minute ? 0,"0, ",04 @. A study o& " women with AB &ound that the

average mean heart rate was 1 beats per minute, and that bradycardia was present in "

percent and hypotension in "1 percent ?"0 @. 6he reduced cardiac &unction and use o& energy

represent an adaptive, compensatory response to caloric deprivation. 6he cause appears to be

increased parasympathetic 8vagal; activity with unchanged sympathetic tone ? 0 @.


31/49

de&inition, all &emale patients with AB have amenorrhea ? @. 2n contrast, an epidemiologic study o&

!0 healthy, premenopausal women aged "4 to 0 years &ound that $ percent had anovulatory

menstrual cycles ? @.

entral nervous system reproductive &unctions are disrupted in AB ? $, 1 @. Bormally, nerve

impulses within the hypothalamus trigger the pulsatile secretion o& gonadotropin releasinghormone, which acts upon the pituitary. 6his initiates the release o& luteini*ing hormone and

&ollicle=stimulating hormone, which in turn determine the onset o& normal menstrual &unction. 2n

patients with AB, secretion o& gonadotropin releasing hormone is reduced, which ultimately

prevents ovulation and causes a &unctional hypothalamic amenorrhea. 8See 9Etiology, diagnosis,

and treatment o& secondary amenorrhea9, section on )Functional hypothalamic amenorrhea) .;

(eight loss o& between "! to "$ percent o& normal weight disrupts the menstrual cycle in most

women ? 0@. owever, amenorrhea may precede weight loss in up to ! percent o& women with

AB. 2n addition, rigorous e5ercise in patients with AB contributes to the secondary amenorrhea

? , 4@.

onversely, normal menstrual cycles usually resume with weight gain ? @. 6he time course and

amount o& weight re3uired &or resumption o& menses has varied among di&&erent studies. A two=

year cohort study o& "!! adolescent &emales with AB &ound that menses resumed in a mean

average o& nine months, re3uired a weight o& .$ pounds 8 g; more than the weight at which

menses were lost, and that 41 percent resumed their menses within si5 months o& achieving a

weight appro5imately ! percent o& ideal body weight ? @. +ther studies support a goal o&

attaining ! percent o& ideal body weight in order to restore normal menses ? 0@. Another cohort

study &ollowed $1 adolescent &emales with AB and &ound that a return o& menses occurred in 1

percent by one=year &ollow=up ? $! @. +ne study &ound the weight re3uirement &or resumption o&menses varied considerably and was predicted by the weight at which menstruation ceased ? $" @.

Amenorrhea persists in about "! to 0! percent o& patients with AB despite weight gain, because

o& ongoing abnormal eating behaviors 8binge eating and purging;, e5ercise, or stress ? 0,$ @. For

patients distressed by persistent amenorrhea, eventual recovery o& menstrual periods may occur

&ollowing psychotherapy. (e do not suggest use o& se5 hormones &or the purpose o& treating

amenorrhea in patients with AB. 6he etiology, diagnosis, and treatment o& secondary amenorrhea

are discussed separately. 8See 9Etiology, diagnosis, and treatment o& secondary amenorrhea9 .;

"ertility %


32/49

higher percentage o& the 1 patients with AB, compared with the 1", 4 women with no eating

disorder 8$! versus " percent;. Signi&icantly more patients also had a history o& induced abortion

8 versus "$ percent;.

Fertility is usually restored in patients who recover &rom AB and remain stable ? ",$$ @. 2& pregnancy

does occur, both pregnancy and lactation stress the maternal s eleton &or minerali*ation o& the&etus and newborn. /ased upon clinical e5perience, clinicians should provide vitamin D and

calcium supplementation, and suggest a diet enriched in protein and phosphate. 2n addition,

pregnancy in AB is associated with a greater incidence o& complications including miscarriages,

premature birth, smaller head circum&erence, and low=birth=weight in&ants, especially i& the

disease is active ? $ @. Butrition during pregnancy and pregnancy outcomes in women with eating

disorders are discussed separately. 8See 9Butrition in pregnancy9 and 9Eating disorders in

pregnant women9, section on )


33/49

reduced testosterone leads to a diminished anabolic state and libido. 6here is no therapeutic role

&or testosterone replacement therapy ? 11 @. 8See)+steoporosis) below.;

2n addition, many patients with AB have elevated growth hormone levels and decreased

production o& 2OF=2, a pro&ile observed in starvation ? $4=1!,1 ,14 @. -educed 2OF=2 levels impede

bone &ormation ? 1!,1 @. 8See )+steoporosis) below.;

Antidiuretic hormone levels are also low, which may rarely cause central diabetes insipidus, with

&ailure to concentrate urine, and resultant hypernatremia and polyuria. 8See 9Diagnosis o& polyuria

and diabetes insipidus9 .;

ypothalamic abnormalities in thermoregulation are apparent with hypothermia ? 1 @. +ne study

&ound hypothermia in percent o& patients with AB ? "0 @.

Osteoporosis % At least 0! percent o& &emale patients with AB have osteoporosis, which

increases their ris o& &ractures ? "0, !, " @. An epidemiologic study identi&ied !4 patients with AB,

and &ound that they were nearly three times more li ely to su&&er a &racture, compared with thegeneral population ? @, and an observational study &ound a seven=&old ris o& &ractures ? 0@. 2n

addition, osteoporosis in AB may result in irreversible s eletal damage and long=term disability

such as pain, yphosis, and short stature ? 0, , $ @.

+steoporosis in AB is characteri*ed by increased bone resorption without concomitant increased

bone &ormation ? $@. 6rabecular bone, &ound in the spine and hips, is a&&ected more than cortical

bone ? " @. 6he most severely a&&ected site is the lumbar spine ? $@. /one loss occurs at a rate o&

to "! percent per year ? " @.

Multiple &actors contribute to osteoporosis in AB.


34/49

bene&it in providing patients their DE A results, because visual evidence that patients are at ris

&or &ractures may lead to positive behavioral changes ? 4@.

6he epidemiology and etiology o& osteoporosis in premenopausal women are discussed

separately. 8See 9Epidemiology and etiology o& premenopausal osteoporosis9 .;

Treatment % (eight gain and resumption o& menstrual &unction is the best established treatment

&or osteoporosis in patients with AB ? $, =4 @. 6here is limited evidence supporting the use o&

hormone therapy in the &orm o& estrogen, recombinant human insulin=li e growth &actor " 82OF=";,

or both. A systematic review identi&ied &ive types o& treatment that have been investigated: weight

gain, hormone therapy, bisphosphonates, calcium, and e5ercise ? $@.

-estoration o& weight and menses is the cornerstone o& treatment &or AB, and is associated with

improved bone mineral density in patients with AB and osteoporosis ? $, =4",40 @. owever, it is

not clear i& bone loss is &ully reversible. Some studies suggest that normal bone mass is restored

&ollowing recovery &rom AB ? 4 @, whereas other studies &ound that deminerali*ation was not &ully

reversible despite weight gain ? 4$ @, even a&ter &ollow=up o& one year ? 1 @.

Supplemental estrogen in the &orm o& oral contraceptive 8estrogen plus progestin; or estrogen

replacement therapy has a secondary role in minimi*ing and perhaps reversing osteoporosis in

patients with AB ? ", $ @. 6here is limited evidence &rom multiple studies to support this

widespread practice ? !, $, ,41 @. 6his contrasts with the une3uivocal bene&its seen in

postmenopausal osteoporosis.

A randomi*ed trial o& "" adolescents with AB &ound that a&ter si5 months, the mean

average increase in bone mineral density was signi&icantly higher in patients who

received oral contraceptive, compared with patients who received placebo ? 4 @. At oneyear, the mean increase was still higher in patients who received oral contraceptive, but

the di&&erence &rom placebo was no longer statistically signi&icant.

A randomi*ed trial o& oral contraceptive in 4 women with AB &ound that a&ter

appro5imately ".$ years, bone mineral density did not di&&er signi&icantly between patients

who received oral contraceptive and patients who received placebo ? 4 @. owever, in

severely ill patients with an initial body weight less than ! percent o& ideal body weight,

patients who received oral contraceptive had a percent increase in mean average bone

density, compared to a ! percent decrease in patients who received placebo.

Furthermore, in control patients who started the study weighing less than ! percent o&

ideal body weight and who spontaneously resumed their menses, there was a " percent

increase in bone mineral density.

An observational study o& "0! women with AB &ound that use o& estrogen did not predict

bone mineral density, but that weight was associated with bone density ? ! @.

An observational study o& $ women with AB &ound that bone mineral density did not

increase in patients receiving oral contraceptives despite a mean average increase in
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weight o& " percent. owever, weight gain and resumption o& menses were each

associated with an increase in bone mineral density ? @.

Himited evidence suggests that recombinant human insulin=li e growth &actor " 82OF="; is

bene&icial ?44 @. A randomi*ed trial assigned 1! women with AB to nine months o& treatment with

2OF=" 80! mcgC g sc twice daily; alone, 2OF=" plus estrogen and progestin, estrogen and

progestin, or placebo. /one mineral density increased signi&icantly in both groups that received

2OF=" compared with placebo ? 4 @. 2n addition, the greatest increase occurred in patients who

received 2OF=" plus estrogen and progestin.

/isphosphonates should not be used routinely in AB ? 0,"! @. Hong=term side e&&ects in young

patients are un nown, and bisphosphonates are teratogenic and can persist in the body &or many

years a&ter discontinuation o& treatment. /isphosphonates have been used &or severe

osteoporosis, especially when AB was unli ely to remit in the near &uture ? $@. 6his is based upon

the nown e&&ectiveness o& bisphosphonates in decreasing bone resorption and increasing bone

mineral density in osteopenic postmenopausal women and adolescent patients with osteogenesis

imper&ecta. Studies o& bisphosphonates include the &ollowing.

A one=year randomi*ed trial in 0 adolescents with AB &ound a nonsigni&icant increase in

bone mineral density in patients treated with alendronate , compared with placebo ? ! @.

An open=label study compared bone mineral density in "! women with AB who received

risedronate $ mg per day and " control patients with AB who did not receive risedronate

? " @. -isedronate increased bone mineral density by percent at si5 months and $

percent at nine months. /y contrast, the controls su&&ered bone loss despite weight gain.

A &ive percent increase in bone mass over a three year period is generally deemed

clinically signi&icant and is associated with a $ percent reduction in &racture ris .

6he use o& bisphosphonates to treat premenopausal and postmenopausal osteoporosis is

discussed separately. 8See 9Evaluation and treatment o& premenopausal osteoporosis9, section

on )/isphosphonates) and 9+verview o& the management o& osteoporosis in postmenopausal

women9, section on )/isphosphonates) .;

Attempts to stimulate bone &ormation with anabolic medications such as dehydroepiandrosterone

8D EA; and transdermal testosterone have &ailed to demonstrate any bene&it &or increasing bone

mineral density ? 0, $ @. Bo randomi*ed trials have &ound a bene&it &or other anabolic agents such

as &luoride, teriparatide, or menatetrenone. 6he use o& androgens &or postmenopausalosteoporosis is discussed separately. 8See 9+verview o& the management o& osteoporosis in

postmenopausal women9, section on )Androgens) .;

alcitonin and ralo5i&ene are used to treat postmenopausal osteoporosis and have been studied

in premenopausal osteoporosis, but there are no credible studies in AB ? $@. 8See 9+verview o&

the management o& osteoporosis in postmenopausal women9, section on ) alcitonin) and
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9+verview o& the management o& osteoporosis in postmenopausal women9, section on )Selective

estrogen receptor modulators) and 9Evaluation and treatment o& premenopausal

osteoporosis9 and 9Evaluation and treatment o& premenopausal osteoporosis9, section on )+ther) .;

alcium and vitamin D are not e&&ective in restoring bone mineral content in patients with AB and

osteoporosis ? $@. 2n addition, studies have &ound no correlation between calcium inta e and bonemineral density in AB, suggesting that ade3uate calcium and vitamin D do not prevent

osteoporosis. owever, calcium is necessary &or bone maintenance and restoration, and is

considered standard treatment &or patients with AB. 6he American Academy o&


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maintain sa&e blood glucose levels ? 4@. An overview o& hypoglycemia is discussed separately.

8See 9 ypoglycemia in adults: linical mani&estations, de&inition, and causes9 .;

Severe complications can occur in patients with comorbid AB and diabetes ? 0@. An overview o&

medical care in diabetes mellitus is discussed separately. 8See 9+verview o& medical care in

adults with diabetes mellitus9 .;

*$#TROINTE#TIN$L % Anore5ia nervosa 8AB; consistently causes gastroparesis 8delayed

emptying o& the stomach; and constipation ? @, and there may be mild elevation o& liver &unction

tests ? 0@. Acute pancreatitis in patients with AB has been described in case reports ? "!! @. 2n

addition, the superior mesenteric artery syndrome is a rare complication o& AB ? "!" @.

*astroparesis % Oastroparesis 8delayed gastric emptying; &re3uently develops with &ood

restriction and a weight loss o& appro5imately "! to ! pounds 8 .$ to ." g; ? ,"! @. 6he main

symptom is bloating 8gas and distension;, which o&ten occurs a&ter eating and may be severe.

/loating is worsened by a high=&iber diet or by &iber=based la5atives. +ther symptoms o&

gastroparesis include early satiety, &ullness, nausea, and vomiting 8not sel&=induced;. eartburn

may also occur as a result o& acidic, vomitus=induced esophagitis &rom &ood remaining in the

stomach &or prolonged periods o& time. 2n some cases it may be di&&icult to tell whether vomiting is

spontaneous andCor sel&=induced. 6he symptoms o& gastroparesis may inhibit the patient &rom

eating and hamper attempts at weight restoration.

Oastroparesis in AB should be managed with the &ollowing conservative measures ? ", ",0$ @:

-eassure patients that eating is not causing gastroparesis, which will eventually resolve

with weight restoration over &our to si5 wee s

Hi3uid &ood supplements should comprise hal& o& the daily calories &or the &irst wee ortwo o& re&eeding

2ngest li3uid components as opposed to solids earlier in the meal

Divide the daily calorie inta e into three small meals and two to three snac s per day

Avoid legume=type &oods, e5cessive &iber, and bran products, which promote gas and

distention

For patients not responding to these measures, clinicians should use metoclopramide , an oral

medication that stimulates stomach contraction and hastens emptying o& the stomach ? " @. A dose

o& $ or "! mg, 0! minutes be&ore meals and at bedtime, is use&ul to treat bloating and early

satiety secondary to weight loss in AB. 2t also acts as an antiemetic medication. Metoclopramide

increases ris &or tardive dys inesia with long=term use.

Oastroparesis induced by weight loss generally improves with partial weight restoration ? 0$,"!0 @.

A signi&icant improvement o&ten occurs with a "! pound 8 .$ g; weight gain and the disorder

largely resolves with weight gain bac to 4! percent o& ideal body weight. owever, symptoms o&

bloating may persist despite weight gain, i& there is ongoing psychopathological distress. 6hus, in
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rare cases it may be necessary to obtain a nuclear medicine gastric emptying study to investigate

persistent symptoms a&ter re&eeding and weight restoration.

Additional in&ormation on gastroparesis is discussed separately. 8See 9Etiology and diagnosis o&

delayed gastric emptying9 and 96reatment o& delayed gastric emptying9 .;

!onstipation % onstipation &re3uently accompanies weight loss in AB ? @. Symptoms include

in&re3uent and small bowel movements and abdominal pain.


39/49

.$ g; can lead to tolerance o& normal &eeding. 6he clinical mani&estations, diagnosis, and

treatment are discussed separately. 8See 9Superior mesenteric artery syndrome9 .;

Acute pancreatitis in patients with AB has been described in multiple case reports ? "!! @. 6he

in&lammation is usually mar ed by acute upper abdominal pain and elevated serum levels o&

pancreatic en*ymes. 6he presumptive etiology is that malnutrition activates proteases, such astrypsin, which damage cells. 2n addition, rapid weight loss may cause retrograde pressure or

re&lu5 o& duodenal contents into the pancreatic duct. 6he etiology, clinical mani&estations and

treatment o& acute pancreatitis are discussed separately. 8See 9 linical mani&estations and

diagnosis o& acute pancreatitis9 and 96reatment o& acute pancreatitis9 and 9Etiology o& acute

pancreatitis9 .;

REN$L $ND ELE!TROL+TE# %


40/49

patients with classic emphysema. 2t is not nown whether this impairment is reversible with

re&eeding.


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NE ROLO*I! % /rain atrophy is a complication o& AB that is evident on neuroimaging

?" !," " @. 6he speci&ic clinical implications o& brain atrophy are not nown. A study &ound that

gray matter volume was signi&icantly smaller in adolescents with AB compared with controls, but

that per&ormance on neuropsychological tests was comparable e5cept &or one test ? " ! @.

Speci&ic &indings on magnetic resonance imaging 8M-2; and computeri*ed tomography 8 6;include gray matter 8neuron cell bodies; volume loss and enlarged ventricles. An M-2 study &ound

that mean average gray matter volume in 0 women with AB was $ percent less than in "

control women, a statistically signi&icant and moderate clinical di&&erence ? " @. 2n addition, an

M-2 study o& "1 women with AB and "1 matched healthy women &ound that the right and le&t

hippocampus were each signi&icantly reduced by 4 percent in the patients ? " 0 @. 2t remains

unclear whether these brain changes are related to the loss o& neurons, glia, and neuropil, or are

merely due to &luid shi&ts.

-esults &rom di&&erent studies suggest that brain atrophy is at least partially reversible with weight

restoration ? " "," @. An M-2 study o& women with AB &ound that during short=termhospitali*ation and weight restoration to ! percent o& ideal body weight, gray matter volumes

increased but remained signi&icantly smaller, compared with control women ? " @. A second M-2

study o& " &emale adolescents with AB and controls &ound that gray matter volumes were

signi&icantly smaller in the patients at the beginning o& their treatment, but that a&ter seven

months, there was no signi&icant di&&erence.

DER)$TOLO*I! % 6he cutaneous mani&estations o& AB are numerous. Symptoms o&

starvation include, in order o& &re3uency ?" ,"" @:

erosis 8dry, scaly s in;

Hanugo=li e body hair 8&ine, downy, dar hair;

6elogen e&&luvium 8hair loss;

arotenoderma 8yellowing;

Acne

yperpigmentation

Seborrheic dermatitis 8erythema and greasy scales;

Acrocyanosis 8cold, blue, and occasionally sweaty hands or &eet;


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