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Hypochondriasis

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Hypochondriasis

o

Author: Glen L Xiong, MD o Chief Editor: David Bienenfeld, MD

Overview

Clinical Presentation

Differential Diagnoses

Workup

Treatment & Management

Medication

Follow-up

Overview

Background

Pathophysiology

Epidemiology

Clinical Presentation

History

Physical

Causes

Workup

Laboratory Studies

Other Tests

Treatment & Management

Medical Care

Surgical Care

Consultations

Diet

Activity

Follow-up

Inpatient & Outpatient Medications

Transfer

Complications

Prognosis

Background

Hypochondriasis and the other somatoform disorders are among the most difficult and most

complex psychiatric disorders to treat in the general medical setting. On the basis of manynew developments in this field, diagnostic criteria have been revised to facilitate clinical care

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and research. Long-awaited randomized, placebo-controlled treatment approaches have

finally emerged. Comparative clinical effectiveness studies are also being developed.

As with all psychiatric disorders, the somatoform disorders demand creative, rich

biopsychosocial treatment planning by a team that includes primary care physicians,

subspecialists, and mental health professionals.[1]

This article describes hypochondriasis, its diagnosis, and an overview of treatment

approaches, with references for details beyond the scope of the article. Finally, the article

reviews new developments in psychopharmacologic and psychotherapeutic treatments.

Case study

A 45-year-old white male engineer presents to a primary care clinic armed with multiple

internet searches on the topic of cancer. He states that he “just knows” he has a GI cancer,

"probably the colon or maybe the pancreas." When asked how long this concern has bothered

him he says "for years I have been concerned that I have cancer." You ask about relevantsymptoms and he is a bit vague, saying "I get some pain or pressure right here (he points to

the left upper quadrant) but it is not there all the time." Upon asking about prior workups he

says “I have had ultrasounds and colonoscopies but they could find anything. I was initially

relieved but a couple of weeks later started to think that they must have just missed

something.”

When you ask about the patient's goals for today’s visit he is emphatic "I think what I really

need is another colonoscopy and abdominal CT scan." His examination is unrevealing. When

you suggest a less invasive approach, he shows the error rates of the other evaluations and

shows literature endorsing how abdominal CT is the criterion standard. He is anxious at

baseline and increasingly irritable when you propose less invasive evaluation. He ends the

encounter by stating that he will “find another doctor who sees my point and will get me what

I need.”

References

Pathophysiology

Neurochemical deficits associated with hypochondriasis and some other somatoform

disorders (eg, somatization, conversion, and body dysmorphic disorders) appear similar to

those of mood and anxiety disorders. See Medscape Reference articles Somatoform Disordersand Conversion Disorders.

For example, Hollander et al posited an "obsessive-compulsive spectrum" to include

obsessive-compulsive disorder (OCD)[2, 3] , body dysmorphic disorder (BDD), anorexia

nervosa, Tourette syndrome, and impulse control disorders (eg, trichotillomania, pathological

gambling).[4] Other authors postulate that somatoform disorders including hypochondriasis

may be a learned unconscious behavior that may serve to avoid internal conflicts and external

stressors.[5]

This formulation of obsessive-compulsive (OC) spectrum disorders, while not a part of the

consensus psychiatric diagnostic and classification literature, crosses boundaries of severaldiagnostic categories in the Diagnostic and Statistical Manual of Mental Disorders, Fourth

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Edition-Text Revision ( DSM-IV-TR). In addition, encountering a patient with more than one

of the anxiety spectrum disorders during his or her life is not unusual. Although findings of

studies of these neurochemical deficits are only preliminary, such deficits may explain why

symptoms overlap, why the disorders are commonly comorbid, and why effective treatments

parallel one another (eg, selective serotonin reuptake inhibitors [SSRIs]).

In a recent study of biological markers, subjective who met DSM-IV-TR diagnostic criteria

for hypochondriasis had decreased plasma neurotrophin 3 (NT-3) level and platelet serotonin

(5-HT) levels, compared to healthy control subjects. NT-3 is a marker of neuronal function

and platelet 5-HT is a surrogate marker for serotonergic activity. [6]

References

Epidemiology

Frequency

United States

The prevalence rates for primary hypochondriasis in the primary care setting are 0.8-

4.5%.[7] Some degree of preoccupation with disease is apparently common, because 10-20%

of people who are healthy and 45% of people without a major psychiatric disorder have

intermittent unfounded worries about illness.[8]

International

International rates are similar to those in the United States.[9]

Mortality/Morbidity

Hypochondriasis is usually episodic, with hypochondriacal symptoms that last from months

to years and equally long quiescent periods. Although formal outcome studies have not been

conducted, one third of patients with hypochondriasis are believed to eventually improve

significantly. A good prognosis appears to be associated with high socioeconomic status,

treatment-responsive anxiety or depression, the absence of a personality disorder, and the

absence of a related nonpsychiatric medical condition. Most children are believed to recover

by adolescence or early adulthood, but empiric studies have not been carried out.

Epidemiological studies are lacking, but patients with hypochondriasis appear similar to those

with somatization disorder. These individuals use medical care at high rates, making frequent

visits to the emergency department, the doctor, and other health care providers and

undergoing frequent physical examinations, laboratory testing, and other costly, invasive, and

potentially dangerous procedures.[10]

Cognitive, social learning, and psychodynamic theories imply that patients have significant

psychosocial disturbances in terms of relationships, vocational, and other endeavors.

Exacerbations may occur with psychological stressors and in patients with comorbid

psychiatric conditions.






These high-use patterns differ dramatically from those of nonsomatizing patients and remain

true even when comorbid medical conditions and sociodemographic differences are

accounted for.[11] The medically unexplained complaint is often a symptom of

hypochondriasis[12] and may well be a presentation of associated abnormal illness

behavior.[13]

Patients with hypochondriasis have a high rate of psychiatric comorbidity.[14] In one general

medical outpatient clinic, 88% of patients with hypochondriasis had one or more concurrent

psychiatric disorders, the most common being generalized anxiety disorder (71%), dysthymic

disorder (45.2%), major depression (42.9%), somatization disorder (21.4%), and panic

disorder (16.7%). These patients are 3 times more likely to have a personality disorder than

the general population.[14] Substance abuse or dependence is also a serious comorbid

condition, particularly use of benzodiazepines, though epidemiological studies have not

assessed the exact frequency of this problem. The long-term prognosis of patients with

hypochondriasis is understudied due to the heterogeneity of the disorder. However, higher

severity at baseline is likely associated with worse outcome.

Race

This disorder has not been well studied with respect to race and ethnicity. More information

is needed, too, with regard to its relationship to other medical disorders needing better

definition (eg, neurasthenia, chronic fatigue syndrome, fibromyalgia, and multiple chemical

sensitivity syndrome).

Sex

Hypochondriasis appears to occur equally in men and women.

Age

Hypochondriasis can begin at any age, but the most common age of onset is early adulthood.

References

History

Hypochondriasis is classified as one of the somatoform disorders, a class that was formulated

to accommodate the differential diagnosis of disorders characterized primarily by physicalsymptoms for which no demonstrable organic explanations or physical findings exist.

The DSM-IV-TR stipulates that the symptoms are not under voluntary control (thus excluding

malingering and factitious disorders) and are not fully explained by known physiological

causes (excluding psychological factors affecting the medical condition). The disorders in the

somatoform class include somatization disorder, conversion disorder, pain disorder,

hypochondriasis, BDD, and undifferentiated somatoform disorder.

The core feature of hypochondriasis is not preoccupation with symptoms themselves, but

rather the fear or idea of having a serious disease (see the image below). The fear or idea is

based on the misinterpretation of bodily signs and sensations as evidence of disease. The

illness persists despite appropriate medical evaluations and reassurance.






View Image

Pathological cycle of bodily concern and anxiety in hypochondriasis.

The diagnosis should be considered strongly if the patient has a history of hypochondriasis

(or other somatization disorder) or has had multiple nonproductive clinical workups, and ifthe patient's complaints are markedly inconsistent with objective findings or the examination

yields no abnormal findings. Further psychiatric history should be obtained with regard to a

history of hypochondriasis (or corresponding behaviors) in family members or a sudden,

unexplained loss of function that spontaneously resolved.

Diagnostic criteria for hypochondriasis include the following ( DSM-IV-TR):

The patient has a preoccupying fear of having a serious disease.

The preoccupation persists despite appropriate medical evaluation and reassurance.

The belief is not of delusional intensity (as in delusional disorder, somatic type) and is

not restricted to a concern about appearance (as in persons with BDD). The preoccupation causes clinically significant distress or impairment.

The preoccupation lasts for at least 6 months.

The preoccupation is not explained better by another mood, anxiety, or somatoform

disorder.

References

Physical

The absence of physical findings, particularly after serial examinations, supports the

diagnosis of hypochondriasis. However, the patient must receive a physical examination to

make the psychiatric intervention possible. A mental status examination complements the

physical examination.

General appearance, behavior, and speech

Modestly or well groomed, not grossly disheveled

Cooperative with the examiner, yet ill at ease and not easily reassured

Possible signs of anxiety, including moist hands, perspiring forehead,

strained/tremulous voice, and wide eyes and intense eye contact

Psychomotor status

Restlessness

Frequent shifts in posture

Mild-to-moderate agitation

Slowed (if sleeping poorly)

Mood (the pervasive and sustained emotion that colors the patient's perception of the

world) and affect (what the examiner observes)

Anxious or worried, depressed mood






Restricted, shallow, fearful, or anxious affect, with restricted fluctuations and limited

depth

Thought process

Spontaneous speaking with occasional abrupt changes in topic Circumstantial, scattered at times

Responds to questions but may divert to next worry or revert to an already expressed

concern despite reassurance to the contrary

No latency unless also depressed

No thought blocking or looseness of associations

Concrete focus of thought, but with capacity to abstract in a number of areas when

encouraged or tested

May appear distractible and yet can concentrate independently and with

encouragement

Thought content

Preoccupation with being ill

Anxious themes concerning what in the body is wrong, how it is wrong, and how it is

experienced

May have feelings of despair and/or hopelessness, although these are not usually ofsignificant depth unless little relief has come from seeing multiple providers and/or

the patient concurrently depressed

Catastrophizing tendencies (focused on dire consequences of various symptoms and

obtaining more diagnostic testing)

Uninterested in revealing other aspects of daily functioning or general lifestyle topics

at length

Inflexibility regarding bodily concerns, but only rarely to the point of a delusion (ie,

fixed, false belief), and if so, limited to somatic complaints rather than grandiose or

persecutory complaints

No perceptual disturbances (eg, hallucinations)

No suicidal ideation, unless concurrently depressed

No homicidal ideation

Cognitive function

Attentive

Oriented fully to time, place, and person

Rare difficulties with concentration, memory, and other faculties, but functions in the

normative range with refocusing and encouragement

May have some deficits if concurrently depressed; these also tend to be overcome in

response to encouragement

Interestingly, may have selective attention (eg, the patient is distressed by an ongoing

bodily complaint but not by a newly sprained ankle)

Insight

Able to recognize bodily sensations



Lacking full understanding of underlying psychological concerns and how they

underpin development and maintenance of bodily complaints; tends to see the "trees"

rather than the "forest"

Some awareness of own feelings about people and events, but not always with the

ability to translate that into action, sustained change in mood, or lessening of

preoccupations

Judgment

Capable of social greetings and other behaviors

Persistence in discussing and evaluating continuing preoccupations (due to limited

insight)

May be impaired if concurrently depressed

References

Causes

Developmental and other predisposing factors (see the image below) consistently indicate the

importance of parental attitudes toward disease, previous experience with physical disease,

and culturally acquired attitudes relevant to the etiology of the disorder. [15] Overall however,

few demographic and clinical differences have been found between patients with

hypochondriasis and the general population. Social position, education level, and marital

status do not appear to be factors in this condition.

View Image

Mood, cultural, developmental, and environmental factors that influence

hypochondriasis.

A cognitive model of hypochondriasis suggests that patients misinterpret bodily symptoms by

augmenting and amplifying their somatic sensations. Patients also appear to have lower-than-

usual thresholds for, and tolerance of, physical discomfort. For example, what most people

normally perceive as abdominal pressure, patients with hypochondriasis experience as

abdominal pain. When they do sustain an injury (eg, ankle sprain), it is experienced with

significant anxiety and is taken as confirmation of their worry about being ill. This may be

due to a tendency among patients with hypochondriasis to exaggerate their assessment of

vulnerability to disease and their appraisal of the risk of serious illness.[11]

The social learning theory frames hypochondriasis as a request for admission to the sick role

made by a person facing seemingly insurmountable and insolvable problems. This role may

allow them to avoid noxious obligations, postpone unwelcome challenges, and be relieved

from duties and obligations.[16]

The psychodynamic theory implies that aggressive and hostile wishes toward others are

transferred via repression and displacement into physical complaints. The hypochondriacal

symptoms serve to "undo" guilt felt about the anger and serve as a punishment for being

"bad."

Neurochemical deficits with hypochondriasis and some other somatoform disorders (eg,BDD) appear similar to those of depressive and anxiety disorders. For example, in 1992,






Hollander et al posited an obsessive-compulsive spectrum that includes OCD, BDD, anorexia

nervosa, Tourette syndrome, and impulse control disorders (eg, trichotillomania, pathological

gambling).[4] Although only preliminary data have been reported on these neurochemical

deficits, such deficits may explain why symptoms overlap, why the disorders are commonly

comorbid, and why treatments may parallel one another (eg, SSRIs).

Hypochondriasis has been hypothesized to be an anxiety spectrum disorder. P-wave

dispersion (the difference between the maximum and minimum P-wave duration on the

electrocardiograph) has been found to be significantly higher in patients with panic disorder

and in patients with hypochondriasis, compared with healthy control subjects. The elevated

P-wave dispersion may be an indicator of cardiac autonomic dysfunction in anxiety

disorders.[17]

References

Differential Diagnoses

Anxiety Disorders

Body Dysmorphic Disorder

Conversion Disorders

Delusional Disorder

Depression

Personality Disorders

Schizophrenia

Somatoform Disorders

Laboratory Studies

In patients with hypochondriasis, the abnormal laboratory findings characteristic of the

suggested physical disorder are absent.

References

Other Tests

Screening tools

The Health Anxiety Inventory (HAI) (long version; short version of 14 items, 5 min)

reliably distinguishes patients with hypochondriasis from patients with anxietydisorders or healthy controls.[27]

The Illness Attitude Scale (29 items, 15 min, English only) is used for detection and

to assess severity.[35]

The Whitely Index of Hypochondriasis (14 items, 5 min, >14 languages) is used for

detection, for rating severity, and for measuring change per interventions.[36]

The Somatoform Disorders Symptom Checklist (65 yes-or-no items, 20 min, >5

languages) screens for hypochondriasis, somatization disorder, BDD, and others.[37]

References

Medical Care



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Due to the enigmatic nature of various physical symptoms, occasionally patients with

hypochondriasis are admitted to the general medical-surgical hospital for an extensive work-

up.

When hypochondriasis is suspected in a medical or surgical inpatient, a psychosomatic

medicine consultation should be performed to elucidate the diagnosis and address psychiatriccomorbidity.

If clinically recommended by the psychosomatic medicine consultant, psychotropic

medication interventions can be started.

As in the outpatient care model, patients should not be exposed to high-risk invasive

procedures.

Numerous other strategies appear to benefit patients with hypochondriasis (see the image

below). These strategies may prevent potentially serious complications, including the effects

of unnecessary diagnostic and therapeutic procedures.

View ImageFactors that maintain anxiety in patients with hypochondriasis.

Establish one primary care physician as the patient's main physician.

Review the patient's medical history to build an alliance and rule out medical disorders.

Premature reassurance, prescription of psychotropic medications, and referral for mental

health services may suggest to the patient that he or she is not being taken seriously.

Therefore, while such treatments may be indicated at some time (in the future), prematurely

offering a diagnosis or psychiatric treatment may, in fact, impair the establishment of a

trusting patient-physician relationship.

Acknowledge the patient's pain and suffering.

Couple reassurance statements of normal findings with statements that that the patient will

not be abandoned. For example, “Mr. Smith, it appear s that you are still having concern about

having a “several medical disorder” despite all the workup, which, so far, has not showed any

abnormal finding. I will continue to work with you to maximize you overall well-being andhealth.”

Reassure the patient that evaluation will be ongoing.

Understand the “the fear” of having an unknown medical disorder as a form of emotional

communication.

Search for underlying medical and psychiatric disorders potentially amenable to treatment.

Seek consultation or refer the patient to a colleague if establishing an alliance proves

difficult.



Allow for time-limited structured discussions about somatic concerns.

Spend sufficient time on health care maintenance issues such as diet, experience, smoking

cessation, and cancer detection.

Treat comorbid psychiatric disorders concurrently.

Be aware of emotional reactions toward the patient (ie, anger, hopelessness, helplessness) and

seek frequent informal consultation when possible.

Focus on care of the patient with hypochondriasis, not exclusively on “a cure” for the

disorder.

Psychotherapy

Several authors have suggested a cognitive-educational approach to understand the

development of the severe anxiety associated with hypochondriasis (see thefirst image below)and the factors that maintain the long-term anxiety (see the second image

below).[39] Randomized controlled trials now suggest that cognitive-behavioral therapy (CBT)

is efficacious in the treatment of hypochondriasis[40, 41, 42, 43, 44] and may be the recommended

treatment for patients with hypochondriasis. Bibliotherapy, using CBT principles, may also

be useful.

References

Surgical Care

Psychosurgery is only recommended for patients with severe and intractable hypochondriasis.

References

Consultations

Primary care physicians generally treat hypochondriasis, with psychiatrists providing

consultation.

References

Diet

Patients with hypochondriasis should eat 3 meals per day to feel as healthy as possible. They

should avoid substances that adversely affect mood, exacerbate anxiety symptoms, or reduce

the quality of sleep (eg, caffeine, alcohol, nicotine).

References

Activity

Exercise increases psychological well-being. Patients who are hypochondriacal may bereluctant to follow this advice, but many patients greatly increase their physical activity as















treatment progresses. Exercise helps to improve mood, reduce tension, and improve sleep in

patients with associated depression, anxiety, or both.

References

Medication Medication Summary

Antidepressants

Beta-adrenergic receptor-blocking agents

Benzodiazepines

Antipsychotic medications

Medication Summary

Pharmacotherapy is used as an adjunct to psychotherapy and educational treatments. The

goals of pharmacotherapy are to reduce comorbid symptoms and disorders (eg, depression),

to prevent complications, and, in a few circumstances, to reduce hypochondriacal symptoms.Each medication has advantages and disadvantages.[45]

References

Antidepressants

Class Summary

Fluoxetine (Prozac)

Paroxetine (Paxil)

Sertraline (Zoloft)

Venlafaxine (Effexor XR)

Clomipramine (Anafranil)

Fluvoxamine (Luvox)

Imipramine (Tofranil)

Phenelzine (Nardil)

Citalopram (Celexa)

Escitalopram (Lexapro)

Fluoxetine (Prozac)

Dosing, Interactions, etc.

Clinical Context: Selectively inhibits presynaptic serotonin reuptake with minimal or no

effect on reuptake of norepinephrine or dopamine

References

Paroxetine (Paxil)


Clinical Context: Potent selective inhibitor of neuronal serotonin reuptake. Also has weak

effect on norepinephrine and dopamine neuronal reuptake



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Clinical Context: Usually reserved for patients who do not tolerate or respond to traditional

cyclic or second-generation antidepressants.

References

Citalopram (Celexa)


Clinical Context: Selectively inhibits presynaptic serotonin reuptake, minimal or no effect

on reuptake of norepinephrine.

References

Escitalopram (Lexapro)


Clinical Context: Selective serotonin reuptake inhibitor (SSRI) and S-enantiomer of

citalopram. Used for the treatment of depression. Mechanism of action is thought to be

potentiation of serotonergic activity in CNS resulting from inhibition of CNS neuronal

reuptake of serotonin. Onset of depression relief may be obtained after 1-2 wk, which is

sooner than other antidepressants.

References

Class Summary

These are typically used for depression or anxiety comorbid with hypochondriasis, although

in some cases they alleviate hypochondriacal symptoms in the absence of another disorder.

They are indicated for use in adults with depression, anxiety (eg, panic disorder, OCD, social

phobia, generalized anxiety, posttraumatic stress disorders), and bulimia nervosa disorders.

Off-label uses include insomnia, attention-deficit/hyperactivity disorder, premenstrual

dysphoric disorder, and other conditions. All SSRIs (eg, fluoxetine [Prozac], sertraline

[Zoloft], paroxetine [Paxil], citalopram [Celexa], escitalopram [Lexapro], fluvoxamine[Luvox]), one selective norepinephrine and serotonin inhibitor (ie, venlafaxine [Effexor

XR]), 2 TCAs (ie, clomipramine [Anafranil], imipramine [Tofranil]), and one MAOI (ie,

tranylcypromine [Parnate]) have been listed; the latter should be used with care because of

dietary restrictions and drug interactions. Data on bupropion (Wellbutrin) and mirtazapine

(Remeron) are insufficient to warrant listing, but they may also be used.

Initial doses are listed below. The general principle in these patients is to start at a low dose

and progress slowly, unless a psychiatric emergency (eg, suicidal ideation) is present. Once

established, a well-tolerated and efficacious antidepressant should be continued as indicated

for the comorbid condition (eg, 6-12 mo for a single depression or indefinitely for recurrent

depression and an anxiety disorder). If used for hypochondriasis alone, for maintenance





















dosing, adjust the dose to maintain the patient on the lowest effective dosage, and reassess the

patient periodically to determine the need for continued treatment.

References

Beta-adrenergic receptor-blocking agents Class Summary

Propranolol (Inderal)

Propranolol (Inderal)


Clinical Context: Has membrane-stabilizing activity and decreases automaticity of

contractions.

References

Class Summary

Compete with beta-adrenergic agonists for available beta-receptor sites. Propranolol inhibits

beta-1 receptors (located mainly in cardiac muscle) and beta-2 receptors (located mainly in

bronchial and vascular musculature), inhibiting chronotropic, inotropic, and vasodilatory

responses to beta-adrenergic stimulation.

References

Benzodiazepines

Class Summary

Alprazolam (Xanax)

Alprazolam (Xanax)


Clinical Context: For management of panic attacks. Binds receptors at several sites within

CNS, including limbic system and reticular formation. Effects may be mediated through

GABA receptor system.

References

Class Summary

Indicated for treatment of anxiety disorders and panic attacks, with or without agoraphobia,

which are commonly comorbid with hypochondriasis. Use with caution because patients with

hypochondriasis may have increased risk of substance abuse or dependence.

References

Antipsychotic medications




































Class Summary

Pimozide (Orap)

Risperidone (Risperdal)

Olanzapine (Zyprexa)

Pimozide (Orap)


Clinical Context: Indicated for Tourette syndrome for suppression of motor and phonic tics.

Off-label use for psychosis, hypochondriacal delusions and parasitosis, and Huntington

chorea.

References

Risperidone (Risperdal)


Clinical Context: Binds to dopamine D2 receptor with 20-times lower affinity than for

serotonin receptor. Improves negative symptoms of psychoses and reduces incidence of EPS.

Indicated for treatment of psychotic disorders, including schizophrenia and bipolar disorder

mania; also used for sleep.

References

Olanzapine (Zyprexa)


Clinical Context: Binds to dopamine D2 and serotonin receptors. Improves negative

symptoms of psychoses and reduces incidence of EPS. Indicated for treatment of psychotic

disorders, including schizophrenia and bipolar disorder mania; also used for sleep

References

Class Summary

Have been shown to reduce morbidity associated with this disorder, particularly in presence

of comorbid anxiety or hypochondriacal worries that mimic obsessions or delusions. Because

of potential for serious long-term adverse effects (eg, tardive dyskinesia), consultation with

psychiatrist recommended to evaluate need for antipsychotic medication. Insufficient data to

list other antipsychotics, although they have been used in patients with hypochondriasis.

References

Inpatient & Outpatient Medications

Continue successful long-term trials of medications for patients with hypochondriasis.




































For patients with comorbid disorders, consider maintenance of those trials because

these disorders can initiate and/or exacerbate hypochondriacal symptoms.

References

Transfer

Physician-to-physician dialogue on the nature of the patient's problems and successful

management strategies is useful.

References

Complications

Patients who are hypochondriacal may be significant consumers of medical care,

undergoing repetitive doctor visits, physical examinations, laboratory testing, and

other costly, invasive, and potentially dangerous procedures. Physician concerns regarding workups for somatic complaints also may preclude

diagnosis of common comorbid disorders (eg, depression) that are quite treatable.

References

Prognosis

Hypochondriasis is a common disorder in primary care settings.

The differential diagnosis includes other somatoform, depressive, anxiety (eg,

generalized anxiety disorder, OCD), and psychotic disorders. Biopsychosocial treatment is required to manage this complex disorder, and further

research is required to better understand its pathophysiology and interface with other

psychiatric conditions. Recognizing the biological similarities between these

seemingly disparate disorders may be a useful starting point to begin a more

systematic study of novel treatments for hypochondriasis.[46]

A system review of six studies on hypochondriasis indicated that 30-50% of patients

achieve recovery.[47]

A good prognosis appears to be associated with high socioeconomic status, treatment-

responsive anxiety or depression, the absence of a personality disorder, and the

absence of a related nonpsychiatric medical condition.

Most children recover by adolescence or early adulthood. There is a dearth of long-term follow-up studies examining outcomes of patients with

hypochondriasis. In a prospective study that examined 58 patients with

hypochondriasis who had participated in selective serotonin reuptake inhibitor (SSRI)

treatment for 4-16 years (mean 8.6±4.5 y), 40% continued to meet the diagnosis of

hypochondriasis. Predictors of continued diagnosis of hypochondriasis include longer

duration of hypochondriasis prior to treatment, history of childhood physical

punishment, and lower use of SSRI during the treatment period. A large portion of

patients with hypochondriasis who received SSRI treatment were able to achieve

remission.[48]

References















Author

Glen L Xiong, MD, Associate Clinical Professor, Department of Psychiatry and Behavioral

Sciences, Department of Internal Medicine, University of California Davis School of

Medicine; Attending Psychiatrist, Sacramento Mental Health Treatment Center; Attending

Physician, Sacramento County Primary Care Clinic

Disclosure: Lippincott Williams & Wilkins Royalty Book Editor; National Alliance for

Research in Schizophrenia and Depression Grant/research funds Independent contractor

Coauthor(s)

Donald M Hilty, MD, Professor of Clinical Psychiatry, Vice-Chair of Faculty Development,

Department of Psychiatry and Behavioral Sciences, University of California, Davis School of

Medicine

Disclosure: Nothing to disclose.

James A Bourgeois, OD, MD, MPA, Clinical Professor, Department of Psychiatry,

University of California, San Francisco, School of Medicine; Faculty Psychiatrist,

Consultation-Liaison Division, Department of Psychiatry, Langley Porter Psychiatric

Institute, University of California, San Francisco, Medical Center


Peter M Yellowlees, MD, MBBS, Professor of Psychiatry, Director of Health Informatics

Program, University of California, Davis, School of Medicine

Disclosure: Medscape Consulting fee Independent contractor

Specialty Editors

Sarah C Aronson, MD, Associate Professor, Departments of Psychiatry and Medicine, Case

Western Reserve School of Medicine/University Hospitals of Cleveland


Francisco Talavera, PharmD, PhD, Adjunct Assistant Professor, University of NebraskaMedical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Medscape Salary Employment

Harold H Harsch, MD, Program Director of Geropsychiatry, Department of

Geriatrics/Gerontology, Associate Professor, Department of Psychiatry and Department of

Medicine, Froedtert Hospital, Medical College of Wisconsin

Disclosure: Novartis Honoraria Speaking and teaching; Sunovion Honoraria Speaking and

teaching; Otsuke Grant/research funds reseach; Merck Honoraria Speaking and teaching

Chief Editor



David Bienenfeld, MD, Professor of Psychiatry, Vice-Chair and Director of Residency

Training, Department of Psychiatry, Wright State University, Boonshoft School of Medicine

Disclosure: Lippincott Williams Wilkins Royalty Author

Additional Contributors

The authors and editors of Medscape Reference gratefully acknowledge the contributions of

previous authors Shayna L Marks, BA, MA; Dandan Liu, BA; and Celia Chang, MD to the

development and writing of this article.

References

1. Barsky AJ, Klerman GL. Overview: hypochondriasis, bodily complaints, and somatic

styles. Am J Psychiatry. Mar 1983;140(3):273-83. [View Abstract]

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hypochondriasis.


Factors that maintain anxiety in patients with hypochondriasis.



hypochondriasis.

Factors that maintain anxiety in patients with hypochondriasis.

A cognitive model of the development of anxiety with hypochondriasis.
















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