A hypochondria “checklist” can help you sort through many overlapping medical and psychiatric disorders and increase your chances of making an accurate diagnosis. Then—by addressing hypochondria’s cognitive dysfunction—you can help patients achieve partial or full remission and change their distressing behaviors.

We offer a checklist that is useful in our practice and suggest behavioral therapies and medications that can help calm these patients’ excessive, unwarranted fears.

WORKING AS A TEAM

Ideal approach. Because hypochondriasis has features of medical and mental illness, working with the patient’s primary care physician is ideal. Physicians often consider these patients difficult because they demand a lot of time, support, and reassurance. Together, you can:

• offer the patient a healthy level of compassion and empathy to establish a positive therapeutic alliance
• set appropriate time limits and guidelines for the patient’s care
• dissuade patients from “doctor shopping”
• set limits on how often patients may visit their doctors and request reassurance.

Box

Hypochondriasis: Persistent, unwarranted distress

For example, you may indicate to the patient, “I will reassure you only at office visits (not by phone), the office visits will be limited to once a month, and during each visit I will reassure you no more than once.”

A doctor-patient relationship based on mutual trust and respect is vital when you treat a patient with hypochondriasis. You can help primary care physicians provide more empathic treatment by explaining that patients do not feign or desire this distressing condition.

DIAGNOSTIC FEATURES

Patients with hypochondriasis tend to be hyper-vigilant about normal physiologic fluctuations and bodily sensations, often misinterpreting them as life-threatening or serious enough to require immediate medical attention. This excessive focus on benign symptoms (such as an accelerated heart rate, sweating, or a bump on the skin) and the cognitive distortion of their significance result in increased anxiety, bodily checking, and doctor visits (Box).^1-4

Presentations. Hypochondriasis has three common presentations: disease conviction, disease fear, and bodily preoccupation (Table 1).⁵ Psychiatrists are most likely to see disease fear, as patients with this predominant symptom tend to realize that fear plays too prominent a role in their lives. Physicians in medical practice are more likely to encounter patients with high levels of disease conviction or somatic preoccupation.

Psychiatric comorbidity. Hypochondriasis is highly comorbid with Axis I and Axis II disorders, which complicate treatment. Nearly one-half of patients with hypochondriasis also have dysthymia (45%) or major depression (43%). Other comorbidities include phobias (38%), somatization disorder (21%), panic disorder (17%), and obsessive-compulsive disorder (8%).⁶ Patients with hypochondriasis are three times more likely than the general population to have personality disorders;^6,7 the prognosis is believed to be more promising for patients without personality disorders.

Distinguishing between primary and secondary hypochondriasis is important. Treating a primary psychiatric disorder often alleviates the symptoms of secondary hypochondriasis, particularly when hypochondriasis masks depression.

HYPOCHONDRIASIS CHECKLIST

Underlying medical disorder? Before diagnosing hypochondriasis, review the medical workup for underlying disease or illness. Medical conditions sometimes go undetected when physicians assume that complaints are an expression of longstanding hypochondriasis.

Table 1

Three common presentations of hypochondriasis

Sometimes a patient may become anxious when mild or vague signs and symptoms do not yet meet established diagnostic criteria for a medical disorder. An effective approach is to provide ongoing support, avoid excessive diagnostic tests, and help the patient make the best use of his or her functional capacities while living with uncertainty.

Functional somatic syndrome? Fibromyalgia and chronic fatigue syndrome do not represent hypochondriasis,⁸ although they may be exacerbated by comorbid psychiatric disorders. Both disorders have diagnostic criteria and specified courses and have been studied to identify psychiatric comorbidity.

Transient or sustained? After it is clear that the patient is not suffering from a medical problem, determine whether hypochondriasis is transient or fully diagnostic:

• If transient, the patient may only need to be educated about how overattention may amplify symptoms; reassure him or her that a full medical workup has been negative.
• If fully diagnostic, reassurance may work for only a few days or weeks; the return of the fear or conviction helps establish the diagnosis.

Somatoform disorder? Distinguish hypochondriasis from other somatoform disorders (Table 2). In practice, the terms “hypochondriac” and “somatizer” are commonly used interchangeably, but the distinction needs to be clear. Hypochondriasis is primarily a disorder of abnormal cognition, in which symptom meaning is of greatest concern. Somatization is primarily a disorder of abnormal sensation, in which the symptoms themselves are the overwhelming focus of attention.

Anxiety disorder? Patients with generalized anxiety disorder may worry about illness, but they also worry about other life issues. Patients with panic disorder may have intense hypochondriacal concerns (such as having a heart attack), but these worries tend to be related to panic symptoms and resolve when the panic disorder is treated.

Obsessive compulsive disorder? Like obsessive-compulsive disorder (OCD), hypochondriasis is characterized by recurrent intrusive thoughts that create heightened anxiety and distress. To relieve their anxiety, patients with hypochondriasis engage in compulsions, such as:

• undergoing extensive medical tests
• seeking habitual reassurance from doctors and family
• consulting medical literature
• performing repeated body checks for perceived lumps or bumps
• avoiding activities that trigger their health-related stress.⁹

Table 2

How to distinguish somatoform disorders

OCD and hypochondriasis also may share the diagnostic feature of pathologic doubt; patients’ uncertainty in appraising a situation leads to additional checking and reassurance-seeking behaviors. The immediate relief gained by these compulsions reinforces the patient’s urge to engage in more maladaptive behaviors and sends a stronger message to the brain that these behaviors are needed to prevent harm.

Ironically, the emergence of a real medical ailment—despite hypochondriacal worry—may force the patient to re-evaluate the usefulness of behaviors motivated by trying to avoid harm. A hypochondriacal patient who was diagnosed with optic neuritis and possible multiple sclerosis recently said to these authors, “I had always thought that by being vigilant I could keep illnesses away. Now I know that’s not true.”

Although hypochondriasis and OCD have similarities, certain clinical distinctions exist. Patients with hypochondriasis worry about having an illness, whereas OCD patients with somatic obsessions fear developing or transmitting an illness. A hypochondriacal patient might fear having AIDS or cancer despite reassurance from doctors, while an OCD patient more typically would fear contracting or transmitting the disease (a contamination obsession) and would engage in excessive behaviors to reduce the risk of developing the disease.

Depressive disorder? Unlike the anxious-worrying version of hypochondriasis, the depressive version is more fatalistic. Patients may be convinced they are dying of a dreaded disease, often believing it to be punishment for an indiscretion, such as marital infidelity. Or they may suddenly become hypochondriacal with mild depressive features, unaware that the actual problem is unresolved bereavement (hypochondriasis with secondary depression). The appropriate diagnosis is primary depressive disorder with secondary hypochondriacal features when depression dominates the presentation and preceded the illness fears.

Table 3

Recommended dosages for treating primary hypochondriasis

Delusional disorder? To distinguish hypochondriasis from delusional disorder (somatic type), consider the patient’s pattern of insight:

• Hypochondriacal patients often vacillate between poor and excellent insight, depending on their distress level.¹⁰ They may acknowledge the irrationality of their fears, then later be convinced they have a disease.
• Patients with delusional disorder are convinced they have a serious health threat, despite the absence of medical confirmation. These patients are considered to have a primary psychotic disorder that requires antipsychotic treatment.

TREATING PRIMARY SYMPTOMS

Drug therapy. When hypochondriasis is secondary—such as to depression or panic disorder—treat the primary condition first.^11,12 For primary hypochondriasis, selective serotonin reuptake inhibitors (SSRIs) such as fluoxetine, paroxetine, or fluvoxamine have shown benefit, mostly in open-label studies. An uncontrolled case series suggests that nefazodone—with mixed serotonin reuptake inhibition and agonist properties—also may help patients with hypochondriasis.¹³ In the only published controlled study, fluoxetine was more effective than placebo for treating hypochondriasis.¹⁰

Continue drug therapy, when used, for at least 8 weeks, with each dosage maintained for at least 4 weeks. If patients do not respond to lower SSRI dosages, increase to the higher dosages reported to be more effective for OCD (Table 3).¹⁴

Except for primary illness phobia, hypochondriasis has not been shown to respond to tricyclics, benzodiazepines, or dopaminergic blockers. In our experience, electroconvulsive therapy—although inadequately studied—may help treat patients with severe, treatment-refractory hypochondriasis with marked somatization.

Psychotherapy. Cognitive-behavioral therapy (CBT)—challenging patients’ irrational fears about illness and teaching them problem-solving tools—is effective in treating hypochondriasis.¹⁵ CBT can help patients understand that distorted thoughts lead to their sad or anxious moods.

Instructing patients to keep thought diaries can help them identify irrational fears and use cognitive restructuring to correct their faulty schemas. Tailor your cognitive therapy techniques to target the patient’s level of insight at the time of therapy.

Effective behavioral techniques may include setting limits on doctor visits, checking behaviors, reassurance seeking, etc. Repeated exposure to feared stimuli such as needles, white lab coats, blood pressure cuffs, medical dialogue, or hospital wards can help the patient habituate to the anxiety.

Relaxation techniques, a healthy diet, and exercise are also useful. Relaxation exercises—such as diaphragmatic breathing, progressive muscle relaxation, and visual imagery—may help patients manage anxiety by reducing CNS and autonomic nervous system arousal.

Bottom line

Hypochondriasis’ cognitive dysfunction is treatable, once an accurate diagnosis is made. Using a checklist can help you differentiate hypochondriasis from other medical and psychiatric disorders. A trusting doctor-patient relationship enhances outcome.

Related resources

• Fallon BA., Feinstein SB. Hypochondriasis: clinical, theoretical, and therapeutic aspects. In: Oldham J (ed). Review of psychiatry (vol. 20) Washington, DC: American Psychiatric Press, 2001:27-60.
• Cantor C, Fallon BA. Phantom illness: shattering the myth of hypochondria Boston: Houghton Mifflin Company, 1996.
• Starcevic V, Lipsitt DR (eds). Hypochondriasis: modern perspectives on an ancient malady New York: Oxford University Press, 2001.

Drug brand names

• Fluoxetine • Prozac
• Fluvoxamine • Luvox
• Nefazodone • Serzone
• Paroxetine • Paxil

A hypochondria “checklist” can help you sort through many overlapping medical and psychiatric disorders and increase your chances of making an accurate diagnosis. Then—by addressing hypochondria’s cognitive dysfunction—you can help patients achieve partial or full remission and change their distressing behaviors.

We offer a checklist that is useful in our practice and suggest behavioral therapies and medications that can help calm these patients’ excessive, unwarranted fears.

WORKING AS A TEAM

Ideal approach. Because hypochondriasis has features of medical and mental illness, working with the patient’s primary care physician is ideal. Physicians often consider these patients difficult because they demand a lot of time, support, and reassurance. Together, you can:

• offer the patient a healthy level of compassion and empathy to establish a positive therapeutic alliance
• set appropriate time limits and guidelines for the patient’s care
• dissuade patients from “doctor shopping”
• set limits on how often patients may visit their doctors and request reassurance.

Box

Hypochondriasis: Persistent, unwarranted distress

For example, you may indicate to the patient, “I will reassure you only at office visits (not by phone), the office visits will be limited to once a month, and during each visit I will reassure you no more than once.”

A doctor-patient relationship based on mutual trust and respect is vital when you treat a patient with hypochondriasis. You can help primary care physicians provide more empathic treatment by explaining that patients do not feign or desire this distressing condition.

DIAGNOSTIC FEATURES

Patients with hypochondriasis tend to be hyper-vigilant about normal physiologic fluctuations and bodily sensations, often misinterpreting them as life-threatening or serious enough to require immediate medical attention. This excessive focus on benign symptoms (such as an accelerated heart rate, sweating, or a bump on the skin) and the cognitive distortion of their significance result in increased anxiety, bodily checking, and doctor visits (Box).^1-4

Presentations. Hypochondriasis has three common presentations: disease conviction, disease fear, and bodily preoccupation (Table 1).⁵ Psychiatrists are most likely to see disease fear, as patients with this predominant symptom tend to realize that fear plays too prominent a role in their lives. Physicians in medical practice are more likely to encounter patients with high levels of disease conviction or somatic preoccupation.

Psychiatric comorbidity. Hypochondriasis is highly comorbid with Axis I and Axis II disorders, which complicate treatment. Nearly one-half of patients with hypochondriasis also have dysthymia (45%) or major depression (43%). Other comorbidities include phobias (38%), somatization disorder (21%), panic disorder (17%), and obsessive-compulsive disorder (8%).⁶ Patients with hypochondriasis are three times more likely than the general population to have personality disorders;^6,7 the prognosis is believed to be more promising for patients without personality disorders.

Distinguishing between primary and secondary hypochondriasis is important. Treating a primary psychiatric disorder often alleviates the symptoms of secondary hypochondriasis, particularly when hypochondriasis masks depression.

HYPOCHONDRIASIS CHECKLIST

Underlying medical disorder? Before diagnosing hypochondriasis, review the medical workup for underlying disease or illness. Medical conditions sometimes go undetected when physicians assume that complaints are an expression of longstanding hypochondriasis.

Table 1

Three common presentations of hypochondriasis

Sometimes a patient may become anxious when mild or vague signs and symptoms do not yet meet established diagnostic criteria for a medical disorder. An effective approach is to provide ongoing support, avoid excessive diagnostic tests, and help the patient make the best use of his or her functional capacities while living with uncertainty.

Functional somatic syndrome? Fibromyalgia and chronic fatigue syndrome do not represent hypochondriasis,⁸ although they may be exacerbated by comorbid psychiatric disorders. Both disorders have diagnostic criteria and specified courses and have been studied to identify psychiatric comorbidity.

Transient or sustained? After it is clear that the patient is not suffering from a medical problem, determine whether hypochondriasis is transient or fully diagnostic:

• If transient, the patient may only need to be educated about how overattention may amplify symptoms; reassure him or her that a full medical workup has been negative.
• If fully diagnostic, reassurance may work for only a few days or weeks; the return of the fear or conviction helps establish the diagnosis.

Somatoform disorder? Distinguish hypochondriasis from other somatoform disorders (Table 2). In practice, the terms “hypochondriac” and “somatizer” are commonly used interchangeably, but the distinction needs to be clear. Hypochondriasis is primarily a disorder of abnormal cognition, in which symptom meaning is of greatest concern. Somatization is primarily a disorder of abnormal sensation, in which the symptoms themselves are the overwhelming focus of attention.

Anxiety disorder? Patients with generalized anxiety disorder may worry about illness, but they also worry about other life issues. Patients with panic disorder may have intense hypochondriacal concerns (such as having a heart attack), but these worries tend to be related to panic symptoms and resolve when the panic disorder is treated.

Obsessive compulsive disorder? Like obsessive-compulsive disorder (OCD), hypochondriasis is characterized by recurrent intrusive thoughts that create heightened anxiety and distress. To relieve their anxiety, patients with hypochondriasis engage in compulsions, such as:

• undergoing extensive medical tests
• seeking habitual reassurance from doctors and family
• consulting medical literature
• performing repeated body checks for perceived lumps or bumps
• avoiding activities that trigger their health-related stress.⁹

Table 2

How to distinguish somatoform disorders

OCD and hypochondriasis also may share the diagnostic feature of pathologic doubt; patients’ uncertainty in appraising a situation leads to additional checking and reassurance-seeking behaviors. The immediate relief gained by these compulsions reinforces the patient’s urge to engage in more maladaptive behaviors and sends a stronger message to the brain that these behaviors are needed to prevent harm.

Ironically, the emergence of a real medical ailment—despite hypochondriacal worry—may force the patient to re-evaluate the usefulness of behaviors motivated by trying to avoid harm. A hypochondriacal patient who was diagnosed with optic neuritis and possible multiple sclerosis recently said to these authors, “I had always thought that by being vigilant I could keep illnesses away. Now I know that’s not true.”

Although hypochondriasis and OCD have similarities, certain clinical distinctions exist. Patients with hypochondriasis worry about having an illness, whereas OCD patients with somatic obsessions fear developing or transmitting an illness. A hypochondriacal patient might fear having AIDS or cancer despite reassurance from doctors, while an OCD patient more typically would fear contracting or transmitting the disease (a contamination obsession) and would engage in excessive behaviors to reduce the risk of developing the disease.

Depressive disorder? Unlike the anxious-worrying version of hypochondriasis, the depressive version is more fatalistic. Patients may be convinced they are dying of a dreaded disease, often believing it to be punishment for an indiscretion, such as marital infidelity. Or they may suddenly become hypochondriacal with mild depressive features, unaware that the actual problem is unresolved bereavement (hypochondriasis with secondary depression). The appropriate diagnosis is primary depressive disorder with secondary hypochondriacal features when depression dominates the presentation and preceded the illness fears.

Table 3

Recommended dosages for treating primary hypochondriasis

Delusional disorder? To distinguish hypochondriasis from delusional disorder (somatic type), consider the patient’s pattern of insight:

• Hypochondriacal patients often vacillate between poor and excellent insight, depending on their distress level.¹⁰ They may acknowledge the irrationality of their fears, then later be convinced they have a disease.
• Patients with delusional disorder are convinced they have a serious health threat, despite the absence of medical confirmation. These patients are considered to have a primary psychotic disorder that requires antipsychotic treatment.

TREATING PRIMARY SYMPTOMS

Drug therapy. When hypochondriasis is secondary—such as to depression or panic disorder—treat the primary condition first.^11,12 For primary hypochondriasis, selective serotonin reuptake inhibitors (SSRIs) such as fluoxetine, paroxetine, or fluvoxamine have shown benefit, mostly in open-label studies. An uncontrolled case series suggests that nefazodone—with mixed serotonin reuptake inhibition and agonist properties—also may help patients with hypochondriasis.¹³ In the only published controlled study, fluoxetine was more effective than placebo for treating hypochondriasis.¹⁰

Continue drug therapy, when used, for at least 8 weeks, with each dosage maintained for at least 4 weeks. If patients do not respond to lower SSRI dosages, increase to the higher dosages reported to be more effective for OCD (Table 3).¹⁴

Except for primary illness phobia, hypochondriasis has not been shown to respond to tricyclics, benzodiazepines, or dopaminergic blockers. In our experience, electroconvulsive therapy—although inadequately studied—may help treat patients with severe, treatment-refractory hypochondriasis with marked somatization.

Psychotherapy. Cognitive-behavioral therapy (CBT)—challenging patients’ irrational fears about illness and teaching them problem-solving tools—is effective in treating hypochondriasis.¹⁵ CBT can help patients understand that distorted thoughts lead to their sad or anxious moods.

Instructing patients to keep thought diaries can help them identify irrational fears and use cognitive restructuring to correct their faulty schemas. Tailor your cognitive therapy techniques to target the patient’s level of insight at the time of therapy.

Effective behavioral techniques may include setting limits on doctor visits, checking behaviors, reassurance seeking, etc. Repeated exposure to feared stimuli such as needles, white lab coats, blood pressure cuffs, medical dialogue, or hospital wards can help the patient habituate to the anxiety.

Relaxation techniques, a healthy diet, and exercise are also useful. Relaxation exercises—such as diaphragmatic breathing, progressive muscle relaxation, and visual imagery—may help patients manage anxiety by reducing CNS and autonomic nervous system arousal.

Bottom line

Hypochondriasis’ cognitive dysfunction is treatable, once an accurate diagnosis is made. Using a checklist can help you differentiate hypochondriasis from other medical and psychiatric disorders. A trusting doctor-patient relationship enhances outcome.

Related resources

• Fallon BA., Feinstein SB. Hypochondriasis: clinical, theoretical, and therapeutic aspects. In: Oldham J (ed). Review of psychiatry (vol. 20) Washington, DC: American Psychiatric Press, 2001:27-60.
• Cantor C, Fallon BA. Phantom illness: shattering the myth of hypochondria Boston: Houghton Mifflin Company, 1996.
• Starcevic V, Lipsitt DR (eds). Hypochondriasis: modern perspectives on an ancient malady New York: Oxford University Press, 2001.

Drug brand names

• Fluoxetine • Prozac
• Fluvoxamine • Luvox
• Nefazodone • Serzone
• Paroxetine • Paxil

A hypochondria “checklist” can help you sort through many overlapping medical and psychiatric disorders and increase your chances of making an accurate diagnosis. Then—by addressing hypochondria’s cognitive dysfunction—you can help patients achieve partial or full remission and change their distressing behaviors.

We offer a checklist that is useful in our practice and suggest behavioral therapies and medications that can help calm these patients’ excessive, unwarranted fears.

WORKING AS A TEAM

Ideal approach. Because hypochondriasis has features of medical and mental illness, working with the patient’s primary care physician is ideal. Physicians often consider these patients difficult because they demand a lot of time, support, and reassurance. Together, you can:

• offer the patient a healthy level of compassion and empathy to establish a positive therapeutic alliance
• set appropriate time limits and guidelines for the patient’s care
• dissuade patients from “doctor shopping”
• set limits on how often patients may visit their doctors and request reassurance.

Box

Hypochondriasis: Persistent, unwarranted distress

For example, you may indicate to the patient, “I will reassure you only at office visits (not by phone), the office visits will be limited to once a month, and during each visit I will reassure you no more than once.”

A doctor-patient relationship based on mutual trust and respect is vital when you treat a patient with hypochondriasis. You can help primary care physicians provide more empathic treatment by explaining that patients do not feign or desire this distressing condition.

DIAGNOSTIC FEATURES

Patients with hypochondriasis tend to be hyper-vigilant about normal physiologic fluctuations and bodily sensations, often misinterpreting them as life-threatening or serious enough to require immediate medical attention. This excessive focus on benign symptoms (such as an accelerated heart rate, sweating, or a bump on the skin) and the cognitive distortion of their significance result in increased anxiety, bodily checking, and doctor visits (Box).^1-4

Presentations. Hypochondriasis has three common presentations: disease conviction, disease fear, and bodily preoccupation (Table 1).⁵ Psychiatrists are most likely to see disease fear, as patients with this predominant symptom tend to realize that fear plays too prominent a role in their lives. Physicians in medical practice are more likely to encounter patients with high levels of disease conviction or somatic preoccupation.

Psychiatric comorbidity. Hypochondriasis is highly comorbid with Axis I and Axis II disorders, which complicate treatment. Nearly one-half of patients with hypochondriasis also have dysthymia (45%) or major depression (43%). Other comorbidities include phobias (38%), somatization disorder (21%), panic disorder (17%), and obsessive-compulsive disorder (8%).⁶ Patients with hypochondriasis are three times more likely than the general population to have personality disorders;^6,7 the prognosis is believed to be more promising for patients without personality disorders.

Distinguishing between primary and secondary hypochondriasis is important. Treating a primary psychiatric disorder often alleviates the symptoms of secondary hypochondriasis, particularly when hypochondriasis masks depression.

HYPOCHONDRIASIS CHECKLIST

Underlying medical disorder? Before diagnosing hypochondriasis, review the medical workup for underlying disease or illness. Medical conditions sometimes go undetected when physicians assume that complaints are an expression of longstanding hypochondriasis.

Table 1

Three common presentations of hypochondriasis

Sometimes a patient may become anxious when mild or vague signs and symptoms do not yet meet established diagnostic criteria for a medical disorder. An effective approach is to provide ongoing support, avoid excessive diagnostic tests, and help the patient make the best use of his or her functional capacities while living with uncertainty.

Functional somatic syndrome? Fibromyalgia and chronic fatigue syndrome do not represent hypochondriasis,⁸ although they may be exacerbated by comorbid psychiatric disorders. Both disorders have diagnostic criteria and specified courses and have been studied to identify psychiatric comorbidity.

Transient or sustained? After it is clear that the patient is not suffering from a medical problem, determine whether hypochondriasis is transient or fully diagnostic:

• If transient, the patient may only need to be educated about how overattention may amplify symptoms; reassure him or her that a full medical workup has been negative.
• If fully diagnostic, reassurance may work for only a few days or weeks; the return of the fear or conviction helps establish the diagnosis.

Somatoform disorder? Distinguish hypochondriasis from other somatoform disorders (Table 2). In practice, the terms “hypochondriac” and “somatizer” are commonly used interchangeably, but the distinction needs to be clear. Hypochondriasis is primarily a disorder of abnormal cognition, in which symptom meaning is of greatest concern. Somatization is primarily a disorder of abnormal sensation, in which the symptoms themselves are the overwhelming focus of attention.

Anxiety disorder? Patients with generalized anxiety disorder may worry about illness, but they also worry about other life issues. Patients with panic disorder may have intense hypochondriacal concerns (such as having a heart attack), but these worries tend to be related to panic symptoms and resolve when the panic disorder is treated.

Obsessive compulsive disorder? Like obsessive-compulsive disorder (OCD), hypochondriasis is characterized by recurrent intrusive thoughts that create heightened anxiety and distress. To relieve their anxiety, patients with hypochondriasis engage in compulsions, such as:

• undergoing extensive medical tests
• seeking habitual reassurance from doctors and family
• consulting medical literature
• performing repeated body checks for perceived lumps or bumps
• avoiding activities that trigger their health-related stress.⁹

Table 2

How to distinguish somatoform disorders

OCD and hypochondriasis also may share the diagnostic feature of pathologic doubt; patients’ uncertainty in appraising a situation leads to additional checking and reassurance-seeking behaviors. The immediate relief gained by these compulsions reinforces the patient’s urge to engage in more maladaptive behaviors and sends a stronger message to the brain that these behaviors are needed to prevent harm.

Ironically, the emergence of a real medical ailment—despite hypochondriacal worry—may force the patient to re-evaluate the usefulness of behaviors motivated by trying to avoid harm. A hypochondriacal patient who was diagnosed with optic neuritis and possible multiple sclerosis recently said to these authors, “I had always thought that by being vigilant I could keep illnesses away. Now I know that’s not true.”

Although hypochondriasis and OCD have similarities, certain clinical distinctions exist. Patients with hypochondriasis worry about having an illness, whereas OCD patients with somatic obsessions fear developing or transmitting an illness. A hypochondriacal patient might fear having AIDS or cancer despite reassurance from doctors, while an OCD patient more typically would fear contracting or transmitting the disease (a contamination obsession) and would engage in excessive behaviors to reduce the risk of developing the disease.

Depressive disorder? Unlike the anxious-worrying version of hypochondriasis, the depressive version is more fatalistic. Patients may be convinced they are dying of a dreaded disease, often believing it to be punishment for an indiscretion, such as marital infidelity. Or they may suddenly become hypochondriacal with mild depressive features, unaware that the actual problem is unresolved bereavement (hypochondriasis with secondary depression). The appropriate diagnosis is primary depressive disorder with secondary hypochondriacal features when depression dominates the presentation and preceded the illness fears.

Table 3

Recommended dosages for treating primary hypochondriasis

Delusional disorder? To distinguish hypochondriasis from delusional disorder (somatic type), consider the patient’s pattern of insight:

• Hypochondriacal patients often vacillate between poor and excellent insight, depending on their distress level.¹⁰ They may acknowledge the irrationality of their fears, then later be convinced they have a disease.
• Patients with delusional disorder are convinced they have a serious health threat, despite the absence of medical confirmation. These patients are considered to have a primary psychotic disorder that requires antipsychotic treatment.

TREATING PRIMARY SYMPTOMS

Drug therapy. When hypochondriasis is secondary—such as to depression or panic disorder—treat the primary condition first.^11,12 For primary hypochondriasis, selective serotonin reuptake inhibitors (SSRIs) such as fluoxetine, paroxetine, or fluvoxamine have shown benefit, mostly in open-label studies. An uncontrolled case series suggests that nefazodone—with mixed serotonin reuptake inhibition and agonist properties—also may help patients with hypochondriasis.¹³ In the only published controlled study, fluoxetine was more effective than placebo for treating hypochondriasis.¹⁰

Continue drug therapy, when used, for at least 8 weeks, with each dosage maintained for at least 4 weeks. If patients do not respond to lower SSRI dosages, increase to the higher dosages reported to be more effective for OCD (Table 3).¹⁴

Except for primary illness phobia, hypochondriasis has not been shown to respond to tricyclics, benzodiazepines, or dopaminergic blockers. In our experience, electroconvulsive therapy—although inadequately studied—may help treat patients with severe, treatment-refractory hypochondriasis with marked somatization.

Psychotherapy. Cognitive-behavioral therapy (CBT)—challenging patients’ irrational fears about illness and teaching them problem-solving tools—is effective in treating hypochondriasis.¹⁵ CBT can help patients understand that distorted thoughts lead to their sad or anxious moods.

Instructing patients to keep thought diaries can help them identify irrational fears and use cognitive restructuring to correct their faulty schemas. Tailor your cognitive therapy techniques to target the patient’s level of insight at the time of therapy.

Effective behavioral techniques may include setting limits on doctor visits, checking behaviors, reassurance seeking, etc. Repeated exposure to feared stimuli such as needles, white lab coats, blood pressure cuffs, medical dialogue, or hospital wards can help the patient habituate to the anxiety.

Relaxation techniques, a healthy diet, and exercise are also useful. Relaxation exercises—such as diaphragmatic breathing, progressive muscle relaxation, and visual imagery—may help patients manage anxiety by reducing CNS and autonomic nervous system arousal.

Bottom line

Hypochondriasis’ cognitive dysfunction is treatable, once an accurate diagnosis is made. Using a checklist can help you differentiate hypochondriasis from other medical and psychiatric disorders. A trusting doctor-patient relationship enhances outcome.

Related resources

• Fallon BA., Feinstein SB. Hypochondriasis: clinical, theoretical, and therapeutic aspects. In: Oldham J (ed). Review of psychiatry (vol. 20) Washington, DC: American Psychiatric Press, 2001:27-60.
• Cantor C, Fallon BA. Phantom illness: shattering the myth of hypochondria Boston: Houghton Mifflin Company, 1996.
• Starcevic V, Lipsitt DR (eds). Hypochondriasis: modern perspectives on an ancient malady New York: Oxford University Press, 2001.

Drug brand names

• Fluoxetine • Prozac
• Fluvoxamine • Luvox
• Nefazodone • Serzone
• Paroxetine • Paxil

Existing drug treatments for narcolepsy enhance daytime alertness, and most improve cataplexy, sleep paralysis, and hypnagogic/hypnopompic hallucinations. None of these agents, however, target the nocturnal sleep deficits that lead to daytime symptoms.

Sodium oxybate, one of the most controversial medications to receive FDA approval in recent years (Table 1), has been found to reduce daytime sleepiness and cataplexy by improving nighttime sleep in patients with narcolepsy.

ABOUT SODIUM OXYBATE

Sodium oxybate is also known as gamma-hydroxybutyrate (GHB). An illegal form of GHB—the so-called “date rape drug”—is produced and used illicitly, typically at parties and nightclubs. Some users hide the fast-acting, sedating drug in a cocktail, rendering victims unable to defend against an assault or to recall details leading to the assault.¹

Some athletes believe GHB enhances on-field performance by increasing production of growth hormone. Enhanced growth hormone release has no known clinical significance or effect on athletic performance, however.

Table 1

Sodium oxybate: Fast facts

The U.S. Drug Enforcement Agency (DEA) considers GHB a Schedule 1 (illegal) drug. DEA considers the prescription version a Schedule 3 drug, meaning it can be prescribed with refills as long as a DEA number is listed on the prescription. To prevent misuse, a central pharmacy dispenses sodium oxybate and mandates use of a specific prescription form to verify the physician’s familiarity with the medication. Psychiatrists can call (866) 997-3688 to obtain the form.

Table 2

Sodium oxybate dosing recommendations for patients

Sodium oxybate is the only agent FDA-approved for treating cataplexy—muscle weakness common among patients with narcolepsy.

HOW IT WORKS

Developed as an anesthetic, sodium oxybate induces deep sleep and at higher doses causes amnesia.

Derived from gamma-aminobutyric acid (GABA), sodium oxybate’s mechanism of action is unknown. Some believe it binds to the GABA B receptor and partially inhibits the NMDA and AMPA receptor-mediated excitatory neurons in the hippocampus.²

Food alters its bioavailability, so sodium oxybate should be taken several hours after meals to prevent delays in absorption and effect. Patients taking it should not eat at bedtime.

The agent’s pharmacokinetics are nonlinear, meaning that if the dose is doubled, the medication effect is tripled or quadrupled. For this reason, dosage increases must be small (no more than 0.75 grams for each dose) and gradual (at intervals of at least 2 weeks). The medication reaches peak plasma concentration within 30 to 75 minutes, so patients should not take the medication until they are in bed. Its 1-hour half-life explains its brief duration of action and need for repeat dosing overnight (Table 2).

Sodium oxybate does not modify the activity of any cytochrome P-450 enzymes. The medication is high in sodium (0.5 grams in a 3-gram dose) and has a salty taste. Use caution when considering the agent for patients with hypertension or on low-sodium diets.

Sodium oxybate’s safety has not been adequately tested in patients younger than 18 or older than 65 or in those with dementia and other disease processes. Because the drug is metabolized by the liver, the manufacturer recommends prescribing one-half the starting dosage to patients with significant hepatic impairment.

EFFICACY

Sodium oxybate has been shown to indirectly reduce frequency of cataplexy by improving nocturnal sleep:

• In a placebo-controlled, 4-week trial, 136 patients received either placebo or sodium oxybate at bedtime and again overnight in two equally divided doses of 3, 6, or 9 grams each. Patients who received the medication experienced less-frequent cataplexy, reduced daytime sleepiness, and fewer unplanned daytime naps and nocturnal awakenings.³
• A placebo-controlled trial that followed 55 patients for more than 3 years demonstrated long-term efficacy based on the patients’ cataplexy diaries (mean duration of treatment 21 months). Cataplexy returned after abrupt discontinuation.⁴

Unlike patients with most other disorders, those with narcolepsy generally are willing to repeat a medication overnight. They awaken easily at night—often without an alarm. Patients taking the medication report that they fall asleep again more readily and experience dramatically improved sleep quality and duration.

TOLERABILITY

Sodium oxybate has been well tolerated in relatively small clinical trials.

In the 4-week, placebo-controlled trial,³ nausea, headache, dizziness, and enuresis were most frequently reported. Out of 136 participants, 1 withdrew because of acute confusion and 9 others left because of mild to moderate adverse events. Twelve others experienced one episode of enuresis—probably because they did not fully awaken from deep sleep when developing urinary urgency. Advise patients taking sodium oxybate to urinate before going to bed.

The medication’s propensity to increase slow-wave sleep may cause sleepwalking. Sleepwalking was reported in 32% of patients in one long-term, uncontrolled study.⁵ If a patient with a history of sleepwalking needs sodium oxybate, advise against sleeping in upper bunks and other dangerous settings, and recommend precautions such as locking doors.

Because of sodium oxybate’s sedating properties, concomitant use of alcohol, barbiturates, and benzodiazepines should be discouraged.

ABUSE POTENTIAL

As discussed, GHB has a high abuse potential with effects such as euphoria, relaxation, and heightened sexual feelings.

Tolerance and dependence has not been reported with sodium oxybate when used as prescribed. A withdrawal state—similar to alcohol and sedative/hypnotic withdrawal and marked by anxiety, tremor, agitation, and delirium—has been reported with GHB abuse (although other chemicals often are used simultaneously in such cases). Narcolepsy patients in clinical trials have abruptly discontinued sodium oxybate after months of use without significant withdrawal.⁴

Related resources

• Narcolepsy Network Inc. www.narcolepsynetwork.org

Disclosure

Dr. Krahn reports no financial relationship with Orphan Medical or with manufacturers of competing products.

Existing drug treatments for narcolepsy enhance daytime alertness, and most improve cataplexy, sleep paralysis, and hypnagogic/hypnopompic hallucinations. None of these agents, however, target the nocturnal sleep deficits that lead to daytime symptoms.

Sodium oxybate, one of the most controversial medications to receive FDA approval in recent years (Table 1), has been found to reduce daytime sleepiness and cataplexy by improving nighttime sleep in patients with narcolepsy.

ABOUT SODIUM OXYBATE

Sodium oxybate is also known as gamma-hydroxybutyrate (GHB). An illegal form of GHB—the so-called “date rape drug”—is produced and used illicitly, typically at parties and nightclubs. Some users hide the fast-acting, sedating drug in a cocktail, rendering victims unable to defend against an assault or to recall details leading to the assault.¹

Some athletes believe GHB enhances on-field performance by increasing production of growth hormone. Enhanced growth hormone release has no known clinical significance or effect on athletic performance, however.

Table 1

Sodium oxybate: Fast facts

The U.S. Drug Enforcement Agency (DEA) considers GHB a Schedule 1 (illegal) drug. DEA considers the prescription version a Schedule 3 drug, meaning it can be prescribed with refills as long as a DEA number is listed on the prescription. To prevent misuse, a central pharmacy dispenses sodium oxybate and mandates use of a specific prescription form to verify the physician’s familiarity with the medication. Psychiatrists can call (866) 997-3688 to obtain the form.

Table 2

Sodium oxybate dosing recommendations for patients

Sodium oxybate is the only agent FDA-approved for treating cataplexy—muscle weakness common among patients with narcolepsy.

HOW IT WORKS

Developed as an anesthetic, sodium oxybate induces deep sleep and at higher doses causes amnesia.

Derived from gamma-aminobutyric acid (GABA), sodium oxybate’s mechanism of action is unknown. Some believe it binds to the GABA B receptor and partially inhibits the NMDA and AMPA receptor-mediated excitatory neurons in the hippocampus.²

Food alters its bioavailability, so sodium oxybate should be taken several hours after meals to prevent delays in absorption and effect. Patients taking it should not eat at bedtime.

The agent’s pharmacokinetics are nonlinear, meaning that if the dose is doubled, the medication effect is tripled or quadrupled. For this reason, dosage increases must be small (no more than 0.75 grams for each dose) and gradual (at intervals of at least 2 weeks). The medication reaches peak plasma concentration within 30 to 75 minutes, so patients should not take the medication until they are in bed. Its 1-hour half-life explains its brief duration of action and need for repeat dosing overnight (Table 2).

Sodium oxybate does not modify the activity of any cytochrome P-450 enzymes. The medication is high in sodium (0.5 grams in a 3-gram dose) and has a salty taste. Use caution when considering the agent for patients with hypertension or on low-sodium diets.

Sodium oxybate’s safety has not been adequately tested in patients younger than 18 or older than 65 or in those with dementia and other disease processes. Because the drug is metabolized by the liver, the manufacturer recommends prescribing one-half the starting dosage to patients with significant hepatic impairment.

EFFICACY

Sodium oxybate has been shown to indirectly reduce frequency of cataplexy by improving nocturnal sleep:

• In a placebo-controlled, 4-week trial, 136 patients received either placebo or sodium oxybate at bedtime and again overnight in two equally divided doses of 3, 6, or 9 grams each. Patients who received the medication experienced less-frequent cataplexy, reduced daytime sleepiness, and fewer unplanned daytime naps and nocturnal awakenings.³
• A placebo-controlled trial that followed 55 patients for more than 3 years demonstrated long-term efficacy based on the patients’ cataplexy diaries (mean duration of treatment 21 months). Cataplexy returned after abrupt discontinuation.⁴

Unlike patients with most other disorders, those with narcolepsy generally are willing to repeat a medication overnight. They awaken easily at night—often without an alarm. Patients taking the medication report that they fall asleep again more readily and experience dramatically improved sleep quality and duration.

TOLERABILITY

Sodium oxybate has been well tolerated in relatively small clinical trials.

In the 4-week, placebo-controlled trial,³ nausea, headache, dizziness, and enuresis were most frequently reported. Out of 136 participants, 1 withdrew because of acute confusion and 9 others left because of mild to moderate adverse events. Twelve others experienced one episode of enuresis—probably because they did not fully awaken from deep sleep when developing urinary urgency. Advise patients taking sodium oxybate to urinate before going to bed.

The medication’s propensity to increase slow-wave sleep may cause sleepwalking. Sleepwalking was reported in 32% of patients in one long-term, uncontrolled study.⁵ If a patient with a history of sleepwalking needs sodium oxybate, advise against sleeping in upper bunks and other dangerous settings, and recommend precautions such as locking doors.

Because of sodium oxybate’s sedating properties, concomitant use of alcohol, barbiturates, and benzodiazepines should be discouraged.

ABUSE POTENTIAL

As discussed, GHB has a high abuse potential with effects such as euphoria, relaxation, and heightened sexual feelings.

Tolerance and dependence has not been reported with sodium oxybate when used as prescribed. A withdrawal state—similar to alcohol and sedative/hypnotic withdrawal and marked by anxiety, tremor, agitation, and delirium—has been reported with GHB abuse (although other chemicals often are used simultaneously in such cases). Narcolepsy patients in clinical trials have abruptly discontinued sodium oxybate after months of use without significant withdrawal.⁴

Related resources

• Narcolepsy Network Inc. www.narcolepsynetwork.org

Disclosure

Dr. Krahn reports no financial relationship with Orphan Medical or with manufacturers of competing products.

Existing drug treatments for narcolepsy enhance daytime alertness, and most improve cataplexy, sleep paralysis, and hypnagogic/hypnopompic hallucinations. None of these agents, however, target the nocturnal sleep deficits that lead to daytime symptoms.

Sodium oxybate, one of the most controversial medications to receive FDA approval in recent years (Table 1), has been found to reduce daytime sleepiness and cataplexy by improving nighttime sleep in patients with narcolepsy.

ABOUT SODIUM OXYBATE

Sodium oxybate is also known as gamma-hydroxybutyrate (GHB). An illegal form of GHB—the so-called “date rape drug”—is produced and used illicitly, typically at parties and nightclubs. Some users hide the fast-acting, sedating drug in a cocktail, rendering victims unable to defend against an assault or to recall details leading to the assault.¹

Some athletes believe GHB enhances on-field performance by increasing production of growth hormone. Enhanced growth hormone release has no known clinical significance or effect on athletic performance, however.

Table 1

Sodium oxybate: Fast facts

The U.S. Drug Enforcement Agency (DEA) considers GHB a Schedule 1 (illegal) drug. DEA considers the prescription version a Schedule 3 drug, meaning it can be prescribed with refills as long as a DEA number is listed on the prescription. To prevent misuse, a central pharmacy dispenses sodium oxybate and mandates use of a specific prescription form to verify the physician’s familiarity with the medication. Psychiatrists can call (866) 997-3688 to obtain the form.

Table 2

Sodium oxybate dosing recommendations for patients

Sodium oxybate is the only agent FDA-approved for treating cataplexy—muscle weakness common among patients with narcolepsy.

HOW IT WORKS

Developed as an anesthetic, sodium oxybate induces deep sleep and at higher doses causes amnesia.

Derived from gamma-aminobutyric acid (GABA), sodium oxybate’s mechanism of action is unknown. Some believe it binds to the GABA B receptor and partially inhibits the NMDA and AMPA receptor-mediated excitatory neurons in the hippocampus.²

Food alters its bioavailability, so sodium oxybate should be taken several hours after meals to prevent delays in absorption and effect. Patients taking it should not eat at bedtime.

The agent’s pharmacokinetics are nonlinear, meaning that if the dose is doubled, the medication effect is tripled or quadrupled. For this reason, dosage increases must be small (no more than 0.75 grams for each dose) and gradual (at intervals of at least 2 weeks). The medication reaches peak plasma concentration within 30 to 75 minutes, so patients should not take the medication until they are in bed. Its 1-hour half-life explains its brief duration of action and need for repeat dosing overnight (Table 2).

Sodium oxybate does not modify the activity of any cytochrome P-450 enzymes. The medication is high in sodium (0.5 grams in a 3-gram dose) and has a salty taste. Use caution when considering the agent for patients with hypertension or on low-sodium diets.

Sodium oxybate’s safety has not been adequately tested in patients younger than 18 or older than 65 or in those with dementia and other disease processes. Because the drug is metabolized by the liver, the manufacturer recommends prescribing one-half the starting dosage to patients with significant hepatic impairment.

EFFICACY

Sodium oxybate has been shown to indirectly reduce frequency of cataplexy by improving nocturnal sleep:

• In a placebo-controlled, 4-week trial, 136 patients received either placebo or sodium oxybate at bedtime and again overnight in two equally divided doses of 3, 6, or 9 grams each. Patients who received the medication experienced less-frequent cataplexy, reduced daytime sleepiness, and fewer unplanned daytime naps and nocturnal awakenings.³
• A placebo-controlled trial that followed 55 patients for more than 3 years demonstrated long-term efficacy based on the patients’ cataplexy diaries (mean duration of treatment 21 months). Cataplexy returned after abrupt discontinuation.⁴

Unlike patients with most other disorders, those with narcolepsy generally are willing to repeat a medication overnight. They awaken easily at night—often without an alarm. Patients taking the medication report that they fall asleep again more readily and experience dramatically improved sleep quality and duration.

TOLERABILITY

Sodium oxybate has been well tolerated in relatively small clinical trials.

In the 4-week, placebo-controlled trial,³ nausea, headache, dizziness, and enuresis were most frequently reported. Out of 136 participants, 1 withdrew because of acute confusion and 9 others left because of mild to moderate adverse events. Twelve others experienced one episode of enuresis—probably because they did not fully awaken from deep sleep when developing urinary urgency. Advise patients taking sodium oxybate to urinate before going to bed.

The medication’s propensity to increase slow-wave sleep may cause sleepwalking. Sleepwalking was reported in 32% of patients in one long-term, uncontrolled study.⁵ If a patient with a history of sleepwalking needs sodium oxybate, advise against sleeping in upper bunks and other dangerous settings, and recommend precautions such as locking doors.

Because of sodium oxybate’s sedating properties, concomitant use of alcohol, barbiturates, and benzodiazepines should be discouraged.

ABUSE POTENTIAL

As discussed, GHB has a high abuse potential with effects such as euphoria, relaxation, and heightened sexual feelings.

Tolerance and dependence has not been reported with sodium oxybate when used as prescribed. A withdrawal state—similar to alcohol and sedative/hypnotic withdrawal and marked by anxiety, tremor, agitation, and delirium—has been reported with GHB abuse (although other chemicals often are used simultaneously in such cases). Narcolepsy patients in clinical trials have abruptly discontinued sodium oxybate after months of use without significant withdrawal.⁴

Related resources

• Narcolepsy Network Inc. www.narcolepsynetwork.org

Disclosure

Dr. Krahn reports no financial relationship with Orphan Medical or with manufacturers of competing products.

Supplement Editor:
Roger M. Mills, MD

Contents

Beyond drugs alone: Pacing, ablation, and surgery for atrial fibrillation
R.M. Mills, MD, MPH

Basic mechanisms of atrial fibrillation
D.R. Van Wagoner, PhD

Current clinical issues in atrial fibrillation
M.K. Chung, MD

Approaches to restoring and maintaining normal sinus rhythm
I. Pharmacologic management: Often insufficient, but still first-line
D.O. Martin, MD, MPH

II. Pacing and devices: Progress toward a preventive role
W. Saliba, MD

III. Surgical approaches: At the 'tipping point'
P.M. McCarthy, MD, and A.M. Gillinov, MD

IV. Catheter ablation: A less invasive path to potential cure
W. Belden, MD; N.F. Marrouche, MD; and A. Natale, MD

Managing chronic atrial fibrillation: Strategies to control symptoms and prevent embolism
D.O. Martin, MD, MPH

Supplement Editor:
Roger M. Mills, MD

Contents

Beyond drugs alone: Pacing, ablation, and surgery for atrial fibrillation
R.M. Mills, MD, MPH

Basic mechanisms of atrial fibrillation
D.R. Van Wagoner, PhD

Current clinical issues in atrial fibrillation
M.K. Chung, MD

Approaches to restoring and maintaining normal sinus rhythm
I. Pharmacologic management: Often insufficient, but still first-line
D.O. Martin, MD, MPH

II. Pacing and devices: Progress toward a preventive role
W. Saliba, MD

III. Surgical approaches: At the 'tipping point'
P.M. McCarthy, MD, and A.M. Gillinov, MD

IV. Catheter ablation: A less invasive path to potential cure
W. Belden, MD; N.F. Marrouche, MD; and A. Natale, MD

Managing chronic atrial fibrillation: Strategies to control symptoms and prevent embolism
D.O. Martin, MD, MPH

Supplement Editor:
Roger M. Mills, MD

Contents

Beyond drugs alone: Pacing, ablation, and surgery for atrial fibrillation
R.M. Mills, MD, MPH

Basic mechanisms of atrial fibrillation
D.R. Van Wagoner, PhD

Current clinical issues in atrial fibrillation
M.K. Chung, MD

Approaches to restoring and maintaining normal sinus rhythm
I. Pharmacologic management: Often insufficient, but still first-line
D.O. Martin, MD, MPH

II. Pacing and devices: Progress toward a preventive role
W. Saliba, MD

III. Surgical approaches: At the 'tipping point'
P.M. McCarthy, MD, and A.M. Gillinov, MD

IV. Catheter ablation: A less invasive path to potential cure
W. Belden, MD; N.F. Marrouche, MD; and A. Natale, MD

Managing chronic atrial fibrillation: Strategies to control symptoms and prevent embolism
D.O. Martin, MD, MPH

Tinea capitis is a common problem among refugee children in Iraq. A recent study of school-aged children in Iraq found a 2.7% prevalence rate of the disorder.1 Although tinea capitis was common in children attending urban, as well as rural, schools, its prevalence was highest in those with poor hygiene and overcrowded living conditions, with new settlers to the area accounting for 23.3% of total cases.¹

Dermatophytes encountered in the Persian Gulf region differ from those commonly found in the United States. In a study of 204 clinical cases of tinea capitis among school-aged children in Iraq, Trichophyton verrucosum was the most common organism, and both Trichophyton rubrum and Trichophyton mentagrophytes var mentagrophytes were more common than Trichophyton tonsurans.² Dermatologists providing services to the Iraqi population, as well as those treating individuals returning from the conflict in Iraq, should be aware of the dermatophytes common to that area. US dermatologists who encounter unusual organisms should consider the possibility of imported disease. A recent study in New Zealand found 63 isolates of Trichophyton violaceum and 5 isolates of Trichophyton soudanense among fungal cultures taken from patients in one city. Fifty-eight of the isolates were from scalp specimens, and the vast majority were from children. All but one of these patients were identified as refugees from East Africa. Nine patients with unusual organisms had presented with tinea corporis. Six of these patients were refugees from the same area.³ As T verrucosum, T rubrum, and T mentagrophytes are common agents of tinea capitis in Iraq, isolates of these organisms from scalp lesions should suggest the possibility of imported disease.

Cutaneous leishmaniasis due to Leishmania tropica is a problem in northeast Afghanistan and northwest Pakistan, as well as in Iraq. As long as US servicemen and volunteers are involved in the region, they are at risk of exposure to leishmaniasis. Timargara, an Afghan refugee camp in northwest Pakistan, experienced a major outbreak of cutaneous leishmaniasis in 1997. Nearly 38% of the 9200 inhabitants had active lesions, and the sandfly Phlebotomus sergenti was implicated as the major vector. The Afghan capital, Kabul, also has experienced recent epidemics of cutaneous leishmaniasis.⁴ Both Afghanistan and Iraq are likely to be important sites for exposure to Leishmania.

Cutaneous manifestations of malnutrition are likely to present to healthcare workers in the region. During the recent conflicts in the Balkan Peninsula, hemorrhagic pellagra was reported in an Albanian refugee who had walked for 3 days in intense sunlight as he traveled from his country to Greece. This case was notable for the atypical appearance of some of the lesions, including gangrenous-appearing hemorrhagic lesions involving the skin of the palms and digits.⁵

Scabies is a common problem among refugees. Between March and May 1999, Albania received almost 500,000 refugees from Kosovo. Roughly 4% of these refugees had scabies and lice.⁶ A study of refugee children from South Vietnam and Bangladesh found their most common problems to include malnutrition, gastroenteritis, pneumonia, scabies, and furunculosis.⁷

Although adults will carry the scabies mite, most clinical cases can be expected to present in young children.⁸ Targeted treatment of affected children is not likely to control an epidemic. Early treatment of large numbers of individuals will be needed. Crowded living conditions favor the spread of scabies. Direct skin-to-skin contact accounts for many cases, but fomites may play a role in the spread of scabies, as evidenced by an outbreak of scabies among employees in a hospital-associated commercial laundry.⁹ Live mites also have been found on chairs and couches in the homes of patients with scabies, suggesting that spread by fomites is a real concern.¹⁰ In situations where malnutrition is common, cases of crusted scabies are likely to occur. These cases are the most likely to spread via fomites.

Effective control of scabies epidemics among refugees often requires mass treatment. This is not much different from the situation in western countries where groups work or live in crowded conditions. Groups of employees living and working in close quarters also have been found to require mass treatment to end epidemics of scabies.^11,12 Day-care centers, prisons, nursing homes, and hospital wards are well-known sites for scabies epidemics.^13-18 Mass treatment often is needed in each of these settings to eliminate persistent infestation.

Many skin diseases will cause morbidity among refugee populations, but some, like measles, will kill large numbers of people. Among internally displaced populations in northern Iraq, Somalia, and Sudan, crude death rates have ranged from 12 to 25 times the baseline death rate. Death rates among children younger than 5 years are particularly high. Most deaths are the result of diarrheal diseases, measles, and acute respiratory infections. Malnutrition greatly increases the mortality from these infectious agents.^19,20 During the 1992 famine in Somalia, an estimated 74% of the refugee children less than 5 years old died. Again, preventable infectious diseases such as measles and diarrhea were the primary causes of death.²¹

To reduce the death rate from infectious diseases, improvements in infrastructure and nutritional status are vital. Our role in humanitarian aid missions includes more than the provision of essential medical services. Sustained benefits to the population will only come from rebuilding the national infrastructure. The death toll from common diseases, and the potential good that can be done through simple interventions, cannot be underestimated. In Bhutanese refugee camps in the lowlands between Nepal and India, the leading causes of death were, again, measles, diarrhea, and acute respiratory infections. Measles vaccination, vitamin-A supplementation, and diarrhea control programs reduced the mortality rate in these camps by 75%.²² Between September 1991 and January 1992, there was a measles epidemic in a refugee camp for Vietnamese “boat people” living in Hong Kong. Measles complications affected 234 children, but the case fatality rate was only 0.76%.²³ This low mortality rate was due in large measure to a favorable nutritional status and the availability of medical care.

Malaria also is likely to be a problem in Iraq. Malaria control programs were started in Iraq in 1957, and the country was largely free of the disease at one time. However, since 1991, several Plasmodium vivax epidemics have occurred. There were 49,840 cases of malaria in 1995. Treatment and vector control measures reduced the incidence to 4134 cases in 1999.²⁴ The disruption of health services and vector control efforts during the recent conflict in Iraq raises the possibility of renewed epidemics. Displaced populations are at particular risk. In Afghan refugee camps, malaria proved to be an important problem.²⁵ After the Soviet invasion of Afghanistan, 2.3 million Afghan refugees arrived in Pakistan. Within a decade, the prevalence of malaria among refugees had risen 10-fold. The number of cases among refugees in these camps was greater than that for the entire Pakistani population.²⁶

In addition to malaria, tuberculosis (TB) also is expected to be encountered in Iraq because it proved to be a significant problem among Afghan refugees. The results of 1000 lymph node biopsies from Afghan refugees revealed that 69% had morphologic evidence of TB. Of these patients, 72% were between 10 and 30 years of age.²⁷

Congo-Brazzaville, a country of 3 million people, experienced war from 1997 to 1999. Before this time, the annual increase in the number of TB cases averaged 20%; in 2000, it was 84%. The greatest increase was seen in the country’s 2 main cities, Brazzaville and Pointe-Noire, where refugees had fled from the rural areas.²⁸ Cessation of TB control activities during the war contributed to the problem because compliance with treatment regimens are quite difficult in times of crisis.²⁹ The situation is likely to be similar in Iraq.

In the coming months, the United States and international aid agencies will shoulder much of the burden of disease surveillance and treatment in Iraq. We have an opportunity to ease the suffering of a nation burdened by years of political oppression and economic collapse, and we have an obligation to help rebuild Iraqi infrastructure and allow displaced families to return to their homes. Past humanitarian missions have taught us some of what we can expect and that vector control efforts and improved nutrition will be critical to the success of public health efforts in the months to come. The effort should be international in nature. US Army presence should be replaced by an international (largely Arab) peacekeeping force. International efforts can then focus on rebuilding a badly damaged country.

Tinea capitis is a common problem among refugee children in Iraq. A recent study of school-aged children in Iraq found a 2.7% prevalence rate of the disorder.1 Although tinea capitis was common in children attending urban, as well as rural, schools, its prevalence was highest in those with poor hygiene and overcrowded living conditions, with new settlers to the area accounting for 23.3% of total cases.¹

Dermatophytes encountered in the Persian Gulf region differ from those commonly found in the United States. In a study of 204 clinical cases of tinea capitis among school-aged children in Iraq, Trichophyton verrucosum was the most common organism, and both Trichophyton rubrum and Trichophyton mentagrophytes var mentagrophytes were more common than Trichophyton tonsurans.² Dermatologists providing services to the Iraqi population, as well as those treating individuals returning from the conflict in Iraq, should be aware of the dermatophytes common to that area. US dermatologists who encounter unusual organisms should consider the possibility of imported disease. A recent study in New Zealand found 63 isolates of Trichophyton violaceum and 5 isolates of Trichophyton soudanense among fungal cultures taken from patients in one city. Fifty-eight of the isolates were from scalp specimens, and the vast majority were from children. All but one of these patients were identified as refugees from East Africa. Nine patients with unusual organisms had presented with tinea corporis. Six of these patients were refugees from the same area.³ As T verrucosum, T rubrum, and T mentagrophytes are common agents of tinea capitis in Iraq, isolates of these organisms from scalp lesions should suggest the possibility of imported disease.

Cutaneous leishmaniasis due to Leishmania tropica is a problem in northeast Afghanistan and northwest Pakistan, as well as in Iraq. As long as US servicemen and volunteers are involved in the region, they are at risk of exposure to leishmaniasis. Timargara, an Afghan refugee camp in northwest Pakistan, experienced a major outbreak of cutaneous leishmaniasis in 1997. Nearly 38% of the 9200 inhabitants had active lesions, and the sandfly Phlebotomus sergenti was implicated as the major vector. The Afghan capital, Kabul, also has experienced recent epidemics of cutaneous leishmaniasis.⁴ Both Afghanistan and Iraq are likely to be important sites for exposure to Leishmania.

Cutaneous manifestations of malnutrition are likely to present to healthcare workers in the region. During the recent conflicts in the Balkan Peninsula, hemorrhagic pellagra was reported in an Albanian refugee who had walked for 3 days in intense sunlight as he traveled from his country to Greece. This case was notable for the atypical appearance of some of the lesions, including gangrenous-appearing hemorrhagic lesions involving the skin of the palms and digits.⁵

Scabies is a common problem among refugees. Between March and May 1999, Albania received almost 500,000 refugees from Kosovo. Roughly 4% of these refugees had scabies and lice.⁶ A study of refugee children from South Vietnam and Bangladesh found their most common problems to include malnutrition, gastroenteritis, pneumonia, scabies, and furunculosis.⁷

Although adults will carry the scabies mite, most clinical cases can be expected to present in young children.⁸ Targeted treatment of affected children is not likely to control an epidemic. Early treatment of large numbers of individuals will be needed. Crowded living conditions favor the spread of scabies. Direct skin-to-skin contact accounts for many cases, but fomites may play a role in the spread of scabies, as evidenced by an outbreak of scabies among employees in a hospital-associated commercial laundry.⁹ Live mites also have been found on chairs and couches in the homes of patients with scabies, suggesting that spread by fomites is a real concern.¹⁰ In situations where malnutrition is common, cases of crusted scabies are likely to occur. These cases are the most likely to spread via fomites.

Effective control of scabies epidemics among refugees often requires mass treatment. This is not much different from the situation in western countries where groups work or live in crowded conditions. Groups of employees living and working in close quarters also have been found to require mass treatment to end epidemics of scabies.^11,12 Day-care centers, prisons, nursing homes, and hospital wards are well-known sites for scabies epidemics.^13-18 Mass treatment often is needed in each of these settings to eliminate persistent infestation.

Many skin diseases will cause morbidity among refugee populations, but some, like measles, will kill large numbers of people. Among internally displaced populations in northern Iraq, Somalia, and Sudan, crude death rates have ranged from 12 to 25 times the baseline death rate. Death rates among children younger than 5 years are particularly high. Most deaths are the result of diarrheal diseases, measles, and acute respiratory infections. Malnutrition greatly increases the mortality from these infectious agents.^19,20 During the 1992 famine in Somalia, an estimated 74% of the refugee children less than 5 years old died. Again, preventable infectious diseases such as measles and diarrhea were the primary causes of death.²¹

To reduce the death rate from infectious diseases, improvements in infrastructure and nutritional status are vital. Our role in humanitarian aid missions includes more than the provision of essential medical services. Sustained benefits to the population will only come from rebuilding the national infrastructure. The death toll from common diseases, and the potential good that can be done through simple interventions, cannot be underestimated. In Bhutanese refugee camps in the lowlands between Nepal and India, the leading causes of death were, again, measles, diarrhea, and acute respiratory infections. Measles vaccination, vitamin-A supplementation, and diarrhea control programs reduced the mortality rate in these camps by 75%.²² Between September 1991 and January 1992, there was a measles epidemic in a refugee camp for Vietnamese “boat people” living in Hong Kong. Measles complications affected 234 children, but the case fatality rate was only 0.76%.²³ This low mortality rate was due in large measure to a favorable nutritional status and the availability of medical care.

Malaria also is likely to be a problem in Iraq. Malaria control programs were started in Iraq in 1957, and the country was largely free of the disease at one time. However, since 1991, several Plasmodium vivax epidemics have occurred. There were 49,840 cases of malaria in 1995. Treatment and vector control measures reduced the incidence to 4134 cases in 1999.²⁴ The disruption of health services and vector control efforts during the recent conflict in Iraq raises the possibility of renewed epidemics. Displaced populations are at particular risk. In Afghan refugee camps, malaria proved to be an important problem.²⁵ After the Soviet invasion of Afghanistan, 2.3 million Afghan refugees arrived in Pakistan. Within a decade, the prevalence of malaria among refugees had risen 10-fold. The number of cases among refugees in these camps was greater than that for the entire Pakistani population.²⁶

In addition to malaria, tuberculosis (TB) also is expected to be encountered in Iraq because it proved to be a significant problem among Afghan refugees. The results of 1000 lymph node biopsies from Afghan refugees revealed that 69% had morphologic evidence of TB. Of these patients, 72% were between 10 and 30 years of age.²⁷

Congo-Brazzaville, a country of 3 million people, experienced war from 1997 to 1999. Before this time, the annual increase in the number of TB cases averaged 20%; in 2000, it was 84%. The greatest increase was seen in the country’s 2 main cities, Brazzaville and Pointe-Noire, where refugees had fled from the rural areas.²⁸ Cessation of TB control activities during the war contributed to the problem because compliance with treatment regimens are quite difficult in times of crisis.²⁹ The situation is likely to be similar in Iraq.

In the coming months, the United States and international aid agencies will shoulder much of the burden of disease surveillance and treatment in Iraq. We have an opportunity to ease the suffering of a nation burdened by years of political oppression and economic collapse, and we have an obligation to help rebuild Iraqi infrastructure and allow displaced families to return to their homes. Past humanitarian missions have taught us some of what we can expect and that vector control efforts and improved nutrition will be critical to the success of public health efforts in the months to come. The effort should be international in nature. US Army presence should be replaced by an international (largely Arab) peacekeeping force. International efforts can then focus on rebuilding a badly damaged country.

Tinea capitis is a common problem among refugee children in Iraq. A recent study of school-aged children in Iraq found a 2.7% prevalence rate of the disorder.1 Although tinea capitis was common in children attending urban, as well as rural, schools, its prevalence was highest in those with poor hygiene and overcrowded living conditions, with new settlers to the area accounting for 23.3% of total cases.¹

Dermatophytes encountered in the Persian Gulf region differ from those commonly found in the United States. In a study of 204 clinical cases of tinea capitis among school-aged children in Iraq, Trichophyton verrucosum was the most common organism, and both Trichophyton rubrum and Trichophyton mentagrophytes var mentagrophytes were more common than Trichophyton tonsurans.² Dermatologists providing services to the Iraqi population, as well as those treating individuals returning from the conflict in Iraq, should be aware of the dermatophytes common to that area. US dermatologists who encounter unusual organisms should consider the possibility of imported disease. A recent study in New Zealand found 63 isolates of Trichophyton violaceum and 5 isolates of Trichophyton soudanense among fungal cultures taken from patients in one city. Fifty-eight of the isolates were from scalp specimens, and the vast majority were from children. All but one of these patients were identified as refugees from East Africa. Nine patients with unusual organisms had presented with tinea corporis. Six of these patients were refugees from the same area.³ As T verrucosum, T rubrum, and T mentagrophytes are common agents of tinea capitis in Iraq, isolates of these organisms from scalp lesions should suggest the possibility of imported disease.

Cutaneous leishmaniasis due to Leishmania tropica is a problem in northeast Afghanistan and northwest Pakistan, as well as in Iraq. As long as US servicemen and volunteers are involved in the region, they are at risk of exposure to leishmaniasis. Timargara, an Afghan refugee camp in northwest Pakistan, experienced a major outbreak of cutaneous leishmaniasis in 1997. Nearly 38% of the 9200 inhabitants had active lesions, and the sandfly Phlebotomus sergenti was implicated as the major vector. The Afghan capital, Kabul, also has experienced recent epidemics of cutaneous leishmaniasis.⁴ Both Afghanistan and Iraq are likely to be important sites for exposure to Leishmania.

Cutaneous manifestations of malnutrition are likely to present to healthcare workers in the region. During the recent conflicts in the Balkan Peninsula, hemorrhagic pellagra was reported in an Albanian refugee who had walked for 3 days in intense sunlight as he traveled from his country to Greece. This case was notable for the atypical appearance of some of the lesions, including gangrenous-appearing hemorrhagic lesions involving the skin of the palms and digits.⁵

Scabies is a common problem among refugees. Between March and May 1999, Albania received almost 500,000 refugees from Kosovo. Roughly 4% of these refugees had scabies and lice.⁶ A study of refugee children from South Vietnam and Bangladesh found their most common problems to include malnutrition, gastroenteritis, pneumonia, scabies, and furunculosis.⁷

Although adults will carry the scabies mite, most clinical cases can be expected to present in young children.⁸ Targeted treatment of affected children is not likely to control an epidemic. Early treatment of large numbers of individuals will be needed. Crowded living conditions favor the spread of scabies. Direct skin-to-skin contact accounts for many cases, but fomites may play a role in the spread of scabies, as evidenced by an outbreak of scabies among employees in a hospital-associated commercial laundry.⁹ Live mites also have been found on chairs and couches in the homes of patients with scabies, suggesting that spread by fomites is a real concern.¹⁰ In situations where malnutrition is common, cases of crusted scabies are likely to occur. These cases are the most likely to spread via fomites.

Effective control of scabies epidemics among refugees often requires mass treatment. This is not much different from the situation in western countries where groups work or live in crowded conditions. Groups of employees living and working in close quarters also have been found to require mass treatment to end epidemics of scabies.^11,12 Day-care centers, prisons, nursing homes, and hospital wards are well-known sites for scabies epidemics.^13-18 Mass treatment often is needed in each of these settings to eliminate persistent infestation.

Many skin diseases will cause morbidity among refugee populations, but some, like measles, will kill large numbers of people. Among internally displaced populations in northern Iraq, Somalia, and Sudan, crude death rates have ranged from 12 to 25 times the baseline death rate. Death rates among children younger than 5 years are particularly high. Most deaths are the result of diarrheal diseases, measles, and acute respiratory infections. Malnutrition greatly increases the mortality from these infectious agents.^19,20 During the 1992 famine in Somalia, an estimated 74% of the refugee children less than 5 years old died. Again, preventable infectious diseases such as measles and diarrhea were the primary causes of death.²¹

To reduce the death rate from infectious diseases, improvements in infrastructure and nutritional status are vital. Our role in humanitarian aid missions includes more than the provision of essential medical services. Sustained benefits to the population will only come from rebuilding the national infrastructure. The death toll from common diseases, and the potential good that can be done through simple interventions, cannot be underestimated. In Bhutanese refugee camps in the lowlands between Nepal and India, the leading causes of death were, again, measles, diarrhea, and acute respiratory infections. Measles vaccination, vitamin-A supplementation, and diarrhea control programs reduced the mortality rate in these camps by 75%.²² Between September 1991 and January 1992, there was a measles epidemic in a refugee camp for Vietnamese “boat people” living in Hong Kong. Measles complications affected 234 children, but the case fatality rate was only 0.76%.²³ This low mortality rate was due in large measure to a favorable nutritional status and the availability of medical care.

Malaria also is likely to be a problem in Iraq. Malaria control programs were started in Iraq in 1957, and the country was largely free of the disease at one time. However, since 1991, several Plasmodium vivax epidemics have occurred. There were 49,840 cases of malaria in 1995. Treatment and vector control measures reduced the incidence to 4134 cases in 1999.²⁴ The disruption of health services and vector control efforts during the recent conflict in Iraq raises the possibility of renewed epidemics. Displaced populations are at particular risk. In Afghan refugee camps, malaria proved to be an important problem.²⁵ After the Soviet invasion of Afghanistan, 2.3 million Afghan refugees arrived in Pakistan. Within a decade, the prevalence of malaria among refugees had risen 10-fold. The number of cases among refugees in these camps was greater than that for the entire Pakistani population.²⁶

In addition to malaria, tuberculosis (TB) also is expected to be encountered in Iraq because it proved to be a significant problem among Afghan refugees. The results of 1000 lymph node biopsies from Afghan refugees revealed that 69% had morphologic evidence of TB. Of these patients, 72% were between 10 and 30 years of age.²⁷

Congo-Brazzaville, a country of 3 million people, experienced war from 1997 to 1999. Before this time, the annual increase in the number of TB cases averaged 20%; in 2000, it was 84%. The greatest increase was seen in the country’s 2 main cities, Brazzaville and Pointe-Noire, where refugees had fled from the rural areas.²⁸ Cessation of TB control activities during the war contributed to the problem because compliance with treatment regimens are quite difficult in times of crisis.²⁹ The situation is likely to be similar in Iraq.

In the coming months, the United States and international aid agencies will shoulder much of the burden of disease surveillance and treatment in Iraq. We have an opportunity to ease the suffering of a nation burdened by years of political oppression and economic collapse, and we have an obligation to help rebuild Iraqi infrastructure and allow displaced families to return to their homes. Past humanitarian missions have taught us some of what we can expect and that vector control efforts and improved nutrition will be critical to the success of public health efforts in the months to come. The effort should be international in nature. US Army presence should be replaced by an international (largely Arab) peacekeeping force. International efforts can then focus on rebuilding a badly damaged country.