What is kleptomania? An independent illness, a symptom of other psychiatric disorders, or merely criminal behavior? Kleptomania—a disorder defined by an inability to resist the impulse to steal—is one of psychiatry’s most poorly understood diagnoses, even though it has been recognized in the literature for almost 200 years.

Kleptomania causes notable distress and impaired functioning.¹ People with kleptomania often suffer from comorbid mood, anxiety, substance use, and other impulse-control disorders.¹⁴ They experience the humiliation of repeated arrests, which leads to guilt, depression, and even suicide.^1,5 Yet kleptomania usually goes undiagnosed and untreated, despite a lifetime prevalence as high as 0.6%.⁶

Case report: ‘I’m a thief’

“I’m a thief,” began Susan, age 39. “I steal something four or five times every week. I steal from grocery stores and clothing stores. Sometimes I might steal something like vanilla extract; other times an expensive men’s tie. I probably steal $200 worth of items every week.

“You probably won’t believe this, but I don’t want or need the stuff I take. I have plenty of money. I have no idea why I take the things I do. That’s why I’m so depressed. What kind of person does something like this?

The urge to steal “I was probably 14 when I started stealing. I would go to stores with my mother. When I saw certain objects, I would get urges to steal them. The odd thing was that the items I stole were so ridiculous. I remember stealing key chains for several months, maybe three or four times a week. When I got older, things got worse. I was having urges more often, and so I needed to steal more often.

Box

“My entire life has been torment. Each day I worry about having the urges, and then I worry about being caught stealing. I can’t relax. I’ve been married for 17 years, and I haven’t told my husband. My secrecy is tearing our marriage apart. My husband thinks I’m having an affair because I’ve distanced myself emotionally from him.”

Table 1

SCREENING TEST FOR KLEPTOMANIA

Susan described urges to steal almost every day. When the urges were mild, she could resist them. Other days they were severe, and Susan felt unable to control her behavior. At work, her urges distracted her from completing projects, and her performance suffered. The urge to steal would often compel Susan to leave work early so she could get to a store.

Calm, then guilt “Every time I steal something I feel both a thrill and a great sense of calm,” she said. “It feels good. The problem is that almost immediately after each theft, I feel guilty and ashamed. After I steal, I usually donate the items to the Salvation Army, throw them away, or give them away as gifts.”

Drug trials We started treating Susan with the selective serotonin reuptake inhibitor (SSRI), citalopram. She reported notable improvement in her mood after 3 weeks on a dosage of 60 mg/d and she had been attending weekly psychotherapy, although her stealing continued unchanged. The addition of naltrexone, 200 mg/d for 2 weeks, decreased the frequency of Susan’s stealing and reduced her urges to steal, but her symptoms continued to interfere significantly with her overall functioning.

We then added the atypical antipsychotic quetiapine, 100 mg bid, and Susan’s urges to steal and stealing behavior went into remission within 3 weeks. She has refrained from stealing for the last 9 months.

Making the diagnosis

In our clinic, we have treated more than 50 patients with kleptomania. Rather than coming to us through the criminal justice system, they are usually self-referred. Often they contact us after discovering on the Internet that we specialize in treating persons with this disorder.

In our experience, kleptomania typically goes undiagnosed in clinical settings, in part because patients are ashamed and embarrassed to discuss their symptoms with physicians unless specifically asked.¹ If left untreated, however, kleptomania frequently becomes chronic.⁴ If persons with kleptomania are to seek treatment, it is important that family, friends, and mental health professionals understand the myths and facts about this disorder (Box).

To make the diagnosis, we use the simple screening instrument shown in Table 1.⁷ In general, because of high comorbidity with certain disorders, we screen every patient presenting to our clinic with a mood, substance use, anxiety, or eating disorder, or who has a problem with impulse control. Kleptomania is likely if the patient answers “yes” to questions 1 through 4 and to question 5 or 6. Stealing may be a symptom of several other psychiatric disorders, however, and misdiagnosis is fairly common (Table 2).^6-8

Data suggest that the female-to-male ratio in kleptomania is approximately 2:1, with onset in adolescence. Typical individuals with kleptomania steal because they have urges to steal, often triggered by specific stimuli such as the sights and sounds of stores or feelings of loneliness or stress.¹ Most patients with kleptomania are fairly specific about the types of stores from which they steal and the items they steal, and most hoard stolen items.¹

Although many patients with kleptomania function quite well, others are severely debilitated in social and occupational realms. In a series of 22 patients with kleptomania:

• 64% had been apprehended
• 23% had served jail time
• 27% had been hospitalized because of their kleptomania symptoms
• 18% had considered or attempted suicide because of the distress associated with their kleptomania.¹

Treatment recommendations

Patient history With patients who steal, we begin by identifying the motivation behind the stealing. Most patients with kleptomania report urges to steal. Some of these patients may have comorbid depression; for them, stealing makes them feel less depressed. Anger or irritability may point to borderline personality disorder. Stealing for the enjoyment of risk may suggest bipolar disorder.

Table 2

DIFFERENTIAL DIAGNOSIS: DISORDERS THAT MAY INVOLVE STEALING

Many patients with kleptomania have comorbid mood, substance, or anxiety disorders. Treating these other symptoms while ignoring the symptoms of kleptomania may be unsuccessful. Comorbidity also may influence the choice of medication.

Medical assessment Case reports have associated the onset of kleptomania with a variety of medical conditions, including presenile cortical atrophy in a 25-year-old, a parietal tumor that caused blackouts and obliterated any memory of stealing episodes, narcolepsy, and an insulinoma that caused severe hypoglycemia.⁹ The relationship of these conditions with the onset of kleptomania is unclear, but the reports suggest that medical causes—although unlikely—should be ruled out before you consider kleptomania as a psychiatric illness.

Patient education Persons with kleptomania often feel that no one else has the same problem. They do not think of their behavior as being an illness. It is helpful to explain that kleptomania is treatable and to connect patients with educational books, self-help groups, and Web sites providing information and support (see “Related resources”).

Cognitive-behavioral therapy (CBT) Although the evidence is quite limited, covert sensitization, exposure and response prevention, and imaginal desensitization have all been shown effective in case reports.¹⁰

What medications are effective?

Only case reports, a case series of five subjects, and a single open-label treatment study involving 10 subjects with kleptomania have been done.

So far, uses of tricyclic antidepressants (imipramine, nortriptyline), SSRIs (fluoxetine, fluvoxamine, paroxetine), the opioid antagonist naltrexone, and mood stabilizers (lithium, valproate) have met with varying degrees of success. Strategies targeting urge and behavior reduction and mechanisms for coping with urges and behavior (e.g., cognitive-behavioral therapies) may represent important adjunctive components.^2,11-17

No medications are FDA-approved for treating kleptomania. Therefore, it is important to inform patients of any off-label use of medications for this disorder, as well as the empirical basis for considering pharmacologic treatment.

SSRIs Only case reports exist on the use of SSRIs in treating kleptomania. The disorder may share a common pathology with pathologic gambling, and in our clinical experience appears to respond to similar treatments.¹⁸ We draw on research of pathologic gambling as well as our clinical experience in choosing SSRIs as first-line treatment, especially for patients with significant mood symptoms.¹⁹

We suggest titrating SSRIs to the maximum recommended dosage. As in the treatment of pathologic gambling, dosages of SSRIs required to treat kleptomania symptoms appear to be higher than average dosages required to treat depressive disorders. An SSRI should not be considered ineffective unless it has been tried for at least 10 to 12 weeks and the highest dosage tolerated or recommended by the manufacturer has been reached.

Response to SSRIs usually is characterized by decreased thoughts about stealing, decreased stealing behavior, and improvement in social and occupational functioning. If an SSRI is only partially effective, we consider augmentation with naltrexone, buspirone, or a mood stabilizer.

Naltrexone Patients taking naltrexone often report less-intense urges to steal. The urges may not disappear but are often sufficiently reduced so that the patient can resist them more easily. Patients also report that the thrill associated with stealing is reduced or eliminated.

Naltrexone was used in the first medication study of kleptomania and showed a significant decline in the intensity of urges to steal, stealing thoughts, and stealing behavior. Average dosage was 150 mg/d;¹¹ a reduced dosage (e.g., 50 mg/d) may work in adolescents with kleptomania.²⁰

Nausea as a side effect can be reduced by starting patients on 25 mg/d for the first 3 or 4 days and possibly adding ondansetron, 4 to 8 mg/d. Nausea and diarrhea are usually mild and resolve within the first week. Clinically, most patients respond to naltrexone within 2 weeks. After that, the dosage usually needs to be adjusted.

In patients with comorbid depression, augmentation with an SSRI may prevent worsening of untreated depressive symptoms. It is prudent to obtain liver function tests prior to naltrexone administration and again 3 to 4 weeks after starting the drug.²¹ Repeat testing should be performed at 2-to 4-week intervals for the next 2 months, then once a month for the following 3 months. After 6 months, testing three to four times a year is usually sufficient.

Nonsteroidal analgesics should not be used with high dosages of naltrexone (>50 mg/d), as concurrent use may increase the risk of hepatic transaminase elevation.²¹

Mood stabilizers Responses to lithium and valproate have been described in two case reports of patients with kleptomania.^14,15 In the case of valproate, the effective dosage was 2,000 mg/d, whereas lithium reduced stealing urges at a serum level of 0.5 mEq/L.

Although it would be premature to recommend the use of mood stabilizers, their possible benefit may be related to their efficacy in bipolar disorder treatment and the existence of features (e.g., impulsivity) shared by kleptomania and bipolar disorder.

Atypical antipsychotics Although there is no evidence that atypical antipsychotics are useful in kleptomania, augmenting an SSRI with an atypical neuroleptic may be beneficial. Atypical antipsychotics have been explored as augmenting agents in the treatment of nonpsychotic disorders and behaviors, including pathologic gambling and obsessive-compulsive disorder.

The role of psychotherapy

Cognitive-behavioral therapy Based on the evidence of its effectiveness in treating pathologic gambling, CBT may hold promise as monotherapy for mild cases of kleptomania.

Combination therapy Combined pharmacologic and behavioral therapy may be the optimal treatment strategy for kleptomania. In our experience, patients who respond only partially or fail to respond to pharmacotherapy alone are more likely to find relief with a combination of drug and cognitive-behavioral therapies.

Related resource

• Goldman MJ. Kleptomania: the compulsion to steal—what can be done? Far Hills, N New Horizon Press, 1998.
• Shoplifters Alternative http://www.shoplifters.org
• Impulse Control Disorders Clinic, University of Minnesota http://www.med.umn.edu/psychiatry/research/impulse.htm

Drug brand names

• Citalopram • Celexa
• Fluvoxamine • Luvox
• Imipramine • Tofranil
• Naltrexone • Revia
• Nortriptyline • Aventyl, Pamelor
• Paroxetine • Paxil
• Quetiapine • Seroquel
• Valproic acid • Depakote

Disclosure

The authors report no affiliation or financial arrangement with any of the companies whose products are mentioned in this article.

What is kleptomania? An independent illness, a symptom of other psychiatric disorders, or merely criminal behavior? Kleptomania—a disorder defined by an inability to resist the impulse to steal—is one of psychiatry’s most poorly understood diagnoses, even though it has been recognized in the literature for almost 200 years.

Kleptomania causes notable distress and impaired functioning.¹ People with kleptomania often suffer from comorbid mood, anxiety, substance use, and other impulse-control disorders.¹⁴ They experience the humiliation of repeated arrests, which leads to guilt, depression, and even suicide.^1,5 Yet kleptomania usually goes undiagnosed and untreated, despite a lifetime prevalence as high as 0.6%.⁶

Case report: ‘I’m a thief’

“I’m a thief,” began Susan, age 39. “I steal something four or five times every week. I steal from grocery stores and clothing stores. Sometimes I might steal something like vanilla extract; other times an expensive men’s tie. I probably steal $200 worth of items every week.

“You probably won’t believe this, but I don’t want or need the stuff I take. I have plenty of money. I have no idea why I take the things I do. That’s why I’m so depressed. What kind of person does something like this?

The urge to steal “I was probably 14 when I started stealing. I would go to stores with my mother. When I saw certain objects, I would get urges to steal them. The odd thing was that the items I stole were so ridiculous. I remember stealing key chains for several months, maybe three or four times a week. When I got older, things got worse. I was having urges more often, and so I needed to steal more often.

Box

“My entire life has been torment. Each day I worry about having the urges, and then I worry about being caught stealing. I can’t relax. I’ve been married for 17 years, and I haven’t told my husband. My secrecy is tearing our marriage apart. My husband thinks I’m having an affair because I’ve distanced myself emotionally from him.”

Table 1

SCREENING TEST FOR KLEPTOMANIA

Susan described urges to steal almost every day. When the urges were mild, she could resist them. Other days they were severe, and Susan felt unable to control her behavior. At work, her urges distracted her from completing projects, and her performance suffered. The urge to steal would often compel Susan to leave work early so she could get to a store.

Calm, then guilt “Every time I steal something I feel both a thrill and a great sense of calm,” she said. “It feels good. The problem is that almost immediately after each theft, I feel guilty and ashamed. After I steal, I usually donate the items to the Salvation Army, throw them away, or give them away as gifts.”

Drug trials We started treating Susan with the selective serotonin reuptake inhibitor (SSRI), citalopram. She reported notable improvement in her mood after 3 weeks on a dosage of 60 mg/d and she had been attending weekly psychotherapy, although her stealing continued unchanged. The addition of naltrexone, 200 mg/d for 2 weeks, decreased the frequency of Susan’s stealing and reduced her urges to steal, but her symptoms continued to interfere significantly with her overall functioning.

We then added the atypical antipsychotic quetiapine, 100 mg bid, and Susan’s urges to steal and stealing behavior went into remission within 3 weeks. She has refrained from stealing for the last 9 months.

Making the diagnosis

In our clinic, we have treated more than 50 patients with kleptomania. Rather than coming to us through the criminal justice system, they are usually self-referred. Often they contact us after discovering on the Internet that we specialize in treating persons with this disorder.

In our experience, kleptomania typically goes undiagnosed in clinical settings, in part because patients are ashamed and embarrassed to discuss their symptoms with physicians unless specifically asked.¹ If left untreated, however, kleptomania frequently becomes chronic.⁴ If persons with kleptomania are to seek treatment, it is important that family, friends, and mental health professionals understand the myths and facts about this disorder (Box).

To make the diagnosis, we use the simple screening instrument shown in Table 1.⁷ In general, because of high comorbidity with certain disorders, we screen every patient presenting to our clinic with a mood, substance use, anxiety, or eating disorder, or who has a problem with impulse control. Kleptomania is likely if the patient answers “yes” to questions 1 through 4 and to question 5 or 6. Stealing may be a symptom of several other psychiatric disorders, however, and misdiagnosis is fairly common (Table 2).^6-8

Data suggest that the female-to-male ratio in kleptomania is approximately 2:1, with onset in adolescence. Typical individuals with kleptomania steal because they have urges to steal, often triggered by specific stimuli such as the sights and sounds of stores or feelings of loneliness or stress.¹ Most patients with kleptomania are fairly specific about the types of stores from which they steal and the items they steal, and most hoard stolen items.¹

Although many patients with kleptomania function quite well, others are severely debilitated in social and occupational realms. In a series of 22 patients with kleptomania:

• 64% had been apprehended
• 23% had served jail time
• 27% had been hospitalized because of their kleptomania symptoms
• 18% had considered or attempted suicide because of the distress associated with their kleptomania.¹

Treatment recommendations

Patient history With patients who steal, we begin by identifying the motivation behind the stealing. Most patients with kleptomania report urges to steal. Some of these patients may have comorbid depression; for them, stealing makes them feel less depressed. Anger or irritability may point to borderline personality disorder. Stealing for the enjoyment of risk may suggest bipolar disorder.

Table 2

DIFFERENTIAL DIAGNOSIS: DISORDERS THAT MAY INVOLVE STEALING

Many patients with kleptomania have comorbid mood, substance, or anxiety disorders. Treating these other symptoms while ignoring the symptoms of kleptomania may be unsuccessful. Comorbidity also may influence the choice of medication.

Medical assessment Case reports have associated the onset of kleptomania with a variety of medical conditions, including presenile cortical atrophy in a 25-year-old, a parietal tumor that caused blackouts and obliterated any memory of stealing episodes, narcolepsy, and an insulinoma that caused severe hypoglycemia.⁹ The relationship of these conditions with the onset of kleptomania is unclear, but the reports suggest that medical causes—although unlikely—should be ruled out before you consider kleptomania as a psychiatric illness.

Patient education Persons with kleptomania often feel that no one else has the same problem. They do not think of their behavior as being an illness. It is helpful to explain that kleptomania is treatable and to connect patients with educational books, self-help groups, and Web sites providing information and support (see “Related resources”).

Cognitive-behavioral therapy (CBT) Although the evidence is quite limited, covert sensitization, exposure and response prevention, and imaginal desensitization have all been shown effective in case reports.¹⁰

What medications are effective?

Only case reports, a case series of five subjects, and a single open-label treatment study involving 10 subjects with kleptomania have been done.

So far, uses of tricyclic antidepressants (imipramine, nortriptyline), SSRIs (fluoxetine, fluvoxamine, paroxetine), the opioid antagonist naltrexone, and mood stabilizers (lithium, valproate) have met with varying degrees of success. Strategies targeting urge and behavior reduction and mechanisms for coping with urges and behavior (e.g., cognitive-behavioral therapies) may represent important adjunctive components.^2,11-17

No medications are FDA-approved for treating kleptomania. Therefore, it is important to inform patients of any off-label use of medications for this disorder, as well as the empirical basis for considering pharmacologic treatment.

SSRIs Only case reports exist on the use of SSRIs in treating kleptomania. The disorder may share a common pathology with pathologic gambling, and in our clinical experience appears to respond to similar treatments.¹⁸ We draw on research of pathologic gambling as well as our clinical experience in choosing SSRIs as first-line treatment, especially for patients with significant mood symptoms.¹⁹

We suggest titrating SSRIs to the maximum recommended dosage. As in the treatment of pathologic gambling, dosages of SSRIs required to treat kleptomania symptoms appear to be higher than average dosages required to treat depressive disorders. An SSRI should not be considered ineffective unless it has been tried for at least 10 to 12 weeks and the highest dosage tolerated or recommended by the manufacturer has been reached.

Response to SSRIs usually is characterized by decreased thoughts about stealing, decreased stealing behavior, and improvement in social and occupational functioning. If an SSRI is only partially effective, we consider augmentation with naltrexone, buspirone, or a mood stabilizer.

Naltrexone Patients taking naltrexone often report less-intense urges to steal. The urges may not disappear but are often sufficiently reduced so that the patient can resist them more easily. Patients also report that the thrill associated with stealing is reduced or eliminated.

Naltrexone was used in the first medication study of kleptomania and showed a significant decline in the intensity of urges to steal, stealing thoughts, and stealing behavior. Average dosage was 150 mg/d;¹¹ a reduced dosage (e.g., 50 mg/d) may work in adolescents with kleptomania.²⁰

Nausea as a side effect can be reduced by starting patients on 25 mg/d for the first 3 or 4 days and possibly adding ondansetron, 4 to 8 mg/d. Nausea and diarrhea are usually mild and resolve within the first week. Clinically, most patients respond to naltrexone within 2 weeks. After that, the dosage usually needs to be adjusted.

In patients with comorbid depression, augmentation with an SSRI may prevent worsening of untreated depressive symptoms. It is prudent to obtain liver function tests prior to naltrexone administration and again 3 to 4 weeks after starting the drug.²¹ Repeat testing should be performed at 2-to 4-week intervals for the next 2 months, then once a month for the following 3 months. After 6 months, testing three to four times a year is usually sufficient.

Nonsteroidal analgesics should not be used with high dosages of naltrexone (>50 mg/d), as concurrent use may increase the risk of hepatic transaminase elevation.²¹

Mood stabilizers Responses to lithium and valproate have been described in two case reports of patients with kleptomania.^14,15 In the case of valproate, the effective dosage was 2,000 mg/d, whereas lithium reduced stealing urges at a serum level of 0.5 mEq/L.

Although it would be premature to recommend the use of mood stabilizers, their possible benefit may be related to their efficacy in bipolar disorder treatment and the existence of features (e.g., impulsivity) shared by kleptomania and bipolar disorder.

Atypical antipsychotics Although there is no evidence that atypical antipsychotics are useful in kleptomania, augmenting an SSRI with an atypical neuroleptic may be beneficial. Atypical antipsychotics have been explored as augmenting agents in the treatment of nonpsychotic disorders and behaviors, including pathologic gambling and obsessive-compulsive disorder.

The role of psychotherapy

Cognitive-behavioral therapy Based on the evidence of its effectiveness in treating pathologic gambling, CBT may hold promise as monotherapy for mild cases of kleptomania.

Combination therapy Combined pharmacologic and behavioral therapy may be the optimal treatment strategy for kleptomania. In our experience, patients who respond only partially or fail to respond to pharmacotherapy alone are more likely to find relief with a combination of drug and cognitive-behavioral therapies.

Related resource

• Goldman MJ. Kleptomania: the compulsion to steal—what can be done? Far Hills, N New Horizon Press, 1998.
• Shoplifters Alternative http://www.shoplifters.org
• Impulse Control Disorders Clinic, University of Minnesota http://www.med.umn.edu/psychiatry/research/impulse.htm

Drug brand names

• Citalopram • Celexa
• Fluvoxamine • Luvox
• Imipramine • Tofranil
• Naltrexone • Revia
• Nortriptyline • Aventyl, Pamelor
• Paroxetine • Paxil
• Quetiapine • Seroquel
• Valproic acid • Depakote

Disclosure

The authors report no affiliation or financial arrangement with any of the companies whose products are mentioned in this article.

What is kleptomania? An independent illness, a symptom of other psychiatric disorders, or merely criminal behavior? Kleptomania—a disorder defined by an inability to resist the impulse to steal—is one of psychiatry’s most poorly understood diagnoses, even though it has been recognized in the literature for almost 200 years.

Kleptomania causes notable distress and impaired functioning.¹ People with kleptomania often suffer from comorbid mood, anxiety, substance use, and other impulse-control disorders.¹⁴ They experience the humiliation of repeated arrests, which leads to guilt, depression, and even suicide.^1,5 Yet kleptomania usually goes undiagnosed and untreated, despite a lifetime prevalence as high as 0.6%.⁶

Case report: ‘I’m a thief’

“I’m a thief,” began Susan, age 39. “I steal something four or five times every week. I steal from grocery stores and clothing stores. Sometimes I might steal something like vanilla extract; other times an expensive men’s tie. I probably steal $200 worth of items every week.

“You probably won’t believe this, but I don’t want or need the stuff I take. I have plenty of money. I have no idea why I take the things I do. That’s why I’m so depressed. What kind of person does something like this?

The urge to steal “I was probably 14 when I started stealing. I would go to stores with my mother. When I saw certain objects, I would get urges to steal them. The odd thing was that the items I stole were so ridiculous. I remember stealing key chains for several months, maybe three or four times a week. When I got older, things got worse. I was having urges more often, and so I needed to steal more often.

Box

“My entire life has been torment. Each day I worry about having the urges, and then I worry about being caught stealing. I can’t relax. I’ve been married for 17 years, and I haven’t told my husband. My secrecy is tearing our marriage apart. My husband thinks I’m having an affair because I’ve distanced myself emotionally from him.”

Table 1

SCREENING TEST FOR KLEPTOMANIA

Susan described urges to steal almost every day. When the urges were mild, she could resist them. Other days they were severe, and Susan felt unable to control her behavior. At work, her urges distracted her from completing projects, and her performance suffered. The urge to steal would often compel Susan to leave work early so she could get to a store.

Calm, then guilt “Every time I steal something I feel both a thrill and a great sense of calm,” she said. “It feels good. The problem is that almost immediately after each theft, I feel guilty and ashamed. After I steal, I usually donate the items to the Salvation Army, throw them away, or give them away as gifts.”

Drug trials We started treating Susan with the selective serotonin reuptake inhibitor (SSRI), citalopram. She reported notable improvement in her mood after 3 weeks on a dosage of 60 mg/d and she had been attending weekly psychotherapy, although her stealing continued unchanged. The addition of naltrexone, 200 mg/d for 2 weeks, decreased the frequency of Susan’s stealing and reduced her urges to steal, but her symptoms continued to interfere significantly with her overall functioning.

We then added the atypical antipsychotic quetiapine, 100 mg bid, and Susan’s urges to steal and stealing behavior went into remission within 3 weeks. She has refrained from stealing for the last 9 months.

Making the diagnosis

In our clinic, we have treated more than 50 patients with kleptomania. Rather than coming to us through the criminal justice system, they are usually self-referred. Often they contact us after discovering on the Internet that we specialize in treating persons with this disorder.

In our experience, kleptomania typically goes undiagnosed in clinical settings, in part because patients are ashamed and embarrassed to discuss their symptoms with physicians unless specifically asked.¹ If left untreated, however, kleptomania frequently becomes chronic.⁴ If persons with kleptomania are to seek treatment, it is important that family, friends, and mental health professionals understand the myths and facts about this disorder (Box).

To make the diagnosis, we use the simple screening instrument shown in Table 1.⁷ In general, because of high comorbidity with certain disorders, we screen every patient presenting to our clinic with a mood, substance use, anxiety, or eating disorder, or who has a problem with impulse control. Kleptomania is likely if the patient answers “yes” to questions 1 through 4 and to question 5 or 6. Stealing may be a symptom of several other psychiatric disorders, however, and misdiagnosis is fairly common (Table 2).^6-8

Data suggest that the female-to-male ratio in kleptomania is approximately 2:1, with onset in adolescence. Typical individuals with kleptomania steal because they have urges to steal, often triggered by specific stimuli such as the sights and sounds of stores or feelings of loneliness or stress.¹ Most patients with kleptomania are fairly specific about the types of stores from which they steal and the items they steal, and most hoard stolen items.¹

Although many patients with kleptomania function quite well, others are severely debilitated in social and occupational realms. In a series of 22 patients with kleptomania:

• 64% had been apprehended
• 23% had served jail time
• 27% had been hospitalized because of their kleptomania symptoms
• 18% had considered or attempted suicide because of the distress associated with their kleptomania.¹

Treatment recommendations

Patient history With patients who steal, we begin by identifying the motivation behind the stealing. Most patients with kleptomania report urges to steal. Some of these patients may have comorbid depression; for them, stealing makes them feel less depressed. Anger or irritability may point to borderline personality disorder. Stealing for the enjoyment of risk may suggest bipolar disorder.

Table 2

DIFFERENTIAL DIAGNOSIS: DISORDERS THAT MAY INVOLVE STEALING

Many patients with kleptomania have comorbid mood, substance, or anxiety disorders. Treating these other symptoms while ignoring the symptoms of kleptomania may be unsuccessful. Comorbidity also may influence the choice of medication.

Medical assessment Case reports have associated the onset of kleptomania with a variety of medical conditions, including presenile cortical atrophy in a 25-year-old, a parietal tumor that caused blackouts and obliterated any memory of stealing episodes, narcolepsy, and an insulinoma that caused severe hypoglycemia.⁹ The relationship of these conditions with the onset of kleptomania is unclear, but the reports suggest that medical causes—although unlikely—should be ruled out before you consider kleptomania as a psychiatric illness.

Patient education Persons with kleptomania often feel that no one else has the same problem. They do not think of their behavior as being an illness. It is helpful to explain that kleptomania is treatable and to connect patients with educational books, self-help groups, and Web sites providing information and support (see “Related resources”).

Cognitive-behavioral therapy (CBT) Although the evidence is quite limited, covert sensitization, exposure and response prevention, and imaginal desensitization have all been shown effective in case reports.¹⁰

What medications are effective?

Only case reports, a case series of five subjects, and a single open-label treatment study involving 10 subjects with kleptomania have been done.

So far, uses of tricyclic antidepressants (imipramine, nortriptyline), SSRIs (fluoxetine, fluvoxamine, paroxetine), the opioid antagonist naltrexone, and mood stabilizers (lithium, valproate) have met with varying degrees of success. Strategies targeting urge and behavior reduction and mechanisms for coping with urges and behavior (e.g., cognitive-behavioral therapies) may represent important adjunctive components.^2,11-17

No medications are FDA-approved for treating kleptomania. Therefore, it is important to inform patients of any off-label use of medications for this disorder, as well as the empirical basis for considering pharmacologic treatment.

SSRIs Only case reports exist on the use of SSRIs in treating kleptomania. The disorder may share a common pathology with pathologic gambling, and in our clinical experience appears to respond to similar treatments.¹⁸ We draw on research of pathologic gambling as well as our clinical experience in choosing SSRIs as first-line treatment, especially for patients with significant mood symptoms.¹⁹

We suggest titrating SSRIs to the maximum recommended dosage. As in the treatment of pathologic gambling, dosages of SSRIs required to treat kleptomania symptoms appear to be higher than average dosages required to treat depressive disorders. An SSRI should not be considered ineffective unless it has been tried for at least 10 to 12 weeks and the highest dosage tolerated or recommended by the manufacturer has been reached.

Response to SSRIs usually is characterized by decreased thoughts about stealing, decreased stealing behavior, and improvement in social and occupational functioning. If an SSRI is only partially effective, we consider augmentation with naltrexone, buspirone, or a mood stabilizer.

Naltrexone Patients taking naltrexone often report less-intense urges to steal. The urges may not disappear but are often sufficiently reduced so that the patient can resist them more easily. Patients also report that the thrill associated with stealing is reduced or eliminated.

Naltrexone was used in the first medication study of kleptomania and showed a significant decline in the intensity of urges to steal, stealing thoughts, and stealing behavior. Average dosage was 150 mg/d;¹¹ a reduced dosage (e.g., 50 mg/d) may work in adolescents with kleptomania.²⁰

Nausea as a side effect can be reduced by starting patients on 25 mg/d for the first 3 or 4 days and possibly adding ondansetron, 4 to 8 mg/d. Nausea and diarrhea are usually mild and resolve within the first week. Clinically, most patients respond to naltrexone within 2 weeks. After that, the dosage usually needs to be adjusted.

In patients with comorbid depression, augmentation with an SSRI may prevent worsening of untreated depressive symptoms. It is prudent to obtain liver function tests prior to naltrexone administration and again 3 to 4 weeks after starting the drug.²¹ Repeat testing should be performed at 2-to 4-week intervals for the next 2 months, then once a month for the following 3 months. After 6 months, testing three to four times a year is usually sufficient.

Nonsteroidal analgesics should not be used with high dosages of naltrexone (>50 mg/d), as concurrent use may increase the risk of hepatic transaminase elevation.²¹

Mood stabilizers Responses to lithium and valproate have been described in two case reports of patients with kleptomania.^14,15 In the case of valproate, the effective dosage was 2,000 mg/d, whereas lithium reduced stealing urges at a serum level of 0.5 mEq/L.

Although it would be premature to recommend the use of mood stabilizers, their possible benefit may be related to their efficacy in bipolar disorder treatment and the existence of features (e.g., impulsivity) shared by kleptomania and bipolar disorder.

Atypical antipsychotics Although there is no evidence that atypical antipsychotics are useful in kleptomania, augmenting an SSRI with an atypical neuroleptic may be beneficial. Atypical antipsychotics have been explored as augmenting agents in the treatment of nonpsychotic disorders and behaviors, including pathologic gambling and obsessive-compulsive disorder.

The role of psychotherapy

Cognitive-behavioral therapy Based on the evidence of its effectiveness in treating pathologic gambling, CBT may hold promise as monotherapy for mild cases of kleptomania.

Combination therapy Combined pharmacologic and behavioral therapy may be the optimal treatment strategy for kleptomania. In our experience, patients who respond only partially or fail to respond to pharmacotherapy alone are more likely to find relief with a combination of drug and cognitive-behavioral therapies.

Related resource

• Goldman MJ. Kleptomania: the compulsion to steal—what can be done? Far Hills, N New Horizon Press, 1998.
• Shoplifters Alternative http://www.shoplifters.org
• Impulse Control Disorders Clinic, University of Minnesota http://www.med.umn.edu/psychiatry/research/impulse.htm

Drug brand names

• Citalopram • Celexa
• Fluvoxamine • Luvox
• Imipramine • Tofranil
• Naltrexone • Revia
• Nortriptyline • Aventyl, Pamelor
• Paroxetine • Paxil
• Quetiapine • Seroquel
• Valproic acid • Depakote

Disclosure

The authors report no affiliation or financial arrangement with any of the companies whose products are mentioned in this article.

Even with psychiatry’s most effective and best studied agents, many patients with bipolar disorder are inadequately treated and respond insufficiently to available psychopharmacologic agents. To address this problem, the Stanley Foundation Bipolar Network (SFBN) was created to explore acute and long-term response to treatment of bipolar disorder.

For the past 6 years, our group (Box) has followed an international cohort of patients with bipolar disorder and offered them opportunities to participate in clinical trials at seven field centers. We have made considerable progress as we focused on the longitudinal course of bipolar illness and evaluated various combinations of psychopharmacologic therapies. The SFBN also has explored factors that increase the risk of suicide, quantified the incidence of anxiety disorder and substance abuse, and looked at other variables that may affect treatment outcome.

This report for the readers of Current Psychiatry provides a brief state-of-the-art overview of what we have learned about the course and management of bipolar disorder. It brings together and summarizes the findings from studies published, in press, or under review. Our goal is to update current findings, which may help you provide optimum care for these at-risk patients.

Box

In part one, we discuss the demographics of our cohort of 676 community-based bipolar patients, including risk factors for suicide attempts, frequency of comorbid psychiatric diagnoses, problems of overweight and obesity, and preliminary findings about thyroiditis.

In part two, we describe our clinical trials assessing mood stabilizers and adjunctive agents such as atypical antipsychotics, second-generation antidepressants, and anticonvulsants. We also will address a soon-to-be analyzed study of omega-3 fatty acids.

Table 1

CHARACTERISTICS OF THE 676 BIPOLAR OUTPATIENTS

Study population

The SFBN recruited outpatients with bipolar disorders I, II, or not otherwise specified (NOS). We did not exclude patients with comorbid illnesses, except those with active substance abuse disorder requiring treatment in another setting.¹ Patients were recruited almost exclusively from the community and rarely from inpatient hospitalization. The average age was 41, and 43% were college graduates. Most were employed but indicated that their illness limited their employment level or ability to function at work (Table 1).

One striking finding was a decadelong lag between the onset of symptoms reaching thresholds for diagnosis and the onset of first treatment.² This long delay could have adverse consequences for illness outcome and represents a major public health target. Age of onset appeared to have both genetic/familial and environmental determinants.³ Subjects with a history of both extreme early life adversities (i.e., physical or sexual abuse) and a positive family history of mood disorder had the earliest onset of bipolar illness. Those who had neither of these factors had late-onset illness.

Suicide attempts

Prior to network entry, 25 to 50% of our study population had made a serious suicide attempt (defined as requiring medical attention and/or hospitalization), pointing to bipolar disorder’s potential lethality.

History of abuse A history of physical or sexual abuse in childhood or adolescence was a prominent risk factor for attempted suicide.⁴ With either type of abuse there was an approximate 15% increase in incidence of suicide attempts over the baseline rate of about 25%. More than 55% of patients with a history of both physical and sexual abuse had made a serious suicide attempt. The frequency of physical and sexual abuse was also positively related to increased incidence of suicide attempts. Taken together, these data suggest a “stressor dose-response” relationship between adverse childhood or adolescent experiences and an increased incidence of suicide attempts.

Table 2

FACTORS THAT APPEAR TO INCREASE SUICIDE RISK IN BIPOLAR DISORDER*

Comorbidities Other factors that appear to be associated with bipolar disorder and increased risk of attempted suicide include anxiety and eating disorders, early onset of symptoms, at least four previous hospitalizations for depression, and medical comorbidity (Table 2). Limited access to psychiatric and medical services and inadequate health insurance also were correlated with having made a serious suicide attempt. Thus, lack of medical care might exacerbate demoralization and increase the risk of suicide.

Family history of suicide or serious suicide attempts and drug abuse were associated with an increase in suicide attempts, but family history of unipolar or bipolar illness were not. These data are consistent with other studies suggesting that vulnerability to suicide may have a separate genetic component from that of mood disorders per se.

Severity of illness Increased severity of bipolar illness also was associated with prior psychosocial stressors³ and serious suicide attempts. We confirmed self-reported history, using daily mood charting, the clinician-rated Inventory of Depressive Symptomatology (IDS-C), and the Young Mania Rating Scale (YMRS) to rate increase in percentage of time ill, percentage of time depressed, and severity of depression.

Clinical implications We are uncertain how directly these data regarding suicide attempts relate to completed suicide. However, patients with bipolar disorder are among those at highest risk for completed suicide, and a prior serious attempt is often a precursor to completed suicide.^5,6

Factors that appear particularly related to increased risk of suicide in patients with bipolar disorder are family history of suicide, history of early psychosocial stressors, comorbid personality disorders, substance abuse, and a relatively severe course of bipolar illness. Patients with these risk factors need support for two types of psychosocial stressors:

• poor access to health care
• stressors related to concurrent events (e.g., occurring with new affective episodes).

It may also be important for clinicians to consider the prophylactic use of lithium because of its demonstrated ability to reduce mortality in bipolar illness.⁷ Additionally, we need data on the efficacy of new drugs in preventing affective episodes and reducing suicidal ideation and acts.

Common comorbidities

We found considerable axis I lifetime comorbidities in the SFBN cohort (Table 3), including a 42% incidence of anxiety disorder and a similarly high rate of substance abuse. In addition to bipolar disorder, patients averaged approximately two lifetime comorbid diagnoses:

• 35% had none
• 65% had one or more
• 42% had two or more
• 24% had three or more.

Table 3

PSYCHIATRIC COMORBIDITY IN BIPOLAR OUTPATIENTS (%)*.

Men with bipolar disorder had a higher absolute prevalence of alcoholism, but the relative risk compared with the general population was much higher in women (odds ratio 7.35) compared with men (odds ratio 2.77). In women, alcohol use and abuse were related to history of social phobia, greater number of depressive episodes prior to network entry, and history of abusing more than one substance. In men, alcohol comorbidity was related to history of alcohol abuse in first-degree relatives and history of early physical abuse.

These data suggest that female patients, in particular, were self-medicating their affective episodes and comorbid anxiety disorders with alcohol. They suggest the importance of asking patients directly about alcohol use to identify the need for primary and secondary prevention. In an adolescent or young adult, affective illness—and bipolar disorder in particular—should be considered a major risk factor for subsequent problems with alcohol and drug abuse. When taking a careful history, the treating physician should include questions regarding any substance abuse.

Overweight and obesity

One-half of the women and two-thirds of the men in the SFBN were overweight at network entry.⁸ Although this rate of overweight sounds alarmingly high, it was not significantly different from rates in the general U.S. population. A greater percentage of women than men in the network had morbid obesity, however.

In our cohort, being overweight or obese was associated with an increased incidence of cardiovascular disease, diabetes, arthritis, hypertension, hypothyroidism, and cancer. The degree of obesity also correlated significantly with past use of the numerous psychotropic drugs that have been associated with weight gain. Also, as might be expected, increased weight was associated with physical inactivity.

Many of the psychotropic drugs routinely used to treat bipolar disorder are associated with weight gain. Among these are the mood stabilizers lithium and valproate and the atypical antipsychotics, with the exception of ziprasidone (and, to follow, aripiprazole). Lithium’s liability to cause weight gain may be counterbalanced by its antisuicide effects and its ability to reverse excess medical mortality associated with affective illness. Thus, lithium should continue to play a major therapeutic role in bipolar disorder.

It may be more effective and easier to prevent weight gain than to attempt to reduce weight that has been gained. Recommending exercise and other weight-reduction measures may be helpful, as may co-administering drugs associated with weight loss, such as topiramate.⁹

Thyroiditis

Antithyroid antibodies were detected in 28% of network patients, compared with rates of 3% in the general population and 18% in psychiatric controls.¹⁰ The increased rate was associated with the need to augment thyroid function in 17% of network patients, but it was not related to age, mood state, rapid cycling status, or lithium treatment.

These data indicate that bipolar patients are prone to autoimmune thyroid changes. Further analysis is required to ascertain whether this finding has therapeutic implications, especially related to adjunctive T3 and T4 treatment.¹¹

Even with psychiatry’s most effective and best studied agents, many patients with bipolar disorder are inadequately treated and respond insufficiently to available psychopharmacologic agents. To address this problem, the Stanley Foundation Bipolar Network (SFBN) was created to explore acute and long-term response to treatment of bipolar disorder.

For the past 6 years, our group (Box) has followed an international cohort of patients with bipolar disorder and offered them opportunities to participate in clinical trials at seven field centers. We have made considerable progress as we focused on the longitudinal course of bipolar illness and evaluated various combinations of psychopharmacologic therapies. The SFBN also has explored factors that increase the risk of suicide, quantified the incidence of anxiety disorder and substance abuse, and looked at other variables that may affect treatment outcome.

This report for the readers of Current Psychiatry provides a brief state-of-the-art overview of what we have learned about the course and management of bipolar disorder. It brings together and summarizes the findings from studies published, in press, or under review. Our goal is to update current findings, which may help you provide optimum care for these at-risk patients.

Box

In part one, we discuss the demographics of our cohort of 676 community-based bipolar patients, including risk factors for suicide attempts, frequency of comorbid psychiatric diagnoses, problems of overweight and obesity, and preliminary findings about thyroiditis.

In part two, we describe our clinical trials assessing mood stabilizers and adjunctive agents such as atypical antipsychotics, second-generation antidepressants, and anticonvulsants. We also will address a soon-to-be analyzed study of omega-3 fatty acids.

Table 1

CHARACTERISTICS OF THE 676 BIPOLAR OUTPATIENTS

Study population

The SFBN recruited outpatients with bipolar disorders I, II, or not otherwise specified (NOS). We did not exclude patients with comorbid illnesses, except those with active substance abuse disorder requiring treatment in another setting.¹ Patients were recruited almost exclusively from the community and rarely from inpatient hospitalization. The average age was 41, and 43% were college graduates. Most were employed but indicated that their illness limited their employment level or ability to function at work (Table 1).

One striking finding was a decadelong lag between the onset of symptoms reaching thresholds for diagnosis and the onset of first treatment.² This long delay could have adverse consequences for illness outcome and represents a major public health target. Age of onset appeared to have both genetic/familial and environmental determinants.³ Subjects with a history of both extreme early life adversities (i.e., physical or sexual abuse) and a positive family history of mood disorder had the earliest onset of bipolar illness. Those who had neither of these factors had late-onset illness.

Suicide attempts

Prior to network entry, 25 to 50% of our study population had made a serious suicide attempt (defined as requiring medical attention and/or hospitalization), pointing to bipolar disorder’s potential lethality.

History of abuse A history of physical or sexual abuse in childhood or adolescence was a prominent risk factor for attempted suicide.⁴ With either type of abuse there was an approximate 15% increase in incidence of suicide attempts over the baseline rate of about 25%. More than 55% of patients with a history of both physical and sexual abuse had made a serious suicide attempt. The frequency of physical and sexual abuse was also positively related to increased incidence of suicide attempts. Taken together, these data suggest a “stressor dose-response” relationship between adverse childhood or adolescent experiences and an increased incidence of suicide attempts.

Table 2

FACTORS THAT APPEAR TO INCREASE SUICIDE RISK IN BIPOLAR DISORDER*

Comorbidities Other factors that appear to be associated with bipolar disorder and increased risk of attempted suicide include anxiety and eating disorders, early onset of symptoms, at least four previous hospitalizations for depression, and medical comorbidity (Table 2). Limited access to psychiatric and medical services and inadequate health insurance also were correlated with having made a serious suicide attempt. Thus, lack of medical care might exacerbate demoralization and increase the risk of suicide.

Family history of suicide or serious suicide attempts and drug abuse were associated with an increase in suicide attempts, but family history of unipolar or bipolar illness were not. These data are consistent with other studies suggesting that vulnerability to suicide may have a separate genetic component from that of mood disorders per se.

Severity of illness Increased severity of bipolar illness also was associated with prior psychosocial stressors³ and serious suicide attempts. We confirmed self-reported history, using daily mood charting, the clinician-rated Inventory of Depressive Symptomatology (IDS-C), and the Young Mania Rating Scale (YMRS) to rate increase in percentage of time ill, percentage of time depressed, and severity of depression.

Clinical implications We are uncertain how directly these data regarding suicide attempts relate to completed suicide. However, patients with bipolar disorder are among those at highest risk for completed suicide, and a prior serious attempt is often a precursor to completed suicide.^5,6

Factors that appear particularly related to increased risk of suicide in patients with bipolar disorder are family history of suicide, history of early psychosocial stressors, comorbid personality disorders, substance abuse, and a relatively severe course of bipolar illness. Patients with these risk factors need support for two types of psychosocial stressors:

• poor access to health care
• stressors related to concurrent events (e.g., occurring with new affective episodes).

It may also be important for clinicians to consider the prophylactic use of lithium because of its demonstrated ability to reduce mortality in bipolar illness.⁷ Additionally, we need data on the efficacy of new drugs in preventing affective episodes and reducing suicidal ideation and acts.

Common comorbidities

We found considerable axis I lifetime comorbidities in the SFBN cohort (Table 3), including a 42% incidence of anxiety disorder and a similarly high rate of substance abuse. In addition to bipolar disorder, patients averaged approximately two lifetime comorbid diagnoses:

• 35% had none
• 65% had one or more
• 42% had two or more
• 24% had three or more.

Table 3

PSYCHIATRIC COMORBIDITY IN BIPOLAR OUTPATIENTS (%)*.

Men with bipolar disorder had a higher absolute prevalence of alcoholism, but the relative risk compared with the general population was much higher in women (odds ratio 7.35) compared with men (odds ratio 2.77). In women, alcohol use and abuse were related to history of social phobia, greater number of depressive episodes prior to network entry, and history of abusing more than one substance. In men, alcohol comorbidity was related to history of alcohol abuse in first-degree relatives and history of early physical abuse.

These data suggest that female patients, in particular, were self-medicating their affective episodes and comorbid anxiety disorders with alcohol. They suggest the importance of asking patients directly about alcohol use to identify the need for primary and secondary prevention. In an adolescent or young adult, affective illness—and bipolar disorder in particular—should be considered a major risk factor for subsequent problems with alcohol and drug abuse. When taking a careful history, the treating physician should include questions regarding any substance abuse.

Overweight and obesity

One-half of the women and two-thirds of the men in the SFBN were overweight at network entry.⁸ Although this rate of overweight sounds alarmingly high, it was not significantly different from rates in the general U.S. population. A greater percentage of women than men in the network had morbid obesity, however.

In our cohort, being overweight or obese was associated with an increased incidence of cardiovascular disease, diabetes, arthritis, hypertension, hypothyroidism, and cancer. The degree of obesity also correlated significantly with past use of the numerous psychotropic drugs that have been associated with weight gain. Also, as might be expected, increased weight was associated with physical inactivity.

Many of the psychotropic drugs routinely used to treat bipolar disorder are associated with weight gain. Among these are the mood stabilizers lithium and valproate and the atypical antipsychotics, with the exception of ziprasidone (and, to follow, aripiprazole). Lithium’s liability to cause weight gain may be counterbalanced by its antisuicide effects and its ability to reverse excess medical mortality associated with affective illness. Thus, lithium should continue to play a major therapeutic role in bipolar disorder.

It may be more effective and easier to prevent weight gain than to attempt to reduce weight that has been gained. Recommending exercise and other weight-reduction measures may be helpful, as may co-administering drugs associated with weight loss, such as topiramate.⁹

Thyroiditis

Antithyroid antibodies were detected in 28% of network patients, compared with rates of 3% in the general population and 18% in psychiatric controls.¹⁰ The increased rate was associated with the need to augment thyroid function in 17% of network patients, but it was not related to age, mood state, rapid cycling status, or lithium treatment.

These data indicate that bipolar patients are prone to autoimmune thyroid changes. Further analysis is required to ascertain whether this finding has therapeutic implications, especially related to adjunctive T3 and T4 treatment.¹¹

Even with psychiatry’s most effective and best studied agents, many patients with bipolar disorder are inadequately treated and respond insufficiently to available psychopharmacologic agents. To address this problem, the Stanley Foundation Bipolar Network (SFBN) was created to explore acute and long-term response to treatment of bipolar disorder.

For the past 6 years, our group (Box) has followed an international cohort of patients with bipolar disorder and offered them opportunities to participate in clinical trials at seven field centers. We have made considerable progress as we focused on the longitudinal course of bipolar illness and evaluated various combinations of psychopharmacologic therapies. The SFBN also has explored factors that increase the risk of suicide, quantified the incidence of anxiety disorder and substance abuse, and looked at other variables that may affect treatment outcome.

This report for the readers of Current Psychiatry provides a brief state-of-the-art overview of what we have learned about the course and management of bipolar disorder. It brings together and summarizes the findings from studies published, in press, or under review. Our goal is to update current findings, which may help you provide optimum care for these at-risk patients.

Box

In part one, we discuss the demographics of our cohort of 676 community-based bipolar patients, including risk factors for suicide attempts, frequency of comorbid psychiatric diagnoses, problems of overweight and obesity, and preliminary findings about thyroiditis.

In part two, we describe our clinical trials assessing mood stabilizers and adjunctive agents such as atypical antipsychotics, second-generation antidepressants, and anticonvulsants. We also will address a soon-to-be analyzed study of omega-3 fatty acids.

Table 1

CHARACTERISTICS OF THE 676 BIPOLAR OUTPATIENTS

Study population

The SFBN recruited outpatients with bipolar disorders I, II, or not otherwise specified (NOS). We did not exclude patients with comorbid illnesses, except those with active substance abuse disorder requiring treatment in another setting.¹ Patients were recruited almost exclusively from the community and rarely from inpatient hospitalization. The average age was 41, and 43% were college graduates. Most were employed but indicated that their illness limited their employment level or ability to function at work (Table 1).

One striking finding was a decadelong lag between the onset of symptoms reaching thresholds for diagnosis and the onset of first treatment.² This long delay could have adverse consequences for illness outcome and represents a major public health target. Age of onset appeared to have both genetic/familial and environmental determinants.³ Subjects with a history of both extreme early life adversities (i.e., physical or sexual abuse) and a positive family history of mood disorder had the earliest onset of bipolar illness. Those who had neither of these factors had late-onset illness.

Suicide attempts

Prior to network entry, 25 to 50% of our study population had made a serious suicide attempt (defined as requiring medical attention and/or hospitalization), pointing to bipolar disorder’s potential lethality.

History of abuse A history of physical or sexual abuse in childhood or adolescence was a prominent risk factor for attempted suicide.⁴ With either type of abuse there was an approximate 15% increase in incidence of suicide attempts over the baseline rate of about 25%. More than 55% of patients with a history of both physical and sexual abuse had made a serious suicide attempt. The frequency of physical and sexual abuse was also positively related to increased incidence of suicide attempts. Taken together, these data suggest a “stressor dose-response” relationship between adverse childhood or adolescent experiences and an increased incidence of suicide attempts.

Table 2

FACTORS THAT APPEAR TO INCREASE SUICIDE RISK IN BIPOLAR DISORDER*

Comorbidities Other factors that appear to be associated with bipolar disorder and increased risk of attempted suicide include anxiety and eating disorders, early onset of symptoms, at least four previous hospitalizations for depression, and medical comorbidity (Table 2). Limited access to psychiatric and medical services and inadequate health insurance also were correlated with having made a serious suicide attempt. Thus, lack of medical care might exacerbate demoralization and increase the risk of suicide.

Family history of suicide or serious suicide attempts and drug abuse were associated with an increase in suicide attempts, but family history of unipolar or bipolar illness were not. These data are consistent with other studies suggesting that vulnerability to suicide may have a separate genetic component from that of mood disorders per se.

Severity of illness Increased severity of bipolar illness also was associated with prior psychosocial stressors³ and serious suicide attempts. We confirmed self-reported history, using daily mood charting, the clinician-rated Inventory of Depressive Symptomatology (IDS-C), and the Young Mania Rating Scale (YMRS) to rate increase in percentage of time ill, percentage of time depressed, and severity of depression.

Clinical implications We are uncertain how directly these data regarding suicide attempts relate to completed suicide. However, patients with bipolar disorder are among those at highest risk for completed suicide, and a prior serious attempt is often a precursor to completed suicide.^5,6

Factors that appear particularly related to increased risk of suicide in patients with bipolar disorder are family history of suicide, history of early psychosocial stressors, comorbid personality disorders, substance abuse, and a relatively severe course of bipolar illness. Patients with these risk factors need support for two types of psychosocial stressors:

• poor access to health care
• stressors related to concurrent events (e.g., occurring with new affective episodes).

It may also be important for clinicians to consider the prophylactic use of lithium because of its demonstrated ability to reduce mortality in bipolar illness.⁷ Additionally, we need data on the efficacy of new drugs in preventing affective episodes and reducing suicidal ideation and acts.

Common comorbidities

We found considerable axis I lifetime comorbidities in the SFBN cohort (Table 3), including a 42% incidence of anxiety disorder and a similarly high rate of substance abuse. In addition to bipolar disorder, patients averaged approximately two lifetime comorbid diagnoses:

• 35% had none
• 65% had one or more
• 42% had two or more
• 24% had three or more.

Table 3

PSYCHIATRIC COMORBIDITY IN BIPOLAR OUTPATIENTS (%)*.

Men with bipolar disorder had a higher absolute prevalence of alcoholism, but the relative risk compared with the general population was much higher in women (odds ratio 7.35) compared with men (odds ratio 2.77). In women, alcohol use and abuse were related to history of social phobia, greater number of depressive episodes prior to network entry, and history of abusing more than one substance. In men, alcohol comorbidity was related to history of alcohol abuse in first-degree relatives and history of early physical abuse.

These data suggest that female patients, in particular, were self-medicating their affective episodes and comorbid anxiety disorders with alcohol. They suggest the importance of asking patients directly about alcohol use to identify the need for primary and secondary prevention. In an adolescent or young adult, affective illness—and bipolar disorder in particular—should be considered a major risk factor for subsequent problems with alcohol and drug abuse. When taking a careful history, the treating physician should include questions regarding any substance abuse.

Overweight and obesity

One-half of the women and two-thirds of the men in the SFBN were overweight at network entry.⁸ Although this rate of overweight sounds alarmingly high, it was not significantly different from rates in the general U.S. population. A greater percentage of women than men in the network had morbid obesity, however.

In our cohort, being overweight or obese was associated with an increased incidence of cardiovascular disease, diabetes, arthritis, hypertension, hypothyroidism, and cancer. The degree of obesity also correlated significantly with past use of the numerous psychotropic drugs that have been associated with weight gain. Also, as might be expected, increased weight was associated with physical inactivity.

Many of the psychotropic drugs routinely used to treat bipolar disorder are associated with weight gain. Among these are the mood stabilizers lithium and valproate and the atypical antipsychotics, with the exception of ziprasidone (and, to follow, aripiprazole). Lithium’s liability to cause weight gain may be counterbalanced by its antisuicide effects and its ability to reverse excess medical mortality associated with affective illness. Thus, lithium should continue to play a major therapeutic role in bipolar disorder.

It may be more effective and easier to prevent weight gain than to attempt to reduce weight that has been gained. Recommending exercise and other weight-reduction measures may be helpful, as may co-administering drugs associated with weight loss, such as topiramate.⁹

Thyroiditis

Antithyroid antibodies were detected in 28% of network patients, compared with rates of 3% in the general population and 18% in psychiatric controls.¹⁰ The increased rate was associated with the need to augment thyroid function in 17% of network patients, but it was not related to age, mood state, rapid cycling status, or lithium treatment.

These data indicate that bipolar patients are prone to autoimmune thyroid changes. Further analysis is required to ascertain whether this finding has therapeutic implications, especially related to adjunctive T3 and T4 treatment.¹¹

ABSTRACT

BACKGROUND: Many individuals with asthma are allergic to house dust mites. The incidence and severity of asthma is increasing. More people are seeking complementary medical care, including homeopathy. Homeopathy attempts to mitigate disease by diluting the treatment without diluting the effect.

POPULATION STUDIED: The investigators recruited 1000 asthmatic outpatients from 38 general practices in Hampshire and Dorset, England. Of these, 327 tested positive for house dust mite allergy. Eighty-five patients were excluded for asthma that was either too mild or too well-controlled. Thus 242 subjects between 18 and 55 years old were randomized into the study. This group included both sexes; no note was made of race.

STUDY DESIGN AND VALIDITY: A double-blind, randomized control design was used. A French manufacturer of homeopathic products prepared the active agent by making 30 sequential 1:100 dilutions of a house dust mite allergen (this “ultramolecular” is a highly diluted solution of allergen molecules). After a 4-week period to assess baseline symptoms, subjects were randomized to receive either an oral homeopathic immunotherapy preparation or a similarly prepared placebo in 3 doses over 24 hours. They were then followed for 16 weeks with 3 clinic visits and every-other-week symptom diaries.

OUTCOMES MEASURED: Primary outcomes were change in lung function as measured by forced expiratory volume in 1 second (FEV₁) and quality of life as measured by proportion of symptom-free days in each 7-day diary period. Other outcomes included peak expiratory flow, scores for asthma visual analogue scale, and average mood scores.

RESULTS: This homeopathic therapy showed no significant improvement over placebo with regard to FEV₁ (0.136 L/sec active agent vs 0.414 L/sec placebo, 95% confidence interval [CI] =0.136–0.693) or mean improvement in quality of life (0.090 active agent vs 0.117 placebo, 95% CI = –.096 to .0150). Neither was there any significant difference in any of the secondary outcomes. These results were independent of the subjects’ belief in complementary medicine. Interestingly, at different times during the study improvement was noted in both the active therapy and placebo groups in FEV₁, quality of life, and mood.

ABSTRACT

BACKGROUND: Many individuals with asthma are allergic to house dust mites. The incidence and severity of asthma is increasing. More people are seeking complementary medical care, including homeopathy. Homeopathy attempts to mitigate disease by diluting the treatment without diluting the effect.

POPULATION STUDIED: The investigators recruited 1000 asthmatic outpatients from 38 general practices in Hampshire and Dorset, England. Of these, 327 tested positive for house dust mite allergy. Eighty-five patients were excluded for asthma that was either too mild or too well-controlled. Thus 242 subjects between 18 and 55 years old were randomized into the study. This group included both sexes; no note was made of race.

STUDY DESIGN AND VALIDITY: A double-blind, randomized control design was used. A French manufacturer of homeopathic products prepared the active agent by making 30 sequential 1:100 dilutions of a house dust mite allergen (this “ultramolecular” is a highly diluted solution of allergen molecules). After a 4-week period to assess baseline symptoms, subjects were randomized to receive either an oral homeopathic immunotherapy preparation or a similarly prepared placebo in 3 doses over 24 hours. They were then followed for 16 weeks with 3 clinic visits and every-other-week symptom diaries.

OUTCOMES MEASURED: Primary outcomes were change in lung function as measured by forced expiratory volume in 1 second (FEV₁) and quality of life as measured by proportion of symptom-free days in each 7-day diary period. Other outcomes included peak expiratory flow, scores for asthma visual analogue scale, and average mood scores.

RESULTS: This homeopathic therapy showed no significant improvement over placebo with regard to FEV₁ (0.136 L/sec active agent vs 0.414 L/sec placebo, 95% confidence interval [CI] =0.136–0.693) or mean improvement in quality of life (0.090 active agent vs 0.117 placebo, 95% CI = –.096 to .0150). Neither was there any significant difference in any of the secondary outcomes. These results were independent of the subjects’ belief in complementary medicine. Interestingly, at different times during the study improvement was noted in both the active therapy and placebo groups in FEV₁, quality of life, and mood.

ABSTRACT

BACKGROUND: Many individuals with asthma are allergic to house dust mites. The incidence and severity of asthma is increasing. More people are seeking complementary medical care, including homeopathy. Homeopathy attempts to mitigate disease by diluting the treatment without diluting the effect.

POPULATION STUDIED: The investigators recruited 1000 asthmatic outpatients from 38 general practices in Hampshire and Dorset, England. Of these, 327 tested positive for house dust mite allergy. Eighty-five patients were excluded for asthma that was either too mild or too well-controlled. Thus 242 subjects between 18 and 55 years old were randomized into the study. This group included both sexes; no note was made of race.

STUDY DESIGN AND VALIDITY: A double-blind, randomized control design was used. A French manufacturer of homeopathic products prepared the active agent by making 30 sequential 1:100 dilutions of a house dust mite allergen (this “ultramolecular” is a highly diluted solution of allergen molecules). After a 4-week period to assess baseline symptoms, subjects were randomized to receive either an oral homeopathic immunotherapy preparation or a similarly prepared placebo in 3 doses over 24 hours. They were then followed for 16 weeks with 3 clinic visits and every-other-week symptom diaries.

OUTCOMES MEASURED: Primary outcomes were change in lung function as measured by forced expiratory volume in 1 second (FEV₁) and quality of life as measured by proportion of symptom-free days in each 7-day diary period. Other outcomes included peak expiratory flow, scores for asthma visual analogue scale, and average mood scores.

RESULTS: This homeopathic therapy showed no significant improvement over placebo with regard to FEV₁ (0.136 L/sec active agent vs 0.414 L/sec placebo, 95% confidence interval [CI] =0.136–0.693) or mean improvement in quality of life (0.090 active agent vs 0.117 placebo, 95% CI = –.096 to .0150). Neither was there any significant difference in any of the secondary outcomes. These results were independent of the subjects’ belief in complementary medicine. Interestingly, at different times during the study improvement was noted in both the active therapy and placebo groups in FEV₁, quality of life, and mood.

ABSTRACT

BACKGROUND: Historically, nebulizers have been preferred over metered-dose inhalers (MDIs) for the treatment of asthma exacerbations, although numerous studies have shown their equivalence. A systematic review of 21 randomized trials supported the equivalence of an MDI with spacer and a nebulizer; the method of albuterol delivery did not affect hospital admission rates, length of stay in the emergency department, or measures of pulmonary function.¹ Advantages of MDIs may include lower costs, less excess drug exposure, and easier use for patients and physicians.

POPULATION STUDIED: The study population consisted of all patients older than 18 years who presented to an emergency department over a 2.5-year period with an asthma exacerbation (2342 visits, 1429 patients). Most patients were African American (75.4%). Most were women (58.6%), and the mean age was 35.5 ± 13.5 years.

STUDY DESIGN AND VALIDITY: The study was a large, prospective, unblinded, and nonrandomized trial consisting of 2 phases. For the first 12 months, physicians, using standard National Institues of Health guidelines, began treatment with a nebulizer (913 visits). Then for the next 18 months, physicians began treatment with albuterol delivered via MDI and spacer (1429 visits). The dose was 5 puffs, then 3 to 5 puffs every 20 minutes as needed. At the time of discharge from the emergency department during the MDI phase of the study, patients received a peak flow meter, an MDI and spacer, an inhaled corticosteroid, written materials, and counseling by emergency department nurses.

OUTCOMES MEASURED: The outcomes measured were PEFR, Sao ₂, heart and respiratory rates, total albuterol dose, and the more patient-oriented outcomes of rate of hospital admission, relapse rate, time in the emergency department, and costs.

RESULTS: In the MDI phase, post-albuterol PEFR was 11.0% higher (342 L/min vs 308 L/min; P = .001) and change in PEFR was 13.3% higher (127 L/min vs 112 L/min; P = .002). Change in Sao ₂ was significant (P = .043), and the total albuterol dose was significantly less in the MDI group (1125 μg vs 6700 μg; P = .001). However, these differences did not result in significantly lower hospital admission rates. Relapse rates were significantly lower at both 14 and 21 days in the MDI phase (6.6% and 10.7% vs 9.6% and 13.5%; P < .01 and P < .05). Patients treated with MDIs spent 6.5% less time in the emergency department (163.6 min vs 175.0 min; P = .007). The difference in visit charges was not significant.

ABSTRACT

BACKGROUND: Historically, nebulizers have been preferred over metered-dose inhalers (MDIs) for the treatment of asthma exacerbations, although numerous studies have shown their equivalence. A systematic review of 21 randomized trials supported the equivalence of an MDI with spacer and a nebulizer; the method of albuterol delivery did not affect hospital admission rates, length of stay in the emergency department, or measures of pulmonary function.¹ Advantages of MDIs may include lower costs, less excess drug exposure, and easier use for patients and physicians.

POPULATION STUDIED: The study population consisted of all patients older than 18 years who presented to an emergency department over a 2.5-year period with an asthma exacerbation (2342 visits, 1429 patients). Most patients were African American (75.4%). Most were women (58.6%), and the mean age was 35.5 ± 13.5 years.

STUDY DESIGN AND VALIDITY: The study was a large, prospective, unblinded, and nonrandomized trial consisting of 2 phases. For the first 12 months, physicians, using standard National Institues of Health guidelines, began treatment with a nebulizer (913 visits). Then for the next 18 months, physicians began treatment with albuterol delivered via MDI and spacer (1429 visits). The dose was 5 puffs, then 3 to 5 puffs every 20 minutes as needed. At the time of discharge from the emergency department during the MDI phase of the study, patients received a peak flow meter, an MDI and spacer, an inhaled corticosteroid, written materials, and counseling by emergency department nurses.

OUTCOMES MEASURED: The outcomes measured were PEFR, Sao ₂, heart and respiratory rates, total albuterol dose, and the more patient-oriented outcomes of rate of hospital admission, relapse rate, time in the emergency department, and costs.

RESULTS: In the MDI phase, post-albuterol PEFR was 11.0% higher (342 L/min vs 308 L/min; P = .001) and change in PEFR was 13.3% higher (127 L/min vs 112 L/min; P = .002). Change in Sao ₂ was significant (P = .043), and the total albuterol dose was significantly less in the MDI group (1125 μg vs 6700 μg; P = .001). However, these differences did not result in significantly lower hospital admission rates. Relapse rates were significantly lower at both 14 and 21 days in the MDI phase (6.6% and 10.7% vs 9.6% and 13.5%; P < .01 and P < .05). Patients treated with MDIs spent 6.5% less time in the emergency department (163.6 min vs 175.0 min; P = .007). The difference in visit charges was not significant.

ABSTRACT

BACKGROUND: Historically, nebulizers have been preferred over metered-dose inhalers (MDIs) for the treatment of asthma exacerbations, although numerous studies have shown their equivalence. A systematic review of 21 randomized trials supported the equivalence of an MDI with spacer and a nebulizer; the method of albuterol delivery did not affect hospital admission rates, length of stay in the emergency department, or measures of pulmonary function.¹ Advantages of MDIs may include lower costs, less excess drug exposure, and easier use for patients and physicians.

POPULATION STUDIED: The study population consisted of all patients older than 18 years who presented to an emergency department over a 2.5-year period with an asthma exacerbation (2342 visits, 1429 patients). Most patients were African American (75.4%). Most were women (58.6%), and the mean age was 35.5 ± 13.5 years.

STUDY DESIGN AND VALIDITY: The study was a large, prospective, unblinded, and nonrandomized trial consisting of 2 phases. For the first 12 months, physicians, using standard National Institues of Health guidelines, began treatment with a nebulizer (913 visits). Then for the next 18 months, physicians began treatment with albuterol delivered via MDI and spacer (1429 visits). The dose was 5 puffs, then 3 to 5 puffs every 20 minutes as needed. At the time of discharge from the emergency department during the MDI phase of the study, patients received a peak flow meter, an MDI and spacer, an inhaled corticosteroid, written materials, and counseling by emergency department nurses.

OUTCOMES MEASURED: The outcomes measured were PEFR, Sao ₂, heart and respiratory rates, total albuterol dose, and the more patient-oriented outcomes of rate of hospital admission, relapse rate, time in the emergency department, and costs.

RESULTS: In the MDI phase, post-albuterol PEFR was 11.0% higher (342 L/min vs 308 L/min; P = .001) and change in PEFR was 13.3% higher (127 L/min vs 112 L/min; P = .002). Change in Sao ₂ was significant (P = .043), and the total albuterol dose was significantly less in the MDI group (1125 μg vs 6700 μg; P = .001). However, these differences did not result in significantly lower hospital admission rates. Relapse rates were significantly lower at both 14 and 21 days in the MDI phase (6.6% and 10.7% vs 9.6% and 13.5%; P < .01 and P < .05). Patients treated with MDIs spent 6.5% less time in the emergency department (163.6 min vs 175.0 min; P = .007). The difference in visit charges was not significant.

ABSTRACT

BACKGROUND: Bolus intravenous (IV) albuterol (salbutamol) improved outcomes in pediatric patients with severe asthma exacerbations in 1 earlier small study. Previous studies demonstrated that the addition of nebulized ipratropium bromide to initial emergency department therapy improves pulmonary function, but it is unclear whether combining the therapies results in earlier hospital discharge. This study compared these 2 approaches to determine their relative benefit in children with acute severe asthma.

POPULATION STUDIED: The researchers studied 55 children (aged 1–14 years) presenting with severe acute asthma to the emergency department of a ter-tiary children’s hospital in Sydney, Australia. Children were classified as having severe asthma if they had all 4 features of respiratory distress (wheezing, sternal retraction, accessory muscle use, and dyspnea) or had any of the absolute criteria (cyanosis, pulsus paradoxus, altered consciousness, or a silent chest auscultation). Baseline demographics and clinical characteristics were similar. Children who were excluded included those with life-threatening asthma, age younger than 12 months, presence of heart disease, family history of Wolff-Parkinson-White or past supraventricular tachycardia, other respiratory disease, or pneumonia, and those who had received inhaled ipratropium bromide that day.

STUDY DESIGN AND VALIDITY: This was a randomized, double-blind, double-dummy trial. The enrolling physician, treating physician, and assessor of outcome were all blinded. All children received 1 dose of nebulized albuterol 2.5 or 5 mg, then were assessed for asthma severity. Children meeting inclusion criteria received oxygen as needed, 1 mg/kg IV bolus methylprednisolone, and nebulized albuterol every 20 minutes for the first hour. The frequency of nebulized albuterol was then decreased based on clinical improvement. Patients were then randomized to receive IV albuterol (15 μg/kg); IV saline and inhaled ipratropium bromide (250 mg) every 20 minutes; or IV albuterol (15 μg/kg) and inhaled ipratropium bromide (250 μg) every 20 minutes. Asthma severity was assessed at 1 and 2 hours into the study using the clinical assessment scale and pulmonary index score. All 55 children completed the study.

OUTCOMES MEASURED: The primary outcomes for this study were mean recovery time (time from randomization to when patients no longer needed nebulized albuterol of a given frequency) and mean discharge time from the hospital. Secondary outcomes included clinical signs of moderate to severe asthma 2 hours after randomization and incidence of medication-related side effects.

RESULTS: Children treated with IV albuterol showed a significant benefit over those treated with inhaled ipratropium in recovery at 90, 120, and 180 minutes (P = .007, .01, and .004, respectively). Children in the IV albuterol group were ready for discharge 28.0 hours earlier than those in the ipratropium group (48.3 vs 76.3 hours; P = .005). The combination of IV albuterol and ipratropium showed a significant benefit over ipratropium alone in recovery time at 90 and 120 minutes (P = .02 and .008, respectively). However, no significant difference was evident between the combination and ipratropium alone in time to discharge (57.6 vs 76.3 hours, respectively; P = .2). The combination demonstrated no significant benefit over IV albuterol for any outcome. No significant adverse effects were documented in any of the patients, including tachycardia of more than 200 beats per minute for at least 5 minutes.

ABSTRACT

BACKGROUND: Bolus intravenous (IV) albuterol (salbutamol) improved outcomes in pediatric patients with severe asthma exacerbations in 1 earlier small study. Previous studies demonstrated that the addition of nebulized ipratropium bromide to initial emergency department therapy improves pulmonary function, but it is unclear whether combining the therapies results in earlier hospital discharge. This study compared these 2 approaches to determine their relative benefit in children with acute severe asthma.

POPULATION STUDIED: The researchers studied 55 children (aged 1–14 years) presenting with severe acute asthma to the emergency department of a ter-tiary children’s hospital in Sydney, Australia. Children were classified as having severe asthma if they had all 4 features of respiratory distress (wheezing, sternal retraction, accessory muscle use, and dyspnea) or had any of the absolute criteria (cyanosis, pulsus paradoxus, altered consciousness, or a silent chest auscultation). Baseline demographics and clinical characteristics were similar. Children who were excluded included those with life-threatening asthma, age younger than 12 months, presence of heart disease, family history of Wolff-Parkinson-White or past supraventricular tachycardia, other respiratory disease, or pneumonia, and those who had received inhaled ipratropium bromide that day.

STUDY DESIGN AND VALIDITY: This was a randomized, double-blind, double-dummy trial. The enrolling physician, treating physician, and assessor of outcome were all blinded. All children received 1 dose of nebulized albuterol 2.5 or 5 mg, then were assessed for asthma severity. Children meeting inclusion criteria received oxygen as needed, 1 mg/kg IV bolus methylprednisolone, and nebulized albuterol every 20 minutes for the first hour. The frequency of nebulized albuterol was then decreased based on clinical improvement. Patients were then randomized to receive IV albuterol (15 μg/kg); IV saline and inhaled ipratropium bromide (250 mg) every 20 minutes; or IV albuterol (15 μg/kg) and inhaled ipratropium bromide (250 μg) every 20 minutes. Asthma severity was assessed at 1 and 2 hours into the study using the clinical assessment scale and pulmonary index score. All 55 children completed the study.

OUTCOMES MEASURED: The primary outcomes for this study were mean recovery time (time from randomization to when patients no longer needed nebulized albuterol of a given frequency) and mean discharge time from the hospital. Secondary outcomes included clinical signs of moderate to severe asthma 2 hours after randomization and incidence of medication-related side effects.

RESULTS: Children treated with IV albuterol showed a significant benefit over those treated with inhaled ipratropium in recovery at 90, 120, and 180 minutes (P = .007, .01, and .004, respectively). Children in the IV albuterol group were ready for discharge 28.0 hours earlier than those in the ipratropium group (48.3 vs 76.3 hours; P = .005). The combination of IV albuterol and ipratropium showed a significant benefit over ipratropium alone in recovery time at 90 and 120 minutes (P = .02 and .008, respectively). However, no significant difference was evident between the combination and ipratropium alone in time to discharge (57.6 vs 76.3 hours, respectively; P = .2). The combination demonstrated no significant benefit over IV albuterol for any outcome. No significant adverse effects were documented in any of the patients, including tachycardia of more than 200 beats per minute for at least 5 minutes.

ABSTRACT

BACKGROUND: Bolus intravenous (IV) albuterol (salbutamol) improved outcomes in pediatric patients with severe asthma exacerbations in 1 earlier small study. Previous studies demonstrated that the addition of nebulized ipratropium bromide to initial emergency department therapy improves pulmonary function, but it is unclear whether combining the therapies results in earlier hospital discharge. This study compared these 2 approaches to determine their relative benefit in children with acute severe asthma.

POPULATION STUDIED: The researchers studied 55 children (aged 1–14 years) presenting with severe acute asthma to the emergency department of a ter-tiary children’s hospital in Sydney, Australia. Children were classified as having severe asthma if they had all 4 features of respiratory distress (wheezing, sternal retraction, accessory muscle use, and dyspnea) or had any of the absolute criteria (cyanosis, pulsus paradoxus, altered consciousness, or a silent chest auscultation). Baseline demographics and clinical characteristics were similar. Children who were excluded included those with life-threatening asthma, age younger than 12 months, presence of heart disease, family history of Wolff-Parkinson-White or past supraventricular tachycardia, other respiratory disease, or pneumonia, and those who had received inhaled ipratropium bromide that day.

STUDY DESIGN AND VALIDITY: This was a randomized, double-blind, double-dummy trial. The enrolling physician, treating physician, and assessor of outcome were all blinded. All children received 1 dose of nebulized albuterol 2.5 or 5 mg, then were assessed for asthma severity. Children meeting inclusion criteria received oxygen as needed, 1 mg/kg IV bolus methylprednisolone, and nebulized albuterol every 20 minutes for the first hour. The frequency of nebulized albuterol was then decreased based on clinical improvement. Patients were then randomized to receive IV albuterol (15 μg/kg); IV saline and inhaled ipratropium bromide (250 mg) every 20 minutes; or IV albuterol (15 μg/kg) and inhaled ipratropium bromide (250 μg) every 20 minutes. Asthma severity was assessed at 1 and 2 hours into the study using the clinical assessment scale and pulmonary index score. All 55 children completed the study.

OUTCOMES MEASURED: The primary outcomes for this study were mean recovery time (time from randomization to when patients no longer needed nebulized albuterol of a given frequency) and mean discharge time from the hospital. Secondary outcomes included clinical signs of moderate to severe asthma 2 hours after randomization and incidence of medication-related side effects.

RESULTS: Children treated with IV albuterol showed a significant benefit over those treated with inhaled ipratropium in recovery at 90, 120, and 180 minutes (P = .007, .01, and .004, respectively). Children in the IV albuterol group were ready for discharge 28.0 hours earlier than those in the ipratropium group (48.3 vs 76.3 hours; P = .005). The combination of IV albuterol and ipratropium showed a significant benefit over ipratropium alone in recovery time at 90 and 120 minutes (P = .02 and .008, respectively). However, no significant difference was evident between the combination and ipratropium alone in time to discharge (57.6 vs 76.3 hours, respectively; P = .2). The combination demonstrated no significant benefit over IV albuterol for any outcome. No significant adverse effects were documented in any of the patients, including tachycardia of more than 200 beats per minute for at least 5 minutes.

Evidence summary

Although several studies have shown the benefit of placing asthmatic and allergic children in highly sanitized hospital and sanitarium environments,¹ benefit has been extremely difficult to prove with measures used in the child’s home. Only reducing tobacco smoke exposure has been shown to be beneficial. In a randomized trial of predominantly poor minority subjects, fewer acute asthma medical visits were needed by children whose household members underwent behavioral education aimed at decreasing smoke exposure.²

Other methods of modifying the environment have not proved beneficial. Although a group of researchers found that home visits by care providers may decrease acute medical visits, specific allergy avoidance steps did not make a difference.³ Two of these authors also reported that the use of chemicals for house dust mite control and the use of synthetic pillows in lieu of feather pillows may actually exacerbate asthma.⁴ A Cochrane review was inconclusive on the risks or benefits of feather bedding.⁵ Benefit from removing cats is difficult to prove because of the ubiquitous nature of cat antigen and the difficulty in eradicating it from the home. Using air filters and reducing indoor humidity have likewise failed to show meaningful improvement in peak flow, medication use, or symptom scores.

The effectiveness of physical methods to reduce house dust mites is unclear. The Cochrane Review of 15 trials noted a small, statistically significant improvement in asthma symptom scores, but the results were not clinically important enough to recommend such measures.⁶ The potential harm of chemical measures was reiterated in this review.

TABLE
Environmental modifications for children with asthma

Recommendations from others

The National Heart, Lung, and Blood Institute continues to recommend physical barriers to reduce house dust mite antigen based on 4 small trials in which the major benefit was decreased bronchial hyperresponsiveness.⁷ Larger trials, now under way, may help resolve the issue.

Clinical Commentary by Nicholas J. Solomos, MD, at http://www.fpin.org.

Evidence summary

Although several studies have shown the benefit of placing asthmatic and allergic children in highly sanitized hospital and sanitarium environments,¹ benefit has been extremely difficult to prove with measures used in the child’s home. Only reducing tobacco smoke exposure has been shown to be beneficial. In a randomized trial of predominantly poor minority subjects, fewer acute asthma medical visits were needed by children whose household members underwent behavioral education aimed at decreasing smoke exposure.²

Other methods of modifying the environment have not proved beneficial. Although a group of researchers found that home visits by care providers may decrease acute medical visits, specific allergy avoidance steps did not make a difference.³ Two of these authors also reported that the use of chemicals for house dust mite control and the use of synthetic pillows in lieu of feather pillows may actually exacerbate asthma.⁴ A Cochrane review was inconclusive on the risks or benefits of feather bedding.⁵ Benefit from removing cats is difficult to prove because of the ubiquitous nature of cat antigen and the difficulty in eradicating it from the home. Using air filters and reducing indoor humidity have likewise failed to show meaningful improvement in peak flow, medication use, or symptom scores.

The effectiveness of physical methods to reduce house dust mites is unclear. The Cochrane Review of 15 trials noted a small, statistically significant improvement in asthma symptom scores, but the results were not clinically important enough to recommend such measures.⁶ The potential harm of chemical measures was reiterated in this review.

TABLE
Environmental modifications for children with asthma

Recommendations from others

The National Heart, Lung, and Blood Institute continues to recommend physical barriers to reduce house dust mite antigen based on 4 small trials in which the major benefit was decreased bronchial hyperresponsiveness.⁷ Larger trials, now under way, may help resolve the issue.

Clinical Commentary by Nicholas J. Solomos, MD, at http://www.fpin.org.

Evidence summary

Although several studies have shown the benefit of placing asthmatic and allergic children in highly sanitized hospital and sanitarium environments,¹ benefit has been extremely difficult to prove with measures used in the child’s home. Only reducing tobacco smoke exposure has been shown to be beneficial. In a randomized trial of predominantly poor minority subjects, fewer acute asthma medical visits were needed by children whose household members underwent behavioral education aimed at decreasing smoke exposure.²

Other methods of modifying the environment have not proved beneficial. Although a group of researchers found that home visits by care providers may decrease acute medical visits, specific allergy avoidance steps did not make a difference.³ Two of these authors also reported that the use of chemicals for house dust mite control and the use of synthetic pillows in lieu of feather pillows may actually exacerbate asthma.⁴ A Cochrane review was inconclusive on the risks or benefits of feather bedding.⁵ Benefit from removing cats is difficult to prove because of the ubiquitous nature of cat antigen and the difficulty in eradicating it from the home. Using air filters and reducing indoor humidity have likewise failed to show meaningful improvement in peak flow, medication use, or symptom scores.

The effectiveness of physical methods to reduce house dust mites is unclear. The Cochrane Review of 15 trials noted a small, statistically significant improvement in asthma symptom scores, but the results were not clinically important enough to recommend such measures.⁶ The potential harm of chemical measures was reiterated in this review.

TABLE
Environmental modifications for children with asthma

Recommendations from others

The National Heart, Lung, and Blood Institute continues to recommend physical barriers to reduce house dust mite antigen based on 4 small trials in which the major benefit was decreased bronchial hyperresponsiveness.⁷ Larger trials, now under way, may help resolve the issue.

Clinical Commentary by Nicholas J. Solomos, MD, at http://www.fpin.org.

Constipation is an often-overlooked problem in primary care practice. It deserves careful evaluation, including consideration of the many possible causes and appropriate diagnostic testing. Fortunately, most patients respond well to conservative measures.

Constipation prompts a visit to a physician by 1.2% of the US population every year (although most persons with constipation do not seek the assistance of a physician).^{What You Should Know About Constipation,” is included with this article. (For your convenience, it may be freely duplicated and distributed.)}

Suggested lifestyle changes include moderate physical activity, increased fluid intake, increased dietary fiber, and sitting on the toilet about 15–20 minutes after breakfast (taking advantage of the gastrocolic reflex). In selected patients, these changes may be useful, although specific benefits of moderate physical activity and increased fluid intake have not been conclusively proven.

Bulk laxatives

Wheat bran is one of the best and least expensive bulk laxatives. Methylcellulose (eg, Citrucel), psyllium (eg, Metamucil), and polycarbophil (eg, FiberCon) are bulk laxatives that are safe, more refined, and more concentrated than wheat bran, but they are also more expensive. Combined with diet and liquids, bulk laxatives are the most effective and “natural” long-term treatment for constipation. However, their slow onset of action (between 12 and 72 hours) limits their usefulness in acute management of constipation.

Saline laxatives

The saline laxatives include magnesium citrate (eg, Citroma) and magnesium hydroxide (eg, Milk of Magnesia). These agents decrease colonic transit time by stimulating cholecystokinin and draw fluid into the colon by their osmotic effect. Their rapid onset of action (between 30 minutes and 3 hours) makes saline laxatives an excellent choice for acute management of constipation. These laxatives commonly cause abdominal cramping and, in patients with renal failure, may cause magnesium toxicity. Nevertheless, saline laxatives are generally safe and effective.

Osmotic laxatives

Polyethylene glycol (eg, MiraLax) is an effective new osmotic laxative. Rapid onset of action (between 24 and 48 hours) makes an osmotic a good choice for patients who have chronic constipation that fails to respond to bulk and saline laxatives. Polyethylene glycol is equally effective, but better tolerated than the older osmotics, lactulose and sorbitol.¹⁶ Because it is not fermented, gas and cramps are minimal. Lactulose (eg, Chronulac) and sorbitol, which are poorly absorbed sugars, likewise have rapid onset of action, but flatulence and abdominal distention may limit tolerance. Sorbitol is generally less expensive than lactulose.

Stimulant laxatives

The oral stimulant laxatives include diphenylmethanes, the anthraquinones, and castor oil (eg, Emulsoil). They are more potent than bulk or osmotic laxatives, but long-term use is safe if limited to 3 days per week. Bisacodyl (eg, Dulcolax), a diphenylmethane, alters electrolyte transportation within intestinal mucosa and stimulates peristalsis. These actions may cause abdominal cramping and hypokalemia. Cascara (mildest), senna (eg, Senokot), and aloe (strongest) are anthraquinones, which are laxatives with actions and side effects similar to bisacodyl. These agents may cause a benign, reversible pigmentation of the colon (melanosis coli). It has been suggested that chronic use of these agents may damage the enteric nervous system, but a causal relationship has not been clearly established. The most prudent approach is to limit use of stimulant laxatives to constipation that is refractory to other laxatives.

Enemas and suppositories

Enemas and suppositories stimulate colonic contractions and soften stools. Water, saline, soap suds, hypertonic sodium phosphate, and mineral oil are used as enemas. Acute water intoxication can occur with water enemas, especially in infants, children, and the elderly, if they have difficulty evacuating the water. Phosphate enemas may cause hyperphosphatemia and hypocalcemic tetany in these patients and should therefore be used with caution in most patients and should not be used in children 3 years of age or younger. Glycerin and bisacodyl are stimulant suppositories that are clinically effective. Bisacodyl and soap suds enemas cause changes in the epithelium of the rectum, and the effect of glycerin on rectal mucosa is unclear. Therefore, these agents should only be used episodically. Mineral oil enemas are used to soften hardened stool in the rectal ampulla.

Other treatment options

More aggressive measures may be necessary for specific types of constipation. These include behavioral therapy and biofeedback for pelvic floor dysfunction, and surgery for slow-transit constipation or Hirschsprung’s disease.

Investigative pharmacologic treatments for constipation include agents that increase colonic contractions (prokinetic drugs) and prostaglandins. These agents have had limited efficacy and troublesome side effects. Therefore, at this time these drugs have limited usefulness in the treatment of constipation.

Fecal impaction

The management of fecal impaction begins with complete evacuation of the colon. Initially, patients with hard stool in the rectum may be given mineral oil retention enemas followed by manual disimpaction. Prior to further treatment, it is important to obtain an abdominal radiograph to rule out mechanical bowel obstruction. If there is no mechanical bowel obstruction, evacuation of the impaction can be accomplished with oral polyethylene glycol (eg, GoLytely) until clear (up to 8 liters or more may be required for complete evacuation).¹⁶ Administration of twice-daily enemas for 3 days or more is an acceptable alternative to oral polyethylene glycol. Lifestyle changes, bulk laxatives, saline, osmotic laxatives, and enemas should be used to maintain regular defecation after the colon has been cleansed. It is reasonable to attempt to withdraw laxatives after several months of regular bowel habits.

Constipation is an often-overlooked problem in primary care practice. It deserves careful evaluation, including consideration of the many possible causes and appropriate diagnostic testing. Fortunately, most patients respond well to conservative measures.

Constipation prompts a visit to a physician by 1.2% of the US population every year (although most persons with constipation do not seek the assistance of a physician).^{What You Should Know About Constipation,” is included with this article. (For your convenience, it may be freely duplicated and distributed.)}

Suggested lifestyle changes include moderate physical activity, increased fluid intake, increased dietary fiber, and sitting on the toilet about 15–20 minutes after breakfast (taking advantage of the gastrocolic reflex). In selected patients, these changes may be useful, although specific benefits of moderate physical activity and increased fluid intake have not been conclusively proven.

Bulk laxatives

Wheat bran is one of the best and least expensive bulk laxatives. Methylcellulose (eg, Citrucel), psyllium (eg, Metamucil), and polycarbophil (eg, FiberCon) are bulk laxatives that are safe, more refined, and more concentrated than wheat bran, but they are also more expensive. Combined with diet and liquids, bulk laxatives are the most effective and “natural” long-term treatment for constipation. However, their slow onset of action (between 12 and 72 hours) limits their usefulness in acute management of constipation.

Saline laxatives

The saline laxatives include magnesium citrate (eg, Citroma) and magnesium hydroxide (eg, Milk of Magnesia). These agents decrease colonic transit time by stimulating cholecystokinin and draw fluid into the colon by their osmotic effect. Their rapid onset of action (between 30 minutes and 3 hours) makes saline laxatives an excellent choice for acute management of constipation. These laxatives commonly cause abdominal cramping and, in patients with renal failure, may cause magnesium toxicity. Nevertheless, saline laxatives are generally safe and effective.

Osmotic laxatives

Polyethylene glycol (eg, MiraLax) is an effective new osmotic laxative. Rapid onset of action (between 24 and 48 hours) makes an osmotic a good choice for patients who have chronic constipation that fails to respond to bulk and saline laxatives. Polyethylene glycol is equally effective, but better tolerated than the older osmotics, lactulose and sorbitol.¹⁶ Because it is not fermented, gas and cramps are minimal. Lactulose (eg, Chronulac) and sorbitol, which are poorly absorbed sugars, likewise have rapid onset of action, but flatulence and abdominal distention may limit tolerance. Sorbitol is generally less expensive than lactulose.

Stimulant laxatives

The oral stimulant laxatives include diphenylmethanes, the anthraquinones, and castor oil (eg, Emulsoil). They are more potent than bulk or osmotic laxatives, but long-term use is safe if limited to 3 days per week. Bisacodyl (eg, Dulcolax), a diphenylmethane, alters electrolyte transportation within intestinal mucosa and stimulates peristalsis. These actions may cause abdominal cramping and hypokalemia. Cascara (mildest), senna (eg, Senokot), and aloe (strongest) are anthraquinones, which are laxatives with actions and side effects similar to bisacodyl. These agents may cause a benign, reversible pigmentation of the colon (melanosis coli). It has been suggested that chronic use of these agents may damage the enteric nervous system, but a causal relationship has not been clearly established. The most prudent approach is to limit use of stimulant laxatives to constipation that is refractory to other laxatives.

Enemas and suppositories

Enemas and suppositories stimulate colonic contractions and soften stools. Water, saline, soap suds, hypertonic sodium phosphate, and mineral oil are used as enemas. Acute water intoxication can occur with water enemas, especially in infants, children, and the elderly, if they have difficulty evacuating the water. Phosphate enemas may cause hyperphosphatemia and hypocalcemic tetany in these patients and should therefore be used with caution in most patients and should not be used in children 3 years of age or younger. Glycerin and bisacodyl are stimulant suppositories that are clinically effective. Bisacodyl and soap suds enemas cause changes in the epithelium of the rectum, and the effect of glycerin on rectal mucosa is unclear. Therefore, these agents should only be used episodically. Mineral oil enemas are used to soften hardened stool in the rectal ampulla.

Other treatment options

More aggressive measures may be necessary for specific types of constipation. These include behavioral therapy and biofeedback for pelvic floor dysfunction, and surgery for slow-transit constipation or Hirschsprung’s disease.

Investigative pharmacologic treatments for constipation include agents that increase colonic contractions (prokinetic drugs) and prostaglandins. These agents have had limited efficacy and troublesome side effects. Therefore, at this time these drugs have limited usefulness in the treatment of constipation.

Fecal impaction

The management of fecal impaction begins with complete evacuation of the colon. Initially, patients with hard stool in the rectum may be given mineral oil retention enemas followed by manual disimpaction. Prior to further treatment, it is important to obtain an abdominal radiograph to rule out mechanical bowel obstruction. If there is no mechanical bowel obstruction, evacuation of the impaction can be accomplished with oral polyethylene glycol (eg, GoLytely) until clear (up to 8 liters or more may be required for complete evacuation).¹⁶ Administration of twice-daily enemas for 3 days or more is an acceptable alternative to oral polyethylene glycol. Lifestyle changes, bulk laxatives, saline, osmotic laxatives, and enemas should be used to maintain regular defecation after the colon has been cleansed. It is reasonable to attempt to withdraw laxatives after several months of regular bowel habits.

Constipation is an often-overlooked problem in primary care practice. It deserves careful evaluation, including consideration of the many possible causes and appropriate diagnostic testing. Fortunately, most patients respond well to conservative measures.

Constipation prompts a visit to a physician by 1.2% of the US population every year (although most persons with constipation do not seek the assistance of a physician).^{What You Should Know About Constipation,” is included with this article. (For your convenience, it may be freely duplicated and distributed.)}

Suggested lifestyle changes include moderate physical activity, increased fluid intake, increased dietary fiber, and sitting on the toilet about 15–20 minutes after breakfast (taking advantage of the gastrocolic reflex). In selected patients, these changes may be useful, although specific benefits of moderate physical activity and increased fluid intake have not been conclusively proven.

Bulk laxatives

Wheat bran is one of the best and least expensive bulk laxatives. Methylcellulose (eg, Citrucel), psyllium (eg, Metamucil), and polycarbophil (eg, FiberCon) are bulk laxatives that are safe, more refined, and more concentrated than wheat bran, but they are also more expensive. Combined with diet and liquids, bulk laxatives are the most effective and “natural” long-term treatment for constipation. However, their slow onset of action (between 12 and 72 hours) limits their usefulness in acute management of constipation.

Saline laxatives

The saline laxatives include magnesium citrate (eg, Citroma) and magnesium hydroxide (eg, Milk of Magnesia). These agents decrease colonic transit time by stimulating cholecystokinin and draw fluid into the colon by their osmotic effect. Their rapid onset of action (between 30 minutes and 3 hours) makes saline laxatives an excellent choice for acute management of constipation. These laxatives commonly cause abdominal cramping and, in patients with renal failure, may cause magnesium toxicity. Nevertheless, saline laxatives are generally safe and effective.

Osmotic laxatives

Polyethylene glycol (eg, MiraLax) is an effective new osmotic laxative. Rapid onset of action (between 24 and 48 hours) makes an osmotic a good choice for patients who have chronic constipation that fails to respond to bulk and saline laxatives. Polyethylene glycol is equally effective, but better tolerated than the older osmotics, lactulose and sorbitol.¹⁶ Because it is not fermented, gas and cramps are minimal. Lactulose (eg, Chronulac) and sorbitol, which are poorly absorbed sugars, likewise have rapid onset of action, but flatulence and abdominal distention may limit tolerance. Sorbitol is generally less expensive than lactulose.

Stimulant laxatives

The oral stimulant laxatives include diphenylmethanes, the anthraquinones, and castor oil (eg, Emulsoil). They are more potent than bulk or osmotic laxatives, but long-term use is safe if limited to 3 days per week. Bisacodyl (eg, Dulcolax), a diphenylmethane, alters electrolyte transportation within intestinal mucosa and stimulates peristalsis. These actions may cause abdominal cramping and hypokalemia. Cascara (mildest), senna (eg, Senokot), and aloe (strongest) are anthraquinones, which are laxatives with actions and side effects similar to bisacodyl. These agents may cause a benign, reversible pigmentation of the colon (melanosis coli). It has been suggested that chronic use of these agents may damage the enteric nervous system, but a causal relationship has not been clearly established. The most prudent approach is to limit use of stimulant laxatives to constipation that is refractory to other laxatives.

Enemas and suppositories

Enemas and suppositories stimulate colonic contractions and soften stools. Water, saline, soap suds, hypertonic sodium phosphate, and mineral oil are used as enemas. Acute water intoxication can occur with water enemas, especially in infants, children, and the elderly, if they have difficulty evacuating the water. Phosphate enemas may cause hyperphosphatemia and hypocalcemic tetany in these patients and should therefore be used with caution in most patients and should not be used in children 3 years of age or younger. Glycerin and bisacodyl are stimulant suppositories that are clinically effective. Bisacodyl and soap suds enemas cause changes in the epithelium of the rectum, and the effect of glycerin on rectal mucosa is unclear. Therefore, these agents should only be used episodically. Mineral oil enemas are used to soften hardened stool in the rectal ampulla.

Other treatment options

More aggressive measures may be necessary for specific types of constipation. These include behavioral therapy and biofeedback for pelvic floor dysfunction, and surgery for slow-transit constipation or Hirschsprung’s disease.

Investigative pharmacologic treatments for constipation include agents that increase colonic contractions (prokinetic drugs) and prostaglandins. These agents have had limited efficacy and troublesome side effects. Therefore, at this time these drugs have limited usefulness in the treatment of constipation.

Fecal impaction

The management of fecal impaction begins with complete evacuation of the colon. Initially, patients with hard stool in the rectum may be given mineral oil retention enemas followed by manual disimpaction. Prior to further treatment, it is important to obtain an abdominal radiograph to rule out mechanical bowel obstruction. If there is no mechanical bowel obstruction, evacuation of the impaction can be accomplished with oral polyethylene glycol (eg, GoLytely) until clear (up to 8 liters or more may be required for complete evacuation).¹⁶ Administration of twice-daily enemas for 3 days or more is an acceptable alternative to oral polyethylene glycol. Lifestyle changes, bulk laxatives, saline, osmotic laxatives, and enemas should be used to maintain regular defecation after the colon has been cleansed. It is reasonable to attempt to withdraw laxatives after several months of regular bowel habits.