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

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

ABOUT SODIUM OXYBATE

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

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

Table 1

Sodium oxybate: Fast facts

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

Table 2

Sodium oxybate dosing recommendations for patients

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

HOW IT WORKS

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

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

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

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

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

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

EFFICACY

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

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

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

TOLERABILITY

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

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

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

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

ABUSE POTENTIAL

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

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

Related resources

• Narcolepsy Network Inc. www.narcolepsynetwork.org

Disclosure

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

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

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

ABOUT SODIUM OXYBATE

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

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

Table 1

Sodium oxybate: Fast facts

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

Table 2

Sodium oxybate dosing recommendations for patients

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

HOW IT WORKS

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

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

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

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

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

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

EFFICACY

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

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

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

TOLERABILITY

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

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

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

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

ABUSE POTENTIAL

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

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

Related resources

• Narcolepsy Network Inc. www.narcolepsynetwork.org

Disclosure

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

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

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

ABOUT SODIUM OXYBATE

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

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

Table 1

Sodium oxybate: Fast facts

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

Table 2

Sodium oxybate dosing recommendations for patients

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

HOW IT WORKS

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

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

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

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

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

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

EFFICACY

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

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

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

TOLERABILITY

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

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

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

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

ABUSE POTENTIAL

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

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

Related resources

• Narcolepsy Network Inc. www.narcolepsynetwork.org

Disclosure

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

Supplement Editor:
Roger M. Mills, MD

Contents

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

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

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

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

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

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

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

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

Supplement Editor:
Roger M. Mills, MD

Contents

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

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

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

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

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

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

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

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

Supplement Editor:
Roger M. Mills, MD

Contents

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

As a psychiatrist specializing in college health, I see 40 to 50 young adults yearly with undiagnosed attention-deficit/hyperactivity disorder (ADHD). I have found that understanding five fundamentals of ADHD is key to recognizing this disorder in adults.

1. There is no “adult onset” ADHD. Although ADHD may manifest itself differently in adults than in children, studies indicate that the disorder is a continuation of childhood ADHD rather than a discrete adult disorder. Clinicians thus need to establish that adult patients exhibited symptomatic and functional impairment before age 7 (as per DSM-IV), although some experts suggest preadolescence as a cutoff.¹
2. Most people do not “outgrow” ADHD. We once assumed that most patients with ADHD became asymptomatic as they matured from adolescence into adulthood. Research reveals that hyperactivity and impulsivity decline over time but inattention and executive dysfunction usually persist into adulthood.² These residual deficits cause continued vocational, academic, and interpersonal difficulties.
3. ADHD can mimic other psychiatric disorders. The hyperkinesis, impulsivity, and inattention that are the essence of ADHD are also commonly observed in adults with anxiety disorders, mood disorders, substance abuse problems, and learning disorders. Patients who present with atypical affective or anxiety symptoms or learning problems, or who do not respond to conventional treatments, should be screened for ADHD.
4. The genetic apple does not fall far from the tree in ADHD. Many adults with ADHD are identified in middle age after their children are diagnosed. Adoption data and multiple twin studies have placed the heritability of ADHD at approximately 75%,³ putting first-degree relatives at fairly high predisposition.
5. Stimulant medications do not promote substance abuse in ADHD patients. Stimulant medication is more likely to reduce the risk of substance abuse in ADHD than enhance it.⁴ For patients at high-risk for substance abuse disorders, however, atomoxetine and bupropion offer nonstimulant alternatives. Also, the newer, longer-acting dextroamphetamine/amphetamine and methylphenidate preparations are more difficult to abuse because of their slow-release mechanisms.

As a psychiatrist specializing in college health, I see 40 to 50 young adults yearly with undiagnosed attention-deficit/hyperactivity disorder (ADHD). I have found that understanding five fundamentals of ADHD is key to recognizing this disorder in adults.

1. There is no “adult onset” ADHD. Although ADHD may manifest itself differently in adults than in children, studies indicate that the disorder is a continuation of childhood ADHD rather than a discrete adult disorder. Clinicians thus need to establish that adult patients exhibited symptomatic and functional impairment before age 7 (as per DSM-IV), although some experts suggest preadolescence as a cutoff.¹
2. Most people do not “outgrow” ADHD. We once assumed that most patients with ADHD became asymptomatic as they matured from adolescence into adulthood. Research reveals that hyperactivity and impulsivity decline over time but inattention and executive dysfunction usually persist into adulthood.² These residual deficits cause continued vocational, academic, and interpersonal difficulties.
3. ADHD can mimic other psychiatric disorders. The hyperkinesis, impulsivity, and inattention that are the essence of ADHD are also commonly observed in adults with anxiety disorders, mood disorders, substance abuse problems, and learning disorders. Patients who present with atypical affective or anxiety symptoms or learning problems, or who do not respond to conventional treatments, should be screened for ADHD.
4. The genetic apple does not fall far from the tree in ADHD. Many adults with ADHD are identified in middle age after their children are diagnosed. Adoption data and multiple twin studies have placed the heritability of ADHD at approximately 75%,³ putting first-degree relatives at fairly high predisposition.
5. Stimulant medications do not promote substance abuse in ADHD patients. Stimulant medication is more likely to reduce the risk of substance abuse in ADHD than enhance it.⁴ For patients at high-risk for substance abuse disorders, however, atomoxetine and bupropion offer nonstimulant alternatives. Also, the newer, longer-acting dextroamphetamine/amphetamine and methylphenidate preparations are more difficult to abuse because of their slow-release mechanisms.

As a psychiatrist specializing in college health, I see 40 to 50 young adults yearly with undiagnosed attention-deficit/hyperactivity disorder (ADHD). I have found that understanding five fundamentals of ADHD is key to recognizing this disorder in adults.

1. There is no “adult onset” ADHD. Although ADHD may manifest itself differently in adults than in children, studies indicate that the disorder is a continuation of childhood ADHD rather than a discrete adult disorder. Clinicians thus need to establish that adult patients exhibited symptomatic and functional impairment before age 7 (as per DSM-IV), although some experts suggest preadolescence as a cutoff.¹
2. Most people do not “outgrow” ADHD. We once assumed that most patients with ADHD became asymptomatic as they matured from adolescence into adulthood. Research reveals that hyperactivity and impulsivity decline over time but inattention and executive dysfunction usually persist into adulthood.² These residual deficits cause continued vocational, academic, and interpersonal difficulties.
3. ADHD can mimic other psychiatric disorders. The hyperkinesis, impulsivity, and inattention that are the essence of ADHD are also commonly observed in adults with anxiety disorders, mood disorders, substance abuse problems, and learning disorders. Patients who present with atypical affective or anxiety symptoms or learning problems, or who do not respond to conventional treatments, should be screened for ADHD.
4. The genetic apple does not fall far from the tree in ADHD. Many adults with ADHD are identified in middle age after their children are diagnosed. Adoption data and multiple twin studies have placed the heritability of ADHD at approximately 75%,³ putting first-degree relatives at fairly high predisposition.
5. Stimulant medications do not promote substance abuse in ADHD patients. Stimulant medication is more likely to reduce the risk of substance abuse in ADHD than enhance it.⁴ For patients at high-risk for substance abuse disorders, however, atomoxetine and bupropion offer nonstimulant alternatives. Also, the newer, longer-acting dextroamphetamine/amphetamine and methylphenidate preparations are more difficult to abuse because of their slow-release mechanisms.

Supplement Editor:
Edy E. Soffer, MD

Contents

Irritable bowel syndrome: An overview of diagnosis and pharmacologic treatment
Kevin W. Olden, MD

Roundtable discussion—Irritable bowel syndrome: New tools and insights for the primary care physician
Edy E. Soffer, MD; Stephen Brunton, MD; J. Harry Isaacson, MD; Kevin W. Olden, MD; and Bo Shen, MD

Supplement Editor:
Edy E. Soffer, MD

Contents

Irritable bowel syndrome: An overview of diagnosis and pharmacologic treatment
Kevin W. Olden, MD

Roundtable discussion—Irritable bowel syndrome: New tools and insights for the primary care physician
Edy E. Soffer, MD; Stephen Brunton, MD; J. Harry Isaacson, MD; Kevin W. Olden, MD; and Bo Shen, MD

Supplement Editor:
Edy E. Soffer, MD

Contents

Irritable bowel syndrome: An overview of diagnosis and pharmacologic treatment
Kevin W. Olden, MD

Roundtable discussion—Irritable bowel syndrome: New tools and insights for the primary care physician
Edy E. Soffer, MD; Stephen Brunton, MD; J. Harry Isaacson, MD; Kevin W. Olden, MD; and Bo Shen, MD