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The patient is empirically diagnosed with AD and eczema herpeticum. A Tzanck smear is done and is positive for multinucleate giant cells with nuclear molding and ballooning degeneration of the keratinocytes. 

Eczema herpeticum, or Kaposi varicelliform eruption, is a rare but potentially life-threatening complication of AD. It is an extensive cutaneous vesicular eruption that arises from pre-existing skin disease — in most cases, AD — and is caused by disseminated cutaneous viral infection, usually with the herpes simplex virus (HSV). The virus can infect the epidermis because of the skin barrier defects that are inherently associated with AD. Patients with AD and filaggrin gene null mutations may have an increased risk for eczema herpeticum. 

Eczema herpeticum is associated with significant morbidity and is considered a medical emergency. Early diagnosis and treatment is essential to prevent or minimize complications. Complications of eczema herpeticum can include keratoconjunctivitis, which may lead to vision loss, as well as multiorgan involvement with meningoencephalitis and/or septic shock. 

Eczema herpeticum occurs on areas of preexisting AD (or other skin disease) and presents as small, dome-shaped, grouped papule-vesicles on an erythematous base. When these vesicles rupture, punched-out ulcers are formed. It is seen most often on the face, neck, and upper trunk. Fever, malaise, and lymphadenopathies may also be present. 

Among patients with severe or poorly controlled AD, even the classic presentation of eczema herpeticum can be challenging to recognize. Clinicians should maintain a high index of suspicion for this complication in any patient with AD who presents with an acute pruritic and painful rash, including pediatric patients, who have the highest risk for the development of eczema herpeticum.

Viral PCR on vesicle fluid can confirm the diagnosis of eczema herpeticum and determine the type of HSV with high sensitivity and specificity. If unavailable, a Tzanck smear of an opened vesicle or erosion can confirm an HSV infection and provide rapid diagnosis, but its sensitivity and specificity can vary. Direct fluorescence antigen testing is a fast and inexpensive method for detecting an HSV antigen and distinguishing between HSV-1 and HSV-2 infections. Bacterial cultures should be performed when there is a concern for impetiginization. A skin biopsy may be indicated in cases involving atypical presentation. 

Immediate treatment with oral acyclovir should be initiated for any patient with eczema herpeticum; patients with severe disease or who are immunocompromised may require hospitalization for administration of systemic antivirals. Because secondary bacterial infections are common, prophylactic antibiotics (eg, cephalexin, clindamycin, doxycycline, or trimethoprim-sulfamethoxazole) may also be indicated. Finally, consultation with an ophthalmologist is indicated when herpes keratitis is suspected. 

Richard Vinson, MD, President, Mountain View Dermatology, El Paso, Texas.

Richard Vinson, MD, has disclosed no relevant financial relationships.

The patient is empirically diagnosed with AD and eczema herpeticum. A Tzanck smear is done and is positive for multinucleate giant cells with nuclear molding and ballooning degeneration of the keratinocytes. 

Eczema herpeticum, or Kaposi varicelliform eruption, is a rare but potentially life-threatening complication of AD. It is an extensive cutaneous vesicular eruption that arises from pre-existing skin disease — in most cases, AD — and is caused by disseminated cutaneous viral infection, usually with the herpes simplex virus (HSV). The virus can infect the epidermis because of the skin barrier defects that are inherently associated with AD. Patients with AD and filaggrin gene null mutations may have an increased risk for eczema herpeticum. 

Eczema herpeticum is associated with significant morbidity and is considered a medical emergency. Early diagnosis and treatment is essential to prevent or minimize complications. Complications of eczema herpeticum can include keratoconjunctivitis, which may lead to vision loss, as well as multiorgan involvement with meningoencephalitis and/or septic shock. 

Eczema herpeticum occurs on areas of preexisting AD (or other skin disease) and presents as small, dome-shaped, grouped papule-vesicles on an erythematous base. When these vesicles rupture, punched-out ulcers are formed. It is seen most often on the face, neck, and upper trunk. Fever, malaise, and lymphadenopathies may also be present. 

Among patients with severe or poorly controlled AD, even the classic presentation of eczema herpeticum can be challenging to recognize. Clinicians should maintain a high index of suspicion for this complication in any patient with AD who presents with an acute pruritic and painful rash, including pediatric patients, who have the highest risk for the development of eczema herpeticum.

Viral PCR on vesicle fluid can confirm the diagnosis of eczema herpeticum and determine the type of HSV with high sensitivity and specificity. If unavailable, a Tzanck smear of an opened vesicle or erosion can confirm an HSV infection and provide rapid diagnosis, but its sensitivity and specificity can vary. Direct fluorescence antigen testing is a fast and inexpensive method for detecting an HSV antigen and distinguishing between HSV-1 and HSV-2 infections. Bacterial cultures should be performed when there is a concern for impetiginization. A skin biopsy may be indicated in cases involving atypical presentation. 

Immediate treatment with oral acyclovir should be initiated for any patient with eczema herpeticum; patients with severe disease or who are immunocompromised may require hospitalization for administration of systemic antivirals. Because secondary bacterial infections are common, prophylactic antibiotics (eg, cephalexin, clindamycin, doxycycline, or trimethoprim-sulfamethoxazole) may also be indicated. Finally, consultation with an ophthalmologist is indicated when herpes keratitis is suspected. 

Richard Vinson, MD, President, Mountain View Dermatology, El Paso, Texas.

Richard Vinson, MD, has disclosed no relevant financial relationships.

The patient is empirically diagnosed with AD and eczema herpeticum. A Tzanck smear is done and is positive for multinucleate giant cells with nuclear molding and ballooning degeneration of the keratinocytes. 

Eczema herpeticum, or Kaposi varicelliform eruption, is a rare but potentially life-threatening complication of AD. It is an extensive cutaneous vesicular eruption that arises from pre-existing skin disease — in most cases, AD — and is caused by disseminated cutaneous viral infection, usually with the herpes simplex virus (HSV). The virus can infect the epidermis because of the skin barrier defects that are inherently associated with AD. Patients with AD and filaggrin gene null mutations may have an increased risk for eczema herpeticum. 

Eczema herpeticum is associated with significant morbidity and is considered a medical emergency. Early diagnosis and treatment is essential to prevent or minimize complications. Complications of eczema herpeticum can include keratoconjunctivitis, which may lead to vision loss, as well as multiorgan involvement with meningoencephalitis and/or septic shock. 

Eczema herpeticum occurs on areas of preexisting AD (or other skin disease) and presents as small, dome-shaped, grouped papule-vesicles on an erythematous base. When these vesicles rupture, punched-out ulcers are formed. It is seen most often on the face, neck, and upper trunk. Fever, malaise, and lymphadenopathies may also be present. 

Among patients with severe or poorly controlled AD, even the classic presentation of eczema herpeticum can be challenging to recognize. Clinicians should maintain a high index of suspicion for this complication in any patient with AD who presents with an acute pruritic and painful rash, including pediatric patients, who have the highest risk for the development of eczema herpeticum.

Viral PCR on vesicle fluid can confirm the diagnosis of eczema herpeticum and determine the type of HSV with high sensitivity and specificity. If unavailable, a Tzanck smear of an opened vesicle or erosion can confirm an HSV infection and provide rapid diagnosis, but its sensitivity and specificity can vary. Direct fluorescence antigen testing is a fast and inexpensive method for detecting an HSV antigen and distinguishing between HSV-1 and HSV-2 infections. Bacterial cultures should be performed when there is a concern for impetiginization. A skin biopsy may be indicated in cases involving atypical presentation. 

Immediate treatment with oral acyclovir should be initiated for any patient with eczema herpeticum; patients with severe disease or who are immunocompromised may require hospitalization for administration of systemic antivirals. Because secondary bacterial infections are common, prophylactic antibiotics (eg, cephalexin, clindamycin, doxycycline, or trimethoprim-sulfamethoxazole) may also be indicated. Finally, consultation with an ophthalmologist is indicated when herpes keratitis is suspected. 

Richard Vinson, MD, President, Mountain View Dermatology, El Paso, Texas.

Richard Vinson, MD, has disclosed no relevant financial relationships.

The patient is diagnosed with atopic dermatitis (AD) on the basis of clinical findings and historical features, morphology and distribution of skin lesions, and associated clinical signs.

AD continues to be a clinical diagnosis. Pruritus and eczema (acute, subacute, or chronic) are essential features for the diagnosis of AD. The eczema should follow characteristic morphology and age-specific patterns (eg, facial/neck/extensor involvement in children, flexural involvement in any age group, sparing of the groin and axillary regions). A personal or family history of atopy is an important historical feature that supports the diagnosis of AD, as are xerosis and early age of onset.

The majority of patients with AD (60%) develop symptoms during the first year of life and 90% experience an eruption by 5 years of age, but disease onset can occur at any age. Some studies have found an association between late-onset AD and persistence of disease into adulthood.

At present, there are no reliable biomarkers that can differentiate AD from other entities. An elevated total and/or allergen-specific serum IgE level is the most commonly associated laboratory feature, but it is not seen in about 20% of individuals with AD. Additionally, elevated allergen-specific IgE levels are found in 55% of the general population in the United States, making it nonspecific for AD. Moreover, while total IgE level usually varies in accordance with disease severity, it is not a reliable marker of disease severity, and it is possible for individuals with severe disease to have normal levels. Nonatopic conditions (eg, parasitic infection, some cancers, and autoimmune disease) may also lead to elevations in IgE levels.

Consistent prognostic markers are also lacking, although elevated total serum IgE levels and filaggrin gene null mutations do tend to be predictive of a more severe and prolonged disease course.

Topical agents including nonpharmacologic moisturizers and topical corticosteroids are the mainstay of treatment for AD; immunomodulatory agents and targeted biologic therapies are also available. For patients with more severe or recalcitrant disease, systemic therapy or phototherapy may be used, often in conjunction with topical therapies.

Richard Vinson, MD, President, Mountain View Dermatology, El Paso, Texas.

Richard Vinson, MD, has disclosed no relevant financial relationships.

The patient is diagnosed with atopic dermatitis (AD) on the basis of clinical findings and historical features, morphology and distribution of skin lesions, and associated clinical signs.

AD continues to be a clinical diagnosis. Pruritus and eczema (acute, subacute, or chronic) are essential features for the diagnosis of AD. The eczema should follow characteristic morphology and age-specific patterns (eg, facial/neck/extensor involvement in children, flexural involvement in any age group, sparing of the groin and axillary regions). A personal or family history of atopy is an important historical feature that supports the diagnosis of AD, as are xerosis and early age of onset.

The majority of patients with AD (60%) develop symptoms during the first year of life and 90% experience an eruption by 5 years of age, but disease onset can occur at any age. Some studies have found an association between late-onset AD and persistence of disease into adulthood.

At present, there are no reliable biomarkers that can differentiate AD from other entities. An elevated total and/or allergen-specific serum IgE level is the most commonly associated laboratory feature, but it is not seen in about 20% of individuals with AD. Additionally, elevated allergen-specific IgE levels are found in 55% of the general population in the United States, making it nonspecific for AD. Moreover, while total IgE level usually varies in accordance with disease severity, it is not a reliable marker of disease severity, and it is possible for individuals with severe disease to have normal levels. Nonatopic conditions (eg, parasitic infection, some cancers, and autoimmune disease) may also lead to elevations in IgE levels.

Consistent prognostic markers are also lacking, although elevated total serum IgE levels and filaggrin gene null mutations do tend to be predictive of a more severe and prolonged disease course.

Topical agents including nonpharmacologic moisturizers and topical corticosteroids are the mainstay of treatment for AD; immunomodulatory agents and targeted biologic therapies are also available. For patients with more severe or recalcitrant disease, systemic therapy or phototherapy may be used, often in conjunction with topical therapies.

Richard Vinson, MD, President, Mountain View Dermatology, El Paso, Texas.

Richard Vinson, MD, has disclosed no relevant financial relationships.

The patient is diagnosed with atopic dermatitis (AD) on the basis of clinical findings and historical features, morphology and distribution of skin lesions, and associated clinical signs.

AD continues to be a clinical diagnosis. Pruritus and eczema (acute, subacute, or chronic) are essential features for the diagnosis of AD. The eczema should follow characteristic morphology and age-specific patterns (eg, facial/neck/extensor involvement in children, flexural involvement in any age group, sparing of the groin and axillary regions). A personal or family history of atopy is an important historical feature that supports the diagnosis of AD, as are xerosis and early age of onset.

The majority of patients with AD (60%) develop symptoms during the first year of life and 90% experience an eruption by 5 years of age, but disease onset can occur at any age. Some studies have found an association between late-onset AD and persistence of disease into adulthood.

At present, there are no reliable biomarkers that can differentiate AD from other entities. An elevated total and/or allergen-specific serum IgE level is the most commonly associated laboratory feature, but it is not seen in about 20% of individuals with AD. Additionally, elevated allergen-specific IgE levels are found in 55% of the general population in the United States, making it nonspecific for AD. Moreover, while total IgE level usually varies in accordance with disease severity, it is not a reliable marker of disease severity, and it is possible for individuals with severe disease to have normal levels. Nonatopic conditions (eg, parasitic infection, some cancers, and autoimmune disease) may also lead to elevations in IgE levels.

Consistent prognostic markers are also lacking, although elevated total serum IgE levels and filaggrin gene null mutations do tend to be predictive of a more severe and prolonged disease course.

Topical agents including nonpharmacologic moisturizers and topical corticosteroids are the mainstay of treatment for AD; immunomodulatory agents and targeted biologic therapies are also available. For patients with more severe or recalcitrant disease, systemic therapy or phototherapy may be used, often in conjunction with topical therapies.

Richard Vinson, MD, President, Mountain View Dermatology, El Paso, Texas.

Richard Vinson, MD, has disclosed no relevant financial relationships.

Based on the patient’s history of asthma, physical examination, and radiograph findings, a diagnosis of right middle lung collapse was determined. Right middle lobe syndrome (RMLS) refers to chronic or recurrent atelectasis in the right middle lobe and can stem from numerous etiologies. It is characterized by wedge-shaped density that extends anteriorly and inferiorly from the hilum of the lung. Atelectasis typically occurs in the right middle lobe, but the lingula may be involved as well.

Asthma may predispose patients to atelectasis, resulting from bronchial inflammation that produces cellular debris, mucus plugs, and edema.Children are also more prone to developing atelectasis than adults because of smaller and more collapsible airways, among other features.

Lateral chest radiography is the most effective imaging technique in patients presenting with RMLS, revealing the condition's hallmark findings: a loss of volume in the right middle lobe and a blurred right heart border.

For appropriate treatment, a precise diagnosis of the pathology underlying the RMLS must be determined. This case represents a complication of uncontrolled asthma. The cornerstone of therapy is chest physical therapy and postural drainage, and the addition of mucolytics and dornase alfa may further clear airways. Children with asthma should be treated with aggressive anti-inflammatory therapy such as inhaled steroids, and the clinician may consider the addition of systemic steroids.  

Cases of RMLS involving neoplastic origin or bronchiectasis should be given special consideration. Diagnosis can be confirmed with high-resolution chest CT scanning, which is safer for younger patients or those with asthma than traditional bronchography. 

If a patient’s symptoms are not responsive to therapy or if the patient has predisposition to airway colonization, the clinician should perform a bronchoalveolar lavage culture to determine an appropriate antibiotic. In children with asthma, there is an association between right middle lobe collapse and infection.

Long-term follow-up has demonstrated that with treatment, RMLS typically resolves within 90 days.Soyer and colleagues also determined that baseline treatment of asthma with anti-inflammatory medications can accelerate the resolution of atelectasis. However, recurrent infections may cause parenchymal damage and bronchiectasis.

Zab Mosenifar, MD, Medical Director, Women's Lung Institute; Executive Vice Chairman, Department of Medicine, Cedars Sinai Medical Center, Los Angeles, California.

Zab Mosenifar, MD, has disclosed no relevant financial relationships.

Based on the patient’s history of asthma, physical examination, and radiograph findings, a diagnosis of right middle lung collapse was determined. Right middle lobe syndrome (RMLS) refers to chronic or recurrent atelectasis in the right middle lobe and can stem from numerous etiologies. It is characterized by wedge-shaped density that extends anteriorly and inferiorly from the hilum of the lung. Atelectasis typically occurs in the right middle lobe, but the lingula may be involved as well.

Asthma may predispose patients to atelectasis, resulting from bronchial inflammation that produces cellular debris, mucus plugs, and edema.Children are also more prone to developing atelectasis than adults because of smaller and more collapsible airways, among other features.

Lateral chest radiography is the most effective imaging technique in patients presenting with RMLS, revealing the condition's hallmark findings: a loss of volume in the right middle lobe and a blurred right heart border.

For appropriate treatment, a precise diagnosis of the pathology underlying the RMLS must be determined. This case represents a complication of uncontrolled asthma. The cornerstone of therapy is chest physical therapy and postural drainage, and the addition of mucolytics and dornase alfa may further clear airways. Children with asthma should be treated with aggressive anti-inflammatory therapy such as inhaled steroids, and the clinician may consider the addition of systemic steroids.  

Cases of RMLS involving neoplastic origin or bronchiectasis should be given special consideration. Diagnosis can be confirmed with high-resolution chest CT scanning, which is safer for younger patients or those with asthma than traditional bronchography. 

If a patient’s symptoms are not responsive to therapy or if the patient has predisposition to airway colonization, the clinician should perform a bronchoalveolar lavage culture to determine an appropriate antibiotic. In children with asthma, there is an association between right middle lobe collapse and infection.

Long-term follow-up has demonstrated that with treatment, RMLS typically resolves within 90 days.Soyer and colleagues also determined that baseline treatment of asthma with anti-inflammatory medications can accelerate the resolution of atelectasis. However, recurrent infections may cause parenchymal damage and bronchiectasis.

Zab Mosenifar, MD, Medical Director, Women's Lung Institute; Executive Vice Chairman, Department of Medicine, Cedars Sinai Medical Center, Los Angeles, California.

Zab Mosenifar, MD, has disclosed no relevant financial relationships.

Based on the patient’s history of asthma, physical examination, and radiograph findings, a diagnosis of right middle lung collapse was determined. Right middle lobe syndrome (RMLS) refers to chronic or recurrent atelectasis in the right middle lobe and can stem from numerous etiologies. It is characterized by wedge-shaped density that extends anteriorly and inferiorly from the hilum of the lung. Atelectasis typically occurs in the right middle lobe, but the lingula may be involved as well.

Asthma may predispose patients to atelectasis, resulting from bronchial inflammation that produces cellular debris, mucus plugs, and edema.Children are also more prone to developing atelectasis than adults because of smaller and more collapsible airways, among other features.

Lateral chest radiography is the most effective imaging technique in patients presenting with RMLS, revealing the condition's hallmark findings: a loss of volume in the right middle lobe and a blurred right heart border.

For appropriate treatment, a precise diagnosis of the pathology underlying the RMLS must be determined. This case represents a complication of uncontrolled asthma. The cornerstone of therapy is chest physical therapy and postural drainage, and the addition of mucolytics and dornase alfa may further clear airways. Children with asthma should be treated with aggressive anti-inflammatory therapy such as inhaled steroids, and the clinician may consider the addition of systemic steroids.  

Cases of RMLS involving neoplastic origin or bronchiectasis should be given special consideration. Diagnosis can be confirmed with high-resolution chest CT scanning, which is safer for younger patients or those with asthma than traditional bronchography. 

If a patient’s symptoms are not responsive to therapy or if the patient has predisposition to airway colonization, the clinician should perform a bronchoalveolar lavage culture to determine an appropriate antibiotic. In children with asthma, there is an association between right middle lobe collapse and infection.

Long-term follow-up has demonstrated that with treatment, RMLS typically resolves within 90 days.Soyer and colleagues also determined that baseline treatment of asthma with anti-inflammatory medications can accelerate the resolution of atelectasis. However, recurrent infections may cause parenchymal damage and bronchiectasis.

Zab Mosenifar, MD, Medical Director, Women's Lung Institute; Executive Vice Chairman, Department of Medicine, Cedars Sinai Medical Center, Los Angeles, California.

Zab Mosenifar, MD, has disclosed no relevant financial relationships.

The patient is probably having a delayed allergenic response to an indoor mold allergen. Early reactions can occur immediately following allergen inhalation but can also manifest 4-10 hours after exposure to wet and damp areas, such as bathrooms and basements.

Allergic asthma represents the most common asthma phenotype. The average age of onset is younger than that of nonallergic asthma, with allergens triggering exacerbations in 60%-90% of children compared with 50% of adults.Triggers can include mold spores, seasonal pollen, dust mites, and animal allergens. There is also an increased incidence of co-occurring allergic rhinoconjunctivitis and atopic dermatitis in patients with allergic asthma.

During an acute asthma exacerbation, lung examination findings may include wheezing, rhonchi, hyperinflation, or a prolonged expiratory phase. In children, supraclavicular and intercostal retractions and nasal flaring, as well as abdominal breathing, are particularly telling. Total serum immunoglobulin E levels are usually higher in allergic vs nonallergic asthma (> 100 IU), although this marker is not specific to asthma.

The allergic asthma phenotype usually responds to inhaled corticosteroid therapy. Although evidence suggests that allergic vs nonallergic asthma is less severe in many cases, compelling data point to a causal relationship between mold allergy and asthma severity in a subgroup of younger asthma patients; specifically, mold sensitization may be associated with asthma attacks requiring hospital admission in this population.

Although spirometry assessments should be obtained as the primary test to establish the asthma diagnosis, to test for allergic sensitivity to specific allergens in the environment, allergy skin tests and blood radioallergosorbent tests may be used. Up to 85% of patients with asthma demonstrate positive skin test results, and in children, this sensitization is reflective of disease activity. Such testing for allergen-specific immunoglobulin E is critical in prescribing allergen avoidance techniques and allergen immunotherapy regimens, although the method shows a relatively high false positive rate and should not be performed during an exacerbation.

Zab Mosenifar, MD, Medical Director, Women's Lung Institute; Executive Vice Chairman, Department of Medicine, Cedars Sinai Medical Center, Los Angeles, California.

Zab Mosenifar, MD, has disclosed no relevant financial relationships.

The patient is probably having a delayed allergenic response to an indoor mold allergen. Early reactions can occur immediately following allergen inhalation but can also manifest 4-10 hours after exposure to wet and damp areas, such as bathrooms and basements.

Allergic asthma represents the most common asthma phenotype. The average age of onset is younger than that of nonallergic asthma, with allergens triggering exacerbations in 60%-90% of children compared with 50% of adults.Triggers can include mold spores, seasonal pollen, dust mites, and animal allergens. There is also an increased incidence of co-occurring allergic rhinoconjunctivitis and atopic dermatitis in patients with allergic asthma.

During an acute asthma exacerbation, lung examination findings may include wheezing, rhonchi, hyperinflation, or a prolonged expiratory phase. In children, supraclavicular and intercostal retractions and nasal flaring, as well as abdominal breathing, are particularly telling. Total serum immunoglobulin E levels are usually higher in allergic vs nonallergic asthma (> 100 IU), although this marker is not specific to asthma.

The allergic asthma phenotype usually responds to inhaled corticosteroid therapy. Although evidence suggests that allergic vs nonallergic asthma is less severe in many cases, compelling data point to a causal relationship between mold allergy and asthma severity in a subgroup of younger asthma patients; specifically, mold sensitization may be associated with asthma attacks requiring hospital admission in this population.

Although spirometry assessments should be obtained as the primary test to establish the asthma diagnosis, to test for allergic sensitivity to specific allergens in the environment, allergy skin tests and blood radioallergosorbent tests may be used. Up to 85% of patients with asthma demonstrate positive skin test results, and in children, this sensitization is reflective of disease activity. Such testing for allergen-specific immunoglobulin E is critical in prescribing allergen avoidance techniques and allergen immunotherapy regimens, although the method shows a relatively high false positive rate and should not be performed during an exacerbation.

Zab Mosenifar, MD, Medical Director, Women's Lung Institute; Executive Vice Chairman, Department of Medicine, Cedars Sinai Medical Center, Los Angeles, California.

Zab Mosenifar, MD, has disclosed no relevant financial relationships.

The patient is probably having a delayed allergenic response to an indoor mold allergen. Early reactions can occur immediately following allergen inhalation but can also manifest 4-10 hours after exposure to wet and damp areas, such as bathrooms and basements.

Allergic asthma represents the most common asthma phenotype. The average age of onset is younger than that of nonallergic asthma, with allergens triggering exacerbations in 60%-90% of children compared with 50% of adults.Triggers can include mold spores, seasonal pollen, dust mites, and animal allergens. There is also an increased incidence of co-occurring allergic rhinoconjunctivitis and atopic dermatitis in patients with allergic asthma.

During an acute asthma exacerbation, lung examination findings may include wheezing, rhonchi, hyperinflation, or a prolonged expiratory phase. In children, supraclavicular and intercostal retractions and nasal flaring, as well as abdominal breathing, are particularly telling. Total serum immunoglobulin E levels are usually higher in allergic vs nonallergic asthma (> 100 IU), although this marker is not specific to asthma.

The allergic asthma phenotype usually responds to inhaled corticosteroid therapy. Although evidence suggests that allergic vs nonallergic asthma is less severe in many cases, compelling data point to a causal relationship between mold allergy and asthma severity in a subgroup of younger asthma patients; specifically, mold sensitization may be associated with asthma attacks requiring hospital admission in this population.

Although spirometry assessments should be obtained as the primary test to establish the asthma diagnosis, to test for allergic sensitivity to specific allergens in the environment, allergy skin tests and blood radioallergosorbent tests may be used. Up to 85% of patients with asthma demonstrate positive skin test results, and in children, this sensitization is reflective of disease activity. Such testing for allergen-specific immunoglobulin E is critical in prescribing allergen avoidance techniques and allergen immunotherapy regimens, although the method shows a relatively high false positive rate and should not be performed during an exacerbation.

Zab Mosenifar, MD, Medical Director, Women's Lung Institute; Executive Vice Chairman, Department of Medicine, Cedars Sinai Medical Center, Los Angeles, California.

Zab Mosenifar, MD, has disclosed no relevant financial relationships.