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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.

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.

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.

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.

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.

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.