<p>Airway remodeling drives progressive and potentially irreversible lung function decline in asthma.<sup>2</sup> Understanding the central role of IL-4 and IL-13 in this process is essential to guiding effective treatment strategies.<sup>1,10</sup></p>

<h3>Listen to Prof. Alberto Papi about Airway remodeling</h3>

<h2>Understanding airway remodeling and hyperresponsiveness<sup>1,3-5</sup></h2>
<p>Asthma involves chronic airway inflammation, structural changes in the lung airway lining, and exaggerated airway constriction in response to stimuli.<sup>3,4</sup> These processes — airway remodeling and airway hyperresponsiveness (AHR) — are the key underlying mechanisms of lung function decline.<sup>1,5</sup></p>

<figure class="table" style="width:100%;">
 <table style="background-color:#23004c;border-color:#fff;border-style:solid;">
  <tbody>
   <tr>
    <td style="background-color:#23004c;border-color:#fff;padding:20px;">
     <h3><span style="color:hsl(0,0%,100%);">Type 2 inflammation, Hyperresponsiveness, and Remodeling contribute to Airway narrowing<sup>6</sup></span></h3></td>
   </tr>
  </tbody>
 </table>
</figure>

<p>What is airway remodeling?</p>

<h3 style="text-align:center;">Remodeling in asthma comprises structural changes to the airways<sup>10-13</sup></h3>

<p>What is airway hyperresponsiveness?</p>

<figure class="table" style="width:100%;">
 <table style="background-color:#23004c;border-color:#fff;border-style:solid;">
  <tbody>
   <tr>
    <td style="background-color:#7A00E6;border-color:#7A00E6;padding:10px;text-align:center;">
     <h3><span style="color:hsl(0,0%,100%);">Key clinical insight</span></h3></td>
   </tr>
   <tr>
    <td style="background-color:#23004c;border-color:#23004c;padding:20px;">
     <h3><span style="color:hsl(0,0%,100%);">AHR is associated with increased risk of lung function decline, persistence of symptoms such as wheezing, and occurrence of future exacerbations. Treatment strategies focused on normalization of AHR can reduce exacerbation risk and prevent further airway inflammation and remodeling.<sup>5</sup></span></h3></td>
   </tr>
  </tbody>
 </table>
</figure>

<h2>The role of type 2 inflammation<sup>10</sup></h2>
<p>Majority of patients with asthma have <strong>type 2 inflammation</strong> as the main causative pathophysiologic process.<sup>10</sup> This type of asthma is driven by type 2 cytokines (primarily IL-4, IL-13, and IL-5) with additional contributions from alarmins like thymic stromal lymphopoietin (TSLP), an epithelial-derived regulator of type 2 inflammation.<sup>10</sup></p>

<h3>How type 2 cytokines drive asthma pathology?<sup>1-2,10-11</sup></h3>

<p>IL-4 and IL-13 facilitate migration and adhesion of eosinophils in the lung airways, stimulate mucus hypersecretion, promote AHR, and directly drive airway remodeling.<sup>1,11</sup></p>

<p>IL-5 mediates eosinophil differentiation in the bone marrow and their subsequent activation in the airways to promote airway inflammation.<sup>1</sup></p>

<p>Alarmins (TSLP and IL33) function as regulators, amplifying the type 2 inflammatory cascade from the epithelial level.<sup>10,11</sup></p>

<p>The cumulative action of IL-4 and IL-13 causes edema, mucus hypersecretion, AHR, and airway remodeling - ultimately leading to decreased lung function.<sup>10</sup></p>

<figure class="table" style="width:100%;">
 <table style="background-color:#23004c;border-color:#fff;border-style:solid;">
  <tbody>
   <tr>
    <td style="background-color:#7A00E6;border-color:#7A00E6;padding:10px;text-align:center;">
     <h3><span style="color:hsl(0,0%,100%);">Did you know?</span></h3></td>
   </tr>
   <tr>
    <td style="background-color:#23004c;border-color:#23004c;padding:20px;">
     <h3><span style="color:hsl(0,0%,100%);">Eosinophils are NOT the primary drivers of airway remodeling. IL-4 and IL-13 are the cytokines mainly responsible for the structural airway changes that lead to lung function decline. Addressing these cytokines is essential to halt lung damage.<sup>1,2</sup></span></h3></td>
   </tr>
  </tbody>
 </table>
</figure>

<p>More info about the role of T2 cytokines in airway remodeling<sup>1,10</sup></p>

<h2>IL-4 and IL-13: The critical therapeutic targets<sup>1,8,9</sup></h2>
<p>While eosinophil count and IL-5 are important markers of asthma exacerbations, IL-4 and IL-13 are the primary drivers of the structural airway changes seen in remodeling.<sup>2</sup> Therapeutic approaches targeting IL-4 and IL-13 can address both the inflammatory cascade and the underlying remodeling processes that contribute to lung function decline.<sup>2</sup></p>
<p>Research evidence supports the direct role of IL-4 and IL-13 in airway inflammation, AHR, and airway remodeling — making them critical therapeutic targets.<sup>1,8,9</sup></p>

<h3 style="text-align:center;">Comparison of therapeutic targets</h3>
<figure class="table" style="width:100%;">
 <table>
  <tbody>
   <tr>
    <td style="background-color:#23004c;border-color:#fff;text-align:center;width:30%;">
     <h3><span style="color:hsl(0,0%,100%);">Target</span></h3></td>
    <td style="background-color:#23004c;border-color:#fff;text-align:center;width:35%;">
     <h3><span style="color:hsl(0,0%,100%);">Mechanism</span></h3></td>
    <td style="background-color:#23004c;border-color:#fff;text-align:center;width:35%;">
     <h3><span style="color:hsl(0,0%,100%);">Impact on Airway Remodeling</span></h3></td>
   </tr>
   <tr>
    <td style="border-color:#000;"><strong>IL-4 &amp; IL-13<sup>1,2,9</sup></strong></td>
    <td style="border-color:#000;">Drive airway inflammation, eosinophil migration and adhesion, mucus hypersecretion, and AHR.</td>
    <td style="border-color:#000;">Direct — address the root cause of remodeling and lung function decline.</td>
   </tr>
   <tr>
    <td style="border-color:#000;"><strong>IL-5<sup>1,2</sup></strong></td>
    <td style="border-color:#000;">Mediates eosinophil differentiation in bone marrow and activation in airways.</td>
    <td style="border-color:#000;">Secondary role — influences remodeling through eosinophil-mediated inflammatory processes.</td>
   </tr>
  </tbody>
 </table>
</figure>
<p>Blocking IL-4 and IL-13 can also suppress eosinophilic inflammation indirectly — reducing airway tissue eosinophilia.<sup>1</sup></p>

<figure class="table" style="width:100%;">
 <table style="background-color:#23004c;border-color:#fff;border-style:solid;">
  <tbody>
   <tr>
    <td style="background-color:#7A00E6;border-color:#7A00E6;padding:10px;text-align:center;">
     <h3><span style="color:hsl(0,0%,100%);">Key message</span></h3></td>
   </tr>
   <tr>
    <td style="background-color:#23004c;border-color:#23004c;padding:20px;">
     <h3><span style="color:hsl(0,0%,100%);">Blocking IL-4 and IL-13 can reduce airway tissue eosinophilia, decrease immune infiltrates associated with type 2 inflammation, and extend therapeutic benefits beyond eosinophil count reduction alone.<sup>1,2</sup></span></h3></td>
   </tr>
  </tbody>
 </table>
</figure>

<h2>Clinical implications: The importance of early intervention<sup>7</sup></h2>
<p>Airway remodeling is a progressive process. Early detection and intervention targeting the underlying inflammatory drivers can reduce acute asthma attacks and minimize irreversible lung function decline.<sup>7</sup></p>
<p>Identifying the type of inflammation present in each patient is key to effective disease management.</p>
<p>The following <strong>type 2 inflammation biomarkers</strong> should be assessed:<sup>7</sup></p>
<ul>
 <li><strong>Blood eosinophil count</strong> — elevated levels indicate eosinophilic airway inflammation</li>
 <li><strong>Fractional exhaled nitric oxide (FeNO)</strong> — a marker of IL-13-driven airway inflammation</li>
 <li><strong>Serum IgE</strong> — elevated in allergic/type 2-driven asthma</li>
</ul>
<p>Early biomarker assessment enables physicians to identify patients at highest risk of remodeling and to select treatment strategies that target the root cause of disease progression.<sup>7</sup></p>

<figure class="table" style="width:100%;">
 <table style="background-color:#23004c;border-color:#fff;border-style:solid;">
  <tbody>
   <tr>
    <td style="background-color:#7A00E6;border-color:#7A00E6;padding:10px;text-align:center;">
     <h3><span style="color:hsl(0,0%,100%);">Clinical action</span></h3></td>
   </tr>
   <tr>
    <td style="background-color:#23004c;border-color:#23004c;padding:20px;">
     <h3><span style="color:hsl(0,0%,100%);">Identify your patients at risk of airway remodeling — assess type 2 inflammation biomarkers early. Proactive phenotyping and targeted intervention can improve the trajectory of disease progression.<sup>7</sup></span></h3></td>
   </tr>
  </tbody>
 </table>
</figure>

<h3>Listen to Prof. Alberto Papi about the importance of early intervention</h3>

<p>Referenties</p>

Airway remodeling in asthma: Why targeting IL-4 and IL-13 matters

SPECIALTY-CARE

DUPIXENT

ASTHMA

RESPIRATORY

<p data-font="small">▼ This medicinal product is subject to additional monitoring.</p>
<p>Beyfortus<sup>®</sup> is indicated for the prevention of Respiratory Syncytial Virus (RSV) lower respiratory tract disease in:<sup>1</sup></p>
<ul>
 <li>Neonates and infants during their first RSV season;</li>
 <li>Children up to 24 months of age who remain vulnerable to severe RSV disease through their second RSV season.</li>
</ul>
<p>Beyfortus<sup>®</sup> should be used in accordance with official recommendations.<sup>1</sup></p>

<h2>Beyfortus<sup>® </sup>has an unparalleled body of real-world evidence against RSV disease, including hospitalizations<sup>2–60</sup></h2>

<figure class="table" style="width:100%;">
 <table style="background-color:#7e81d2;border-color:#fff;border-style:solid;">
  <tbody>
   <tr>
    <td style="background-color:#7e81d2;border-color:#fff;padding:10px;">
     <h3><span style="color:hsl(0,0%,100%);">&gt; 50 real-world studies in over 400,000 Beyfortus<sup>®</sup>-immunized infants across the Northern and Southern Hemispheres<sup>*,2-60</sup></span></h3></td>
   </tr>
  </tbody>
 </table>
</figure>

<h2>A meta-analysis of 27 studies assessed the effectiveness of Beyfortus<sup>®</sup> against RSV-related outcomes in the real world<sup>61</sup></h2>
<p>The 27 studies included after screening/eligibility, was conducted in Spain, France, US, Italy and Luxembourg. Beyfortus<sup>®</sup> was associated with high effectiveness against RSV-related outcomes<sup>61</sup>:</p>

<p data-font="small">Length of hospital stay: No difference between Beyfortus<sup>®</sup>-immunized infants and non-immunized infants was observed (weighted mean difference [WMD]: 0.10; 95% CI: -0.63–0.65; p=0.97)</p>

<h2>The NIRSE-GAL study: A real-world effectiveness and impact study from Galicia, Spain<sup>60</sup></h2>
<p>Galicia, a region in northwestern Spain, became one of the first places in the world to introduce nirsevimab as part of its regional immunization program for infants. The study was conducted between September 25, 2023, and ended March 31, 2024. It included over 13,300 infants.<sup>2,60</sup></p>

<figure class="table" style="width:100%;">
 <table style="background-color:#c065ba;border-color:#fff;border-style:solid;">
  <tbody>
   <tr>
    <td style="background-color:#c065ba;border-color:#fff;padding:10px;">
     <h3><span style="color:hsl(0, 0%, 100%);">After Beyfortus<sup>®</sup> implementation, RSV LRTI hospitalization decreased substantially by 89,2%<sup>¶</sup> vs. five previous seasons for infants in the overall cohort (infants born before and during RSV season).<sup>60</sup></span></h3></td>
   </tr>
  </tbody>
 </table>
</figure>

<p>In this real-world study, high coverage was achieved in the seasonal and catch-up groups. High effectiveness and public health impact were seen with Beyfortus. The findings from this study support clinical trial efficacy and safety data.<sup>1,60,62,63</sup></p>
<h3 style="text-align:center;">Watch the video below to learn more about the findings of the study:</h3>

VACCINES

BEYFORTUS

RESPIRATORY-SYNCYTIAL-VIRUS

Beyfortus®▼(nirsevimab): effectiveness and public health impact in the real world

<h3><sup>▼</sup>Beyfortus had a favorable safety profile in clinical trials.<sup>1,62-65</sup></h3>
<p>Safety has been studied in a broad population, including healthy premature infants and children at higher risk of RSV infections of the lower respiratory tract. The type and frequency of adverse reactions with Beyfortus were comparable to placebo in the Phase 2b and Phase 3 studies.<sup>1,62-65</sup></p>

<h3><span style="color:hsl( 186, 100%, 43% );">Rash</span></h3>
<p>within 14 days of dosing</p>

<h3><span style="color:hsl( 238, 48%, 66% );">Pyrexia</span></h3>
<p>within 7 days of dosing</p>

<h3><span style="color:hsl( 304, 42%, 57% );">Injection site reactions</span></h3>
<p>within 7 days of dosing</p>

<p>Hypersensitivity reactions have been spontaneously reported after marketing authorisation; The frequency is unknown.<sup>1</sup></p>
<p>In the study in infants at higher risk of severe RSV, the safety profile of Beyfortus was comparable to that of the comparator medicinal product palivizumab and consistent with the safety profile of nirsevimab in full-term and preterm infants at GA ≥ 29 weeks.<sup>1,62,65</sup></p>

<p>Footnotes</p>

<p>Compulsory Information</p>

<p>Heeft&nbsp;u vragen&nbsp;of wilt u meer weten? Wij zorgen dat&nbsp;u zo snel mogelijk geholpen wordt.</p>

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<h2>Classification and early presentation</h2>
<p>Gaucher disease is an autosomal recessive lysosomal storage disorder caused by pathogenic variants in the <i>GBA1</i> gene, resulting in deficient activity of the enzyme acid β glucosidase. This deficiency leads to accumulation of glucosylceramide and related lipids within macrophages, forming characteristic Gaucher cells.<sup>1-5</sup> These lipid laden cells infiltrate multiple organs, particularly the spleen, liver, bone marrow and lungs.<sup>1,2</sup></p>

<h2>Why early recognition of Gaucher disease matters</h2>
<p>Early recognition in paediatric patients enables timely intervention, preventing irreversible skeletal, hematologic, and visceral complications.<sup>1,2</sup> Various types of treatment are available for patients with Gaucher disease, which focuses on addressing the underlying metabolic defect to reduce disease burden and improve organ function, alongside supportive care for hematologic, skeletal, and growth-related complications. Therapy is individualized based on disease severity, symptoms, and progression, with regular monitoring to guide initiation and adjustment of treatment strategies.<sup>1</sup></p>

<p>Gaucher disease should be considered in children</p>
<ul>
 <li>frequently presenting with splenomegaly which often emerges before other symptoms and sometimes as the only early sign<sup>4</sup> &nbsp;</li>
 <li>with hepatomegaly, thrombocytopenia, and anaemia if there is no alternative explanation<sup>2,3</sup></li>
 <li>with bone manifestations, including bone pain, delayed growth, Erlenmeyer-flask deformity, and bone crises<sup>1,4</sup></li>
 <li>with growth delay and delayed puberty<sup>2</sup></li>
</ul>

<h2>Clinical types</h2>
<p>Gaucher disease comprises three major clinical types ranging from neuronopathic to severe neuronopathic forms, of which type 1 is the most seen form in children (table 1).<sup>3,6-9</sup></p>

<figure class="table" style="width:100%;">
 <table class="ck-table-resized" style="border-color:#F5F5F5;border-style:solid;">
  <colgroup>
   <col style="width:30.12%;">
   <col style="width:21.63%;">
   <col style="width:24.65%;">
   <col style="width:23.6%;">
  </colgroup>
  <tbody>
   <tr>
    <td style="background-color:#23004C;border-color:#fff;padding:15px;text-align:center;">
     <h3><span style="color:hsl(0,0%,100%);">Type</span></h3></td>
    <td style="background-color:#23004C;border-color:#fff;padding:15px;text-align:center;">
     <h3><span style="color:hsl(0,0%,100%);">Neurologic involvement</span></h3></td>
    <td style="background-color:#23004C;border-color:#fff;padding:15px;text-align:center;">
     <h3><span style="color:hsl(0,0%,100%);">Typical onset</span></h3></td>
    <td style="background-color:#23004C;border-color:#fff;padding:15px;text-align:center;">
     <h3><span style="color:hsl(0,0%,100%);">Key features</span></h3></td>
   </tr>
   <tr>
    <td style="border-color:#000;padding:15px;text-align:center;"><strong>Type 1 (non neuropathic)</strong></td>
    <td style="border-color:#000;padding:15px;text-align:center;">None</td>
    <td style="border-color:#000;padding:15px;text-align:center;">Childhood to adulthood</td>
    <td style="border-color:#000;padding:15px;text-align:center;">Hepatosplenomegaly, cytopenias, bone disease</td>
   </tr>
   <tr>
    <td style="border-color:#000;padding:15px;text-align:center;"><strong>Type 2 (acute neuropathic)</strong></td>
    <td style="border-color:#000;padding:15px;text-align:center;">Severe, early</td>
    <td style="border-color:#000;padding:15px;text-align:center;">Infancy</td>
    <td style="border-color:#000;padding:15px;text-align:center;">Rapid neurological decline, death in early childhood</td>
   </tr>
   <tr>
    <td style="border-color:#000;padding:15px;text-align:center;"><strong>Type 3 (chronic neuropathic)</strong></td>
    <td style="border-color:#000;padding:15px;text-align:center;">Slowly progressive</td>
    <td style="border-color:#000;padding:15px;text-align:center;">Childhood</td>
    <td style="border-color:#000;padding:15px;text-align:center;">Neurologic impairment + systemic manifestations</td>
   </tr>
  </tbody>
 </table>
</figure>
<p style="text-align:center;" data-font="small">Table 1. Clinical types of Gaucher disease<sup>3,6-9</sup></p>

<h2>Clinical presentation in children</h2>
<p>Children with Gaucher disease almost always (95%) present with splenomegaly, appearing earlier than bone manifestations. In half of young children, splenomegaly is the only initial symptom.<sup>1,4</sup><br>
  Hepatomegaly (present in 87% of cases), thrombocytopenia (50%) and anaemia (40%) are among the most common presenting combinations in children with Gaucher disease.<sup>1,2,4</sup></p>
<p>Gaucher disease should be considered when splenomegaly coexists with cytopenias or bone pain.<sup>1,4</sup></p>

<h2>Key early symptoms<sup>1,2,3</sup></h2>

<h2>Age at which symptoms may occur</h2>
<p>Symptoms of Gaucher disease can begin in infancy, especially in the more severe forms like Gaucher disease type 2, which often presents prenatally, perinatally, or in the first few months of life, and typically leads to death in infancy. For Gaucher disease type 3, children often show symptoms within the first year and later in childhood, including neurological issues like seizures and saccadic gaze abnormalities. In contrast, GD1 (non-neuronopathic form) tends to have more variable onset, but still typically appears in childhood, with symptoms such as hepatosplenomegaly, thrombocytopenia, anaemia and bone pain. Due to the variability in symptoms and lack of awareness, diagnosis can be significantly delayed. About 1 in 6 patients experienced a delay of ≥7 years or more from the first medical consultation to diagnosis.<sup>1</sup></p>

<h2>Diagnostic algorithm for pediatric patients without a family history of the disease<sup>10</sup></h2>

<h2>Differential diagnosis in children</h2>
<p>Gaucher disease may be initially mistaken for:</p>
<ul>
 <li>Hematologic malignancies<sup>1,2</sup></li>
 <li>Immune thrombocytopenia<sup>4</sup></li>
 <li>Thalassemia<sup>4</sup></li>
 <li>Other disorders (e.g., ASMD)<sup>1,3</sup></li>
</ul>

<p>Would you like to know more about the diagnostics of Gaucher disease?</p>

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Gaucher disease is an autosomal recessive lysosomal storage disorder caused by pathogenic variants in the GBA1 gene, resulting in deficient activity of the enzyme acid β glucosidase.

Gaucher disease in children

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