*IL-4 induces naive Th0 cells to differentiate into Th2 cells, which secrete IL-4, IL-5, and IL-13 in EoE5 ; ILC2 cells are increased in EoE and also secrete IL-5 and IL-137 ; † IL-4 and IL-13 induce B-cell isotype switching to produce IgE, activating mast cells and basophils, resulting in degranulation,4,19 while IL-4 can also directly activate mast cells15,16; ‡ Not approved for EoE; § Topical swallowed steroids include swallowed puffs from inhalers, suspension, viscous slurry, and effervescent tablets.3 IL=interleukin; ILC2=type 2 innate lymphoid cell; Th0=naive T helper; Th2=Type 2 helper. 1. O’Shea KM, et al. Gastroenterology. 2018;154(2):333-345. 2. Dellon ES, Hirano I. Gastroenterology. 2018;154(2):319-332.e3. 3. Lucendo AJ, et al. United European Gastroenterol J. 2017;5(3):335-358. 4. Aceves SS. Gastroenterology. 2019;157(1):17-20. 5. Davis BP, Rothenberg ME. Annu Rev Pathol. 2016;11:365-393. 6. Davis BP, et al. JCI Insight. 2016;1(4):e86355. 7. Doherty TA, et al. J Allergy Clin Immunol. 2015;136(3):792-794. 8. Chen JW, Kao JY. BMJ. 2017;359:j4482. 9. Miller E, et al. G3 (Bethesda). 2019;9(3):729-736. 10. Muir AB, et al. J Gastroenterol. 2019;54(1):10-18. 11. Aceves SS, et al. J Allergy Clin Immunol. 2010;126:1198-1204. 12. Ozdemir C, et al. Chem Immunol Allergy. 2010;95:22-44. 13. Abonia JP, et al. J Allergy Clin Immunol. 2010;126(1):140-149. 14. Stone KD, et al. J Allergy Clin Immunol. 2010;125(2 Suppl 2):S73-S80. 15. Nilsson G, Nilsson K. Eur J Immunol. 1995;25(3):870-873. 16. McLeod JJA, et al. Cytokine. 2015;75(1):57-61. 17. Noti M, et al. Nat Med. 2013;19(8):1005-1013. 18. Cheng E, et al. Am J Physiol Gastrointest Liver Physiol. 2012;303(11):G1175-G1187. 19. Wechsler JB, Bryce PJ. Gastroenterol Clin North Am. 2014;43:281-296. 20. Muir AB, et al. Clin Exp Gastroenterol. 2019;12:391-399. 21. Wang R, et al. Dig Dis Sci. 2018;63(7):1756-1762. 22. Chehade M, et al. J Allergy Clin Immunol Pract. 2018;6(5):1534-1544. 23. Capucilli P, Hill DA. Allergy Immunol. 2019;57(1):111-127. 24. Hirano I, et al. Gastroenterology. 2020;158(6):1775-1786.

EOSINOPHILIC-ESOPHAGITIS-EOE

GASTROENTEROLOGY

EoE Pathophysiology

<ul>
 <li>Currently asthma and COPD are considered different obstructive respiratory diseases, sharing some clinical and pathobiology characteristics1,2</li>
 <li>GOLD 2024 and GINA 2024 reports no longer recognize “asthma-COPD overlap” (ACO) as a single disease entity1,2,a</li>
</ul>

CHRONIC-OBSTRUCTIVE-PULMONARY-DISEASE-(COPD)

RESPIRATORY

Type 2 Inflammation in the Pathophysiology of the Lower Airways

<h3>Elements in the periphery and the CNS each have their own distinct roles and players in the onset and progression of MS1</h3>

MS has historically been considered a disease mediated by adaptive immune cells from the periphery (B cells and T cells)2
Our current understanding is that innate immune cells residing in the CNS (including microglia) potentially play a pivotal role in disease progression that results in disability accumulation

<figure class="table" style="width:100%;">
 <table>
 <tbody>
 <tr>
 <td style="background-color:#CC4818;width:30%;">Periphery</td>
 <td style="background-color:#F5E6DA;width:70%;">
 <ul>
 <li>B cells</li>
 <li>T cells</li>
 <li>Monocytes</li>
 </ul></td>
 </tr>
 </tbody>
 </table>
</figure>

<figure class="table" style="width:100%;">
 <table>
 <tbody>
 <tr>
 <td style="background-color:#CC4818;width:30%;">CNS</td>
 <td style="background-color:#F5E6DA;width:70%;">
 <ul>
 <li>Microglia</li>
 <li>CNS-resident B cells</li>
 <li>Astrocytes</li>
 </ul></td>
 </tr>
 </tbody>
 </table>
</figure>

CNS, central nervous system; MS, multiple sclerosis.

References

<h3>These form 2 pathways: acute neuroinflammation driven by peripheral B cells and the microglia-driven pathway inside the CNS involved in smoldering neuroinflammation1-3</h3>

<h4>How do you think the peripheral pathway is involved in MS?</h4>

PIRA, progression independent of relapse activity.

<h3>Acute neuroinflammation in MS is driven primarily by activated B cells in the periphery</h3>

<figure class="table" style="width:100%;">
 <table>
 <tbody>
 <tr>
 <td style="background-color:#cc4818;" rowspan="3">
 Acute Neuroinflammation</td>
 <td style="background-color:#f5e6da;">
 <ul>
 <li>Activation and proliferation of autoreactive/ self-recognizing lymphocytes (ie, B cells)</li>
 </ul></td>
 </tr>
 <tr>
 <td style="background-color:#f5e6da;">
 <ul>
 <li>Infiltration of autoreactive lymphocytes across the blood-brain barrier (BBB)</li>
 <li>Secretion of proinflammatory cytokines</li>
 </ul></td>
 </tr>
 <tr>
 <td style="background-color:#f5e6da;">
 <ul>
 <li>Demyelination</li>
 <li>Formation of acute lesions</li>
 </ul></td>
 </tr>
 </tbody>
 </table>
</figure>

CD4, cluster of differentiation 4.

<h3>…Unlike smoldering neuroinflammation, which is primarily driven by microglia in the CNS1</h3>

<figure class="table" style="width:100%;">
 <table>
 <tbody>
 <tr>
 <td style="background-color:#f5e6da;">
 <ul>
 <li>Focal and diffuse microglial inflammation in the CNS1</li>
 </ul></td>
 <td style="background-color:#cc4818;" rowspan="3">
 Smoldering Neuroinflammation</td>
 </tr>
 <tr>
 <td style="background-color:#f5e6da;">
 <ul>
 <li>Pathogenic microglia act at the edges of lesions causing them to slowly expand as chronic active lesions2,3</li>
 </ul></td>
 </tr>
 <tr>
 <td style="background-color:#f5e6da;">
 <ul>
 <li>Smoldering neuroinflammation manifests as disability accumulation1</li>
 </ul></td>
 </tr>
 </tbody>
 </table>
</figure>

BTK, Burton’s tyrosine kinase.

<h3>The BBB is a selective layer protecting the CNS from external solutes, materials, and pathogens</h3>

The BBB selectively inhibits trafficking into the CNS
Crossing the BBB is a highly regulated process dependent on:
<ul>
 <li>Solute size and charge</li>
 <li>Selective active transport</li>
</ul>

mAb, monoclonal antibodies.

<h3>BTK plays a pivotal role in both peripheral and CNS pathways in MS1,2</h3>

<figure class="table" style="width:100%;">
 <table class="ck-table-resized">
 <colgroup>
 <col style="width:100%;">
 </colgroup>
 <tbody>
 <tr>
 <td style="background-color:#F5E6DA;">
 BTK expression is increased in lesion tissue in people with progressive MS7</td>
 </tr>
 </tbody>
 </table>
</figure>

<h3>Comprehensive clinical management of MS includes targeting both smoldering and acute neuroinflammation1-3</h3>

<figure class="table" style="width:100%;">
 <table class="ck-table-resized">
 <colgroup>
 <col style="width:100%;">
 </colgroup>
 <tbody>
 <tr>
 <td style="background-color:#F5E6DA;">
 Early control of disability accumulation in addition to relapses and acute lesion activity may improve long-term outcomes1,2</td>
 </tr>
 </tbody>
 </table>
</figure>

Do you agree or disagree with this? Why or why not?

<figure class="table" style="width:100%;">
 <table class="ck-table-resized">
 <colgroup>
 <col style="width:100%;">
 </colgroup>
 <tbody>
 <tr>
 <td style="background-color:#F5E6DA;">
 Elements in the periphery and CNS each have their own distinct roles and players in the onset and progression of MS1
 <ul>
 <li>B cells, located in the periphery, and microglia, located in the CNS, are the main drivers of MS2</li>
 </ul></td>
 </tr>
 </tbody>
 </table>
</figure>
<figure class="table" style="width:100%;">
 <table class="ck-table-resized">
 <colgroup>
 <col style="width:100%;">
 </colgroup>
 <tbody>
 <tr>
 <td style="background-color:#F5E6DA;">Because it is located inside the BBB within the CNS, smoldering inflammation has been largely inaccessible to date1,3,4</td>
 </tr>
 </tbody>
 </table>
</figure>
<figure class="table" style="width:100%;">
 <table class="ck-table-resized">
 <colgroup>
 <col style="width:100%;">
 </colgroup>
 <tbody>
 <tr>
 <td style="background-color:#F5E6DA;">
 BTK is involved in the activation of both B cells, as well as microglia1,5
 <ul>
 <li>For microglia, this may result in a shift from a homeostatic to pathogenic state4</li>
 </ul></td>
 </tr>
 </tbody>
 </table>
</figure>
<figure class="table" style="width:100%;">
 <table class="ck-table-resized">
 <colgroup>
 <col style="width:100%;">
 </colgroup>
 <tbody>
 <tr>
 <td style="background-color:#F5E6DA;">
 Optimal management of MS includes controlling relapses, lesions, and disability progression caused by both acute and smoldering neuroinflammation1
 <ul>
 <li>Because microglia reside in the CNS, any potential treatment would need to cross the blood-brain barrier to affect them1,3,6</li>
 </ul></td>
 </tr>
 </tbody>
 </table>
</figure>

The Role of the CNS and Periphery in MS and Disease Accumulation

MULTIPLE-SCLEROSIS

NEUROLOGY

<h2>Atopic Dermatitis Prevalence</h2>

Atopic dermatitis (AD) is a common chronic inflammatory skin disease affecting approximately 20% to 25% of children and about 10% of adults
worldwide1. The onset of AD typically occurs in infancy or early childhood, with around 60% of cases starting within the first year of life and up to
85% before the age of five2. However, adult-onset AD accounts for 20-25% of adult cases, highlighting that the disease can also develop later in
life3. Prevalence varies regionally, with higher rates reported in industrialized countries and urban areas, likely due to environmental and lifestyle
factors4. The Global Burden of Disease Study 2021 estimated that over 129 million people worldwide are affected by AD, with pediatric cases
reaching approximately 72 million, predominantly in children aged 5 to 9 years5.
&nbsp;
Atopic dermatitis prevalence in the GCC region is considerably higher than the global average, especially among children and adolescents, with rates
ranging roughly from 12% to 30% depending on the country and age group. This elevated prevalence highlights the necessity to increase awareness, diagnosis, and management efforts tailored to the regional population.

<ul>
 <li>The United Arab Emirates (UAE) shows notably high AD prevalence rates compared to global averages. For the general population, UAE has an estimated prevalence of about 12.0%, with children showing even higher rates around 19.7%6.</li>
 <li>Saudi Arabia shows an adult AD prevalence of about 30%, indicating a significant disease burden in the adult population7.</li>
</ul>

OTHER-TOPICS

DERMATOLOGY

Epidemiology

<h2>Disease Overview</h2>
Atopic dermatitis (AD), is a common chronic inflammatory skin condition characterized by dry, itchy, and inflamed skin that can flare periodically throughout life. It most often begins in childhood but can affect individuals of any age.1-3
Diagnostic Criteria for Atopic Dermatitis (AD)
Atopic dermatitis is diagnosed clinically, based on a combination of essential, important, and supportive features, as well as by excluding
other similar skin conditions. There is no single definitive laboratory test for AD4-6.

Essential Features (Must Be Present)
Pruritus (itching): Persistent itching is the hallmark of 4,5
Eczema: This includes acute, subacute, or chronic skin changes such as erythema and scaling, with a typical age-specific distribution (e.g., cheeks and extensor surfaces in infants; flexural areas in older children and adults) 4,5
Chronic or Relapsing Course: Symptoms must have a history of chronicity or recurring flares4,5

Important Features (Support Diagnosis)
<ul>
 <li>Personal or Family History of Atopy: Includes atopic diseases such as asthma, allergic rhinitis, or food allergies4,5,7</li>
 <li>Early Age at Onset: Most cases begin in childhood, often before age five4,5</li>
 <li>Immunoglobulin E (IgE) Reactivity: Elevated IgE levels are common but not required4</li>
 <li>Xerosis: Dry skin is frequently observed4,5</li>
</ul>

Associated Features (Suggestive but Nonspecific)
<ul>
 <li>Atypical Vascular Responses: Such as facial pallor or white dermographism.5</li>
 <li>Skin Findings: Keratosis pilaris, pityriasis alba, hyperlinear palms, ichthyosis, lichenification, prurigo lesions.5</li>
 <li>Ocular or Periorbital Changes: Such as Dennie-Morgan folds.5</li>
</ul>

Exclusionary Conditions
<ul>
 <li>Diagnosis also requires exclusion of other conditions that can mimic AD, including:</li>
 <li>Seborrheic dermatitis</li>
 <li>Psoriasis</li>
 <li>Contact dermatitis</li>
 <li>Scabies</li>
 <li>Tinea (fungal) infections</li>
 <li>Immunodeficiency syndromes</li>
 <li>Cutaneous T-cell lymphoma</li>
</ul>

<h2>Clinical Features of Patients With AD</h2>
<ul>
 <li>Clinical diagnosis can be difficult in infants, toddlers and in elderly people8</li>
 <li>Skin biopsies in adults help exclude malignant diseases (e.g. cutaneous T cell lymphoma)8</li>
 <li>AD lesions typically show an age-related distrubution8,9</li>
</ul>

AD Disease Overview

<h2>Understanding the Burden of Atopic Dermatitis on Patients</h2>
Atopic dermatitis (AD) places a significant burden on patients’ lives, impacting much more than just the skin. For millions worldwide, AD causes
ongoing discomfort, affects mental and social well-being, and leads to both direct and indirect economic challenges.1-3
<h2>Chronic Symptoms of Atopic Dermatitis</h2>
Chronic atopic dermatitis is marked by a persistent and evolving set of symptoms that can severely impact patients’ daily lives. These symptoms often
last for months or years and are characterized by both their physical appearance and their impact on comfort and function.3

<h2>Key Chronic Symptoms</h2>

Lichenification

Persistent Itching (Pruritus)

Dry, Scaly Skin (Xerosis)

Skin Thickening and Hyperpigmentation

Eczematous Lesions

Cracked or Fissured Skin

Secondary Infections

Other Chronic Features

Chronic atopic dermatitis symptoms not only cause physical discomfort but are also associated with substantial psychosocial and quality-of-life
burdens, highlighting the need for comprehensive, ongoing management.5,7,8
&nbsp;
<h2>Impact of Atopic Dermatitis on Quality of Life</h2>
Atopic dermatitis (AD) goes far beyond the skin, reducing quality of life (QoL) in profound and lasting ways for both patients and their families.10,11

Physical and Emotional Burden
<ul>
 <li>
 Persistent itch and discomfort are the most distressing symptoms, reported as severe by most patients, leading to constant scratching,
 pain, and skin damage.10,11,15</li>
 <li>
 Sleep disturbances are common, with poor sleep quality affecting up to 92% of patients, resulting in daytime fatigue, impaired
 concentration, and decreased school or work performance.10,11</li>
 <li>
 Emotional consequences such as depression, anxiety, embarrassment, and low self-esteem are frequently reported, especially in those
 with severe or visible disease.10,15,16</li>
 <li>Over half of adult AD patients report a moderate to extremely large impact on their overall quality of life.12,13,16</li>
 <li>In children and adolescents, AD can lead to social isolation, bullying, and fewer friendships, especially for those with severe disease.11</li>
</ul>

Social and Daily Functioning
<ul>
 <li>Social withdrawal and limitations: The visibility of lesions and constant need for treatment cause many patients and families to avoid social activities or alter their routines.10,11</li>
 <li>Academic and work impact: Nearly one-third of adults with AD have experienced challenges at school or work, and 14% believe their academic or career advancement has been hindered by their disease.11</li>
 <li>Family burden: Caregivers—especially parents of children with AD—report significant stress, time commitment for treatments, and emotional distress related to their child’s condition.11,13,15</li>
</ul>

Severity Matters
The impact of AD on all quality of life measures increases sharply with disease severity. In studies using quality of life indexes, children
and adults with moderate-to-severe AD report a “very large” or “extremely large” effect on daily life more than twice as often as those
with mild disease.12-14,16
Long-term and Lifelong Impact
<ul>
 <li>Severe, uncontrolled AD from childhood into adulthood leads to enduring difficulties in school, work, and forming social relationships, sometimes even influencing career paths.10</li>
 <li>The burden can accumulate over a lifetime, contributing to poorer long-term health and social outcomes.10,11</li>
</ul>

<h2>Comorbidities17-22:</h2>

<h2>Economic Burden of Atopic Dermatitis on Patients</h2>
Atopic dermatitis (AD) imposes a substantial financial and productivity burden on patients, families, and society. The costs are both direct—arising
from medical care—and indirect, resulting from reduced productivity and impaired daily functioning.
Direct Costs
The impact of AD on all quality of life measures increases sharply with disease severity. In studies using quality of life indexes, children
and adults with moderate-to-severe AD report a “very large” or “extremely large” effect on daily life more than twice as often as those
with mild disease.12-14,16
<ul>
 <li>Medical Expenses: Patients with AD face significantly higher health care expenditures than those without AD. In adults, annual direct health care costs can be nearly $5,000 higher per patient, encompassing physician visits, hospitalization, prescription medications (including costly newer therapies), and outpatient services.23</li>
 <li>Treatment-Related Costs: Frequent clinic appointments, management of complications, and long-term use of topical or systemic therapies further increase financial strain.24</li>
 <li>Out-of-Pocket Expenses: Patients and families often pay for moisturizers, special skin care products, specific clothing or bedding, and transportation to healthcare providers.23,24</li>
</ul>
Indirect Costs
Lost Productivity: AD leads to increased absenteeism and loss of workdays. Adults with AD report more missed work or school days and higher utilization of short-term disability benefits compared to the general population.23
Reduced Work Capacity: The physical discomfort and sleep disturbances from AD negatively impact concentration, work efficiency,
and even career choices or advancement.23
Family Burden: Beyond the patient, family members may incur additional costs for caregiving and experience productivity loss due to
time devoted to ongoing care needs.25
Healthcare utilization: Patients with AD have increased physician office visits and outpatient pharmacy use.26
Severity dependence: Economic burden intensifies with increasing severity of AD, leading to more interventions, treatment changes,
and lost workdays.26

AD Burden on Patients

Smoldering disease is a key unaddressed component of MS, driving disease progressions1-3
<h3>The Silent Progression in MS: Smoldering neuroinflammation and PIRA&nbsp;</h3>

Acute Neuroinflammation

Acute neuroinflammation is driven in party by activated B cells and T cells derived from the periphery 
 &nbsp; &nbsp;&nbsp;• Leads to relapses,acute lesions, and RAW1,8,11

10%-20% of disability accumulation in treated patients is driven by relapses and acute lesions&nbsp;12,13

Smoldering Neuroinflammation

Smoldering neuroinflammation is driven in primarily by disease-associated microglia found in the CNS1,8,11 
 &nbsp; &nbsp;&nbsp;• Leads to PIRA,resulting in physical disability and cognitive worsening1,8,11

80%-90% of disability accumulation in treated patients is relapse-independent and driven by smoldering neuroinflammation.12,13

<h3>Both concurrent neuroinflammatory processes drive disability accumulation in MS 1,14-16</h3>
Smoldering neuroinflammation starts at disease onset and increasingly drives disability accumulation1

The relative contribution of both acute and smoldering neuroinflammation shifts as patients progress from RRMS to nrSPMS1,14
<ul>
 <li>Smoldering neuroinflammation presents early and throughout:the spectrum of MS, before initial clinical symptoms.1,11</li>
 <li>Over the course of MS, acute neuroinflammation may decline, but smoldering neuroinflammation persists in the absence of relapses and acute lesions1</li>
 <li>Disability accumulation driven by smoldering neuroinflammation can: 
 <ul>
 <li>Happen throughout the disease spectrum9</li>
 <li>Affect any patient, regardless of the type of MS or if patients have a history of taking DMTs1</li>
 </ul></li>
 <li>Smoldering neuronflammation is driven primarily by disease-associated microglia found in the CNS and contributes to both physical and cognitive disability accumulation1,17</li>
</ul>

For more information about Acute and Smoldering Inflammation, click on this link:

Acute &amp; Smoldering Neuroinflammation

Abbreviations

References

Smoldering Disease Overview

<h3>Despite effective control of relapses and acute lesions, many people with MS continue to accumulate disability.1,2</h3>

PIRA is responsible for up to&nbsp;80% to 90% of disability accumulation in treated RRMS patients4,5*

*As documented by an observational study and pooled data from 2 randomized clinical trials.6,7

Many patients still progress from RRMS to SPMS and accumulate significant disability despite current treatments that effectively address relapses and acute lesions.1,2,15

<h4 style="text-align:center;">Approximately 30% to 40% 
 of treated patients will transition to SPMS within 12 years of RRMS diagnosis6</h4>

*As documented by an observational study and pooled data from 2 randomized clinical trials.4,5
<h3>PIRA can occur early in the course of MS3,7&nbsp;</h3>

65% of RRMS patients reported experiencing PIRA8,9

PIRA can be seen in treated RRMS patients as early as 3 years after diagnosis3,7

*As seen in real-world data (patient-reported outcomes). PIRA was defined as continuous worsening of symptoms independent of relapses in the previous 12 months.9

<h3>The damage from smoldering neuroinflammation can accumulate slowly and manifest as gradual physical and/or cognitive changes over years prior to transitioning to nrSPMS2,12</h3>

Physical decline may present as13,14
<ul>
 <li>Reduced mobility and having to stop or decrease playing sports, such as tennis, running, etc</li>
 <li>Debilitating fatigue</li>
 <li>Worsening bladder and bowel control, vision, speech, and spasticity/dexterity</li>
 <li>Sexual dysfunction</li>
 <li>Pain</li>
</ul>

Cognitive decline may present as13:
<ul>
 <li>Trouble concentrating</li>
 <li>Experiencing difficulty multitasking</li>
 <li>Being less productive at work, or having more difficulty completing activities at work</li>
 <li>Brain "fog" and memory impairment</li>
 <li>Changes in mood/personality and reduced social activities</li>
</ul>

<figure class="table" style="width:100%;">
 <table class="ck-table-resized">
 <colgroup>
 <col style="width:100%;">
 </colgroup>
 <tbody>
 <tr>
 <td style="background-color:#f0d7c3;padding:20px;">
 <h3 style="text-align:center;">Symptoms could be gradually building before revealing themselves as clinically detectable disability accumulation, so it is important to continue monitoring patients for changes over time.2</h3></td>
 </tr>
 </tbody>
 </table>
</figure>

Smoldering Disease Burden

<h3>Radiological manifestation of smoldering disease&nbsp;</h3>
Chronic active lesions, including SELs and PRLs, represent the evolution of acute lesions via CNS resident processes.1–4 They occur early and throughout the disease course.1,2

Chronic active lesions undergo ongoing demyelination; may slowly expand, change shape or fuse with neighboring lesions4–7
Chronic active WM lesion4

<h3>Detecting smoldering disease clinically during routine clinical practice&nbsp;</h3>

<h3>Multimodal approach to uncover disability accumulation resulting from smoldering disease in MS</h3>

Smoldering Disease Detection

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The ADCT gives a measure of how controlled the eczema is. Answer these 6 simple questions with your patient to find the ADCT score. It will indicate proper course of action.

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