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Eosinophilic Granulomatosis with Polyangiitis (EGPA)

Eosinophilic Granulomatosis with Polyangiitis (EGPA)

Eosinophils in EGPA
Diagnosis & Clinical Presentation
Unmet Need in EGPA Management
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AstraZeneca Medical's ambition is to address unmet needs for people living with inflammatory diseases driven by eosinophilic inflammation.

Watch Eosinophils in Action in EGPA

What is EGPA?

EGPA is a complex, rare, multisystem disease characterized by necrotizing vasculitis and eosinophilic inflammation, which is associated with adult-onset asthma and nasal polyps.^1-3 The US incidence rate is estimated at 1 to 3 cases per 100,000 adults per year.⁴

EGPA is the rarest subgroup among the AAVs, although the majority of patients with EGPA are ANCA negative.^1,2

Characteristics of the 3 Diseases of AAV

AAV Diseases	Key clinical manifestations^1-3,5,6	ANCA positivity^2,7,a
EGPA	Asthma, eosinophilia, and nasal polyps are common^b Necrotizing vasculitis of small to medium-sized blood vessels and eosinophilic granulomatous inflammation	30-47%
MPA	Necrotizing arteritis involving small and medium arteries may be present Necrotizing glomerulonephritis is very common Inflammation that is not centered on vessels, including granulomatous inflammation, is absent Skin involvement is common	70-90%
GPA	Necrotizing glomerulonephritis and granulomatous and non-granulomatous extravascular inflammation are very common Nasal crusting, stuffiness and bleeding, and eye involvement are common	70-90%

^aANCA are autoantibodies directed against antigens found in the cytoplasmic granules of neutrophils and monocytes; ^bThese characteristics are rare in MPA and GPA.

What are Eosinophils?

Eosinophils are terminally differentiated granulocytes that have a role in inflammation and tissue injury in multiple diseases and across many organ systems.^8-10

Eosinophils can have reciprocal interactions with other immune cells to perpetuate chronic inflammation.^8,10 They exert inflammatory effects by releasing cytotoxic granules (eg, EDN, ECP, EPO, MBP), extracellular traps, and lipid body inflammatory mediators.¹⁰

Eosinophils contribute to inflammation both directly and indirectly³

Cytotoxicity and Microenvironment Manipulation

Eosinophils can produce diverse cytotoxic proteins that cause organ damage through direct cytotoxic effects.¹¹

Eosinophils produce thrombin and can induce a prothrombotic environment.

Chronic Inflammation

Eosinophils can drive cytotoxicity by interacting with other inflammatory cell types to perpetuate chronic inflammation.¹¹

Ischemic Damage

Eosinophils may contribute to ischemic damage via inflammation and thrombosis, irrespective of ANCA status.^3,8,12

Eosinophils Are Involved in All Phases of EGPA

These phases may not appear in every patient, may not appear in a defined order, or may partially overlap.^7,13

Prodromal

Characteristics

Severe adult-onset asthma^7,13
Upper respiratory symptoms^a
Non-specific symptoms^b

Role of Eosinophils

Increased numbers of eosinophils contribute to respiratory and ENT manifestations³

Eosinophilic Infiltrative

Characteristics

Peripheral blood eosinophilia^13,14,c
Tissue eosinophilia, particularly in the lungs, heart, and GI system

Role of Eosinophils

Eosinophilic infiltration contributes to organ damage³

Vasculitic

Characteristics

Systemic blood vessel vasculitis with granulomatous inflammation^13,14

Role of Eosinophils

Eosinophilic vasculitis of small arteries and veins³
Extravascular eosinophilic granulomas contribute to organ damage

^aSuch as allergic rhinitis and nasal polyps.

^bIncluding malaise, fever, migrating polyarthralgia, and weight loss.

^cTypically defined as 5.0-9.0 x 10⁹/L.

Spectrum of Clinical Manifestations of EGPA

Although EGPA has historically been segregated into 2 distinct phenotypes based on the underlying pathophysiological mechanisms, it may present as a spectrum of disease phenotypes with overlapping pathological mechanisms that cannot be defined by a single serological or clinical parameter.^7,11

Note: Mononeuritis multiplex is a form of peripheral neuropathy, involving damage to at least 2 different areas of the peripheral nervous system.

AAV	antineutrophil cytoplasmic antibody-associated vasculitis
ANCA	antineutrophil cytoplasmic antibody
ECP	eosinophilic cationic protein
EDN	eosinophil-derived neurotoxin
EGPA	eosinophilic granulomatosis with polyangiitis
ENT	ear, nose, and throat
EPO	eosinophil peroxidase
GI	gastrointestinal
GPA	granulomatosis with polyangiitis
ILC2	type 2 innate lymphoid cell(s)
MBP	major basic protein
MPA	microscopic polyangiitis
US	United States

1. Jennette JC, Falk RJ, Bacon PA, et al. 2012 revised International Chapel Hill Consensus Conference nomenclature of vasculitides. Arthritis Rheum. 2013;65(1):1-11. doi:10.1002/art.37715

2. Furuta S, Iwamoto T, Nakajima H. Update on eosinophilic granulomatosis with polyangiitis. Allergol Int. 2019;68(4):430-436. doi:10.1016/j.alit.2019.06.004

3. Khoury P, Grayson PC, Klion AD. Eosinophils in vasculitis: characteristics and roles in pathogenesis. Nat Rev Rheumatol. 2014;10(8):474-483. doi:10.1038/nrrheum.2014.98

4. Vasculitis Foundation. Pediatric vasculitis. Who gets EGPA? Vasculitis Foundation website. Accessed February 11, 2026. https://www.vasculitisfoundation.org/pediatrics-vasculitis/pediatric-types/pediatric-eosinophilic-granulomatosis-with-polyangiitis/

5. Yates M, Watts R. ANCA-associated vasculitis. Clin Med (Lond). 2017;17(1):60-64. doi:10.7861/clinmedicine.17-1-60

6. Chung SA, Seo P. Microscopic polyangiitis. Rheum Dis Clin North Am. 2010;36(3):545-558. doi:10.1016/j.rdc.2010.04.003

7. Trivioli G, Terrier B, Vaglio A. Eosinophilic granulomatosis with polyangiitis: understanding the disease and its management. Rheumatology (Oxford). 2020;59(suppl 3):iii84-iii94. doi:10.1093/rheumatology/kez570

8. Ramirez GA, Yacoub MR, Ripa M, et al. Eosinophils from physiology to disease: a comprehensive review. BioMed Res Int. 2018;2018:9095275. doi:10.1155/2018/9095275

9. Rosenberg HF, Dyer KD, Foster PS. Eosinophils: changing perspectives in health and disease. Nat Rev Immunol. 2013;13(1):9-22. doi:10.1038/nri3341

10. Jacobsen EA, Jackson DJ, Heffler E, et al. Eosinophilic knockout humans: uncovering the role of eosinophils through eosinophil-directed biologic therapies. Annu Rev Immunol. 2021;39:719-757. doi:10.1146/annurev-immunol-093019-125918

11. Fagni F, Bello F, Emmi G. Eosinophilic granulomatosis with polyangiitis: dissecting the pathophysiology. Front Med (Lausanne). 2021;8:627776. doi:10.3389/fmed.2021.627776

12. Koike H, Nishi R, Furukawa S, et al. In vivo visualization of eosinophil secretion in eosinophilic granulomatosis with polyangiitis: an ultrastructural study. Allergol Int. 2022;71(3):373-382. doi:10.1016/j.alit.2022.02.009

13. Chakraborty RK, Aeddula NR. Eosinophilic granulomatosis with polyangiitis (Churg-Strauss syndrome). In: StatPearls [Internet]. StatPearls Publishing; March 23, 2023.

14. Gioffredi A, Maritati F, Oliva E, et al. Eosinophilic granulomatosis with polyangiitis: an overview. Front Immunol. 2014;5:549. doi:10.3389/fimmu.2014.00549

AstraZeneca Medical's ambition is to address unmet needs for people living with inflammatory diseases driven by eosinophilic inflammation.

Diagnosis of EGPA Is a Complex Clinical Challenge

Patients can experience a variety of manifestations that impact multiple organ systems simultaneously.^1-3

Proportion of EGPA patients with clinical signs/symptoms^1-4

Most Common EGPA Manifestations

Eosinophilic Asthma

In most cases of EGPA, asthma is the first disease manifestation with >90% of patients having eosinophilic asthma. Asthma precedes the onset of systemic disease by a mean of 12 years.^2-4

Eosinophilic asthma in EGPA is classically severe, adult onset, and OCS dependent. At the time of diagnosis, the majority of patients with EGPA have severe asthma.^3,5

ENT Involvement

About 60 to 80% of patients with EGPA experience ENT manifestations. These manifestations typically emerge during the early phases of the disease.^4,6,7

Delayed and Missed Diagnoses

There are no commonly accepted diagnostic criteria for EGPA, and there is a lack of definitive biomarkers for EGPA.^2,8,9 These may factor into the frequent delayed or missed diagnoses as mean time from symptom onset to diagnosis is 12 years.^2,3

Common Differential Diagnoses Should Be Ruled Out

Symptomatic overlap with other diseases, including other forms of AAV, HES, and infection, can suggest that differential diagnoses need to be considered.^2,10,11

Other Forms of AAV

EGPA is distinct from MPA and GPA in that it is characterized by eosinophilia, asthma, and nasal polyps.^2,12

HES

The distinction between EGPA and HES is challenging as both conditions are characterized by eosinophilia and widespread organ involvement.^2,10

Patients with HES usually do not have asthma or vasculitic complications, and they are ANCA negative.¹⁰

Infection and Other Exposures

Helminthic infections should be ruled out, particularly in patients with GI involvement.

Eosinophilia and respiratory symptoms are major features of allergic bronchopulmonary aspergillosis and eosinophilic pneumonia.²

Assessment Tools of EGPA

The BVAS is used to assess disease activity in EGPA, and it is often used to assess disease remission.
The BVAS (version 3) is currently used for the assessment of systemic vasculitis.^13,14
Importantly, items of disease activity should only be recorded in the BVAS if they have been active in the previous 4 weeks and are directly attributed to active vasculitis.
Activity attributed to comorbidities or infection, or induced by treatment, is not recorded on the BVAS.

The 9 organ-based systems measured by the BVAS¹⁴

The VDI is an assessment of longitudinal organ damage in EGPA^14,15
The VDI includes 64 items of damage, grouped into 11 organ systems^14,15
The VDI records organ damage that has accrued since the onset of vasculitis; it requires that disease manifestations be present for at least 3 months before being scored as damage rather than ongoing activity^14,15
Use of the VDI in patients with vasculitis has shown that the accumulation of damage is bimodal, with an earlier phase due to vasculitis and a later phase due to treatment-related toxicity¹⁴

The FFS is a tool used to assess (a) a patient's prognosis according to clinical and biologic parameters and (b) the severity of the manifestations at the time of diagnosis¹⁶
The FFS assesses 5 parameters, each of which is associated with an increased risk of death
These parameters include proteinuria, renal insufficiency, cardiomyopathy, severe GI manifestations, and CNS involvement^16,a
It is important to note that the parameters included in the FFS are based on their assessed impact on patient survival. The impact on function and QoL is not considered¹⁶
The FFS does not assess vasculitis evolution or organ damage¹⁶

^aAlthough the original 1996 FFS remains the most commonly used prognostic assessment, in 2011, the parameters of the FFS were re-evaluated in a larger cohort of patients, including 230 patients with EGPA. The revised 2011 FFS comprises 4 factors associated with a poorer prognosis (scored +1) and 1 factor associated with better outcomes (scored −1): age ≥65 years, cardiac insufficiency, renal insufficiency, severe GI manifestations (each scored +1), and ENT manifestations (scored -1).

Organ Damage Is Frequent in Patients with EGPA

Organ damage accumulates over time in patients with EGPA.¹
Age, duration of OCS use, and prior relapse are associated with worse organ damage in patients with EGPA, as evidenced by higher VDI scores.¹
Organ damage substantially contributes to disease burden and mortality in patients with EGPA, as reflected by higher FFS.^1,16
- For example, patients with EGPA and cardiac insufficiency have a significantly increased risk of mortality (HR, 2.8; 95% CI, 1.2-5.9; p=0.02).

The most commonly reported manifestations of organ damage in patients with EGPA^1,a

^aVDI items present after at least 1 year of follow-up after diagnosis in a longitudinal cohort study (n=268).

AAV	antineutrophil cytoplasmic antibody-associated vasculitis
ANCA	antineutrophil cytoplasmic antibody
BVAS	Birmingham Vasculitis Activity Score
CI	confidence interval
BR	bendamustine +rituximab
EGPA	eosinophilic granulomatosis with polyangiitis
ENT	ear, nose, and throat
FFS	Five Factor Score
GI	gastrointestinal
GPA	granulomatosis with polyangiitis
HES	hypereosinophilic syndrome
HR	hazard ratio
MPA	microscopic polyangiitis
OCS	oral corticosteroid(s)
QoL	quality of life
VDI	Vasculitis Damage Index

1. Doubelt I, Cuthbertson D, Carette S, et al. Clinical manifestations and long-term outcomes of eosinophilic granulomatosis with polyangiitis in North America. ACR Open Rheumatol. 2021;3(6):404-412. doi:10.1002/acr2.11263

2. Trivioli G, Terrier B, Vaglio A. Eosinophilic granulomatosis with polyangiitis: understanding the disease and its management. Rheumatology (Oxford). 2020;59(suppl 3):iii84-iii94. doi:10.1093/rheumatology/kez570

3. Cottin V, Bel E, Bottero P, et al. Respiratory manifestations of eosinophilic granulomatosis with polyangiitis (Churg-Strauss). Eur Respir J. 2016;48(5):1429-1441. doi:10.1183/13993003.00097-2016

4. Emmi G, Bettiol A, Gelain E, et al. Evidence-based guideline for the diagnosis and management of eosinophilic granulomatosis with polyangiitis. Nat Rev Rheumatol. 2023;19(6):378-393. doi:10.1038/s41584-023-00958-w

5. Khoury P, Grayson PC, Klion AD. Eosinophils in vasculitis: characteristics and roles in pathogenesis. Nat Rev Rheumatol. 2014;10(8):474-483. doi:10.1038/nrrheum.2014.98

6. Baldwin C, Wolter NE, Pagnoux C. Ear, nose, and throat involvement in eosinophilic granulomatosis with polyangiitis. Adv Cell Mol Otolaryngol. 2015;3(1):27181. doi:10.3402/acmo.v3.27181

7. Srouji I, Lund V, Andrews P, et al. Rhinologic symptoms and quality-of-life in patients with Churg-Strauss syndrome vasculitis. Am J Rhinol. 2008;22(4):406-409. doi:10.2500/ajr.2008.22.3204

8. Grayson PC, Ponte C, Suppiah R, et al. 2022 American College of Rheumatology/European Alliance of Associations for Rheumatology classification criteria for eosinophilic granulomatosis with polyangiitis. Ann Rheum Dis. 2022;81(3):309-314. doi:10.1136/annrheumdis-2021-221794

9. Jennette JC, Falk RJ, Bacon PA, et al. 2012 revised International Chapel Hill Consensus Conference nomenclature of vasculitides. Arthritis Rheum. 2013;65(1):1-11. doi:10.1002/art.37715

10. Gioffredi A, Maritati F, Oliva E, et al. Eosinophilic granulomatosis with polyangiitis: an overview. Front Immunol. 2014;5:549. doi:10.3389/fimmu.2014.00549

11. Jackson DJ, Akuthota P, Roufosse F. Eosinophils and eosinophilic immune dysfunction in health and disease. Eur Respir Rev. 2022;31(163):210150. doi:10.1183/16000617.0150-2021

12. Yates M, Watts R. ANCA-associated vasculitis. Clin Med (Lond). 2017;17(1):60-64. doi:10.7861/clinmedicine.17-1-60

13. Mukhtyar C, Lee R, Brown D, et al. Modification and validation of the Birmingham Vasculitis Activity Score (version 3). Ann Rheum Dis. 2009;68(12):1827-1832. doi:10.1136/ard.2008.101279

14. Flossmann O, Bacon P, de Groot K, et al. Development of comprehensive disease assessment in systemic vasculitis. Ann Rheum Dis. 2007;66(3):283-292. doi:10.1136/ard.2005.051078

15. Exley AR, Bacon PA, Luqmani RA, et al. Development and initial validation of the Vasculitis Damage Index for the standardized clinical assessment of damage in the systemic vasculitides. Arthritis Rheum. 1997;40(2):371-380. doi:10.1002/art.1780400222

16. Guillevin L, Pagnoux C, Seror R, et al. The Five-Factor Score revisited: assessment of prognoses of systemic necrotizing vasculitides based on the French Vasculitis Study Group (FVSG) cohort. Medicine (Baltimore). 2011;90(1):19-27. doi:10.1097/MD.0b013e318205a4c6

AstraZeneca Medical's ambition is to address unmet needs for people living with inflammatory diseases driven by eosinophilic inflammation.

Managing EGPA

There is an unmet need for earlier, optimized management of EGPA.^1-6

EGPA treatment considerations include controlling inflammation, achieving long-term remission^a, and preventing disease relapse, while minimizing dose- and drug-related toxicity.

Eosinophilic Inflammation Is a Defining Feature of EGPA^7,8

GOAL: Reduce eosinophilic inflammation

EGPA Is a Chronic Condition^9,10

GOAL: Achieve long-term remission, using well-tolerated treatments, with minimal drug toxicity^a

Disease Relapse Is Common^11,12

GOAL: Prevent disease relapse, particularly during steroid tapering

^aNote that definitions for remission vary between established guidelines and clinical trials.

Early Collaboration Can Help Optimize Disease Management

EGPA is most frequently diagnosed by rheumatologists and pulmonologists¹³; however, other disciplines may also be involved in diagnosis.^5,14,15 Early collaboration can help optimize disease management to enhance outcomes for patients.⁴

The 2022 EULAR guidelines deem multidisciplinary management by specialist centers with expertise in vasculitis a fundamental principle for the management of EGPA.⁴

Patients with EGPA experience substantial disease burden^1-3,9,16

Treatment Strategies

OCS and Non-Specific Immunosuppressants

High-dose OCS therapy is a cornerstone of treatment for EGPA, while non-specific immunosuppressants are used to induce and/or maintain remission.

Most patients are prescribed OCS and receive them long term.^3,4,17

Adverse events that may be associated with long-term use of OCS^18-20

Adverse events typically associated with long-term use of non-specific immunosuppressants^21,22

OCS and immunosuppressants can be associated with a risk of side effects to patients, and the disease frequently remains uncontrolled. To prevent or reduce toxicity, it is recommended to taper OCS dose once remission has been achieved; however, disease relapse is common during tapering.^3,4,11

Advances in Therapy

Advances in the understanding of EGPA pathophysiology have led to additional treatment approaches. Biologics targeting eosinophils are an emerging treatment strategy.¹⁴

Treatment Algorithms for EGPA

EGPA treatment is individualized based on disease severity and organ involvement. Given the heterogeneity of EGPA and evolving evidence base, clinicians are encouraged to consult the full ACR/Vasculitis Foundation guidelines for further information.³

ACR	American College of Rheumatology
ED	emergency department
ENT	ear, nose, and throat
EULAR	European Alliance of Associations for Rheumatology
GI	gastrointestinal
HRQoL	health-related quality of life
OCS	oral corticosteroid(s)
SF-36	36-item short form health survey

1. Jackson DJ, Akuthota P, Roufosse F. Eosinophils and eosinophilic immune dysfunction in health and disease. Eur Respir Rev. 2022;31(163):210150. doi:10.1183/16000617.0150-2021

2. Jakes RW, Kwon N, Nordstrom B, et al. Burden of illness associated with eosinophilic granulomatosis with polyangiitis: a systematic literature review and meta-analysis. Clin Rheumatol. 2021;40(12):4829-4836. doi:10.1007/s10067-021-05783-8

3. Chung SA, Langford CA, Maz M, et al. 2021 American College of Rheumatology/Vasculitis Foundation guideline for the management of antineutrophil cytoplasmic antibody-associated vasculitis. Arthritis Rheumatol. 2021;73(8):1366-1383. doi:10.1002/art.41773

4. Hellmich B, Sanchez-Alamo B, Schirmer JH, et al. EULAR recommendations for the management of ANCA-associated vasculitis: 2022 update. Ann Rheum Dis. 2024;83(1):30-47. doi:10.1136/ard-2022-223764

5. Bloom JL, Langford CA, Wechsler ME. Therapeutic advances in eosinophilic granulomatosis with polyangiitis. Rheum Dis Clin North Am. 2023;49(3):563-584. doi:10.1016/j.rdc.2023.03.006

6. Yates M, Watts R. ANCA-associated vasculitis. Clin Med (Lond). 2017;17(1):60-64. doi:10.7861/clinmedicine.17-1-60

7. Jennette JC, Falk RJ, Bacon PA, et al. 2012 revised International Chapel Hill Consensus Conference nomenclature of vasculitides. Arthritis Rheum. 2013;65(1):1-11. doi:10.1002/art.37715

8. Fagni F, Bello F, Emmi G. Eosinophilic granulomatosis with polyangiitis: dissecting the pathophysiology. Front Med (Lausanne). 2021;8:627776. doi:10.3389/fmed.2021.627776

9. Sokołowska B, Szczeklik W, Piłat O, et al. The impact of current health-related quality of life on future health outlook in patients with eosinophilic granulomatosis with polyangiitis (Churg-Strauss syndrome). Clin Rheumatol. 2013;32(6):779-785. doi:10.1007/s10067-013-2169-7

10. Benarous L, Terrier B, Laborde-Casterot H, et al. Employment, work disability and quality of life in patients with ANCA-associated vasculitides. The EXPOVAS study. Clin Exp Rheumatol. 2017;35(suppl 103):40-46.

11. Ribi C, Cohen P, Pagnoux C, et al. Treatment of Churg-Strauss syndrome without poor-prognosis factors: a multicenter, prospective, randomized, open-label study of seventy-two patients. Arthritis Rheum. 2008;58(2):586-594. doi:10.1002/art.23198

12. Yates M, Watts RA, Bajema IM, et al. EULAR/ERA-EDTA recommendations for the management of ANCA-associated vasculitis. Ann Rheum Dis. 2016;75(9):1583-1594. doi:10.1136/annrheumdis-2016-209133

13. Chen LF, Qianhua LI, Zheng DH, et al. Comparison of clinical characteristics of eosinophilic granulomatosis with polyangiitis between rheumatology and respiratory medicine: a single center, retrospective study [abstract]. Ann Rheum Dis. 2019;78(suppl 2):1751-1752. Abs AB0579. doi:10.1136/annrheumdis-2019-eular.5369

14. Emmi G, Bettiol A, Gelain E, et al. Evidence-based guideline for the diagnosis and management of eosinophilic granulomatosis with polyangiitis. Nat Rev Rheumatol. 2023;19(6):378-393. doi:10.1038/s41584-023-00958-w

15. Vasculitis Foundation. Pediatric vasculitis. Who gets EGPA? Vasculitis Foundation website. Accessed February 11, 2026. https://www.vasculitisfoundation.org/pediatrics-vasculitis/pediatric-types/pediatric-eosinophilic-granulomatosis-with-polyangiitis/

16. Cottin V, Bel E, Bottero P, et al. Respiratory manifestations of eosinophilic granulomatosis with polyangiitis (Churg-Strauss). Eur Respir J. 2016;48(5):1429-1441. doi:10.1183/13993003.00097-2016

17. Jakes R, Kwon N, Huynh L, et al. Characterisation and burden of eosinophilic granulomatosis with polyangiitis: a European retrospective study [abstract]. Eur Respir J. 2022;60(suppl 66):2254. doi:10.1183/13993003.congress-2022.2254

18. Rice JB, White AG, Scarpati LM, et al. Long-term systemic corticosteroid exposure: a systematic literature review. Clin Ther. 2017;39(11):2216-2229. doi:10.1016/j.clinthera.2017.09.011

19. Baldini C, Talarico R, Della Rossa A, et al. Clinical manifestations and treatment of Churg-Strauss syndrome. Rheum Dis Clin North Am. 2010;36(3):527-543. doi:10.1016/j.rdc.2010.05.003

20. Scherbacher PJ, Hellmich B, Feng Y-S, et al. Prospective study of complications and sequelae of glucocorticoid therapy in ANCA-associated vasculitis. RMD Open. 2024;10(1):e003956. doi:10.1136/rmdopen-2023-003956

21. Alam V, Nanzer AM. Eosinophilic granulomatosis with polyangiitis: case report and literature review. Breathe (Sheff). 2022;18(4):220170. doi:10.1183/20734735.0170-2022

22. Hsu DC, Katelaris CH. Long-term management of patients taking immunosuppressive drugs. Aust Prescr. 2009;32(3):68-71. doi:10.18773/austprescr.2009.035

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Eosinophilic Granulomatosis with Polyangiitis (EGPA)

AstraZeneca Medical's ambition is to address unmet needs for people living with inflammatory diseases driven by eosinophilic inflammation.

Watch Eosinophils in Action in EGPA

What is EGPA?

Characteristics of the 3 Diseases of AAV

What are Eosinophils?

Eosinophils contribute to inflammation both directly and indirectly3

Direct Mechanisms of Inflammation

Cytotoxicity and Microenvironment Manipulation

Indirect Mechanisms of Inflammation

Chronic Inflammation

Ischemic Damage

Eosinophils Are Involved in All Phases of EGPA

Prodromal

Eosinophilic Infiltrative

Vasculitic

Spectrum of Clinical Manifestations of EGPA

Abbreviations

References

AstraZeneca Medical's ambition is to address unmet needs for people living with inflammatory diseases driven by eosinophilic inflammation.

Diagnosis of EGPA Is a Complex Clinical Challenge

Proportion of EGPA patients with clinical signs/symptoms1-4

Most Common EGPA Manifestations

Delayed and Missed Diagnoses

Common Differential Diagnoses Should Be Ruled Out

Other Forms of AAV

HES

Infection and Other Exposures

Assessment Tools of EGPA

Birmingham Vasculitis Activity Score (BVAS)

The 9 organ-based systems measured by the BVAS14

Vasculitis Damage Index (VDI)

Five Factor Score (FFS)

Organ Damage Is Frequent in Patients with EGPA

The most commonly reported manifestations of organ damage in patients with EGPA1,a

Abbreviations

References

Eosinophilic Inflammation Is a Defining Feature of EGPA7,8

EGPA Is a Chronic Condition9,10

Disease Relapse Is Common11,12

Early Collaboration Can Help Optimize Disease Management

OCS and Non-Specific Immunosuppressants

Abbreviations

References

Connect with an MSL

Welcome to AstraZeneca Medical Information

Eosinophils contribute to inflammation both directly and indirectly³

Proportion of EGPA patients with clinical signs/symptoms^1-4

The 9 organ-based systems measured by the BVAS¹⁴

The most commonly reported manifestations of organ damage in patients with EGPA^1,a

Eosinophilic Inflammation Is a Defining Feature of EGPA^7,8

EGPA Is a Chronic Condition^9,10

Disease Relapse Is Common^11,12