Dupilumab-Associated Ocular Surface Disease

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Article initiated by:
Michele Lee, MD, Minh T Nguyen, MD
All contributors:
Michele Lee, Minh T Nguyen, MD, Sezen Karakus, MD, Marcus L. Turner, MD
Assigned editor:
Sezen Karakus, MD
Review:
Assigned status Up to Date
 by Sezen Karakus, MD on May 30, 2026.


Disease Entity

Disease

Dupilumab (Dupixent® by Regeneron & Sanofi, USA), is the first FDA-approved biologic systemic treatment for moderate-to-severe atopic dermatitis. Its indications have since expanded to include asthma, chronic rhinosinusitis with nasal polyps (CRSwNP), eosinophilic esophagitis, prurigo nodularis, COPD with eosinophilic phenotype, chronic spontaneous urticaria, and bullous pemphigoid. This human monoclonal antibody binds to interleukin-4 receptor subunit alpha (IL-4Ra) and effectively blocks IL-4 and IL-13 signaling, which induces the inflammatory process responsible for asthma, atopic dermatitis, and chronic sinusitis with nasal polyps.[1][2] In Phase 3 of clinical trials, the incidence of conjunctivitis (including viral, bacterial, allergic conjunctivitis, and atopic keratoconjunctivitis) was higher in patients treated with dupilumab and topical corticosteroids compared to the control group treated with placebo and topical corticosteroids (8% vs 14-19%). Most cases of conjunctivitis in clinical trials were reportedly mild, and only one patient discontinued dupilumab due to severe unilateral atopic keratoconjunctivitis.[1] However, since its FDA approval in March 2017, there has been an increasing number of reports of severe dupilumab-induced conjunctivitis, with real-world studies reporting incidence rates of approximately 26–38%, substantially higher than clinical trial estimates. [3][4] While most cases are manageable with topical therapy, vision-threatening complications have been reported in approximately 1% of patients, and dupilumab discontinuation due to this side effect occurs in 4–5% of cases, which warrants a closer look at this disease entity. [3] [4]

Risk Factors

Dupilumab dosage, the severity of atopic dermatitis, and the presence of conjunctivitis before dupilumab treatment were found to be independent risk factors for dupilumab-induced conjunctivitis. [5]

  • History of asthma (OR 2.94; 95% CI 1.26–6.87) and family history of AD (OR 2.58; 95% CI 1.08–6.17) [4]
  • Prolonged AD duration: patients who developed DAOSD had significantly longer AD duration (median 41.5–44 years vs. 33 years, p=0.005) [3]
  • Facial/eyelid AD lesions: 91% of patients with conjunctivitis had a history of facial lesions during AD flares, and 65% had periocular eczematous rash, compared to 18% in those without conjunctivitis [6]
  • Comorbid rhinitis: more frequent among DAOSD patients (49–53% vs. 37%, p=0.031) [3]
  • Elevated biomarkers including TARC, IgE, and eosinophils [5]
  • Pre-existing ocular surface disease [3]

Pathology

Conjunctival biopsies of patients with ophthalmologist-confirmed conjunctivitis during dupilumab treatment revealed a scarcity of intraepithelial goblet cells with a median density of 3.3 cells/mm vs. 32.3 cells/mm in control groups. CD3+/CD4+ T cells and eosinophils were also found migrating into the conjunctival epithelium. Interestingly, this is different from histopathological findings of atopic keratoconjunctivitis and allergic conjunctivitis, in which there is an increased density of goblet cells.[7]

However, a more recent prospective study using impression cytology found that goblet cell numbers remained stable during conjunctivitis, but the percentage of CK19⁻CD45⁻MUC5AC⁺ cells decreased, suggesting functional impairment of goblet cells (reduced mucin production) rather than outright goblet cell depletion. [8] In vitro studies have further demonstrated that IL-13 and IL-4 promote proliferation of primary human conjunctival goblet cells and increase expression of MUC2 and MUC5AC mucins, providing a direct mechanistic link between IL-4Rα blockade and goblet cell dysfunction. [9]

Pathophysiology

There have been a few proposed mechanisms to explain the development of conjunctivitis in patients with atopic dermatitis treated with dupilumab. A multifactorial model is now favored, involving a complex interplay of goblet cell dysfunction, mucin deficiency, immune dysregulation, epithelial barrier dysfunction, and microbiome alterations.

  • Thyssen theorized that suppressing IL-4 and IL-13 signaling led to an increased number of Demodex, which in turn caused an IL-17-mediated rosacea-like inflammation.[10]
  • Bakker et al. thought the decreased density of conjunctival goblet cells in the settings of increased lymphocytes, as well as eosinophils, plays a key role in the inflammatory process.[7]
  • Akinlade et al, through pharmacokinetic data, suggested that the lower tissue distribution of dupilumab in the eyes might be related to more inflammation here compared to elsewhere.[11] This theory is consistent with the fact conjunctivitis is specific to atopic dermatitis treated with dupilumab, as this side effect has not been reported in other conditions treated with this drug.[12]
  • In vitro studies have demonstrated that IL-13 and IL-4 promote proliferation of primary human conjunctival goblet cells and increase expression of MUC2 and MUC5AC mucins, while IFN-γ negatively impacts goblet cell growth. This provides a direct mechanistic link: blocking IL-4/IL-13 signaling via dupilumab removes trophic support for conjunctival goblet cells. [13]
  • Using a murine model of skin inflammation-evoked conjunctivitis, it has been demonstrated that blockade of IL-4Rα partially attenuated conjunctivitis but led to significant augmentation of genes encoding tear proteins and enzymes, which may represent candidate mediators of the increased conjunctivitis frequency in dupilumab-treated atopic dermatitis patients. [14]
  • Due to the functional redundancy of IL-13 and IL-4 on conjunctival goblet cell biology, targeted treatment with monoclonal antibodies that specifically neutralize IL-13 alone (e.g., lebrikizumab) may be associated with a lower incidence of conjunctivitis compared to dual IL-4/IL-13 blockade with dupilumab. [15]

Diagnosis

Dupilumab-induced conjunctivitis, now more commonly referred to as dupilumab-associated ocular surface disease, ranges from mild to severe blepharitis, conjunctivitis, and keratoconjunctivitis. Rare but serious manifestations include intraocular inflammation and cicatrizing conjunctivitis. [16] The diagnosis is made clinically based on history and ophthalmic examination. Validated scoring tools such as the Utrecht Ophthalmic Inflammatory and Allergic disease (UTOPIA) score have been developed to standardize severity assessment, defining dupilumab-associated ocular surface disease as an increase in UTOPIA score of ≥3 points from baseline. [8]

History

Patients must have a history of moderate to severe atopic dermatitis (also known as eczema) recalcitrant to topical therapy, and have recently started dupilumab treatment. There is frequently known ocular surface disease before starting dupilumab, as this is a well-known comorbidity of atopic disorders, including eczema, asthma, and allergic rhinitis.[17][18][19][20][21][22][23][24][25] Notably, baseline ocular surface disease has been found in up to 91% of moderate-to-severe AD patients before dupilumab initiation. Symptoms develop quickly in patients on dupilumab monotherapy (after about 2 weeks on average) vs. dupilumab + topical corticosteroids (after about 4-8 weeks).[11] In a large real-world cohort, 75% of dupilumab-associated ocular surface disease cases presented before week 9 of treatment. [4]

Symptoms

Figure 1. Papillary conjunctivitis in upper lids in a patient with dupilumab-induced keratoconjunctivitis

Patients typically present with these symptoms:

  • Redness
  • Irritation
  • Itching
  • Foreign body sensation
  • Photophobia
  • Tearing
  • Discharge
  • Decreased vision
  • Intermittent monocular diplopia
Figure 2. SPK found in a patient with dupilumab-induced keratoconjunctivitis

Physical Examination

Providers should pay attention to the anterior segment and note any sign of inflammation, which is usually bilateral but asymmetric. The most frequent signs include conjunctival injection (62%), superficial punctate keratitis (55%), and papillary reaction (28%). [26] Blepharoconjunctivitis is the most common clinical presentation, reported in 68% of patients in a multicenter cohort. [4]

1. Early stage:

  • Meibomian gland dysfunction
  • Conjunctival hyperemia
  • Papillary conjunctivitis (Figure 1)
  • Superficial punctate keratopathy (Figure 2)
    Figure 3. Thick symblepharon band in a patient with dupilumab-induced keratoconjunctivitis

2. Intermediate stage:

  • Symblepharon (Figure 3)
  • Madarosis
  • Shortening of fornices
  • Limbitis
  • Periorbital skin changes (eczematous rash)

3. Advanced stage:

  • Ankyloblepharon (Figure 4)
  • Complete loss of fornices
  • Ocular surface keratinization
  • Corneal scarring
  • Conjunctival cicatrization
  • Cicatricial ectropion


In addition, a few special tests could be performed in-office to determine the stage and prognosis:

  • Corneal sensation test using cotton tip applicator or Cochet-Bonnet esthesiometer
  • Schirmer's test: Less than 10 mm of moisture may indicate the involvement of lacrimal glands in an advanced disease
  • Ocular surface staining with fluorescein and lissamine green, which is useful to assess conjunctival integrity
  • Tear break-up time (TBUT)
  • Delayed tear clearance
Figure 4. Lateral ankyloblepharon in a patient with dupilumab-induced keratoconjunctivitis


In cases with risk factors such as pre-existing ocular surface disease or severe atopic dermatitis of eyelids, a baseline ophthalmic examination and frequent follow-up with an ophthalmologist after initiation of treatment may be useful. The 2023 AAAAI/ACAAI guidelines note that some protocols suggest a baseline eye examination by an ophthalmologist and prophylactic lubricant eye drops (artificial tears) twice daily when dupilumab is initiated, though practice varies. [27]Close monitoring with treatment in the setting of active inflammation may be warranted, given the reversible nature of the early disease. Slit-lamp photographs should be considered at each visit to document baseline, progression/improvement, and response to treatment. Red flags warranting urgent ophthalmology referral include blurred vision, decreased visual acuity, purulent discharge, photophobia, or eye pain. [27]

Laboratory test

Diagnosis is based on clinical history and examination. No laboratory test or biopsy is indicated. Conjunctival impression cytology may be performed in research settings to assess goblet cell function but is not required for clinical diagnosis. [8]

Differential diagnosis

It is important to rule out other etiologies through history and physical examination to tailor the best course of treatment:

  • Dry eye syndrome
  • Chemical burn
  • Scleritis
  • Episcleritis
  • Viral conjunctivitis
  • Bacterial conjunctivitis
  • Allergic conjunctivitis
  • Atopic keratoconjunctivitis
  • Rosacea-associated ocular disease
  • Ocular cicatricial pemphigoid
  • Ocular graft-versus-host disease
  • Ocular Stevens-Johnson syndrome/toxic epidermal necrolysis

Management

Medical treatment

The main goal of treatment is to halt the inflammatory process. A stepwise approach is recommended based on disease severity. [28] [27]

Mild dupilumab-associated ocular surface disease (manageable by dermatologists/allergists):

  • Warm compresses for meibomian gland dysfunction
  • Artificial tears/lubricant eye drops
  • Topical antihistamine/mast cell stabilizer eye drops (if concomitant allergen exposure)
  • Lid hygiene and patient education (minimize eye-rubbing, allergen exposure, dry environments, and screen time)

Moderate-to-severe dupilumab-associated ocular surface disease (requires ophthalmology referral):

  • Topical corticosteroids (fluorometholone 0.1%–0.25%, dexamethasone 0.1%, or prednisolone acetate 1.0%)
  • Topical calcineurin inhibitors (tacrolimus 0.03% ointment, cyclosporine 0.05% drops) as steroid-sparing maintenance therapy
  • Lifitegrast 5.0% ophthalmic solution (included in the 2023 AAAAI/ACAAI guidelines as an immunomodulatory option)
  • Periocular tacrolimus ointment or pimecrolimus cream for eyelid eczema

Wollenberg et al. reported 11 cases of mild to severe dupilumab-induced conjunctivitis that showed excellent results with topical fluorometholone and tacrolimus, a calcineurin inhibitor. Among 5 patients treated with fluorometholone 0.1% drop, 2 patients had complete resolution of conjunctivitis, while 3 significantly improved. In 4 cases treated with tacrolimus 0.03% ointment, 2 patients had complete resolution, whereas the other 2 significantly improved in both signs and symptoms. The remaining patients were treated with either dexamethasone, hydrocortisone, or an antibiotic and steroid combination topical medication, and all cases reported improvement. In another report, two cases were treated successfully with an initial dose of prednisolone acetate 1% eye drops with concurrent cyclosporine 0.05% eye drops, a calcineurin inhibitor, for maintenance without recurrence of conjunctivitis despite the continuation of dupilumab injections.[29] It is postulated that if a lower number of goblet cells play a meaningful role in the mechanism of the disease process, calcineurin inhibitors such as cyclosporine may reverse this process by increasing goblet cells while preventing epithelial cell death.[30]

Wollenberg et al. reported 11 cases of mild to severe dupilumab-induced conjunctivitis that showed excellent results with topical fluorometholone and tacrolimus, a calcineurin inhibitor. Among 5 patients treated with fluorometholone 0.1% drop, 2 patients had complete resolution of conjunctivitis, while 3 significantly improved. In 4 cases treated with tacrolimus 0.03% ointment, 2 patients had complete resolution, whereas the other 2 significantly improved in both signs and symptoms. The remaining patients were treated with either dexamethasone, hydrocortisone, or an antibiotic and steroid combination topical medication, and all cases reported improvement. In another report, two cases were treated successfully with an initial dose of prednisolone acetate 1% eye drops with concurrent cyclosporine 0.05% eye drops, a calcineurin inhibitor, for maintenance without recurrence of conjunctivitis despite the continuation of dupilumab injections.[29] It is postulated that if a lower number of goblet cells play a meaningful role in the mechanism of the disease process, calcineurin inhibitors such as cyclosporine may reverse this process by increasing goblet cells while preventing epithelial cell death.[31]

In a large prospective observational study, most patients (88%) received multiple ophthalmic treatments for conjunctivitis. Investigators assessed topical corticosteroids and topical calcineurin inhibitors, administered either as eye drops or ointment, as the most effective treatments. [6] [32]Treatment regimens including corticosteroid eye drops have been shown to be effective within 3 to 12 months in approximately 75% of patients. Tacrolimus ointment (0.03%–0.1%) applied periocularly has shown rapid resolution of blepharoconjunctivitis signs and symptoms within days in some series. [33]

Since other therapies such as topical antihistamines and artificial tears were ineffective for moderate-to-severe disease, lower dose steroids such as fluorometholone and/or a non-steroid immunomodulatory agent such as tacrolimus and cyclosporine should be initially considered to prevent the adverse effects of topical steroids such as the development of cataract or glaucoma.[29] The 2023 AAAAI/ACAAI guidelines recommend that patients with symptoms of severe ocular disease (blurred vision, decreased visual acuity, purulent discharge, photophobia, or eye pain) should be urgently or emergently evaluated by ophthalmology. [27]

Discontinuation of dupilumab

Discontinuation of dupilumab is generally avoided where possible. Across multiple studies, discontinuation rates due to dupilumab-associated ocular surface disease range from 0% to 12%. [32]In a large Danish nationwide cohort (n = 382), 5% of patients discontinued dupilumab due to dupilumab-associated ocular surface disease despite receiving lubricating eye drops and topical steroids. [3] In most cases, temporary interruption with optimization of ophthalmic treatment allows resumption of dupilumab at optimal doses. [32] Switching to an IL-13-selective agent (e.g., tralokinumab or lebrikizumab) may be considered in refractory cases, as these agents appear to carry a lower risk of conjunctivitis. [28]

Surgical treatment

There are no reports of surgical treatment for dupilumab-induced conjunctivitis. However, rare advanced cases with cicatricial complications (ankyloblepharon, symblepharon, cicatricial ectropion) may theoretically require surgical intervention, though this has not been formally studied. [4]

Prognosis

Nearly all cases of dupilumab-induced conjunctivitis and ocular surface disease resolved or improved with the initiation of medical treatment and/or discontinuation of dupilumab. However, discontinuation is usually not needed. In a prospective study, 84% of conjunctivitis events recovered/resolved and 12% were resolving at study end, with a mean time to recovery of approximately 172 days. No participants discontinued dupilumab. [6]

However, long-term data suggest that a substantial proportion of patients require ongoing maintenance therapy. Popiela et al. found that 67% of patients with dupilumab-associated ocular surface disease needed continued anti-inflammatory drops at a mean of 16 months of follow-up. [34] Felfeli et al. reported that 46.3% of patients with dupilumab-associated ocular surface disease at 16 weeks still had symptoms at 52 weeks, and an additional 17% developed new-onset dupilumab-associated ocular surface disease between weeks 16 and 52, suggesting that late-onset disease can occur. [4]

Vision-threatening complications are rare but documented, including corneal scarring and cicatricial ectropion in approximately 1% of patients in a large multicenter cohort. [4] Conjunctival cicatrisation has also been reported as a long-term sequela. [34] Early recognition and treatment are therefore critical, as the early stages of dupilumab-associated ocular surface disease are reversible, whereas advanced cicatricial changes may not be. [8]

References

  1. ↑ 1.0 1.1 Blauvelt A, Bruin-Weller M, Gooderham M, et al., Long-term management of moderate-to-severe atopic dermatitis with dupilumab and concomitant topical corticosteroids (LIBERTY AD CHRONOS): a 1-year, randomised, double-blinded, placebo-controlled, phase 3 trial. Lancet. 2017;389:2287–2303. 
  2. ↑ Gandhi N, Bennett B, Graham N, Pirozzi G, Stahl, Yancopoulos G. Targeting key proximal drivers of type 2 inflammation in disease. Nature Reviews Drug Discovery. 2016;15(1):35-50.
  3. ↑ 3.0 3.1 3.2 3.3 3.4 3.5 Nøhr AMH, Hansen PM, Møller-Hansen M, Larsen HHP, Rønnstad ATM, Thomsen SF, Zachariae COC, Ibler K, Mortz CG, Bindslev-Jensen C, Deleuran MS, Vestergaard C, Bjerring P, Thyssen JP, Heegaard S. Dupilumab-Associated Ocular Surface Disease in Patients with Atopic Dermatitis Is Frequent: A Nationwide Real-World Evidence Study. Dermatology. 2025;241(5-6):415-424. doi: 10.1159/000548467.
  4. ↑ 4.0 4.1 4.2 4.3 4.4 4.5 4.6 4.7 Felfeli T, Georgakopoulos JR, Jo CE, Mimouni M, Piguet V, Drucker AM, Yeung J, Chan CC. Prevalence and Characteristics of Dupilumab-Induced Ocular Surface Disease in Adults With Atopic Dermatitis. Cornea. 2022 Oct 1;41(10):1242-1247.
  5. ↑ 5.0 5.1 Akinlade B, Guttman-Yassky E, de Bruin-Weller M, Simpson EL, Blauvelt A, Cork MJ, Prens E, Asbell P, Akpek E, Corren J, Bachert C, Hirano I, Weyne J, Korotzer A, Chen Z, Hultsch T, Zhu X, Davis JD, Mannent L, Hamilton JD, Teper A, Staudinger H, Rizova E, Pirozzi G, Graham NMH, Shumel B, Ardeleanu M, Wollenberg A. Conjunctivitis in dupilumab clinical trials. Br J Dermatol. 2019 Sep;181(3):459-473.
  6. ↑ 6.0 6.1 6.2 Asbell P, Akpek E, Chamberlain W, Chen Z, Lawless E, Van Spall M, Ozturk ZE, Shumel B. Conjunctivitis in Adults with Atopic Dermatitis Treated with Dupilumab: An Observational Study of Clinical Characteristics, Symptomatology, and Treatment. Adv Ther. 2025 Jul;42(7):3285-3305.
  7. ↑ 7.0 7.1 Bakker DS, Ariens LFM, van Luijk C, van der Schaft J, Thijs JL, Schuttelaar MLA, et al. Goblet cell scarcity and conjunctival inflammation during treatment with dupilumab in patients with atopic dermatitis. Br J Dermatol. 2019;180(5):1248-9. 
  8. ↑ 8.0 8.1 8.2 8.3 Achten R, Thijs J, van der Wal M, et al. "Dupilumab-Associated Ocular Surface Disease in Atopic Dermatitis Patients: Clinical Characteristics, Ophthalmic Treatment Response and Conjunctival Goblet Cell Analysis." Allergy. 2023;78(8):2266-2276 (PMID: 36934403).
  9. ↑ Chiricozzi A, Di Nardo L, Gori N, et al. Dupilumab-associated ocular adverse events are predicted by low tear break-up time and correlate with high IL-33 tear concentrations in patients with atopic dermatitis. Exp Dermatol. 2023;32(9):1531-1537.
  10. ↑ Thyssen JP. Could conjunctivitis in patients with atopic dermatitis treated with dupilumab be caused by colonization with Demodex and increased interleukin‐17 levels? Br J Dermatol 2018; 178: 1220.
  11. ↑ 11.0 11.1 Akinlade B, Guttman-Yassky E, de Bruin-Weller M, Simpson EL, Blauvelt A, Cork MJ, et al. Conjunctivitis in dupilumab clinical trials. Br J Dermatol. 2019;181(3):459-73. 
  12. ↑ Rabe KF, Nair P, Brusselle G, Maspero JF, Castro M, Sher L, Zhu H, Hamilton JD, Swanson BN, Khan A, Chao J, Staudinger H, Pirozzi G, Antoni C, Amin N, Ruddy M, Akinlade B, Graham NMH, Stahl N, Yancopoulos GD, Teper A. Efficacy and Safety of Dupilumab in Glucocorticoid-Dependent Severe Asthma. N Engl J Med. 2018 Jun 28; 378(26):2475-2485.
  13. ↑ Tollenaere MAX, Rævdal P, Hedengran A, et al. IL-13 and IL-4 promote proliferation and mRNA expression of MUC2 and MUC5AC in primary human conjunctival goblet cells. Abstract presented at: 4th Inflammatory Skin Disease Summit; November 3-6, 2021; New York, NY. Exp Dermatol. 2021;30(suppl 2):3-43. doi:10.1111/exd.14457
  14. ↑ Han H, Cummings S, Shade KC, et al. Cellular mechanisms and effects of IL-4 receptor blockade in experimental conjunctivitis evoked by skin inflammation. JCI Insight. 2023;8(3):e163495.
  15. ↑ Silverberg JI, Guttman-Yassky E, Thaçi D, et al. Two phase 3 trials of lebrikizumab for moderate-to-severe atopic dermatitis. N Engl J Med. 2023;388(12):1080-1091.
  16. ↑ Wu D, Daniel BS, Lai AJX, Wong N, Lim DKA, Murrell DF, Lim BXH, Mehta JS, Lim CHL. Dupilumab-associated ocular manifestations: A review of clinical presentations and management. Surv Ophthalmol. 2022 Sep-Oct;67(5):1419-1442.
  17. ↑ Bousquet J, Devillier P, Anto JM et al. Daily allergic multimorbidity in rhinitis using mobile technology: a novel concept of the MASK study. Allergy 2018; 73: 1622– 31.
  18. ↑ Rosario N, Bielory L. Epidemiology of allergic conjunctivitis. Curr Opin Allergy Clin Immunol 2011; 11: 471– 6.
  19. ↑ Maio S, Baldacci S, Bresciani M et al. RItA: the Italian severe/uncontrolled asthma registry. Allergy 2018; 73: 683– 95.
  20. ↑ Lemmetyinen RE, Karjalainen JV, But A et al. Higher mortality of adults with asthma: a 15‐year follow‐up of a population‐based cohort. Allergy 2018; 73: 1479– 88.
  21. ↑ Vehof J, Kozareva D, Hysi PG, Hammond CJ. Prevalence and risk factors of dry eye disease in a British female cohort. Br J Ophthalmol 2014; 98: 1712– 17.
  22. ↑ Kim M, Oh J‐H, Park CY, Lee SW. Dry eye disease and allergic conditions: a Korean nationwide population‐based study. Am J Rhinol Allergy 2016; 30: 397– 401.
  23. ↑ Cingi C, Gevaert P, Mösges R et al. Multi‐morbidities of allergic rhinitis in adults: European Academy of Allergy and Clinical Immunology Task Force Report. Clin Transl Allergy 2017; 7: 17.
  24. ↑ Michailopoulos P, Almaliotis D, Georgiadou I et al. Allergic conjunctivitis in patients with respiratory allergic symptoms; a retrospective study in Greece. Med Hypothesis Discov Innov Ophthalmol 2017; 6: 3– 9.
  25. ↑ Wang X, Shi X‐D, Li L‐F et al. Prevalence and clinical features of adult atopic dermatitis in tertiary hospitals of China. Medicine (Baltimore) 2017; 96: e6317.
  26. ↑ Bohner A, Topham C, Strunck J, Haynes D, Brazil M, Clements J, Simpson E, Chamberlain W. Dupilumab-Associated Ocular Surface Disease: Clinical Characteristics, Treatment, and Follow-Up. Cornea. 2021 May 1;40(5):584-589.
  27. ↑ 27.0 27.1 27.2 27.3 Chu DK, Schneider L, Asiniwasis RN, et al. Atopic dermatitis (eczema) guidelines: 2023 American Academy of Allergy, Asthma and Immunology/American College of Allergy, Asthma and Immunology Joint Task Force on Practice Parameters GRADE- and Institute of Medicine-based recommendations. Ann Allergy Asthma Immunol. 2024;132(3):274-312.
  28. ↑ 28.0 28.1 Mickevicius T, Pink AE, Bhogal M, O'Brart D, Robbie SJ. Dupilumab-Induced, Tralokinumab-Induced, and Belantamab Mafodotin-Induced Adverse Ocular Events-Incidence, Etiology, and Management. Cornea. 2023 Apr 1;42(4):507-519.
  29. ↑ 29.0 29.1 29.2 Wollenberg A, Ariens L, Thurau S, van Luijk C, Seegräber M, de Bruin-Weller M. Conjunctivitis occurring in atopic dermatitis patients treated with dupilumab-clinical characteristics and treatment. J Allergy Clin Immunol Pract. 2018;5–8.
  30. ↑ Maudinet A, Law-Koune S, Duretz C, Lasek A, Modiano P, Tran THC. Ocular Surface Diseases Induced by Dupilumab in Severe Atopic Dermatitis. Ophthalmol Ther. 2019;8(3):485-490.
  31. ↑ Maudinet A, Law-Koune S, Duretz C, Lasek A, Modiano P, Tran THC. Ocular Surface Diseases Induced by Dupilumab in Severe Atopic Dermatitis. Ophthalmol Ther. 2019;8(3):485-490.
  32. ↑ 32.0 32.1 32.2 Yap AXY, Tan D, Koh MJ, et al. Dupilumab-associated ocular surface disease in pediatric atopic dermatitis: a single-center Asian experience. Pediatr Dermatol. 2025;42(3):481-486. doi:10.1111/pde.15814
  33. ↑ Nahum Y, Mimouni M, Livny E, Bahar I, Hodak E, Leshem YA. Dupilumab-induced ocular surface disease (DIOSD) in patients with atopic dermatitis: clinical presentation, risk factors for development and outcomes of treatment with tacrolimus ointment. Br J Ophthalmol. 2020 Jun;104(6):776-779.
  34. ↑ 34.0 34.1 Popiela MZ, Barbara R, Turnbull AMJ, Corden E, Martinez-Falero BS, O'Driscoll D, Ardern-Jones MR, Hossain PN. Dupilumab-associated ocular surface disease: presentation, management and long-term sequelae. Eye (Lond). 2021 Dec;35(12):3277-3284.
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