Autoimmune Dry Eye

Mary Andrews,* a 50-year-old female, presented for a comprehensive dry eye assessment with a history of chronic ocular surface symptoms. She had undergone bilateral laser-assisted in situ keratomileusis (LASIK) surgery in 2013 for a preoperative refractive error of -4.50D of myopia and had been a long-term contact lens wearer prior to refractive surgery. In 2017, she developed persistent symptoms of dry eyes, followed by xerostomia (dry mouth). At that time, she underwent systemic investigations and was informed that testing for Sjögren’s syndrome was negative. Previous ocular management included punctal plug insertion, which provided minimal symptomatic relief.

On examination, slit lamp biomicroscopy demonstrated well-positioned LASIK flaps in both eyes without evidence of epithelial ingrowth or guttering. Mild bulbar conjunctival hyperaemia was noted bilaterally (Efron grade 1), while corneal evaluation revealed inferior superficial punctate epithelial erosions, more pronounced in the right eye and along the LASIK flap margins, consistent with Efron grade 2 staining. Tear film assessment demonstrated marked instability, with invasive tear break-up time (ITBUT) of four seconds in the right eye and five seconds in the left, accompanied by significantly reduced tear volume, with central lower tear meniscus height (TMH) of 0.15 mm bilaterally. Eyelid and meibomian gland evaluation revealed pronounced lid margin telangiectasia, tarsal conjunctival hyperaemia, and capped inferior glands with frothy, turbid meibum at the orifices. Meibography, when performed, confirmed partial inferior gland dropout. The anterior chambers were deep and quiet with no evidence of intraocular inflammation.

Management was initiated using an inflammation-focused approach consistent with DEWS III recommendations. The patient underwent an initial session of intense pulsed light (IPL) therapy, which demonstrated improved expressibility of meibomian gland secretions. Topical ciclosporin 0.09% was prescribed twice daily to address chronic ocular surface inflammation, alongside a short induction course of topical fluorometholone using a 4-3-2-1 weekly taper. Preservative-free artificial tears were advised at least four times daily, with dietary omega-3supplementation, lid hygiene, and lifestyle modifications also discussed. The patient was scheduled for review in two weeks for a second session of combination therapy and repeat systemic assessment for Sjögren’s syndrome.1,4,5

At follow up and during the third IPL session, the patient reported that a rheumatologist had formally diagnosed Sjögren’s syndrome based on clinical findings and exclusion criteria, despite persistently negative serological markers. She had commenced systemic methotrexate therapy two weeks prior. Ocular management continued with combination therapy (RF with IPL and MGX), lid hygiene, and topical ciclosporin. Punctal occlusion was discussed but deferred until improved control of ocular surface inflammation could be achieved.1,5

This case reflects a well-documented challenge in the diagnosis of Sjögren’s syndrome. Up to 30–40% of patients with clinically confirmed disease may be seronegative for anti-Sjögren’s syndrome-related antigen A and anti-Sjogren’s syndrome B antibodies, resulting in delayed diagnosis and management.5,7 Current literature emphasises that Sjögren’s syndrome remains a clinical diagnosis supported – but not excluded – by laboratory testing. Persistent ocular dryness accompanied by xerostomia should prompt repeat evaluation and appropriate referral, particularly when symptoms of dry eye are reported more severely on symptom surveys such as OSDI.²

From a pathophysiological perspective, autoimmune dry eye is characterised by lymphocytic infiltration and dysfunction of the lacrimal glands, leading to irreversible aqueous tear deficiency and chronic ocular surface inflammation.8 Inflammatory mediators cause epithelial damage, tear film instability, and neurosensory dysfunction, creating a self-sustaining cycle of disease.8 Randomised controlled trials have demonstrated that topical ciclosporin reduces inflammatory markers, increases tear production, and improves goblet cell density, supporting its early use in moderate to severe disease.8

The inclusion of combination therapy with RF with IPL and MGX, in this case, reflects evolving evidence for multimodal intervention in mixed mechanism dry eye. IPL has been evaluated in multiple clinical studies and meta-analyses, and has generally demonstrated improvement in patient symptoms, clinical signs of meibomian gland dysfunction (MGD), and evaporative dry eye disease. Systematic reviews and meta-analyses have reported significant reductions in symptom scores such as the OSDI and improvements in tear break-up time (TBUT) following IPL treatment, although the evidence base varies in quality and consistency.3 Additionally, IPL combined with MGX has been shown to improve tear film parameters and reduce ocular surface staining in refractory cases of aqueous deficient and MGD-related dry eye.⁶

Radiofrequency therapy is a more recent adjunctive treatment aimed at improving gland function by delivering controlled thermal energy to the tarsal plate, thereby facilitating clearance of obstructed glands and assisting periglandular inflammation. Emerging clinical evidence suggests that combining RF with IPL and MGX can produce larger improvements in gland function and symptom scores compared with IPL and MGX alone. In one prospective cohort, combination RF with IPL and MGX significantly decreased modified meibomian gland scores and OSDI scores, and when compared with a historical control, the addition of RF resulted in greater reduction in gland dysfunction metrics.6

While randomised controlled trials directly comparing RF with IPL and MGX with IPL and MGX alone are still limited, preliminary data indicate enhanced meibum quality, increased expressible gland count, and greater symptomatic relief with combination therapy. Case series and early studies also report significant improvements in gland expressibility, and patient-reported outcomes following RF inclusive treatment protocols.6 Given this context, the combination of RF with IPL and MGX represents a therapeutically plausible and increasingly studied approach that closely aligns with recommendations in TFOS DEWS III for moderate-to-severe mixed mechanism dry eye disease.

Laser refractive surgery disrupts corneal innervation and can reduce reflex tearing, predisposing patients to persistent or exacerbated dry eye symptoms.2,3 Evidence suggests that individuals with pre-existing dry eye or underlying autoimmune disease are at increased risk of chronic post-LASIK dry eye and neuropathic ocular pain. In some cases, systemic autoimmune disease may be subclinical at the time of surgery. Therefore, thorough preoperative screening is important, including assessment of dry eye severity and contact lens intolerance, as well as systemic symptoms such as dry mouth or fatigue, before proceeding with laser vision correction.2,8

Optometrists play a pivotal role in the early identification of autoimmune dry eye. Reliance on single-point serological testing may lead to missed or delayed diagnoses, whereas detailed assessment and clinical vigilance can facilitate earlier referral and collaborative management. Early recognition of systemic disease has implications, not only for ocular outcomes but also for broader patient health and surgical decision making. Dry eye disease may represent the initial manifestation of Sjögren’s syndrome, even in the absence of positive serology. Emerging literature supports the combined use of IPL, RF, and MGX for the treatment of moderate-to-severe dry eye disease, particularly noting improvements in the expressibility of meibum.