Dry Eye
Meibomian gland dysfunction (MGD): Prevalence is 15% higher than in healthy individuals. It causes evaporative dry eye.
Tear film instability: Shortened tear break-up time (TBUT) and decreased Schirmer test values are observed.
Psoriasis is a chronic immune-mediated skin disease caused by overactivation of the adaptive immune system. It affects 1–3% of the US population and approximately 125 million people worldwide.
The most common type is plaque psoriasis (psoriasis vulgaris), accounting for 80% of all cases. Other types include nail psoriasis, guttate psoriasis, inverse psoriasis, pustular psoriasis, and erythrodermic psoriasis.
Approximately 10% of psoriasis patients develop ocular symptoms. The main ocular complications are as follows:
Ocular symptoms are particularly associated with psoriatic arthritis and pustular psoriasis, and are more common in men. They often appear following exacerbation of skin lesions.
Ocular symptoms associated with psoriasis are diverse and vary depending on the affected site.
The intensity of symptoms may fluctuate in response to stress, temperature changes, and flares of skin lesions.
Dry Eye
Meibomian gland dysfunction (MGD): Prevalence is 15% higher than in healthy individuals. It causes evaporative dry eye.
Tear film instability: Shortened tear break-up time (TBUT) and decreased Schirmer test values are observed.
Blepharitis
Changes in the eyelid margin: Accompanied by redness, scaling, crusting, and ulcer formation.
Changes in bacterial flora: The normal eyelid bacterial flora may be disrupted, leading to overgrowth of Staphylococcus species.
Uveitis
Primarily anterior uveitis: Often non-granulomatous. Cases with arthritis may present with hypopyon.
Complications: May include macular edema and optic nerve swelling.
Cataract
Inflammatory mechanism: Oxidative stress from TNF-α and IL-6 promotes lens opacification.
Iatrogenic factors: Long-term steroid use and PUVA therapy also increase cataract risk.
Psoriatic uveitis is slightly more common in men, with an average age in the early 40s. Psoriasis vulgaris is the most common type, followed by association with psoriatic arthritis. In Japan, HLA-A2 positivity is reported to be frequent.
An analysis of uveitis associated with psoriasis and psoriatic arthritis showed that anterior uveitis was the most common, with complications including vitreous opacity 41.1%, cataract 29.7%, posterior vitreous detachment 25.9%, elevated intraocular pressure 17%, and dry eye 13.3%1).
Patients with psoriasis should see an ophthalmologist when symptoms such as eye redness, pain, photophobia, blurred vision, or dry eyes appear. Since eye symptoms are often not reported spontaneously, regular ophthalmologic screening is recommended during dermatology visits. For details, see the “Standard Treatment” section.
The core of psoriasis pathogenesis is overactivation of the IL-23/Th17 pathway. Plasmacytoid dendritic cells release type I interferon, activating myeloid dendritic cells. Myeloid dendritic cells secrete IL-12 to promote differentiation into Th1 cells and IL-23 to induce proliferation of Th17 and Th22 cells.
IL-17, IL-22, and TNF-α secreted from Th17 cells cause excessive proliferation of keratinocytes, forming a positive feedback loop that recruits more immune cells. This pathway promotes transcription of inflammatory genes via the TYK2/JAK/STAT pathway.
Risk factors for ocular symptoms include the following:
Long-term systemic use of steroids increases the risk of cataracts and glaucoma. PUVA therapy (psoralen plus ultraviolet A irradiation) has also been reported to be associated with cataract development. Biologics (such as TNF-α inhibitors) are also used to treat uveitis, but rarely may cause ocular side effects.
Diagnosis of ocular complications of psoriasis is based on clinical findings. Skin psoriasis often precedes, and the presence of well-demarcated erythematous scaly plaques provides a diagnostic clue.
The following diseases need to be differentiated.
If ocular symptoms improve with systemic treatment (e.g., methotrexate), it supports the diagnosis of psoriatic ocular complications.
Treatment of ocular symptoms of psoriasis is performed stepwise according to the site and severity of the lesion. Collaboration between dermatologists and ophthalmologists is essential.
Treatment of psoriatic uveitis is performed in a stepwise manner.
Response to steroid treatment is generally good, and visual prognosis is relatively favorable. However, uveitis tends to recur; in case of recurrence, consider adding immunosuppressive drugs or biologic agents. Systemic treatment should be performed in consultation with a dermatologist.
Dry eye and blepharitis can be well controlled with appropriate management. Uveitis responds well to steroids and has a relatively good visual prognosis, but it tends to recur, so long-term follow-up is necessary. Since psoriasis itself is a chronic disease, continuous management of ocular symptoms is also required.
Ocular complications of psoriasis arise from systemic immune abnormalities spreading to ocular tissues.
T cells and cytokines (TNF-α, IL-17) that are hyperactivated in psoriasis are also deeply involved in the pathogenesis of uveitis. The activation cascade of plasmacytoid dendritic cells → myeloid dendritic cells → IL-23 → Th17 cells triggers inflammation in both the skin and eyes.
IL-17 produced by Th17 cells promotes keratinocyte proliferation and chemokine production, recruiting more immune cells. IL-22 causes differentiation disorders of keratinocytes. TNF-α increases the expression of adhesion molecules on vascular endothelium, promoting tissue infiltration of inflammatory cells.
According to a review by Rojas-Carabali et al. (2023), dry eye and uveitis share multiple molecular signaling pathways, including involvement of Th1 lymphocytes, IL-17/Th17 expression, activation of matrix metalloproteinases, and infiltration of macrophages and dendritic cells1).
In the tear fluid of uveitis patients, concentrations of IL-1β and IL-23 are significantly higher than in healthy controls. IL-23 plays an important role in the long-term memory of Th17 cells and mediates chronic inflammation in autoimmune diseases including dry eye1).
Epithelial cells produce and release TNF-α, IL-1, IL-6, and IL-8, amplifying immune responses and attracting inflammatory cells. This mechanism is centrally involved in the pathogenesis of dry eye1).
Inflammasomes, including NLRP3, are also suggested to be involved in the pathogenesis of both dry eye and uveitis1).
Cataracts associated with psoriasis arise through multiple mechanisms. Inflammatory cytokines such as TNF-α and IL-6 increase oxidative stress and promote degeneration of lens proteins. In addition, posterior subcapsular cataracts due to long-term systemic steroid use and lens damage from UV exposure in PUVA therapy are also involved.
Serum osteopontin has been reported to be potentially associated with ocular complications in psoriasis. Whether it can serve as a biomarker for early detection or severity prediction of ocular complications awaits future validation.
Studies using optical coherence tomography angiography (OCTA) have shown that retinal vascular changes may be detected even in psoriasis patients without clinical eye disease. It is expected to become a tool for disease severity classification in the future.
Rojas-Carabali et al. (2023) pointed out that the coexistence of dry eye and uveitis may be more frequent than previously assumed, and recommended that ophthalmologists actively search for dry eye (both aqueous-deficient and evaporative types) in patients with anterior uveitis. They also emphasized the need for longitudinal studies to clarify which disease precedes the other 1).