Medications and Dry Eye

There is no single mechanism. Different medications can affect different parts of the ocular-surface system. Depending on the drug, possible effects may involve:

• •tear secretion
• •meibomian gland function
• •blinking
• •corneal or conjunctival tissues
• •inflammation
• •or the overall stability of the tear film

Some medications act systemically and indirectly affect the eyes. Others are applied directly to the eye and can influence the ocular surface locally. This is why the term medication-induced dry eye actually covers several quite different biological situations.

Several medication groups have been associated with dry-eye disease or ocular-surface abnormalities. Examples include:

• •antihistamines
• •some antidepressants
• •some antipsychotic and anxiolytic medications
• •beta-blockers
• •some diuretics
• •isotretinoin
• •and some other systemic treatments

A recent international position paper on drug-induced ocular-surface disorders specifically identifies antihistamines, beta-blockers, antipsychotics, antidepressants and isotretinoin among medications associated with dry-eye disease. But there is an important word in that sentence: associated. The strength of evidence, mechanism and size of effect are not identical for every drug.

Some systemic antihistamines can reduce secretions through their anticholinergic effects. That can potentially affect tear production. In the DREAM study, people taking antihistamines had, on average, shorter tear break-up time and higher dry-eye symptom scores than non-users after adjustment for several relevant factors.

That does not mean that antihistamine plus dry eye equals “the antihistamine caused it.” Someone taking antihistamines may also have allergy, for example, and allergy itself can affect the ocular surface. This is exactly why medication history has to be interpreted in context.

Some antidepressants have repeatedly been associated with dry-eye disease. Depending on the medication, anticholinergic and other neurochemical effects may influence tear secretion and ocular-surface function. But “antidepressants cause dry eye” is too broad a statement. There are several classes of antidepressants, different drugs within those classes, different doses and very different patients.

So the useful information for your doctor is not simply “I take an antidepressant.” It is which medication, what dose, for how long, and whether the eye symptoms changed after starting or changing it.

Isotretinoin deserves special attention because its relationship with the meibomian glands is particularly relevant to dry eye. Meibomian glands are modified sebaceous glands. Isotretinoin acts on sebaceous glands, and studies have found changes in meibomian gland structure and function during treatment. A 2026 systematic review including 43 studies found that worsening dry-eye symptoms and objective ocular-surface abnormalities were frequently reported during isotretinoin treatment, particularly changes involving meibomian gland structure and function. This gives us a very different potential mechanism from, for example, a medication that primarily reduces aqueous tear secretion.

Meibomian Glands & Lipids

This is where we should be careful. There are reports and studies suggesting that meibomian-gland alterations can persist after isotretinoin exposure. But the new systematic review concludes that while persistent sebaceous-gland changes may occur in some patients, the long-term extent and clinical significance remain uncertain.

So it would be too strong to say:

“Isotretinoin permanently destroys meibomian glands.”

But it would also be incorrect to dismiss the ocular effects as necessarily temporary or insignificant. The evidence is still evolving.

Some cardiovascular medications, particularly beta-blockers and diuretics, have historically been associated with dry-eye disease. However, this is another good example of why medication lists can be misleading.

People taking these medications are often older and may have other health conditions that independently increase the likelihood of dry eye. So an epidemiological association does not necessarily tell us what happened in one individual. Medication history is a clue, not a diagnosis.

Age, Hormones and Dry Eye

Yes. And this deserves just as much attention as systemic medication. Long-term topical eye treatments can sometimes affect the ocular surface through:

• •the active medication itself
• •preservatives
• •or repeated exposure to the formulation

This is particularly relevant for people using chronic topical therapy, such as some glaucoma medications. The 2025 EAACI position paper notes that topical antibiotics, antiglaucoma medications and preservatives can produce toxic or allergic ocular-surface disease. So when someone develops dry-eye symptoms, the medication history should include eye drops, not just tablets.

Multi-dose eye drops often contain preservatives to prevent microbial contamination. One of the best-known is benzalkonium chloride (BAK). With repeated exposure, preservatives can affect the ocular surface in susceptible patients, particularly when drops are used frequently or over long periods. That does not mean:

• •preserved drops are automatically harmful
• •or that everyone needs preservative-free medication

The concentration, frequency, duration of exposure, formulation and condition of the ocular surface all matter. But preservative exposure is something worth considering when a person uses multiple topical medications every day.

Sometimes. An artificial tear may contain ingredients or preservatives that do not suit a particular ocular surface. But irritation after a drop does not automatically mean that the product is “toxic.” Formulation, osmolarity, viscosity, preservatives, allergies or sensitivities and the underlying condition of the ocular surface can all influence how a drop feels. We will discuss artificial tears separately in the treatment section because choosing a tear substitute is more complicated than simply finding the bottle labelled “for dry eyes.”

Treating Dry Eye: start with the target

Potentially. The tear system depends partly on normal neurological control and blinking. Some medications that influence the nervous system may alter blink behaviour or other protective ocular responses. This matters because, as we discussed earlier, blinking is part of the tear system.

A medication does not necessarily need to directly “dry out the lacrimal gland” to influence the ocular surface.

Why Blinking Matters

Usually there is no single test. Instead, clinicians can look for a pattern. Useful questions include:

• •Did the symptoms begin after starting the medication?
• •Did they worsen after increasing the dose?
• •Did something change after switching medications?
• •Is the known biological effect of the medication consistent with the ocular findings?
• •Are there stronger alternative explanations?

This is essentially a causality problem. Timing can strengthen the suspicion. But timing alone does not prove it.

That makes the relationship less obvious, but it does not automatically exclude it. Dry-eye disease can develop gradually. Other factors may also accumulate over time:

• •age
• •hormonal changes
• •screen use
• •MGD
• •contact-lens exposure
• •systemic disease
• •environmental stress

A medication might therefore be one contributor within a changing system rather than the single event that suddenly “caused” dry eye. This is another reason why searching for one root cause can sometimes be misleading.

Dry Eye Is Often Mixed

Not on your own. This is particularly important. A medication prescribed for depression, cardiovascular disease, allergy, autoimmune disease or another systemic condition may be far more important to your overall health than its possible contribution to dry eye. If a medication is genuinely suspected, the prescribing doctor may sometimes consider:

• •changing the dose
• •switching to another medication
• •changing the route of administration
• •or continuing the medication while treating the ocular-surface problem

Which option makes sense depends on the medication and why you need it. Earlier TFOS guidance explicitly described dose adjustment, substitution or route changes as possible approaches to systemic medication-associated dry eye, but these are prescribing decisions, not something a patient should do independently.

Sometimes ocular effects may improve after the medication is withdrawn or changed. But there is no universal rule. It depends on:

• •the medication
• •the mechanism
• •how long it was used
• •what structures were affected
• •what other dry-eye drivers are present

For some medications, long-term reversibility is not completely understood. Isotretinoin is a good example: persistent meibomian-gland changes have been reported, but current evidence does not allow us to predict reliably who will have lasting abnormalities.

So we should avoid both extremes:

“Just stop the drug and everything will return to normal.”

“The damage is permanent.”

Neither statement can be generalized.

Bring a complete medication list. That includes:

• •prescription medications
• •over-the-counter medications
• •eye drops
• •and relevant topical treatments around the eyes

And if possible, mention when you started them. The timeline can sometimes be more informative than the name of the medication itself.

How Dry Eye Is Diagnosed