Steroids — The Good, The Bad, and the Ugly Truth About a Powerful Drug

Steroids are a good drug. I want to be clear about that from the start. They reduce inflammation remarkably well. They shrink nasal polyps. They can work synergistically with antibiotics to break through infections that are hard to treat on their own. In the right patient, at the right time, for the right duration, they are one of the most effective tools in sinus and allergy medicine.

But they have a very narrow spectrum of benefit before they become a serious concern. And when they are used without limits — prescribed indefinitely, repeated four or five times a year, layered on top of each other without a plan — they can cause diabetes, obesity, avascular necrosis of long bones, and death. That is not a theoretical risk. I have watched it happen.

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What Steroids Are Actually Doing

Steroids work by suppressing the inflammatory cascade — the immune response that produces swelling, mucus overproduction, and tissue hypertrophy in the nose and sinuses. In patients with nasal polyps, this effect is particularly striking. Steroids reduce the eosinophilic inflammation driving polyp growth, shrink existing polyps, and help prevent recurrence after surgery. Patients who have been congested and unable to smell for months experience dramatic relief within days. It is easy to understand why both patients and physicians reach for them repeatedly.

The problem is that steroids do not fix the underlying driver of the inflammation. They suppress the immune response temporarily. When the course ends, the inflammatory environment that was driving the symptoms is still there — and the symptoms return. This is why patients end up on repeated prednisone bursts. Each one works. And each one creates the impression that steroids are the solution rather than what they actually are: a powerful suppressor of a process that has not been addressed at its source.

The Spectrum of Steroid Delivery — Risk Increases With Systemic Absorption

Not all steroids are equal in their risk profile, and my approach is always to start at the lowest systemic exposure and escalate only when the severity of disease demands it.

Nasal steroid sprays are the starting point for most patients. They deliver corticosteroid directly to the nasal mucosa with minimal systemic absorption — the least likely of all steroid formulations to produce systemic effects. That said, they are not without risk. Epistaxis — nosebleeds — is the most common side effect, typically from improper technique directing spray toward the septum. Patients on long-term nasal steroid sprays should also have regular eye checks, as there is a recognized association with increased intraocular pressure and cataracts.

Steroid rinses — budesonide added to a saline irrigation solution — deliver a higher concentration of corticosteroid directly to the sinus cavities and posterior nasal mucosa than a spray can reach. This makes them more effective for patients with significant mucosal disease, but the higher concentration means higher potential for systemic absorption. I monitor blood glucose in patients on long-term steroid rinses, particularly those with any risk factors for diabetes.

Oral steroids carry the full systemic burden. Weight gain, irritability, sleep disruption and insomnia, blood glucose elevation, and over time — with repeated or prolonged use — the risk of diabetes, avascular necrosis of the femoral head and other long bones, adrenal suppression, and immune compromise. These are not rare side effects in patients who are prescribed oral steroids repeatedly over years. They are the expected consequences of sustained systemic cortisol elevation.

Injected steroids — depot corticosteroids — carry the same systemic risks as oral steroids and in some respects more, because the release cannot be controlled once the injection is administered. If a patient develops a significant adverse effect, there is no way to stop it. I use injectable steroids with considerable caution and for specific, time-limited indications.

The Patient I Think About Every Time I Prescribe a Steroid

Early in my career I had a patient — a farmer — who had been diagnosed with significant nasal polyposis by an ENT department chairman at an academic center. The chairman told him he needed to stay on oral steroids indefinitely. He came to me after years on that regimen. I tapered him off the oral steroids and transitioned him to a budesonide saline rinse. He did well. The disease was controlled. He did not need the systemic burden he had been carrying.

I also think about another patient — a woman with asthma who had been placed on long-term systemic steroids by her primary care physician. She became obese as a direct consequence of that steroid use. She developed diabetes. She needed a pulmonologist but the relationship with the one she was referred to broke down badly — a clinical encounter that ended in a way that left her traumatized and unwilling to try again. She never got the specialist care she needed. She died of complications from her diabetes, which was a consequence of the steroids she was placed on and never adequately tapered from.

I believe that was preventable. I believe better coordination, better specialist access, and a more honest conversation about the long-term risks of chronic systemic steroid use would have changed that outcome. I share this story with colleagues and patients not to assign blame but because it illustrates what happens when steroids are used as a permanent solution to a problem that demands a different approach.

When Steroids Are the Right Answer — And When They Are Not

There are patients for whom steroid therapy is genuinely appropriate — patients with severe eosinophilic disease, significant polyposis, or asthma where the inflammatory burden is high and the alternatives have been exhausted. For those patients, the biologic therapies that have emerged in recent years — dupilumab and others that target the Type 2 inflammatory pathway directly — have been transformative. They address the immune mechanism driving the disease without the systemic steroid burden.

But the patient who receives four or five prednisone bursts a year from their primary care physician because they keep getting “sinus infections” that respond to steroids is not a patient who needs more steroids. That is a patient who needs a complete evaluation, a root cause assessment, and a treatment plan that addresses what is actually driving the recurrent inflammation. Whether that is anatomy, allergy, immune dysregulation, biofilm, or pepsin-driven posterior mucosal injury — the answer is not an indefinite prescription for a drug with a narrow window of safety.

Steroids are a powerful tool. They deserve to be used with the precision and caution that power demands.

Want to Understand More?

This post is part of the Why Sinus Treatments Fail — And What Starts Before Them section of the Airway & Sinus Wellness Review.

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About the Author

Franklyn R. Gergits, DO, MBA, FAOCO is an otolaryngologist and rhinologist with over 30 years of clinical experience. He is the founder of the Sinus & Allergy Wellness Center of North Scottsdale, where he performs in-office balloon sinuplasty, turbinate reduction, NEUROMARK® posterior nasal nerve ablation (Neurent Medical, FDA-cleared radiofrequency ablation system), and Eustachian tube dilation under local anesthesia. He performed the first balloon sinuplasty in Pennsylvania and holds dual Entellus Centers of Excellence certifications. Dr. Gergits is the originator of the Posterior Sinonasal Syndrome (PSS) hypothesis, with a preprint available at Preprints.org (DOI: 10.20944/preprints202603.0858.v1). ORCID: 0009-0000-4893-6332.

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This content is for educational purposes only and does not constitute medical advice. If you are experiencing sinus or allergy symptoms or have questions about steroid therapy, please consult a qualified physician for evaluation and individualized treatment recommendations.