Actinic Keratosis in Houston: Treatment and When to Act

This article is educational and does not replace an evaluation by a board-certified dermatologist. If you have a concerning skin change, please book a visit.

By the end of a Houston summer, a lot of scalps, ears, and forearms feel different than they did in April. Rough spots appear that you notice with your fingertips before you see them, and moisturizer does nothing for them. Many are actinic keratoses, the most common precancer dermatologists treat and the earliest point at which the squamous cell carcinoma pathway can be interrupted. Actinic keratosis is a cumulative-dose disease, and Houston delivers that dose year round. Here is how dermatologists identify these lesions, what the progression data show, and how treatment works.

What actinic keratosis is (and is not)

An actinic keratosis, often abbreviated AK, is a lesion of atypical, sun-damaged keratinocytes confined to the epidermis. The National Cancer Institute defines it plainly as a thick, scaly patch of skin that may become cancer (NCI). A typical AK is a 2 to 6 mm erythematous macule or thin papule topped by adherent, gritty scale, and the defining feature is texture: AKs are easier to feel than to see, which is why dermatologists palpate sun-exposed skin rather than only inspecting it. They cluster where cumulative UV dose is highest: the balding scalp, forehead, temples, ears, nose, cheeks, dorsal forearms and hands, and the lower legs in women. Hypertrophic AKs are thicker and more keratotic, sometimes forming a cutaneous horn, and respond poorly to superficial treatment. Actinic cheilitis is the same process on the lower lip.

How AKs differ from seborrheic keratoses and solar lentigines

These three look similar to patients and quite different under a dermatoscope. A seborrheic keratosis is benign, waxy, sharply demarcated, and classically "stuck on," greasy rather than gritty. A solar lentigo, the flat brown spot most people call a sun spot, is uniformly pigmented and smooth, with no scale. An actinic keratosis is the rough one: erythematous base, dry adherent scale, sandpaper texture. On dermatoscopy, facial AKs often show the "strawberry pattern," an erythematous pseudonetwork with white-yellow scale and prominent targetoid follicular openings. A lesion behaving differently from its neighbors, tender, indurated, growing quickly, ulcerated, or bleeding, raises concern for invasive squamous cell carcinoma and is sorted out by biopsy.

Why Houston's UV pattern drives actinic keratosis

A UV index with no off-season

The National Weather Service Houston/Galveston office records a summer UV index that routinely sits between 10 and 11, which the agency classifies as extreme, and a UV index that does not fall below 3, or moderate, in any month of the year (National Weather Service). Most of the country banks a real winter break from meaningful UV. Houston does not. That is why fall is our busiest season for AK treatment: lesions a long summer produced become obvious in September, and the cooler months are the easiest time to finish a course that leaves skin photosensitive.

Outdoor work and water reflection

Houston's construction, shipping, and refining sectors keep a large share of the workforce outdoors through the highest-index months, and occupational UV is chronic rather than recreational, the exposure pattern most closely tied to AK and squamous cell carcinoma. Water adds to it: sunlight off the bay or a boat deck delivers a second dose from below, striking the underside of the chin, the nose, and the lower lip. Our sun damage page covers how we assess cumulative exposure.

The risk that matters: AK to squamous cell carcinoma

What the progression numbers actually say

The published range here is enormous, and honest framing matters. The American Academy of Dermatology's 2021 guidelines of care for the management of actinic keratosis note that estimates for a single AK progressing to invasive squamous cell carcinoma span roughly 0.025% to 20% (Eisen et al., JAAD 2021), a spread reflecting differences in study design, follow-up, and patient risk. The practical translation: any individual AK is far more likely to persist or regress than to become cancer, while a patient carrying dozens across a damaged field carries a meaningfully elevated risk of a squamous cell carcinoma somewhere in that field. Treatment is about lowering total lesion burden, not the odds on one spot.

Field cancerization versus the isolated lesion

Sun-damaged skin does not sustain injury in neat, visible islands. Between the AKs you can see lies subclinical dysplasia, keratinocytes with the same UV signature that have not yet raised a palpable scale. Dermatologists call this field cancerization, and it explains how treatment is structured. Freezing four visible spots on a scalp with forty square centimeters of damage treats what is apparent and leaves what is not, which is why widespread damage is steered toward field-directed therapy while three discrete lesions are better targeted individually.

How dermatologists confirm it is an AK

Diagnosis is usually clinical. We take a history covering sun exposure, prior skin cancers, tanning bed use, and any immunosuppression, including transplant medications, which sharply increases both AK burden and progression risk. We then palpate the sun-exposed surfaces, using dermatoscopy to separate AKs from pigmented mimics and to judge keratin thickness. We biopsy when a lesion does not behave like a precancer: tenderness, induration, diameter over about a centimeter, rapid growth, ulceration, bleeding, or failure to clear after treatment. If pathology returns squamous cell carcinoma, the conversation shifts to treating a cancer, which may involve Mohs surgery for high-risk sites or image-guided superficial radiation therapy for selected patients who are not good surgical candidates. Our skin cancer page covers that pathway.

Treatment decisions depend on your individual skin, medical history, and goals. The information below describes how dermatologists evaluate options; it is not a prescription or a recommendation for any specific person.

Lesion-directed treatments

Cryotherapy with liquid nitrogen

Cryotherapy is the most common in-office AK treatment and carries a strong recommendation in the AAD guideline. Liquid nitrogen at roughly minus 196 degrees Celsius freezes and lyses the atypical keratinocytes, and freeze duration drives the result: complete clearance was about 39% with freeze times under 5 seconds, 69% at 5 to 20 seconds, and 83% beyond 20 seconds (Thai et al., cited in Eisen et al., JAAD 2021). Longer freezes clear more lesions and also raise the risk of blistering and lasting hypopigmentation, a real consideration in Fitzpatrick types IV through VI. Expect erythema and edema for 24 to 72 hours, sometimes a blister, then a crust that separates over one to two weeks.

Curettage with electrodesiccation

For hypertrophic AKs and cutaneous horns, freezing often cannot penetrate the keratin. Curettage scrapes the lesion away and electrodesiccation treats the base. Its advantage is tissue for histology, which matters precisely in the thick lesions where occult invasion is most plausible. Healing takes one to three weeks.

Tirbanibulin (Klisyri) 1% ointment

Tirbanibulin (Klisyri) is a microtubule inhibitor with Src kinase signaling activity, applied once daily for five consecutive days to a field of up to about 25 square centimeters on the face or scalp. In two Phase 3 trials, complete clearance at day 57 reached 44% versus 5% on vehicle in the first trial and 54% versus 13% in the second (Blauvelt et al., NEJM 2021). Local erythema and flaking peak near day 8 and largely resolve by day 29. The limitation is durability, since the same trials reported substantial recurrence at one year.

Field-directed treatments for widespread damage

These four are not interchangeable. They differ in mechanism, course length, how inflamed the skin becomes, and what the twelve-month data show.

5-fluorouracil (5-FU) cream

5-FU inhibits thymidylate synthase, starving rapidly dividing atypical keratinocytes of the nucleotides they need for DNA synthesis. The 5% formulation is applied twice daily for two to four weeks and produces the briskest reaction of any field therapy: erythema, erosion, crusting, and discomfort peaking in weeks two to three, then settling over the next two to four weeks. Patients need that warning up front, because a course that looks alarming halfway through is working as designed. It also has the best comparative data: in a four-arm randomized trial, 74.7% of patients treated with 5% fluorouracil achieved at least a 75% reduction in lesion count twelve months later, versus 53.9% with imiquimod, 37.7% with methyl aminolevulinate photodynamic therapy, and 28.9% with ingenol mebutate (Jansen et al., NEJM 2019). A 4% once-daily formulation is generally better tolerated.

Imiquimod

Imiquimod is a toll-like receptor 7 agonist. Rather than killing keratinocytes directly, it recruits the innate immune system to clear them, which makes its reaction inflammatory and somewhat unpredictable between patients. The 5% cream is dosed intermittently in cycles with rest periods; a 3.75% formulation uses a two-weeks-on, two-weeks-off, two-weeks-on schedule. It reached 53.9% success at twelve months, and flu-like symptoms occur in a minority of patients.

Photodynamic therapy (PDT)

PDT is a two-step in-office treatment. A photosensitizer, aminolevulinic acid or methyl aminolevulinate, is preferentially converted to protoporphyrin IX inside metabolically active atypical keratinocytes; illumination with blue light near 417 nm or red light near 630 nm then generates reactive oxygen species that destroy them. The course finishes in the office rather than depending on weeks of home adherence, but illumination is genuinely uncomfortable, the area stays red and swollen for several days, and strict photo-avoidance is required for roughly 48 hours, which is easier in a Houston November than a Houston July. Twelve-month efficacy above was 37.7%, though protocols vary and other studies report higher clearance.

Diclofenac 3% gel

Diclofenac gel works through COX-2 inhibition, applied twice daily for 60 to 90 days. It is the gentlest field therapy and carries a weaker recommendation in the AAD guideline because its efficacy is more modest. It suits patients who cannot tolerate a brisk inflammatory course.

How we decide what to recommend, and what recovery looks like

At Bayou City Dermatology the recommendation follows the field, not a default. Three or four discrete lesions on a limited area usually means cryotherapy the same visit. Thick or hypertrophic lesions usually mean curettage with histology. Confluent damage across a scalp, face, or pair of forearms usually means field therapy, most often 5-FU given the twelve-month data, with imiquimod or PDT chosen when 5-FU is not a good fit. Season factors in, since courses that leave skin inflamed are easier to complete between October and April, and so does immune status: transplant recipients need more aggressive treatment and tighter follow-up.

Aftercare is the same either way. Expect the area to look worse before it looks better, keep it bland and moisturized, protect it from sun completely while it heals, and return for reassessment at 8 to 12 weeks. Treatment reduces lesion count; it does not repair the underlying photoaging, so the field stays under surveillance rather than being declared finished.

Preventing new AKs during a Houston year, and when to come in

• Daily broad-spectrum SPF 30 or higher, every month of the year. A UV index that never drops below 3 means no season in which the damage pauses.
• Cover the sites that produce AKs. A wide-brim hat protects the scalp, ears, and nose better than any sunscreen application people realistically maintain; UPF sleeves solve the forearms.
• Ask about nicotinamide. In the ONTRAC trial, oral nicotinamide 500 mg twice daily reduced new keratinocyte carcinomas by about 23% over 12 months in high-risk patients (Chen et al., NEJM 2015). That is a conversation with your dermatologist, not a self-prescription.
• Check your own skin monthly using our monthly skin cancer self-exam guide for Texas. Texture finds AKs earlier than sight does.
• Come in promptly for a spot that is tender, firm, growing, bleeding, ulcerated, or not healing, or for a rough patch on the lower lip.

Frequently Asked Questions

Does actinic keratosis always turn into cancer?

No. Most individual actinic keratoses persist or regress rather than becoming cancer. The AAD's 2021 guideline notes published estimates for a single lesion progressing to invasive squamous cell carcinoma ranging from roughly 0.025% to 20%, a wide spread reflecting different study designs and patient risk. We still treat because a patient with many lesions across a sun-damaged field has a meaningfully elevated risk of a squamous cell carcinoma somewhere in that field.

Can I remove actinic keratosis at home?

No. Over-the-counter acid products, freeze kits, and picking can flatten the surface scale without treating the atypical cells underneath, which makes a lesion harder to assess and can mask an early squamous cell carcinoma. Treatment also depends on an accurate diagnosis, since seborrheic keratoses and solar lentigines look similar to patients and need no treatment at all.

Is cryotherapy or 5-FU better for actinic keratosis?

They answer different questions. Cryotherapy is lesion-directed and best for a few discrete AKs, done in one visit. 5-fluorouracil is field-directed and treats a whole region including subclinical damage you cannot see, which is why it is preferred when lesion counts are high. In the four-arm comparison of field treatments, 5% fluorouracil produced the highest twelve-month success rate at 74.7%.

How long does 5-FU cream take to work?

The course runs two to four weeks of twice-daily application for the 5% cream. Redness, erosion, and crusting build through weeks two and three, which is the expected reaction rather than a complication, then settle over the following two to four weeks. Results are assessed roughly 8 to 12 weeks after finishing.

Are actinic keratosis treatments covered by insurance?

Actinic keratosis is a precancerous lesion, so treatment is generally handled as medically necessary rather than cosmetic, and most plans cover it. Coverage rules, prior authorization for specific topicals, and your own deductible and copay vary by plan. Our office can help verify benefits before a course starts.

Book a full-body skin exam

Actinic keratoses are the most treatable step on the squamous cell carcinoma pathway, and far easier to manage as a handful of lesions than as a field. If you have rough, scaly spots on your scalp, face, ears, or forearms after this summer, book a full-body skin exam at Bayou City Dermatology.

References

1. Eisen DB, et al. Guidelines of care for the management of actinic keratosis. JAAD. 2021. jaad.org
2. Blauvelt A, et al. Phase 3 trials of tirbanibulin ointment for actinic keratosis. NEJM. 2021;384(6):512-520. nejm.org
3. Jansen MHE, et al. Randomized trial of four treatment approaches for actinic keratosis. NEJM. 2019;380(10):935-946. nejm.org
4. Chen AC, et al. A phase 3 randomized trial of nicotinamide for skin-cancer chemoprevention. NEJM. 2015;373(17):1618-1626. nejm.org
5. National Cancer Institute. Actinic keratosis. cancer.gov
6. Skin Cancer Foundation. Actinic keratosis. Accessed August 2026. skincancer.org
7. FDA. Klisyri (tirbanibulin) prescribing information. accessdata.fda.gov
8. U.S. Preventive Services Task Force. Skin cancer: screening, 2023. uspreventiveservicestaskforce.org
9. National Weather Service Houston/Galveston. UV index and climate data. weather.gov/hgx