Periungual inflammation: paronychia

 

Paronychia: acute or chronic, what should you do?

Paronychia is inflammation of the tissues surrounding the nail and one of the most common nail disorders. Although different forms may look similar at first, distinguishing acute paronychia from chronic paronychia is essential because their mechanisms and treatment are different.

Practical rule:
Pus or abscess → think acute paronychia.
Loss of the cuticle → think chronic paronychia.

 

This blog was created to present common clinical situations encountered in general practice in an accessible, practical and engaging way. It includes both clinical cases involving frequently seen conditions and the questions or uncertainties that often arise when assessing and treating a patient.

Its aim is to serve as a helpful resource for everyday clinical practice. The topics are drawn directly from routine consultations and do not follow a predetermined order, reflecting the way patients —and the questions they bring— arrive in the consulting room.

Our intention is to move away from overly academic discussions and to avoid focusing on rare or particularly complex conditions, for which referral to a dermatology specialist remains an appropriate option.

We hope this blog will be useful to both general practitioners and medical students.

Nicotinamide in the prevention of cutaneous squamous cell carcinoma

 

Skin cancer prevention

When should I use nicotinamide to prevent new cutaneous squamous cell carcinomas?

In patients with several previous skin cancers, nicotinamide may be used as an additional measure to reduce the development of new tumours. It does not replace photoprotection, treatment of actinic keratoses or dermatological follow-up.

Practical answer. Oral nicotinamide 500 mg every 12 hours may be offered to immunocompetent patients with a history of two or more cutaneous squamous cell carcinomas. The benefit is maintained while treatment is continued. I would not routinely recommend it in solid-organ transplant recipients.

Who is a good candidate?

The best-studied profile is a patient who is:

Immunocompetent

The strongest evidence comes from patients without immunosuppression.

Has previous tumours

Particularly if they have had two or more cutaneous squamous cell carcinomas in recent years.

Has persistent risk

Extensive photodamage, numerous actinic keratoses or repeated development of new carcinomas.

This is not primary prevention. There is insufficient evidence to recommend it generally to anyone with photodamage or isolated actinic keratoses who has never had skin cancer.

What benefit can I explain?

In the ONTRAC trial, 386 high-risk patients received nicotinamide 500 mg every 12 hours or placebo for 12 months. Nicotinamide reduced the development of new cutaneous squamous cell carcinomas by approximately 30%.

The important nuance: the effect disappeared after treatment was stopped. It should therefore not be presented as a one-year intervention that provides permanent protection.

How do I use it in practice?

1. Confirm the risk profile: an immunocompetent patient with two or more previous cutaneous squamous cell carcinomas.
2. Maintain the basic measures: photoprotection, self-examination, follow-up visits and treatment of actinic keratoses and early carcinomas.
3. Prescribe nicotinamide 500 mg every 12 hours. The studied regimen lasted 12 months.
4. Review tolerability and adherence. The benefit depends on the patient continuing treatment.

Safety

It is generally well tolerated. The most common adverse effects are gastrointestinal and usually improve after dose reduction or discontinuation.

Laboratory tests

At the dose used for chemoprevention, specific laboratory monitoring is not usually required.

Duration

The main evidence covers 12 months. The optimal duration beyond this period is not well defined.

What about transplant recipients?

In solid-organ transplant recipients, the ONTRANS trial included 158 patients and found no reduction in new keratinocyte cancers, cutaneous squamous cell carcinomas, basal cell carcinomas or actinic keratoses with nicotinamide 500 mg every 12 hours for 12 months.

Practical conclusion: do not use nicotinamide as a standard chemoprevention strategy in transplant recipients. The lack of recommendation is mainly due to the absence of a demonstrated clinical benefit, rather than major toxicity concerns.

Pocket algorithm

Situation	Practical approach
Immunocompetent patient with 2 or more previous carcinomas	Consider nicotinamide 500 mg every 12 hours as an additional measure.
Photodamage or actinic keratoses only, with no previous skin cancer	Do not recommend it routinely.
Solid-organ transplant recipient	Do not use it routinely; prioritise specialist follow-up and other preventive strategies.
Patient who stops treatment	Explain that the preventive benefit is not maintained after discontinuation.

Knowledge gaps

• The optimal treatment duration beyond 12 months is not well established.
• It has not been shown to reduce aggressive cutaneous squamous cell carcinomas, metastases or mortality.
• In transplant recipients, the data are conflicting and further trials are needed.

Take-home message

Nicotinamide 500 mg every 12 hours is a simple and well-tolerated option for secondary prevention in immunocompetent patients with two or more previous cutaneous squamous cell carcinomas. It may reduce the development of new cutaneous squamous cell carcinomas while treatment is continued. It does not replace standard preventive measures and should not be used routinely in transplant recipients.

Main sources

1. Chen AC et al. A Phase 3 Randomized Trial of Nicotinamide for Skin-Cancer Chemoprevention. N Engl J Med. 2015;373:1618-1626. Open.
2. Allen NC et al. Nicotinamide for Skin-Cancer Chemoprevention in Transplant Recipients. N Engl J Med. 2023;388:804-812. Open.
3. Stratigos AJ et al. European consensus-based interdisciplinary guideline for invasive cutaneous squamous cell carcinoma. Part 1: Diagnostics and prevention — Update 2026. Eur J Cancer. 2026. doi:10.1016/j.ejca.2026.116763.

Content intended for healthcare professionals. Individualise the indication and always maintain photoprotection, treatment of precursor lesions and clinical follow-up.

Doctor, please don’t take me off the cream—it’s the only thing that’s really worked for me…

 

Clinical presentation

Easy. Moderate frequency.

A 52-year-old patient has had facial lesions for about eight months; they began as small papules and pustules.

The patient had tried several topical treatments, but obtained only temporary relief with a cream containing clobetasol 0.05%, initially prescribed for a foot problem. They have been applying it daily to the face for three months.

Despite this, the condition continues to worsen and is accompanied by an intense burning sensation.

Diagnosis: steroid-induced rosacea-like dermatitis or steroid rosacea.

Steroid rosacea

Prolonged application of potent topical corticosteroids to the face can cause a condition that mimics or worsens rosacea.

It may present with persistent erythema, burning, flushing, papules, pustules, or inflammatory plaques. In some patients, it follows a predominantly perioral, periocular, or perinasal pattern.

The corticosteroid initially reduces inflammation and provides rapid improvement. However, continued use leads to dependence, loss of efficacy, and progressive worsening.

Key point: the immediate relief produced by the corticosteroid may conceal the fact that, in the medium term, it is perpetuating and worsening the condition.

The cycle of dependence

1. Initial improvement

The corticosteroid rapidly reduces erythema and the burning sensation.

2. Rebound effect

When its use is reduced or stopped, vasodilation, burning, and a severe inflammatory flare develop.

3. Reapplication

The patient uses it again to relieve the flare, establishing a cycle of dependence.

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Clues to recognition

Clinical feature	What it suggests
Use of a potent corticosteroid on the face	This is the key history finding.
Rapid but temporary improvement	Encourages the patient to continue applying it.
Erythema, papules, and pustules	Produces an appearance similar to inflammatory rosacea.
Intense burning or stinging	Common, especially during the rebound effect.
Worsening after discontinuation	Suggests corticosteroid-induced dependence and rebound.

Practical diagnosis

In any rosacea-like facial eruption, always ask what products the patient is applying and for which areas they were originally prescribed.

1

Ask

Review creams, ointments, and treatments used in recent months.

2

Link

Link onset or worsening to facial corticosteroid use.

3

Warn

Explain that temporary worsening may occur during withdrawal.

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Management

The essential measure is to withdraw the topical corticosteroid. However, after prolonged use, abrupt discontinuation can trigger a very severe flare and prompt the patient to apply it again.

Corticosteroid withdrawal

• Explain the possibility of a rebound effect in advance.
• Taper gradually when use has been prolonged.
• Avoid restarting the corticosteroid in response to temporary worsening.
• A topical calcineurin inhibitor may be considered as bridging therapy.

Treatment of the rosacea-like inflammation

• Topical metronidazole.
• Topical ivermectin.
• Topical azelaic acid.
• Oral doxycycline in moderate or severe cases.

Take-home message

Potent topical corticosteroids should not be used continuously on the face. They may provide initial improvement, but can also cause dependence, rebound, and progressively more severe rosacea-like dermatitis.

Final summary

• Cause: prolonged use of topical corticosteroids, especially high-potency agents, on the face.
• Clinical features: erythema, burning, flushing, papules, pustules, or inflammatory plaques.
• Main clue: temporary improvement with the corticosteroid and worsening after discontinuation.
• Problem: a cycle of dependence and reapplication may develop.
• Management: corticosteroid withdrawal, counselling about rebound, and specific treatment of the rosacea-like component.

When rosacea improves briefly with corticosteroids but subsequently worsens, consider steroid rosacea.

Clinical question

Which topical treatment should I choose for a patient with actinic keratoses?

In patients with multiple actinic keratoses on photodamaged skin, the aim is to treat the field of cancerisation, not only the visible lesions. In practice, the choice usually comes down to 5-fluorouracil (5-FU), imiquimod and tirbanibulin.

5-FU is the reference option when efficacy and clinical experience are the priorities. Imiquimod is an established alternative. Tirbanibulin is particularly useful when a very short, well-tolerated course is needed.

Before starting. Do not automatically treat a lesion that is indurated, painful, ulcerated, bleeding, markedly hyperkeratotic or clearly different. In these cases, Bowen disease or invasive squamous cell carcinoma should be excluded, and biopsy or referral considered.

1. 5-FU, imiquimod or tirbanibulin

5% 5-FU has the strongest comparative evidence at 12 months: in a direct trial it was more effective than imiquimod and also more cost-effective. This makes it a reasonable starting point in many patients, although the final choice depends on tolerability, regimen and patient preference.

Issue	5-FU	Imiquimod	Tirbanibulin 1%
When to choose it	When field control is the main priority.	When 5-FU is unsuitable or another first-line option is preferred.	When treatment duration and tolerability are the main priorities.
Regimen	4%: once daily for 4 weeks. 5%: according to product information and local protocol.	Intermittent regimens or cycles lasting several weeks, depending on formulation.	Once daily for 5 days.
Advantage	Strongest comparative support and extensive experience.	Effective and well-established alternative.	Very short course and usually shorter-lived local reactions.
Limitation	Visible inflammation, sometimes marked.	Longer regimen and less predictable inflammatory response.	Small treatment field, narrow indication and less comparative evidence.

In practice: choose 5-FU when efficacy is the priority; imiquimod when 5-FU is unsuitable; tirbanibulin when a five-day course may substantially improve adherence.

2. If I choose 5-FU: 4% or 5%?

The difference in concentration does not translate into a proportional difference in efficacy. In the direct comparison, complete clearance was 54.4% with once-daily 4% and 57.9% with twice-daily 5%. Clearance of at least 75% of lesions was virtually identical.

4% 5-FU

Once daily for 4 weeks. Very similar short-term efficacy, greater convenience and, overall, better tolerability.

5% 5-FU

The formulation with the strongest 12-month comparative evidence against other field treatments.

Practical choice

4% is very reasonable when adherence and tolerability are priorities. 5% is particularly relevant when aiming to reproduce the option with the best comparative evidence.

With either formulation, patients should expect erythema, scaling, crusting and possible erosion. Explain what is expected and when medical advice is needed.

3. Where should tirbanibulin be positioned?

Its main advantage is a five-day course. Under the European product information, it is indicated for Olsen grade I, non-hyperkeratotic and non-hypertrophic actinic keratoses on the face or scalp, within a field of up to 25 cm².

It is particularly suitable when

• the field is small and located on the face or scalp;
• lesions are thin and non-hyperkeratotic;
• the patient is unlikely to complete several weeks of treatment;
• prolonged visible inflammation would create work or social difficulties.

It would not be my first choice when

• the field is extensive;
• lesions are thick, infiltrated or clinically suspicious;
• the strongest evidence for sustained control is the main priority;
• automatic repeat courses are being considered or the patient is immunocompromised.

Review response at approximately 8 weeks. If complete clearance has not been achieved, reassess the diagnosis and management plan.

Pocket algorithm

1. Confirm that there are several thin actinic keratoses.
2. Remove any suspicious lesion from the algorithm.
3. Choose according to the main priority: efficacy, tolerability or treatment duration.
4. Explain the expected reaction and arrange follow-up.

Knowledge gaps

• Immunocompromised patients: too few trials define the best strategy.
• Prevention of squamous cell carcinoma: reducing actinic keratoses is not the same as proving a sustained reduction in invasive carcinoma.
• Tirbanibulin: direct comparisons with 5-FU and imiquimod are lacking, as are stronger data on retreatment and long-term control.

Take-home message

In an immunocompetent patient with several thin actinic keratoses, 5-FU is usually the most practical first choice. The 4% formulation improves convenience and tolerability; 5% has the strongest comparative evidence. Imiquimod remains a valid alternative. Tirbanibulin is especially useful when a five-day course may clearly improve adherence.

Main sources

1. Jansen MHE et al. Randomized Trial of Four Treatment Approaches for Actinic Keratosis. N Engl J Med. 2019;380:935-946. Open source.
2. Jansen MHE et al. Trial-based cost-effectiveness analysis of topical field treatments. Br J Dermatol. 2020;183:738-744. Open source.
3. AEMPS-CIMA. Tolak 40 mg/g crema: ficha técnica. Open source.
4. Blauvelt A et al. Phase 3 Trials of Tirbanibulin Ointment for Actinic Keratosis. N Engl J Med. 2021;384:512-520. Open source.
5. European Medicines Agency. Klisyri: European product information. Open source.

Content intended for healthcare professionals. Always adapt treatment to current product information and the individual patient.

 

Controversy

Photoprotection and vitamin D: how can we sunbathe safely without falling short

Photoprotection is one of the most important measures for preventing cumulative sun damage, premature skin aging, and skin cancer.

But a reasonable question often comes up: if we protect ourselves a lot from the sun, can we develop vitamin D deficiency?

The practical answer is that it is possible to maintain good photoprotection without giving up adequate vitamin D levels. The key is understanding that we do not need to burn, tan, or spend a long time exposed to the sun in order to synthesize vitamin D.

Key point: the goal is not to avoid the sun at all costs, but to avoid sun damage. Exposure should be brief, gradual, adapted to skin phototype, and always avoid sunburn.

In cases of suspected onychomycosis, is it always necessary to collect a sample, or can empirical treatment be started?

 

Clinical question

When onychomycosis is suspected, should a sample always be collected, or can empirical treatment be started?

Onychomycosis is a common cause of nail changes, but not every thickened, yellowish, brittle, or dystrophic nail is infected by fungi.

Therefore, when there is clinical suspicion of onychomycosis, the general recommendation is to confirm the diagnosis with a sample, especially if oral antifungal treatment is going to be started.

Key point: clinical diagnosis alone has limited value. Many nails with a compatible appearance are not actually onychomycosis.

Why is it advisable to confirm the diagnosis?

All guidelines recommend collecting a sample, especially before prescribing oral treatment, for two main reasons:

1. Clinical diagnosis alone is unreliable. Only some nails with clinical suspicion are truly fungal.
2. Oral treatments are not harmless. They may cause drug interactions and adverse effects that should be avoided if the diagnosis has not been confirmed.

Are there any exceptions?

Yes. If suspected onychomycosis is accompanied by plantar scaling compatible with tinea pedis, starting treatment without prior microbiological confirmation may be justified, especially if the clinical picture is very typical.

In practice: if oral treatment is going to be used, confirming the diagnosis beforehand is the most prudent approach. If the treatment is topical and the suspicion is very clear, it can be individualized.

Diagnostic tests

• First line: direct examination with KOH + fungal culture.
• If suspicion is high and KOH/culture are negative: prioritize PAS and/or PCR.
• If there has been previous antifungal treatment: consider PAS and PCR, if available.

Comparison of diagnostic methods

Method	What does it demonstrate?	Approximate performance	Main clinical usefulness	Main limitation
Direct examination with KOH	Presence of hyphae or yeasts	Sensitivity 61% / Specificity 95%	Rapid, inexpensive test that is useful if positive	Many false negatives; does not identify the species
Fungal culture	Viable fungus and identification	Sensitivity 56% / Specificity 99%	Allows confirmation and identification of the genus or species	Slow and associated with quite a few false negatives
Histology with PAS	Fungal invasion of the nail plate	Sensitivity 84% / Specificity 89%	Very useful when suspicion is high and KOH/culture are negative	Does not identify the species; may detect nonviable fungi
PCR	Fungal DNA	More often positive than culture; approximately 78% sensitivity and 90% specificity in one study	Rapid and useful if culture is negative or the patient has received previous treatment	Depends on the panel; may detect nonviable DNA

Diagnostic guide for onychomycosis

Effective diagnosis requires understanding that conventional tests have limited sensitivity. The strategic combination of direct methods, culture, histology, and molecular techniques reduces false negatives.

Performance of diagnostic methods

61%

KOH

Rapid and inexpensive test. Useful for confirmation if positive.

56%

Culture

Identifies the fungus, but it is slow and may give false negatives.

84%

PAS

Detects fungal invasion. Very useful when other tests are negative.

78%

PCR

Rapid and useful after previous treatment or with a negative culture.

Recommended practical strategy

Step 1. Basic combination: KOH + culture

This is the recommended initial strategy. KOH provides rapid results, and culture allows identification of the causative agent.

Step 2. If suspicion persists: PAS and/or PCR

If KOH and culture are negative but clinical suspicion is high, PAS and/or PCR should be added. The combination of PAS + PCR may improve diagnostic yield.

Step 3. Pay special attention to patients who have already been treated

In patients who have previously received antifungals, culture may be negative. In these cases, PAS and PCR can be especially useful.

How should the sample be collected correctly?

Sample quality is essential. Many false negatives are due to superficial or insufficient sampling, or to samples taken from a poorly representative area.

For direct examination and culture

1. Clean the nail with alcohol.
2. Cut or remove the most altered part if necessary.
3. Scrape the subungual material with a scalpel blade or curette.
4. Take the sample from the active edge of the lesion, not only from the distal tip.
5. Place the fragments on a slide or in an appropriate dry container.
6. Send the sample to microbiology.

In the superficial white variant, the whitish area of the nail surface should be scraped directly.

For PAS

1. Cut a full-thickness nail fragment.
2. Use nail nippers or appropriate instruments.
3. Send the fragment to the pathology department.

Take-home message

Not every dystrophic nail is onychomycosis. If oral treatment is going to be prescribed, confirming the diagnosis is the prudent approach. The most practical initial strategy is KOH + culture, and if suspicion persists, add PAS and/or PCR.

Final summary

• KOH: rapid, inexpensive, and useful if positive.
• Culture: identifies the fungus, but it is slow and may fail.
• PAS: the most sensitive method for detecting fungal invasion.
• PCR: rapid and useful in previously treated patients or when culture is negative.
• The sample: should be sufficient and taken from the active area of the lesion.

The key is not to choose a perfect test, but to combine diagnostic methods appropriately according to the clinical context.