terbinafine
Regulatory sources consulted
Approved indications
- Fingernail or toenail onychomycosis caused by dermatophytes, confirmed with a nail specimen.
Contraindications
Absolute
- Chronic or active liver disease.
- History of allergic reaction to oral terbinafine.
Clinical warnings
- Major warning · Liver failure, transplantation, and death have occurred. Obtain transaminases before treatment, monitor periodically, and stop for liver injury. Also stop for severe taste or smell disturbance, neutrophils ≤1000/mm³, or a severe skin reaction. — openFDA terbinafine tablets 250 mg set ID 085e0809-6b7f-447e-976e-8276c29daad6
- Major warning · Thrombotic thrombocytopenic purpura and hemolytic uremic syndrome, including fatal cases, have been reported; discontinue if compatible findings develop. Induction or exacerbation of lupus erythematosus and depressive symptoms have also been reported; assess and discontinue according to severity. — openFDA terbinafine tablets 250 mg set ID 085e0809-6b7f-447e-976e-8276c29daad6
Drug interactions
- HighCYP2D6 substrates
Mechanism: Terbinafine inhibits CYP2D6 and may increase exposure to tricyclic antidepressants, SSRIs, beta-blockers, class 1C antiarrhythmics, and MAO-B inhibitors.
Recommendation: Monitor closely and consider reducing the substrate dose.
https://dailymed.nlm.nih.gov/dailymed/drugInfo.cfm?setid=584d1fae-0120-49a0-e063-6394a90a36fc
- HighRifampin
Mechanism: It approximately doubles terbinafine clearance.
Recommendation: Monitor for loss of efficacy and adjust only under clinical supervision.
https://dailymed.nlm.nih.gov/dailymed/drugInfo.cfm?setid=584d1fae-0120-49a0-e063-6394a90a36fc
- ModerateFluconazole
Mechanism: It increases terbinafine exposure through CYP2C9 and CYP3A4 inhibition.
Recommendation: Monitor toxicity; also consider this risk with similar dual inhibitors.
https://dailymed.nlm.nih.gov/dailymed/drugInfo.cfm?setid=584d1fae-0120-49a0-e063-6394a90a36fc
- ModerateCimetidine
Mechanism: Cimetidine decreased terbinafine clearance by 33% and may increase its exposure.
Recommendation: Monitor for terbinafine adverse effects and consider adjustment under clinical supervision.
https://dailymed.nlm.nih.gov/dailymed/drugInfo.cfm?setid=584d1fae-0120-49a0-e063-6394a90a36fc
- ModerateCyclosporine
Mechanism: Terbinafine increased cyclosporine clearance by 15% and may reduce its exposure.
Recommendation: Monitor cyclosporine concentrations and clinical response; adjust under supervision if needed.
https://dailymed.nlm.nih.gov/dailymed/drugInfo.cfm?setid=584d1fae-0120-49a0-e063-6394a90a36fc
- ModerateCaffeine
Mechanism: Terbinafine decreased intravenous caffeine clearance by 19% and may increase its effects.
Recommendation: Monitor for stimulant effects and consider reducing caffeine intake if they occur.
https://dailymed.nlm.nih.gov/dailymed/drugInfo.cfm?setid=584d1fae-0120-49a0-e063-6394a90a36fc
- HighWarfarin
Mechanism: Increases or decreases in prothrombin time have been reported during concomitant use; a causal relationship has not been established.
Recommendation: Monitor prothrombin time or INR when starting, stopping, or changing terbinafine.
https://dailymed.nlm.nih.gov/dailymed/drugInfo.cfm?setid=584d1fae-0120-49a0-e063-6394a90a36fc
Adverse events
Common (≥1%)
Headache · Diarrhea or dyspepsia · Rash or itching · Taste disturbance · Nausea or abdominal pain · Liver enzyme abnormality
Rare but serious
Liver failure · Anaphylaxis or angioedema · Severe neutropenia or pancytopenia · Stevens-Johnson syndrome, toxic epidermal necrolysis, or DRESS
Pregnancy and lactation
Pregnancy data are insufficient. Oral terbinafine is present in human milk; weigh breastfeeding benefits, maternal need, and potential effects on the infant.
Recent literature (PubMed)
Dermatophytes represent the largest and most common group of fungal infections, impacting 25% of the global population. Among them, Trichophyton rubrum has emerged as the predominant species, responsible for a range of conditions such as tinea corporis, tinea pedis, onychomycosis, tinea cruris, and tinea manuum. Although dermatophyte incidence varies geographically, there is a noticeable rise in cases caused by T. indotineae, a strain that exhibits resistance to terbinafine. In the past decade zoophilic dermatophyte T. mentagophytes genotype VII (now known as T. interdigitale) gains a growing importance, due to its increasing frequency, the severity of the clinical manifestation and mode of transmission. Tinea infections present with various clinical symptoms and can affect individuals of all ages, from tinea pedis in adults to tinea capitis in children. Among adults globally, tinea unguium (onychomycosis) is the most common form of dermatophytosis, affecting 5.5% of the general population. Tinea unguium is more frequently seen in developed countries, while tinea capitis is more common in developing nations. The COVID-19 pandemic has led to an increase in cases of tinea faciei, likely due to prolonged mask-wearing. Terbinafine remains the preferred treatment for dermatophyte infections worldwide due to its potent fungicidal properties, minimal risk of drug interactions, and fewer side effects compared to other oral antifungals. Itraconazole and terbinafine appear to be equally effective and safe for treating tinea cruris and tinea corporis. However, the rising resistance of dermatophytes to these antifungal drugs, along with frequent recurrences of dermatophytosis in certain regions, is becoming a significant public health concern.
Tinea pedis is one of the most common superficial fungal infections of the skin, with various clinical manifestations. This review aims to familiarize physicians with the clinical features, diagnosis and management of tinea pedis. A search was conducted in April 2023 in PubMed Clinical Queries using the key terms 'tinea pedis' OR 'athlete's foot'. The search strategy included all clinical trials, observational studies and reviews published in English within the past 10 years. Tinea pedis is most often caused by Trichophyton rubrum and Trichophyton interdigitale. It is estimated that approximately 3% of the world population have tinea pedis. The prevalence is higher in adolescents and adults than in children. The peak age incidence is between 16 and 45 years of age. Tinea pedis is more common amongst males than females. Transmission amongst family members is the most common route, and transmission can also occur through indirect contact with contaminated belongings of the affected patient. Three main clinical forms of tinea pedis are recognized: interdigital, hyperkeratotic (moccasin-type) and vesiculobullous (inflammatory). The accuracy of clinical diagnosis of tinea pedis is low. A KOH wet-mount examination of skin scrapings of the active border of the lesion is recommended as a point-of-care testing. The diagnosis can be confirmed, if necessary, by fungal culture or culture-independent molecular tools of skin scrapings. Superficial or localized tinea pedis usually responds to topical antifungal therapy. Oral antifungal therapy should be reserved for severe disease, failed topical antifungal therapy, concomitant presence of onychomycosis or in immunocompromised patients. Topical antifungal therapy (once to twice daily for 1-6 weeks) is the mainstay of treatment for superficial or localized tinea pedis. Examples of topical antifungal agents include allylamines (e.g. terbinafine), azoles (e.g. ketoconazole), benzylamine, ciclopirox, tolnaftate and amorolfine. Oral an
Onychomycosis is a common chronic fungal infection of the nail that causes discoloration and/or thickening of the nail plate. Oral agents are generally preferred, except in the case of mild toenail infection limited to the distal nail plate. Terbinafine and itraconazole are the only approved oral therapies, and fluconazole is commonly utilized off-label. Cure rates with these therapies are limited, and resistance to terbinafine is starting to develop worldwide. In this review, we aim to review current oral treatment options for onychomycosis, as well as novel oral drugs that may have promising results in the treatment of onychomycosis.
Tinea versicolor is a common superficial fungal infection of the skin with various clinical manifestations. This review aims to familiarize physicians with the clinical features, diagnosis and management of tinea versicolor. A search was conducted in July 2022 in PubMed Clinical Queries using the key terms "tinea versicolor" OR "pityriasis versicolor". The search strategy included all clinical trials, observational studies and reviews published within the past 10 years. Tinea versicolor is caused by Malassezia species, notably M. globosa, M. furfur and M. sympodialis. The condition is characterized by scaly hypopigmented or hyperpigmented macules/patches, primarily located on the upper trunk, neck and upper arms. The diagnosis is usually based on characteristic clinical features. If necessary, a potassium hydroxide preparation test can be performed to reveal numerous short, stubby hyphae intermixed with clusters of spores. Most patients with tinea versicolor respond to topical antifungal therapy, which has a better safety profile (fewer adverse events, fewer drug interactions) and lower cost compared to systemic treatment and is therefore the treatment of choice. Oral antifungal therapy is typically reserved for patients with extensive disease, frequent recurrences or disease that is refractory to topical therapy. Advantages of oral antifungal therapy include increased patient compliance, shorter duration of treatment, increased convenience, less time involved with therapy and reduced recurrence rates. On the other hand, oral antifungal therapy is associated with higher cost, greater adverse events and potential drug-drug interactions and is therefore not the first-line treatment for tinea versicolor. Long-term intermittent prophylactic therapy should be considered for patients with frequent recurrence of the disease. Selection of antifungal agents depends on several factors, including efficacy, safety, local availability, ease of administration, likelihood of compl
Seborrheic dermatitis (SD) is a common chronic inflammatory skin disorder that mostly affects young adults in areas rich in sebaceous glands (scalp, face, and trunk). In adolescents and adults, SD clinical presentation may range from mild patches to diffuse scalp scaling. In infants, it mainly occurs on the scalp as yellowish, scaly patches ("cradle cap"). In adults, several environmental triggers are likely to promote SD development, along with fungal colonization by Malassezia spp., sebaceous gland activity, as well as immunosuppression, endocrine, neurogenic and iatrogenic factors. In children, early occurrence in the first trimester suggests the role of excessive sebaceous gland activity from maternal hormones, along with cutaneous microbiome alterations. The diagnosis of SD is usually clinical, and specific laboratory and/or instrumental investigations are seldom required. Treatment is aimed at modulating sebum production, reducing skin colonization by Malassezia spp., and controlling inflammation. In adults, mild-to-moderate scalp SD forms can be managed with topical antifungals (ketoconazole, ciclopirox, miconazole) or antiinflammatory (mild-to-moderate potency corticosteroids) or keratolytic/humectant (propylene glycol) agents. Recommended topical therapeutic options for mild-to-moderate facial or body areas SD include topical ketoconazole, ciclopirox, clotrimazole, mild-to-moderate potency corticosteroids, lithium succinate/gluconate, and topical calcineurin inihibitors (off-label use). In severe and/or resistant cases, the use of systemic antifungal drugs (terbinafine, itraconazole), as well as UVB phototherapy, may be considered. In children, scant scientific evidence supports the effectiveness and safety of topical drugs, and "cradle cap" is usually successfully managed with baby shampoos enriched with emollient agents and vegetable oils. Alternatively, similarly to adult scalp SD, medical device shampoos with antiinflammatory and antifungal properties,