Oral Terbinafine Dosing and Treatment Duration
For onychomycosis, terbinafine 250 mg once daily for 12 weeks (toenails) or 6 weeks (fingernails) is the recommended treatment, as it achieves superior mycological cure rates compared to other oral antifungals. 1
FDA-Approved Indications and Dosing
The FDA-approved indication for oral terbinafine is specifically for onychomycosis (tinea unguium) of the toenail or fingernail due to dermatophytes 1:
- Toenail onychomycosis: 250 mg once daily for 12 weeks 1
- Fingernail onychomycosis: 250 mg once daily for 6 weeks 1
Dosing for Other Dermatophyte Infections
While not FDA-approved for these indications in the U.S., terbinafine is highly effective for other superficial fungal infections:
Tinea Capitis (Scalp Ringworm)
Terbinafine is particularly effective against Trichophyton species and requires shorter treatment courses than griseofulvin 2:
- < 20 kg body weight: 62.5 mg daily for 2-4 weeks 2
- 20-40 kg body weight: 125 mg daily for 2-4 weeks 2
- > 40 kg body weight: 250 mg daily for 2-4 weeks 2
Important caveat: Terbinafine is more efficacious against Trichophyton species but less effective against Microsporum species, where griseofulvin remains superior 2. Treatment selection should be guided by the causative organism or local epidemiology 2.
Tinea Pedis (Athlete's Foot)
For dermatophyte foot infections, oral terbinafine 250 mg daily for 1-2 weeks achieves mycological cure rates of 80-90% 3. This represents a significantly shorter treatment duration compared to other systemic antifungals 4.
Clinical Efficacy Evidence
The superiority of terbinafine in onychomycosis is well-established. The landmark L.I.ON. study demonstrated that at 72 weeks follow-up, terbinafine achieved mycological cure rates of 76-81% compared to only 38-49% with intermittent itraconazole 5. Complete cure rates were approximately twice as high with terbinafine 5.
The 5-year L.I.ON. Icelandic Extension study further confirmed terbinafine's durability, showing superior complete cure rates (35% vs 14%), mycological cure rates (46% vs 13%), and lower relapse rates (23% vs 53%) compared to itraconazole 5.
Safety Monitoring Requirements
Critical safety considerations that require attention before and during treatment 1:
- Hepatotoxicity: Obtain pretreatment serum transaminases; discontinue if liver injury develops 1
- Baseline monitoring recommended for: Heavy alcohol consumption, pre-existing liver disease, or history of hepatitis 3
- Taste disturbance: Can be severe, prolonged, or permanent; discontinue if it occurs 1
- Smell disturbance: May be prolonged or permanent; discontinue if it occurs 1
- Severe neutropenia: Discontinue if neutrophil count ≤ 1,000 cells/mm³ 1
- Depressive symptoms: Monitor for development during treatment 1
- Severe skin reactions: Stevens-Johnson syndrome, toxic epidermal necrolysis, DRESS syndrome have been reported; discontinue if signs occur 1
Common Adverse Effects
The most frequently reported adverse events (>2% incidence) include headache, diarrhea, rash, dyspepsia, liver enzyme abnormalities, pruritus, taste disturbance, nausea, abdominal pain, and flatulence 1. Gastrointestinal complaints represent 49% of reported side effects, with dermatological reactions accounting for 23% 3.
Drug Interactions
Terbinafine is a CYP2D6 inhibitor and affects metabolism of desipramine, cimetidine, fluconazole, cyclosporine, rifampin, and caffeine 1. However, compared to azole antifungals, terbinafine has a relatively low potential for clinically significant drug interactions 5, 4.
Treatment Failure Management
If treatment fails, consider 2:
- Non-compliance or suboptimal drug absorption
- Relative insensitivity of the organism
- Reinfection
If clinical improvement occurs but mycology remains positive, continue therapy for an additional 2-4 weeks 2. If no initial clinical improvement, switch to second-line therapy (itraconazole for mixed infections, or alternative agents for refractory cases) 2.
Mechanism of Action Advantage
Terbinafine's fungicidal mechanism (inhibition of squalene epoxidase leading to ergosterol depletion and toxic squalene accumulation) provides a key advantage over fungistatic agents 5, 6. This explains why mycological cure rates continue to improve after treatment cessation due to residual drug effect in tissues 4.