Tinea Kruris Bahan
Tinea Kruris Bahan
Tinea Kruris Bahan
Tinea cruris, a pruritic superficial fungal infection of the groin and adjacent
skin, is the second most common clinical presentation for dermatophytosis.
Tinea cruris is a common and important clinical problem that may, at times,
be a diagnostic and therapeutic challenge.
Other Medscape articles on tinea infections include Tinea Barbae, Tinea
Capitis, Tinea Corporis, Tinea Faciei, Tinea Nigra, Tinea Pedis, and Tinea
Versicolor.
Pathophysiology
Epidemiology
Frequency
United States
Dermatophytosis accounts for approximately 10-20% of all visits to
dermatologists.[1]
International
Tinea cruris has a worldwide distribution but is found more commonly in hot
humid climates. [2, 3]
Sex
Tinea cruris is 3 times more common in men than in women.
Age
Adults are affected by tinea cruris much more commonly than are children.
However, the prevalence of several risk factors for tinea cruris, such as
obesity and diabetes mellitus, is rapidly increasing among adolescents. [4]
Prognosis
The prognosis of tinea cruris is excellent with appropriate diagnosis and
treatment; however, recurrence is likely if the groin region is not kept dry.
No mortality is associated with tinea cruris. Associated pruritus leads to
morbidity resulting from lichenification, secondary bacterial infection, and
irritant and allergic contact dermatitis caused by topically applied
medications.
Patient Education
Educate patients about the risks of sharing sheets and undergarments with
others and about the need to keep the groin region dry (see
Deterrence/Prevention).
For patient education resources, visit the Skin Conditions and Beauty
Center. Also, see the patient education article Ringworm on Body.
History
Patients with tinea cruris report pruritus and rash in the groin. A history of
previous episodes of a similar problem usually is elicited. Additional
historical information in patients with tinea cruris may include recently
visiting a tropical climate, wearing tight-fitting clothes (including bathing
suits) for extended periods, sharing clothing with others, participating in
sports, or coexisting diabetes mellitus or obesity. Prison inmates, members
of the armed forces, members of athletic teams, and people who wear tight
clothing may be subject to independent or additional risk for
dermatophytosis.
Physical Examination
Tinea cruris manifests as a symmetric erythematous rash in the groin, as
shown in the images below.
Tinea cruris.
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Tinea cruris.
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Tinea cruris.
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Large patches of erythema with central clearing are centered on the
inguinal creases and extend distally down the medial aspects of the thighs
and proximally to the lower abdomen and pubic area.
Scale is demarcated sharply at the periphery.
In acute tinea cruris infections, the rash may be moist and exudative.
Chronic infections typically are dry with a papular annular or arciform
border and barely perceptible scale at the margin.
Central areas typically are hyperpigmented and contain a scattering of
erythematous papules and a little scale.
The penis and scrotum typically are spared in tinea cruris; however, the
infection may extend to the perineum and buttocks.
Secondary changes of excoriation, lichenification, and impetiginization may
be present as a result of pruritus.
Chronic infections modified by the application of topical corticosteroids are
more erythematous, less scaly, and may have follicular pustules.
Approximately one half of patients with tinea cruris have coexisting tinea
pedis.
Erythematous-scale plaques and erythematous-liquenificated plaques were
the most frequently found clinical types in an excellent Brazilian study. [6] T
rubrum was the prevalent dermatophyte in 90% of the cases, followed by T
tonsurans (6%) and T mentagrophytes (4%).
Causes
The dermatophyte T rubrum is the most common etiologic agent for tinea
cruris. [5]In a Brazilian series, T rubrum was the prevalent dermatophyte in
90% of the tinea cruris cases, followed by T tonsurans (6%) and T
mentagrophytes (4%). [6] Other organisms, including E floccosum and T
verrucosum, cause an identical clinical condition. T rubrum and E
floccosum infections are more apt to become chronic and noninflammatory,
while infection by T mentagrophytes often is associated with an acute
inflammatory clinical presentation.
Complications
Tinea cruris can become infected secondarily by candidal or bacterial
organisms. In addition, the area can become lichenified and
hyperpigmented in the setting of a chronic fungal infection. Mistreatment of
tinea cruris with topical steroids can result in exacerbation of the disease.
Although patients may note initial relief of symptoms, the infection may
spread.
Onychomycosis
250 mg (1 tablet) PO daily for 6 weeks (fingernail) or 12 weeks (toenail)
Tinea Pedis (Off-label)
250 mg/day PO in single dose or divided q12hr for 2-6 weeks
Tinea Corporis, Tinea Cruris
250 mg/day PO in single dose or divided q12hr for 2-4 weeks
Sporotrichosis, Lymphocutaneous and cutaneous (Off-label)
500 mg/day PO q12hr for 2-6 weeks; treat for additional 2-4 weeks after
resolution of all lesions (resolution may take 3-6 months)
Dosing Modifications
Renal impairment: Use not recommended if CrCl <50 mL/min
Hepatic impairment: Use contraindicated in chronic or active liver disease
Butenafine (Mentax)
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Butenafine is a potent antifungal related to the allylamines. It damages
fungal cell membranes, causing fungal cell growth to arrest. It is available
in 1% cream only.
Clotrimazole topical (Lotrimin, Mycelex)
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Clotrimazole topical is often the first-line drug used in the treatment of tinea
cruris. It is a broad-spectrum antifungal agent that inhibits yeast growth by
altering cell membrane permeability, causing the death of fungal cells.
Reevaluate the diagnosis if no clinical improvement after is seen after 4
weeks. It is available without a prescription in 1% cream, solution/spray,
and lotion.
Miconazole (Micatin, Monistat-Derm)
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Miconazole damages the fungal cell wall membrane by inhibiting the
biosynthesis of ergosterol. Membrane permeability is increased, causing
nutrients to leak, resulting in fungal cell death. It is available without a
prescription, and 2% cream, solution/spray, lotion, and powder forms are
available. Lotion is preferred in intertriginous areas. If cream is used, apply
sparingly to avoid maceration effects.
Ketoconazole topical (Nizoral)
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Ketoconazole topical comes as 2% cream. It is an imidazole broad-
spectrum antifungal agent; it inhibits the synthesis of ergosterol, causing
cellular components to leak, resulting in fungal cell death.
Econazole topical (Ecoza)
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Econazole is effective in cutaneous infections. It interferes with RNA and
protein synthesis and metabolism. It disrupts fungal cell wall permeability,
causing fungal cell death.
Luliconazole (Luzu)
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Luliconazole is available as a 1% topical cream administered once daily for
1 week. It is an imidazole antifungal that alters the fungal cell membrane by
interacting with 14-alpha demethylase (an enzyme necessary for
conversion of lanosterol to ergosterol). It is indicated for tinea corporis.
Naftifine (Naftin)
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Naftifine is a broad-spectrum antifungal agent and synthetic allylamine
derivative; it may decrease the synthesis of ergosterol, which, in turn,
inhibits fungal cell growth. It is available in 1% cream or solution. If no
clinical improvement is seen after 4 weeks, reevaluate the patient.
Oxiconazole (Oxistat)
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Oxiconazole is a broad-spectrum antifungal agent. It inhibits the synthesis
of ergosterol, causing cellular components to leak, resulting in fungal cell
death. It is available in 1% cream or lotion.
Tolnaftate (Tinactin)
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Tolnaftate is a nonprescription medication used in the treatment of tinea
cruris. It is available in 1% cream, solution/spray, and powder.
Ciclopirox (Loprox)
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Ciclopirox is a synthetic broad-spectrum antifungal agent. It interferes with
the synthesis of DNA, RNA, and protein by inhibiting the transport of
essential elements in fungal cells. It is available by prescription only in 1%
cream and lotion.
Itraconazole (Sporanox)
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Itraconazole has fungistatic activity. It is a synthetic triazole antifungal
agent that slows fungal cell growth by inhibiting cytochrome P450–
dependent synthesis of ergosterol, a vital component of fungal cell
membranes. It is a widely used and well-studied oral antifungal that can be
used in the treatment of tinea cruris. Studies have shown that it is tolerated
better than griseofulvin. Best results are noted 2-3 weeks after the end of
treatment.
Sulconazole (Exelderm)
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Sulconazole is a broad-spectrum antifungal agent. It inhibits the synthesis
of ergosterol, causing cellular components to leak, resulting in fungal cell
death. It is available as 1% cream or solution.
Griseofulvin (Fulvicin-U/F, Grifulvin-V)
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Griseofulvin has fungistatic activity. Fungal cell division is impaired by
interfering with microtubules. It binds to keratin precursor cells. Keratin
gradually is replaced by noninfected tissue, which is highly resistant to
fungal invasions. It is less effective than itraconazole in the treatment of
tinea cruris.
For isolated plaques on the glabrous skin, topical allylamines, imidazoles, tolnaftate, butenafine, or
ciclopirox are effective. Most are applied twice daily for 2–4 weeks. Oral antifungal agents are
reserved for widespread or more inflammatory eruptions. Comparative studies in adults show that
terbinafine 250 mg daily for 2–4 weeks, itraconazole 200 mg daily for 1 week, and fluconazole 150–
300 mg weekly for 4–6 weeks are preferable over griseofulvin 500 mg dailyuntil cure is reached.73
Safe and effective regimens for children include terbinafine 3–6 mg/kg/day for 2 weeks, itraconazole
5 mg/kg/day for 1 week, and ultramicrosize griseofulvin 10–20 mg/ kg/day for up to 2–4 weeks.