Objective: To provide an update on the current understanding, evaluation, and management of penile warts.
Methods: A PubMed search was completed in Clinical Queries using the key terms 'penile warts' and 'genital warts'. The search strategy included meta-analyses, randomized controlled trials, clinical trials, observational studies, and reviews.
Results: Penile warts are caused by human papillomavirus (HPV), notably HPV-6 and HPV-11. Penile warts typically present as asymptomatic papules or plaques. Lesions may be filiform, exophytic, papillomatous, verrucous, hyperkeratotic, cerebriform, fungating, or cauliflower-like. Approximately one-third of penile warts regress without treatment and the average duration prior to resolution is approximately 9 months. Active treatment is preferable to watchful observation to speed up clearance of the lesions and to assuage fears of transmission and autoinoculation. Patient-administered therapies include podofilox (0.5%) solution or gel, imiquimod 3.75 or 5% cream, and sinecatechins (polypheron E) 15% ointment. Clinician-administered therapies include podophyllin, cryotherapy, bichloroacetic or trichloroacetic acid, oral cimetidine, surgical excision, electrocautery, and carbon dioxide laser therapy. Patients who do not respond to first-line treatments may respond to other therapies or a combination of treatment modalities. Second-line therapies include topical/intralesional/intravenous cidofovir, topical 5-fluorouracil, and topical ingenol mebutate.
Conclusion: No single treatment has been shown to be consistently superior to other treatment modalities. The choice of the treatment method should depend on the physician's comfort level with the various treatment options, the patient's preference and tolerability of treatment, and the number and severity of lesions. The comparative efficacy, ease of administration, adverse effects, cost, and availability of the treatment modality should also be taken into consideration.
Objective: This article aimed to provide a narrative updated review on the evaluation, diagnosis, and treatment of tinea corporis.
Methods: A PubMed search was performed with Clinical Queries using the key term 'tinea corporis.' The search strategy included clinical trials, meta-analyses, randomized controlled trials, observational studies, and reviews. The search was restricted to the English language. The information retrieved from the mentioned search was used in the compilation of the present article.
Results: Tinea corporis typically presents as a well-demarcated, sharply circumscribed, oval or circular, mildly erythematous, scaly patch or plaque with a raised leading edge. Mild pruritus is common. The diagnosis is often clinical but can be difficult with prior use of medications, such as calcineurin inhibitors or corticosteroids. Dermoscopy is a useful and non-invasive diagnostic tool. If necessary, the diagnosis can be confirmed by microscopic examination of potassium hydroxide wet-mount preparations of skin scrapings from the active border of the lesion. Fungal culture is the gold standard to diagnose dermatophytosis especially if the diagnosis is in doubt and results of other tests are inconclusive or the infection is widespread, severe, or resistant to treatment. The standard treatment of tinea corporis is with topical antifungals. Systemic antifungal treatment is indicated if the lesion is multiple, extensive, deep, recurrent, chronic, or unresponsive to topical antifungal treatment, or if the patient is immunodeficient.
Conclusion: The diagnosis of tinea corporis is usually clinical and should pose no problem to the physician provided the lesion is typical. However, many clinical variants of tinea corporis exist, rendering the diagnosis difficult especially with prior use of medications, such as calcineurin inhibitors or corticosteroids. As such, physicians must be familiar with this condition so that an accurate diagnosis can be made and appropriate treatment initiated.
METHODS: A search was conducted in July 2023 in PubMed Clinical Queries using the key term "guttate psoriasis". The search strategy included all observational studies, clinical trials and reviews published within the past 10 years. The information retrieved from the search was used in the compilation of the present article.
RESULTS: Guttate psoriasis typically presents with an abrupt onset of numerous, small, scattered, tear-drop-shaped, scaly, erythematous, pruritic papules and plaques. Sites of predilection include the trunk and proximal extremities. There may be a history of preceding streptococcal infection. Koebner phenomenon is characteristic. Guttate psoriasis may spontaneously remit within 3-4 months with no residual scarring, may intermittently recur and, in 40-50% of cases, may persist and progress to chronic plaque psoriasis. Given the possibility for spontaneous remission within several months, active treatment may not be necessary except for cosmetic purposes or because of pruritus. On the other hand, given the high rates of persistence of guttate psoriasis and progression to chronic plaque psoriasis, some authors suggest active treatment of this condition.
CONCLUSION: Various treatment options are available for guttate psoriasis. Triggering and exacerbating factors should be avoided if possible. Topical corticosteroids alone or in combination with other topical agents (e.g. tazarotene and vitamin D analogues) are the most rapid and efficient treatment for guttate psoriasis and are therefore the first-line treatment for mild cases. Other topical therapies include vitamin D analogues, calcineurin inhibitors, anthralin, coal tar and tazarotene. Ultraviolet phototherapy is the first-line therapy for moderate-to-severe guttate psoriasis, as it is more practical than topical therapy when treating widespread or numerous small lesions. Systemic immunosuppressive and immunomodulatory therapies (e.g. methotrexate, cyclosporine, retinoids, fumaric acid esters and biologics) may be considered for patients with moderate-to-severe guttate psoriasis who fail to respond to phototherapy and topical therapies.
METHODS AND RESULTS: Eleven anonymized case scenarios are described to illustrate issues associated with these fallacies. A literature review is performed and possible solutions to handle or dismiss these fallacies are discussed.
CONCLUSIONS: The first step in patient care is to accurately assess the patient and the family to evaluate possible concerns, anxiety, and phobias that could impede therapeutic efficacy. Education about the disease should be individualized. Conflicting recommendations on the usage of topical steroid have a detrimental effect on management outcomes, which must be avoided.
Methods: A PubMed search was performed with Clinical Queries using the key term "acne". The search strategy included clinical trials, meta-analyses, randomized controlled trials, observational studies and reviews. The search was restricted to articles published in English.
Results: Treatments of acne include proper skin care, topical medications, oral medications and procedural therapies. Topical agents are the first-line treatment for mild-to-moderate acne and can be used as combination therapy for more severe acne. Systemic therapies are usually prescribed for the initial treatment of moderate-to-severe acne as well as for acne that is refractory to topical therapies.
Conclusion: Topical retinoids are the drugs of choice for the treatment and maintenance therapy of patients with mild-to-moderate acne vulgaris. Depending on the severity of the acne, topical retinoids may be used alone or in combination with benzoyl peroxide and topical or oral antibiotics. Oral antibiotics are an important therapy for inflammatory acne unresponsive to topical therapy. Neither topical nor oral antibiotics should be used as monotherapy. Oral contraceptives and/or spironolactone are useful for many women with acne. Oral isotretinoin is the drug of choice for severe, extensive, nodular acne vulgaris but is also often used in moderate cases where scarring is evident, acne-related psychosocial distress is significant or other treatment modalities have failed.
METHODS: 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.
RESULTS: 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.
CONCLUSION: Selection of antifungal agents depends on several factors, including efficacy, safety, local availability, ease of administration, likelihood of compliance and potential drug interactions of the antifungal agent.
METHODS: 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.
RESULTS: 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.
CONCLUSION: 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 antifungal agents used for the treatment of tinea pedis include terbinafine, itraconazole and fluconazole. Combined therapy with topical and oral antifungals may increase the cure rate. The prognosis is good with appropriate antifungal treatment. Untreated, the lesions may persist and progress.