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Drugs Context. 2020; 9: 2020-5-vi.
Tinea corporis: an updated review
Alexander KC Leung, MBBS, FRCPC, FRCP (Britain and Irel), FRCPCH, FAAP, 
1 Joseph M Lam, Doc, FRCPC,2 Kin Fon Leong, MBBS, MRCPCH,three and Kam Lun Hon, Medico, FAAP, FCCM4, v
Alexander KC Leung
oneDepartment of Pediatrics, The University of Calgary, Alberta Children's Infirmary, Calgary, Alberta, Canada
Joseph M Lam
2Department of Pediatrics and Department of Dermatology and Skin Sciences, University of British Columbia, Vancouver, British Columbia, Canada
Kin Fon Leong
3Pediatric Found, Kuala Lumpur Full general Hospital, Kuala Lumpur, Malaysia
Kam Lun Hon
4Section of Paediatrics, The Chinese University of Hong Kong, Shatin, Hong Kong
vDepartment of Paediatrics and Adolescent Medicine, The Hong Kong Children's Infirmary, Hong Kong
Received 2020 May xiii; Revised 2020 Jun 18; Accepted 2020 Jun 25.
Abstruse
Background
Tinea corporis is a common fungal infection that mimics many other annular lesions. Physicians must familiarize themselves with this status and its treatment.
Objective
This commodity 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 central 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 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 border. Mild pruritus is common. The diagnosis is ofttimes clinical only tin can be difficult with prior apply of medications, such every bit calcineurin inhibitors or corticosteroids. Dermoscopy is a useful and not-invasive diagnostic tool. If necessary, the diagnosis can be confirmed past microscopic examination of potassium hydroxide wet-mount preparations of skin scrapings from the active border of the lesion. Fungal civilisation is the gilt standard to diagnose dermatophytosis peculiarly if the diagnosis is in uncertainty 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.
Determination
The diagnosis of tinea corporis is usually clinical and should pose no trouble to the physician provided the lesion is typical. However, many clinical variants of tinea corporis exist, rendering the diagnosis hard especially with prior use of medications, such every bit calcineurin inhibitors or corticosteroids. As such, physicians must be familiar with this condition so that an accurate diagnosis can exist made and advisable treatment initiated.
Keywords: butenafine, dermatophytosis, fluconazole, itraconazole, naftifine, ringworm, terbinafine
Introduction
Tinea corporis, also known as 'ringworm,' is a superficial dermatophyte infection of the skin, other than on the hands (tinea manuum), feet (tinea pedis), scalp (tinea capitis), bearded areas (tinea barbae), face (tinea faciei), groin (tinea cruris), and nails (onychomycosis or tinea unguium).i Tinea corporis is virtually unremarkably caused past dermatophytes belonging to one of the three genera, namely, Trichophyton (which causes infections on pare, pilus, and nails), Microsporum (which causes infections on skin and hair), and Epidermophyton (which causes infections on skin and nails).1–three Dermatophytes are grouped as either anthropophilic, zoophilic, or geophilic, depending on whether their main source is human, animal, or soil, respectively.4,v Because tinea corporis is mutual and many other annular lesions can mimic this fungal infection, physicians must familiarize themselves with its etiology and its handling.
The purpose of this article was to provide a narrative updated review on the evaluation, diagnosis, and handling of tinea corporis. 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 to a higher place search was used in the compilation of the present article.
Etiology
Tinea corporis is almost often caused past Trichophyton rubrum, T. tonsurans, and Microsporum canis.6–12 T. rubrum is past far the almost common cause of dermatophytosis worldwide and is the near common crusade of tinea corporis in Due north America.thirteen–fifteen Tinea corporis secondary to tinea capitis is often caused by T. tonsurans.sixteen On the other hand, tinea corporis resulting from close contact with dogs or cats is often caused by M. canis.8,17–19 Other causative organisms include T. interdigitale (previously known as T. mentagrophytes), T. verrucosum, T. violaceum, T. concentricum, Epidermophyton floccosum, G. audouinii, and M. gypseum.six,20–29 In recent years, T. interdigitale has replaced T. rubrum as the most mutual crusade of tinea corporis in Southeast Asia. Rare causative organisms include T. erinaceid, T. equinum, T. simii, T. schoenleinii, Nannizzia gypsea, N. nana, and Thousand. gallinae and M. fulvum.30–40
Epidemiology
Tinea corporis is the most common dermatophytosis.41 While tinea corporis occurs worldwide, information technology is well-nigh commonly observed in tropical regions.42 The lifetime risk of acquiring tinea corporis is estimated to be 10–xx%.6 Tinea corporis occurs nearly frequently in post-pubertal children and young adults.18,43,44 Rare cases have been reported in the newborn menstruum.45 At that place is no sex predominance.one Humans may go infected through close contact with an infected individual, an infected beast (in particular, domestic dog or cat), contaminated fomites, or contaminated soil.46–48 Infection may exist acquired as a consequence of spread from another site of dermatophyte infection (e.g. tinea capitis, tinea pedis, onychomycosis).49,50 Transmission among household family members is by far the most mutual route; children often become infected past spores shed by an infected household family member.fifteen,48,51 Autoinfection by dermatophytes elsewhere in the torso may besides occur.52 Transmission of the fungus is facilitated past a moist, warm environment, sharing of towels and vesture, and wearing of occlusive clothing.one,52 Predisposing factors include personal history of dermatophytosis (e.g. tinea capitis, tinea pedis, tinea cruris, and tinea unguium), concurrent affected family members, pets in the abode, crowding in dwelling house, recreational exposure (eastward.g. wrestling and marital arts), hyperhidrosis, depression β-defensin four levels, immunodeficiency, diabetes mellitus, genetic predisposition (in particular, tinea imbricata), xerosis, and ichthyosis.2,eighteen,48,53–55
Pathogenesis
Mannans in the cell walls of some dermatophytes, such equally T. rubrum, have immune-inhibitory properties.2 This allows the mucus to stay on the skin without being sloughed off prior to invasion of the skin. The causative fungus can produce proteases (enzymes that digest keratin), serine-subtilisins (enzymes that digest poly peptide past initiating the nucleophilic attack on the peptide bail through a serine residue at the active site), and keratinases (enzymes that penetrate keratinized tissue), which allow the fungus to invade the horny layer of the skin and spread outward.three,56 Infection is unremarkably cutaneous and confined to the outer, non-living, cornified layers of the skin. The fungus is unable to penetrate the deeper tissues in healthy immunocompetent hosts because of host defense mechanisms, such as activation of serum inhibitory factor, polymorphonuclear leukocytes, and complements.3 Scaling of the active border results from increased epidermal prison cell proliferation in response to the fungal infection.56
Clinical manifestations
The incubation period is 1–iii weeks.57 Tinea corporis typically presents as a well-demarcated, sharply circumscribed, oval or round, mildly erythematous, scaly patch or plaque with a raised leading edge (Figure 1).44,52,57 The lesion starts off as a flat scaly spot that spreads centrifugally and clears centrally to class a feature annular lesion giving ascent to the term 'ringworm.'52,58,59 The fundamental area becomes hypopigmented or chocolate-brown and less scaly as the agile border progresses outward.4,58 The border is usually annular and irregular.58 Occasionally, the border can exist papular, vesicular, or pustular.iv,15 Lesions may assume other shapes such as circinate and arcuate. Mild pruritus is common.52,60 In full general, lesions caused by anthropophilic species (due east.g. T. rubrum, T. tonsurans, T. interdigitale, T. schoenleinii, T. soundanense, T. violaceum, M. audouinii, and E. floccosum) are ofttimes less inflammatory/erythematous than those caused past zoophilic species (e.grand. M. canis, M. nanum, Thou. ferrugineum, K. distortum, M. nanum, T. equinum, and T. verrucosum) or geophilic species (e.one thousand. M. gypseum).44 The lesions tend to be asymmetrically distributed. When multiple lesions are present, they may coalesce into polycyclic patterns.15 In adults, tinea corporis most commonly occurs on exposed skin. In children and adolescents, the site of predilection is the trunk.61
An annular, erythematous, scaly plaque with a raised leading edge on the left arm characteristic of tinea corporis.
In tinea gladiatorum, the lesion presents also-demarcated, erythematous, annular, scaling plaques on areas of skin-to-skin contact, such as the caput, neck, and arms.half-dozen Tinea gladiatorum is most oftentimes caused by T. tonsurans.62–66 The condition is most common among those who engage in contact sports such as wrestling and judo.62–66 In a 2020 systematic review and meta-analysis of thirteen studies involving 4818 wrestlers, the prevalence of tinea gladiatorum varied from 2.4 to 96.62%, with an overall prevalence of 34.29% (95% conviction interval: 20.33–48.25).67
Tinea incognito refers to a cutaneous fungal infection that has lost its classical morphological features because of the utilise of calcineurin inhibitors or corticosteroids.68,69 The clinical manifestations of tinea incognito are highly variable. Mostly, compared with the lesion of tinea corporis, the lesion seen in tinea incognito is less erythematous and scaly, with a less defined edge and is typically more widespread (Figure 2).24 Pruritus is commonly balmy or absent.69 The rash tin be eczema-like, rosacea-like, or discoid lupus erythematosus-like, specially on the face, and eczema-like or impetigo-similar on the trunk and limbs.69
Tinea incognito resulting from topical corticosteroid handling of tinea corporis on the medial aspect of the right thigh.
Many clinical variants of tinea corporis exist. Tinea imbricata, caused mainly by a strictly anthropophilic dermatophyte, T. concentricum, typically presents as multiple, scaly, annular, concentric, erythematous rings that can extend to form polycyclic plaques (Figure three).53,60,lxx With time, multiple overlapping lesions develop and the plaques become lamellar with abundant thick scales adhering to the interior of the plaque, giving ascent to the appearance of overlapping roof tiles or lace, fish scales.53,lxx The torso is the site of predilection. Tinea imbricata has a high tendency to generalize and big areas of the body may exist afflicted. Pruritus is common. Tinea imbricata is endemic in Fundamental and Southward America, Southwest Pacific, and Southeast Asia.53
Tinea imbricata. Note the generalized, concentric, annular, lamellar, scaly plaques on the anterior trunk and upper limbs. The undulating lines were composed of overlapping scales.
Majocchi granuloma, also known as nodular granulomatous perifolliculitis, results from penetration of the fungus along the hair follicle to the dermal or subcutaneous tissue, leading to a suppurative folliculitis.71 The condition may exist precipitated past apoplexy of hair follicles or trauma to the pare.24 Majocchi granuloma is most commonly seen in immunocompromised individuals or those treated with topical corticosteroids.72 T. rubum is the virtually common causative organism, followed by T. interdigitale, T. violaceum, and T. tonsurans.72,73 Majocchi granuloma typically presents every bit inflammatory perifollicular papules or pustules, mainly on the face or limbs (Figure 4).24,73,74 Nodular lesion and subcutaneous abscess are more unremarkably seen in immunocompromised individuals.24 The trichophytin skin test is usually positive.74
Erythematous papules located on the glabella in a 5-year-erstwhile girl with a Majocchi granuloma.
Bullous tinea corporis, a rare clinical variant of tinea corporis, is characterized by vesicles or bullae, usually express to the borders of an erythematous scaly plaque.75–77 Rupture of the vesicles or bullae may get out backside erosions and crusts over an erythematous groundwork.
In immunocompromised individuals, tinea corporis may present equally a disseminated pare infection or subcutaneous/deep abscess.78 Rarely, tinea corporis may present as purpuric macules, known as tinea corporis purpurica.79
Diagnosis
The diagnosis of tinea corporis is most often clinical, especially if the lesion is typical.half dozen A well-demarcated, sharply circumscribed, erythematous, annular, scaly plaque with a raised leading border, and scaling and primal clearing on the body is feature. At times, the diagnosis can exist difficult due to the prior utilise of medications, such as calcineurin inhibitors or corticosteroids. Dermoscopy is a useful and non-invasive diagnostic tool. Dermoscopic findings in cases of tinea corporis include lengthened erythema, dotted vessels with peripheral to patchy distribution, white scales with peripheral distribution, 'moth-eaten' scale, peeling in an outward direction, brown spots surrounded past a white-yellow halo, follicular micropustules, wavy hair, and broken hair.80,81 These changes may be seen despite the use of topical corticosteroids or calcineurin inhibitors.82 Reflectance confocal microscopy is another useful diagnostic tool.2,83 With reflectance confocal microscopy, branching fungal hyphae tin can be detected over an erythematous annular scaly patch in individuals with tinea corporis.2,83 Wood lamp examination of the affected expanse is not useful as the lesion of tinea corporis usually does not fluoresce with a Woods lamp.
If necessary, the diagnosis tin can exist confirmed by microscopic exam of potassium hydroxide (KOH) moisture-mountain preparations of skin scrapings from the active border of the lesion.46 The skin scrapings should be transported in a presterilized blackness chart paper and then as to go along the specimen dry out and foreclose overgrowth of bacteria that may exist contaminants.2 To perform the test, a drib of 10–20% KOH is added to the scrapings on a microscopic slide.1 The specimen is gently heated to accelerate the destruction of the squamous cells.1,59 The KOH dissolves the epithelial tissue, leaving behind easily visualized septate hyphae with or without arthroconidiospores (Figure 5).ane,59 The addition of dimethyl sulfoxide to KOH may permit more rapid examination without heating.
Microscopic test of skin scrapings in ten% KOH showed a big amount of branching fungal hyphae.
Fungal civilization 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 unresponsive to treatment.46,56 Fungal culture can assist to differentiate fungal species.84 However, fungal culture is expensive and it commonly takes vii–xiv days for results.2,15 For certain species, it may accept upwards to four weeks for results.16 The most common civilisation medium is Sabouraud peptone–glucose agar (4% peptone, one% glucose).59 However, Sabouraud peptone–glucose agar does not contain antibiotics and thus may let overgrowth of bacterial contaminants. On the other hand, mycosel agar and dermatophyte exam medium both incorporate antibiotics. The antibiotics help to suppress the growth of bacterial species, which may contaminate the civilisation. If the results of the investigations are inconclusive, a polymerase concatenation reaction (PCR) assay for fungal Deoxyribonucleic acid or a PCR-restriction fragment length polymorphism method based on a ribosomal DNA internal transcribed spacer may be considered for fungal identification in bookish settings for research purposes.85–89
Differential diagnosis
Diseases that present with annular lesions may mimic tinea corporis. The differential diagnosis is wide and includes pityriasis rosea (non-itchy herald patch, generalized, bilateral, symmetrical eruption 4–14 days later, characteristic 'Christmas tree' advent on the back and a V-shaped pattern on the upper breast); tinea versicolor (multiple, well-demarcated, finely scaly, brownish macules/patches in blanched individuals and hypopigmented macules/patches in night-skinned individuals, minimal or absent erythema, absent-minded collarette of scales in private lesions, typically asymptomatic); nummular eczema (well-demarcated, pruritic, money-shaped, symmetrical, eczematous, scaly lesions, involvement of the extremities rather than the trunk, serous exudate in astute lesions, no key immigration, rapid response to topical steroids); plaque psoriasis (well-demarcated, sharply circumscribed, annular, erythematous, circular or oval, pruritic plaques with loosely adherent silvery-white micaceous scales, positive Auspitz sign, Koebner phenomenon, smash pitting, arthritis, uveitis, geographic natural language, positive family unit history); atopic dermatitis (flexural involvement in older children and adolescents, highly pruritic, excoriations, lichenification in chronic lesions, chronically relapsing); contact dermatitis (well-demarcated, erythematous lesion localized to the area of contact, immediate pare reaction with called-for, stinging, or discomfort if caused by an irritant, delayed response associated with pruritus caused by an allergen); seborrheic dermatitis (salmon-colored or erythematous, sharply demarcated patches with yellow-white, greasy scales); localized granuloma annulare (asymptomatic, firm, erythematous, violaceous, flesh-colored or brown, non-scaly plaques with central involution, annular configuration, commonly involve the extensor surfaces of distal extremities); fixed drug eruption (history of medication use, well-demarcated, round-to-oval, erythematous or violaceous macules/plaques, absent-minded systemic symptoms, sites of predilection include easily, feet, lips and perianal surface area, usually subsides within 14 days after the offending medication has been discontinued, recurs in the same location with repeat exposure to the medication); subacute cutaneous lupus erythematosus (annular, erythematous, scaly plaques often in sunday-exposed areas); discoid lupus erythematosus (well-demarcated, erythematous, hyperkeratotic, indurated, money-shaped plaques covered past partially adherent, scales in dominicus-exposed areas); urticaria (pruritic, erythematous, and edematous wheals of the superficial layers of the peel, private lesions wax and wane rapidly); urticaria pigmentosa (pruritic, yellow-tan to reddish-brown macules/papules on the trunk and proximal extremities, positive Darier sign); pityriasis lichenoides chronica (polymorphic pink to reddish brownish papular rash with overlying mica-like scales, chronic relapsing course without herald patch, residual hypo- or hyperpigmentation); lichen planus (characterized by 6 Ps: planar (flat-topped), purple (violaceous), polygonal, pruritic, papules/plaques, lesions may be covered with white, lacy, reticular lines [Wickham striae]); erythema migrans (apartment, erythematous, rapidly expanding [days], asymptomatic, annular lesion at the site of a tick bite, central immigration as the lesion expands, 'bull's eye' advent); erythema multiforme (acrally distributed, singled-out targetoid lesions with cardinal erythema); erythema dyschromicum perstans (slowly progressive, symmetrical, ashy gray-colored macules/patches, truncal distribution, slightly raised, erythematous border in the early phase); erythema marginatum (migratory, rapid expanding [hours], evanescent, not-pruritic, arciform/polycyclic/annular, erythematous plaque, lesion extends centrifugally with central immigration, border is irregular, serpiginous, and sharp on the outer edge just diffuse on the inner edge, a major manifestation of acute rheumatic fever); superficial erythema annulare centrifugum (annular or arcuate, erythematous patch/plaque that enlarge centrifugally with key clearing, 'trailing scale' forth the inner portion of the advancing edge, associated with drugs, systemic infection, malignancies, and autoimmune disease); impetigo contagiosum (characteristic xanthous-brown or love-colored 'stuck-on' crust over the superficial erosion, satellite lesions in the vicinity, near mutual on the face); erythema gyratum repens (paraneoplastic eruption, erythematous concentric rings with trailing scale at their edges, characteristic 'forest grain' appearance); and secondary syphilis (asymptomatic, lengthened, symmetrical, round-to-oval, pink-to-cherry-red-brown monomorphous macules or patches on the trunk and extremities including the palms and soles, absence of herald patch, 'moth-eaten' alopecia, lymphadenopathy, history of crabs exposure, and/or chancre).15,49,52,54,56,lx,90–96
Complications
Tinea corporis is contagious and therefore may have significant psychological, social, and occupational health furnishings.84 Secondary bacterial superinfection may occur equally a event of scratching and chafe of the peel. Post-inflammatory hypopigmentation and hyperpigmentation may occur.59 Dermatophytid (id) reaction, likewise known as id reaction, auto-eczematization, or disseminated eczema is a secondary dermatitic eruption that may occur in clan with a fungal infection especially simply after kickoff of systemic antifungal treatment.5 Affected patients frequently develop widespread, intensely pruritic, erythematous, scaly papules, maculopapules, papulovesicles, or pustules. Presumably, the dermatitic eruption is an immunologic reaction to the fungal antigen like a delayed-type (type Four) hypersensitivity response.24 Rarely, psoriatic flares precipitated by tinea corporis take been described.97
Treatment
Non-pharmacologic measures
Equally fungi thrive best in moist and warm environments, patients should be advised to vesture light and loose-fitting article of clothing.59 The skin should be kept make clean and dry.
Pharmacotherapy
The standard handling of tinea corporis is with topical antifungals and there is show of the superiority of topical antifungals over the apply of placebo.84,98 Localized or superficial tinea corporis commonly responds to topical antifungal therapy applied to the lesion and at least 2 cm across the lesion in one case or twice daily for 2–4 weeks.24 Usually used topical antifungal agents include azoles (e.m. econazole, ketoconazole, miconazole, clotrimazole, miconazole, oxiconazole, sulconazole, sertaconazole, eberconazole, and luliconazole), allylamines (e.g. naftifine, terbinafine), benzylamine (butenafine), ciclopirox, and tolnaftate.xviii,24,99–110 In this regard, nystatin, which is an effective handling for Candida infections, is not constructive for tinea corporis.24 In a 2013 meta-analysis of 65 trials (trials with a mutual comparator and caput-to-head trials) involving 14 topical antifungals, there was no significant difference among the antifungals regarding the outcome of mycologic cure at the finish of the treatment.111 Pairwise comparing of topical antifungals showed that butenafine, naftifine, and terbinafine were significantly more efficacious in sustaining the cured effect.111 A 2014 Cochrane review suggests that individual treatments with terbinafine and naftifine are constructive and take few mild agin events.112 Topical antifungal agents are generally well tolerated. Side effects are uncommon, except for rare instances of contact dermatitis. Mutual causes of treatment failure include poor compliance, drug resistance, reinfection from close contact and auto-inoculation, and misdiagnosis.113 Some authors suggest the improver of a topical corticosteroid to the topical antifungal agent, especially in individuals with inflammatory dermatomycosis.114,115
Systemic antifungal handling is indicated if the lesion is all-encompassing, deep (e.yard. Majocchi granuloma), recurrent, chronic, or unresponsive to topical antifungal handling; if the patient is immunodeficient; or if at that place are multiple site lesions.24,52,84 Randomized control trials support the efficacy of systemic treatment with oral antifungal agents.116,117 Oral antifungal agents used for the treatment of tinea corporis include itraconazole (children: 3–5 mg/kg/solar day [maximum 200 mg/day]; adults: 200 mg/mean solar day), fluconazole (children: half-dozen mg/kg one time weekly [maximum: 200 mg once weekly]; adults: 200 mg in one case weekly), terbinafine granules (children: <25 kg, 125 mg/solar day; 25–35 kg, 187.5 mg/twenty-four hours; >35 kg, 250 mg/24-hour interval), and terbinafine tablets (children: 10–20 kg, 62.five mg/day; 21–forty kg, 125 mg/day; >40 mg, 250 mg/day; adults: 250 mg/day).2,24,56,118 The duration of handling varies, depending on the response. The usual duration of treatment is 2–4 weeks only may take longer for recalcitrant cases.84 Oral ketoconazole should exist avoided because of the risk of hepatotoxicity, adrenal insufficiency, and drug interactions.24 Oral griseofulvin (not available in many countries, including Canada) is less effective, has more than agin events, and requires longer duration of therapy.v,50 As such, oral griseofulvin is not the medication of choice in the treatment of tinea corporis. Combined therapy with oral and topical antifungal agents may increase the cure charge per unit.119
In contempo years, the incidence of tinea corporis refractory to terbinafine handling has been on the rise.116,120–124 Terbinafine acts past inhibiting the enzyme squalene epoxidase, which is responsible for synthesis of ergosterol – an essential component of fungal cell wall.122 Resistance to terbinafine has largely been attributed to point mutations in the squalene epoxidase target gene (SQLE).123 Identification of the point mutation tin be achieved by DNA sequencing of the SQLE gene of the fungal isolate. Subtherapeutic dosage, not-compliance to handling, and corruption of over-the-counter topical preparations that combine antifungals with corticosteroids may too exist contributory.116
Prevention
Close contact or sharing of fomites and clothing with an infected private should be avoided.
Prognosis
The prognosis for localized tinea corporis is excellent with appropriate treatment and patient compliance. Recurrence may occur if therapy is stopped too shortly without complete eradication of the fungi. Reinfection may occur if a reservoir (tinea pedis, tinea capitis, onychomycosis) of infection is present.5,50,125
Conclusion
A well-demarcated, sharply circumscribed, mildly erythematous, annular, scaly plaque with a raised leading edge, and scaling and central immigration on the trunk is characteristic of tinea corporis. At times, the diagnosis tin can exist difficult due to the prior use of medications, such equally calcineurin inhibitors or corticosteroids. Furthermore, diseases that present with annular lesions may mimic tinea corporis. Tinea corporis is a common fungal infection and the differential diagnosis is broad and, at times, difficult. Physicians must exist familiar with this status and then that an authentic diagnosis tin can be fabricated and appropriate treatment initiated.
Footnotes
Contributions: Professor Alexander KC Leung was involved in the conceptualization of the manuscript. He wrote the showtime draft of the paper and oversaw the manuscript cosmos. All the authors contributed to drafting and revising the manuscript and approved the final version submitted for publication. All named authors meet the International Committee of Medical Journal Editors (ICMJE) criteria for authorship for this article, take responsibility for the integrity of the work as a whole, and have given their approving for this version to be published.
Disclosure and potential conflicts of involvement: Professor Alexander KC Leung and Professor Kam Lun Hon are associate editors of Drugs in Context and ostend no other conflicts of interest. All other authors declare that they have no conflicts of interest relevant to this manuscript. The International Committee of Medical Journal Editors (ICMJE) Potential Conflicts of Interests grade for the authors is available for download at: https://www.drugsincontext.com/wp-content/uploads/2020/07/dic.2020-5-half dozen-COI.pdf
Funding declaration: Professor Alexander KC Leung, Dr Joseph Lam, Dr Kin Fon Leong, and Professor Kam Lun Hon disclose no relevant funding associated with the preparation of this commodity.
Correct attribution: Copyright © 2020 Leung AKC, Lam JM, Leong KF, Hon KL. https://doi.org/ten.7573/dic.2020-5-6. Published by Drugs in Context under Creative Commons License Human activity CC Past NC ND 4.0.
Article URL: https://www.drugsincontext.com/tinea-corporis:-an-updated-review
Provenance: Invited; externally peer reviewed.
Peer review comments to writer: 8 June 2020
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