- Annular skin lesions are round with central clearing, whereas nummular lesions are round with discrete margins without central clearing.
- Tinea corporis produces well-demarcated, erythematous, dry, and scaly lesions with raised red borders and central clearing.
- Localized granuloma annulare produces annular lesions with smooth, non-scaly contours.
- Pityriasis rosea produces diffuse eruption on the trunk and proximal extremities with oval-shaped, scaly plaques.
- Urticaria produces wheals and well-defined, erythematous superficial swelling of the dermis. As a general rule, the individual lesions last less than 24 hours.
- Psoriasis is suggested when lesions occur on the extensor surfaces of the limbs, umbilical region, and sacrum.
- Nummular eczema is common during the winter months, with crusting, hyperpigmented, coin-shaped plaques on the lower legs, dorsal hands, and extensor surface of the arms.
- In erythema multiforme, the characteristic target lesions remain fixed for multiple days, as opposed to the transient lesions of urticaria.
Like you, I’ve had little training in dermatology; most of what I know was learned on the job and through continuing education. With round rashes, my differential was limited to tinea, if it had been there for a while, or urticaria and erythema multiforme, if it had just started. This article interested me because it broadened my awareness about this type of rash. I trust it will do the same for you.
— J. Stephan Stapczynski, MD, Editor
Although rashes are not usually an emergency, it is common for emergency physicians to see patients come in with a rash. Sometimes the rash is new onset, and sometimes it has been present for a while and refractory to treatment. Among the common presentations seen on a day-to-day basis are annular lesions. The term annular is derived from the Latin word “annulus,” meaning ring shaped.1 These lesions have a characteristic appearance, described as round to oval-shaped patches or plaques with central clearing. In contrast, the term nummular, derived from the Latin word “nummulus,” meaning coin shaped, is used to describe sharply marginated, round to disc-shaped lesions without central clearing. In adults, the most common etiology of annular lesions is tinea, a superficial fungal infection of keratinized tissue. While tinea may be readily identifiable, a wide variety of clinical entities mimic these infections, leading to confusion and, often, misdiagnosis.
Key morphological characteristics of annular lesions can improve diagnostic accuracy, leading to correct initial treatment. (See Table 1.) This review also may be helpful especially in cases of suspected tinea that are refractory to treatment.
Table 1. Summary of Diseases, Clinical Features, and Treatment
Asymmetric, well-demarcated, erythematous lesion with or without central clearing. Often associated with a scaly, palpable edge. KOH microscopy positive.
Topical or systemic antifungal agents
Non-scaly, erythematous to violaceus colored papules or plaques with a thin, smooth border. Favors the dorsal aspects of the extremities.
Topical, intralesional, or oral corticosteroids
Can begin with a herald patch, followed by a diffuse eruption involving the trunk and proximal extremities. Lesions are oval-shaped, scaly, skin- to salmon-colored papules or plaques. Described as a “Christmas-tree distribution” when on the back.
Oral corticosteroids if significant pruritus is present
Erythema annulare centrifugum
Erythematous annular or polycyclic plaques with a trailing scale inside an erythematous border. Favors the trunk and proximal extremities.
Topical corticosteroid creams
Erythema chronicum migrans
Large, evolving erythematous plaque without scale. May have a characteristic “bull’s-eye” appearance.
Doxycycline (adults)/amoxicillin (pregnant women and children)
Well-circumscribed, non-scaly edematous papules or plaques with blanched centers, surrounded by a red flare.
First- or second-generation antihistamines
Small, violaceous, polygonal-shaped papules and plaques with a diffuse network of white streaking.
Topical or intralesional corticosteroids; oral corticosteroids if severe
Cutaneous larva migrans
Erythematous, serpiginous tracts associated with intense pruritus.
Ivermectin (adults)/albendazole (children)
Porokeratosis of Mibelli
Annular, skin- to brown-colored plaque with a raised, ridge-like border.
Topical 5-fluorouracil with or without topical retinoids; cryosurgery
Well-circumscribed, erythematous dry plaques with silvery scale.
Well-demarcated, erythematous or hyperpigmented scaly or crusty coin-shaped plaques.
Subacute cutaneous lupus erythematosus
Red to pink plaques with raised borders and central clearing. Occurs following sun exposure. Favors the face, upper trunk, and backs of arms.
Multiple firm, red to purple to brown colored papules, nodules, or plaques. Favor the face, neck, and areas of trauma. Can have annular lesions.
Intralesional triamcinolone. Oral corticosteroids for systemic disease
Sharply demarcated red to pink to brown patches or thin plaques with greasy scale.
Topical ketoconazole cream or shampoo
Edematous plaques with three distinct zones.
Tuberculoid — erythematous plaques with raised, sharply defined borders and atrophic center. Characteristically anesthetic.
Lepromatous — numerous, poorly defined, hypopigmented macules that are symmetrically distributed.
Dapsone and rifampin
Dapsone, rifampin, and clofazimine
The Superficial Mycoses
Superficial mycotic infections are those limited to keratinized environments such as the skin, hair, and nails. Notoriously, these infections are caused by dermatophytes, a collective term that describes three genera — Microsporum, Trichophyton, and Epidermophyton. In naming dermatophyte infections, the term “tinea” is used, followed by the Latin name for the anatomical area infected.2 Subtypes include tinea corporis (body), cruris (groin), capitis (scalp), faciei (face), barbae (beard), unguium (nail), and manuum (hand).
Tinea infections are caused by close contact with infected persons, animals, or, occasionally, soil, and are spread to multiple body areas via autoinoculation when an infected region is scratched.1 Most infections occur in young adults and affect men more often than women.3 Warm environments, poor hygiene, contact sports, prolonged use of potent topical corticosteroids, and diseases that cause defects in the skin barrier facilitate these infections.4 Additionally, practices such as sharing towels, clothing, and toiletries, commonly seen in young athletes, are other important risk factors.
Tinea can be diagnosed confidently when characteristic lesions described below are observed. When available, the diagnosis can be confirmed by observing branching hyphae under the microscope using a potassium hydroxide (KOH) preparation. Tinea corporis and tinea cruris, the most common subtypes of dermatophytosis, are discussed briefly in this report.
Tinea corporis is a superficial dermatophyte infection of the body, not involving the scalp, face, hands, feet, or groin.4 Classically, tinea corporis is characterized by an asymmetric, well-demarcated, erythematous, dry, and scaly patch with a raised, red advancing border.2,4 Centrally, lesions clear, forming an annular pattern.4 Individual eruptions vary in size, enlarge over time, and often are associated with mild to moderate pruritus, although smaller lesions may be asymptomatic.4
Tinea cruris, or “jock itch,” is dermatophytosis of the groin. Lesions are similar to those of tinea corporis, characterized by an asymmetric, well-defined, mildly erythematous patch with associated scale. The advancing border is raised and may contain vesicles, pustules, or papules.4 Typically, infection begins unilaterally and extends to the medial thighs, perineum, and anus, sparing the scrotum.5 Tinea cruris commonly is found in conjunction with tinea pedis and/or tinea unguium, as the fungus is spread from the infected foot to the groin when clothing is pulled to the waist.2
Treatment of Tinea
For localized tinea corporis or cruris, pedis, and faciei, topical antifungals, such as imidazoles (clotrimazole, miconazole, ketoconazole, econazole, oxiconazole, sulconazole) or allylamines (naftifine, terbinafine), should be used once to twice daily for two to six weeks, including two weeks following clearance.2,6 Nystatin, commonly used to treat Candida infections, should not be used to treat tinea.3
Other Etiologies of Annular Lesions
Granuloma annulare (GA) is a relatively common, self-limiting disorder of the dermis that affects women twice as often as men.7 The eruption has a predilection for young adults and children, with most cases presenting before the third decade of life.1,7 Although the etiology remains unknown, GA is controversially associated with diabetes mellitus and hyperlipidemia.8 Several clinical variants of GA exist; however, localized disease primarily affects the dorsal surfaces of the fingers, hands, elbows, feet, and ankles.1,7 Lesions are characterized by asymptomatic, erythematous to violaceus colored papules or plaques with a thin, smooth border.9 Lesions develop slowly, spread peripherally, and involute centrally, conferring an annular appearance.9 An isolated (< 5 cm) lesion on the hand or arm represents most cases.7
Granuloma annulare can be diagnosed clinically by its unique distribution and morphology. Asymptomatic lesions with smooth, non-scaly contours are differentiated easily from the pruritic, scaly, and rough lesions of tinea. Biopsy with histopathologic correlation can be used to confirm or establish the diagnosis when not clinically obvious.7
Reassurance and observation is appropriate, as GA is benign and self-limiting. If left alone, one half of cases will resolve within two years.8 If treatment is preferred, high-potency topical corticosteroids or intralesional triamcinolone can be used.8,9 Although most cases heal without residual skin findings, recurrence is common regardless of treatment.9
Pityriasis rosea is a common eruption primarily seen in adolescents and young adults.10 The etiology remains unknown, but given its seasonal variation, occurring mostly in the spring and fall, a viral cause is suspected.11 The eruption is aptly named — pityriasis, meaning scaly, and rosea, meaning pink. About half of cases will begin with a “herald patch,” a 2 to 4 cm lesion that occurs mainly on the trunk or neck.11 The herald patch is a pink to brown oval-shaped patch or plaque with slightly raised margins and collarette scale at the periphery.10,12 One to two weeks following the herald patch, numerous, fine scaling papules and patches arise on the trunk and proximal extremities, sparing the face, palms, and soles.10 Subsequent lesions are smaller, oval-shaped, and salmon-colored, although they may be hyperpigmented in darker skinned individuals.10,12 (See Figure 1.) Lesions are mildly pruritic and oriented along cleavage lines.12 When stretched, scale hangs, resulting in the pathognomonic “hanging curtain sign.” Multiple lesions may coalesce, forming a diffuse rash that, when present on the back, exhibits a “Christmas tree” pattern along Langer’s lines, the natural folds of the body. A small subset of patients will experience a prodrome of headache, fever, and generalized malaise days to weeks prior to the initial outbreak.13
Figure 1. Multiple, Oval-shaped Lesions of Pityriasis Rosea
Source: Karl Kellawan, MD
When the rash is localized to the trunk, axillae, or groin, it commonly is mistaken for tinea. Tinea rarely is as widespread, and its lesions generally exude more significant central clearing.12 A negative KOH preparation can be used to exclude tinea.
The classic presentation often is alarming to patients, prompting medical evaluation. However, treatment generally is not required, as the eruption spontaneously remits in three to eight weeks.12 If patients experience intense pruritus, second-generation antihistamines, topical corticosteroids, a short course of systemic corticosteroids, or narrowband ultraviolet B (UVB) phototherapy can provide symptomatic relief.10
Erythema Annulare Centrifugum
Erythema annulare centrifugum (EAC) belongs to a group of disorders characterized by raised, erythematous lesions that form annular, polycyclic, or arcuate arrangements.14 Although the etiology is unclear and most patients do not have an identifiable trigger, an association with leukemias and lymphomas has been reported.15 The eruption is seen in both men and women and peaks in the fifth decade of life.16 Lesions begin as firm, pink papules that expand slowly over weeks, clear centrally, and progress to annular, erythematous, minimally elevated lesions that remain relatively asymptomatic beyond mild pruritis.14,16 Just inside the erythematous border is a trailing white scale that represents desquamation at the inner margin, characteristic of EAC. (See Figure 2.) Lesions have a predilection for the trunk and proximal extremities, sparing the hands, feet, face, and mucosa.14 When pressed, lesions should blanch.
Figure 2. Erythema Annulare Centrifugum With Faint Trailing White Scale Inside the Erythematous Border
Source: Karl Kellawan, MD
Diagnosis relies on clinical presentation. Centrally, lesions lack the associated crusts or vesicles commonly seen with tinea. Annular psoriasis may present similarly, but these lesions have diffuse, thick scaling throughout as opposed to the fine, trailing scale around the margin in EAC.
EAC often has a waxing and waning course that persists for about nine months.1,14 Most cases will subside spontaneously without treatment, leaving no residual scar. While rare, a basic cancer workup is warranted to rule out a paraneoplastic cause. If pruritus is present or treatment is desired, corticosteroids often are effective, but topical applications are preferred, as recurrence upon discontinuation of systemic agents is common.14,16
Erythema Chronicum Migrans
Erythema chronicum migrans (ECM) is the cutaneous manifestation of Lyme disease. In the United States, Borrelia spirochetes are transmitted to humans by an infected Ixodes tick. For most patients, ECM at the site of the tick bite is the first sign of infection.17 However, only about half of patients presenting with ECM will recall a recent bite or exposure to ticks. As with most tick bites, an erythematous, small, round papule will appear at the site of the bite, and within days, the surrounding erythema will migrate peripherally, forming a large, erythematous plaque.17 The expanding border will be warm and slightly raised without an associated scale, while centrally, a ring may clear, resulting in an annular or pathognomonic bull’s-eye appearance.18,19 (See Figure 3.) Primary lesions can reach 15 cm in diameter and commonly are found on the trunk, axilla, groin, and popliteal fossa.17,18 Days to weeks following the primary eruption, a subset of patients will develop secondary lesions that are smaller and less pronounced than the primary lesion. Generally, these secondary lesions will not have the targetoid appearance of the primary lesion and will spare the palms and soles.19 The cutaneous manifestations are self-limiting and, if untreated, will fade within six weeks.17
Figure 3. Classic Bull’s-eye Rash of Erythema Chronicum Migrans on the Lower Extremity
Source: Getty Images
While the skin manifestations are mostly asymptomatic, accompanying symptoms of Lyme disease are common. Early in the disease course, a mild flu-like illness consisting of general malaise, fever, headache, nausea, vomiting, arthralgias, myalgias, and photophobia can occur.19 If untreated, the disease can progress over the course of weeks to months, resulting in significant complications such as chronic arthritis, facial nerve palsy, and varying degrees of atrioventricular block.19
Early recognition and accurate diagnosis can prevent progression of disease and subsequent lifelong rheumatologic, neurologic, and cardiac complications. In a case of suspected Lyme disease, cutaneous findings are the most sensitive sign of early infection.18 Tick bites not associated with infection will begin to regress within a few days, while ECM will persist and progress. A detailed travel history, recent bites, or outdoor exposures should raise clinical suspicion. Lab findings may include an elevated erythrocyte sedimentation rate, elevated liver function tests, and mild anemia.18 Serologic evidence of infection is most sensitive between weeks three and six and commonly involves detection of anti-Borrelia antibodies using enzyme-linked immunosorbent assay (ELISA), followed by a Western blot for confirmation.17
Adults should be treated with a 21-day course of doxycycline.18 Amoxicillin, cefuroxime, and penicillin can be used in pregnant women and children younger than 8 years of age.18 If significant rheumatologic, neurologic, or cardiac complications are present, more aggressive regimens consisting of intravenous antibiotics should be used.18
Often referred to as hives, urticaria is an extremely common skin eruption that occurs in up to 20% of the population.20 Most cases are benign and resolve spontaneously. Rarely, patients experience a chronic course lasting longer than six weeks or progress to anaphylaxis.21 In acute cases, a trigger such as infection or allergic reaction may be identified. Chronic urticaria almost always occurs in adults and often does not have an obvious trigger.20 The eruption is composed of wheals, well-defined superficial swellings of the dermis that are characterized by raised, erythematous papules or plaques surrounded by a red flare.21 (See Figure 4.) Shape varies, but lesions often are round and blanch centrally, conferring an annular appearance.14 Lesions range from a few millimeters to more than 10 cm in size and are accompanied by intense itching, stinging, or burning. The hallmark finding in urticaria is its transient course. As a general rule, individual wheals do not last longer than 24 hours.20 Urticaria may be accompanied by deeper, ill-defined swellings of the dermis and subcutaneous tissue, termed angioedema.21
Figure 4. Edematous Plaque With Red Flare Characteristic of Urticaria
Source: Karl Kellawan, MD
Urticaria can be classified as allergic, physical, or idiopathic. Allergic urticaria can be IgE-mediated, occurring in response to foods (milk, eggs, wheat, shellfish, nuts), inhalants (pollen, dander), medications (penicillin), or complement-mediated in the case of serum sickness. Physical urticarias include dermatographic urticaria, occurring where skin has been stroked; cholinergic urticaria, occurring in response to fever and hot baths; cold urticaria, occurring on distal extremities upon rewarming; pressure urticaria, often occurring on the feet and buttocks hours after pressure has been applied; solar urticaria, occurring after exposure to light; and exercise-induced urticaria, which presents with large lesions five to 30 minutes into exercise.14
Urticaria is a clinical diagnosis based on history and physical exam. Laboratory tests rarely are indicated and generally are not recommended. Difficulty arises when patients present asymptomatically after an eruption, limiting the exam. As mentioned earlier, individual lesions should not last longer than 24 hours, although an attack may last much longer.21 If lesions persist beyond 24 hours, other causes must be considered and a biopsy may be warranted.22 If food is a suspected trigger, a food diary may be helpful. If a physical cause is suspected, provocative testing can uncover the offending stimuli.14
Treatment for acute urticaria involves avoidance of identifiable triggers and use of first- or second-generation antihistamines.14,21 If the patient fails to respond, a three-week tapered course of systemic corticosteroids is effective with a lower risk of recurrence than shorter courses.14
Lichen planus (LP) is an idiopathic, inflammatory disease of the skin and mucus membranes that primarily affects middle-aged adults.23 Mediated by T-lymphocytes, the reaction can be triggered by medications, vaccinations, or viral infections, especially hepatitis C.24 The eruption begins as small, pinpoint papules that expand into plaques that are classically shiny, violaceous, and polygonal-shaped.25 Wickham striae, a diffuse network of white streaking, can be seen embedded throughout the surface.23 Lesions commonly are found on the dorsal hands, flexor wrists, forearms, shins, vulva, and glans penis, but also can be seen in the mouth.23 When lesions are present on the body, patients may be asymptomatic or complain of intense pruritus. Oral lesions typically are painful, especially when ulcerated.
Annular LP is a subtype of LP present in 10% of cases and seen scattered among typical lesions described above. Lesions are characterized by asymptomatic, small, annular papules or plaques with raised borders, typically purple to white in color.24,25 (See Figure 5.) Centrally, lesions may be hyperpigmented or skin-colored.24 LP may mimic tinea, granuloma annulare, or porokeratosis of Mibelli (discussed later). Tinea is classically more erythematous and scaly than LP, while lesions of GA are less numerous and have smooth borders.
Figure 5. Annular Lichen Planus of the Glans Penis
Source: Karl Kellawan, MD
Cutaneous LP often is self-limiting; most cases resolve spontaneously within one year.24 For cutaneous disease, topical corticosteroids under occlusion can be used.24,25 When lesions are symptomatic or when oral lesions are present, intralesional triamcinolone is helpful.25 Widespread disease can be treated with systemic corticosteroids, although relapse may occur when the dose is tapered.25
Cutaneous Larva Migrans
Cutaneous larva migrans is a serpiginous eruption caused by animal hookworm larvae as they migrate through the epidermis.26 In the United States, this disease is most common in warm, southeastern states.27 Percutaneous infection often occurs in those who walk barefoot and children who play in sandboxes. Most cases occur on the feet, hands, and buttocks where larvae can penetrate the skin easily.28 Shortly after infection, patients experience intense pruritus localized to the area of inoculation. Within days, erythematous papules followed by characteristic thin, red, torturous tracts begin to appear.26 (See Figure 6.) Many isolated tracts may be present, each representing the course of an individual larva. Eventually, tracts can coalesce to form annular or ring-shaped lesions. Tracts migrate up to several centimeters a day and may disappear then reappear throughout their course.27 Systemic manifestations are not seen, as larvae are unable to invade deeper tissues.27
Diagnosis is based on clinical findings and supported by a recent history of potential exposure. The eruption can be differentiated from tinea by its lack of scale and distinctive migrating course.
Figure 6. Serpiginous Tracts of Cutaneous Larva Migrans on the Proximal Lower Extremity
Source: Karl Kellawan, MD
The cutaneous infestation is self-
limiting in that humans are “dead-end” hosts. Most eruptions spontaneously resolve in two to eight weeks.28 Treatment with anthelmintics can shorten the course of the disease. Early, localized lesions can be treated with topical thiabendazole. Widespread disease is treated with oral albendazole or invermectin.27
Porokeratosis of Mibelli
Porokeratosis of Mibelli is a rare, genetically inherited disorder of epidermal keratinization that arises during childhood or adolescence.29 Lesions begin as small, skin- to brown-colored papules that enlarge over the course of years, forming plaques with raised, ridge-like borders and atrophic, hyper- or hypopigmented centers.30 (See Figure 7.) Lesions are asymptomatic, measuring up to several centimeters in diameter and having a predilection for the hands, fingers, feet, and ankles.31 When multiple lesions are present, they are almost always unilateral and localized.30
Figure 7. Enlarging Plaque With Raised Border of Porokeratosis of Mibelli
Source: Karl Kellawan, MD
Focusing on the furrowed rim formed by the prominent border and depressed center is key in differentiating the lesion from other annular lesions like tinea. The large, ridge-like border can be accentuated with the application of colored dye, such as crystal violet or povidone-iodine, followed by removal with alcohol.31 In addition, questioning may reveal a family history of similar lesions. Definitive diagnosis can be made with biopsy and histopathological examination showing a cornoid lamella.29
Treatment consists of topical 5-fluorouracil alone or in combination with topical retinoids.30,31 Other possible approaches include cryotherapy with liquid nitrogen.29
Psoriasis is one of the most common skin conditions encountered by primary care physicians. The immune-mediated, hyperproliferative disorder affects approximately 2% of the U.S. population with equal frequency in men and women.32 Psoriasis can begin at any age, although the majority of cases occur in patients younger than 40 years of age.33
Many different types of psoriasis exist. The most common type, chronic plaque psoriasis, accounts for approximately 90% of cases.34 In this variant, lesions present as well-circumscribed, erythematous, dry plaques covered by a silvery scale. During an eruption, lesions begin small then extend peripherally, becoming more erythematous over time.32 As lesions mature, desquamation occurs, leaving a collarette of scale at the margin, which often is accompanied by intense pruritis and burning.32,33
Although characteristic plaques predominate, variations in morphology are not uncommon. Lesions may appear annular when they develop rapidly, forming the active outer margin first, leaving relatively normal skin at the center.34 As plaques regress, margins persist while the center heals, again resulting in annular-shaped lesions.35 (See Figure 8.) A rare form of psoriasis, termed annular pustular psoriasis, also is considered when annular lesions are present. In this variant, lesions are characterized by well-demarcated, erythematous plaques with an active border composed of pustules.
Figure 8. Healing Lesions of Chronic Plaque Psoriasis
Source: Karl Kellawan, MD
In many cases, the diagnosis may not be obvious, even for the experienced clinician. Family history may be helpful in revealing relatives with the disease. The location is suggestive when plaques are confined to the extensor surfaces of limbs, umbilical region, and sacrum.33 Physically removing scale can produce pinpoint bleeding, referred to as the “Auspitz sign,” characteristic of psoriasis.32 Extracutaneous manifestations including nail changes and asymmetric, oligoarthritis of the hands and feet commonly are seen in conjunction with cutaneous findings.34
The chronic nature of the disease often leads to complex treatment regimens requiring combination therapy to achieve control. Therefore, referral to a dermatologist is appropriate. For small, localized lesions, potent topical corticosteroids and vitamin D derivatives in creams, lotions, or ointments can be used.32 When plaques persist, intralesional injections of triamcinolone can be tried.32 Another commonly used, cost-effective modality is phototherapy.32 When the disease is severe or widespread, biologic and oral immunosuppressive agents are options.
Nummular eczema (NE) is a relatively common, inflammatory dermatitis that occurs in the form of coin-shaped lesions.36 The pathogenesis remains poorly understood, but often it is seen in atopic individuals. Clinically, NE follows a chronic course characterized by well-demarcated, erythematous, or hyperpigmented coin-shaped plaques with diffuse crust.37 (See Figure 9.) Acutely, lesions may ooze and have associated vesicles.38 Most will lack central clearing, although in some cases, plaques can expand and clear centrally, conferring an annular appearance.1 Lesions are especially common during winter months when skin is dry and primarily present on the lower legs, dorsal hands, and extensor surface of the arms.39 Excoriations often are prominent because of intense pruritus.36
Figure 9. Nummular Eczema of the Lower Extremity
Source: Karl Kellawan, MD
Nummular eczema should be differentiated from tinea corporis and psoriasis. Tinea corporis is associated with a fine scale and commonly affects the trunk, unlike NE, which has a thick crust and occurs almost exclusively on the extremities. Lesions of psoriasis often are larger and associated with a more silvery scale compared to NE.40 In addition, nail changes and arthritis would not be seen in conjunction with NE.
Treatment consists of potent topical corticosteroids supplemented by daily soaking and greasing with occlusive ointments.36,40 In refractory cases, phototherapy can be used.36
Subacute Cutaneous Lupus Erythematosus
Systemic lupus erythematosus can have dramatic skin involvement that comes in three variants — acute, subacute, and discoid. Acute cutaneous lupus erythematosus refers to the notorious malar rash that is almost always associated with systemic disease.41 Subacute cutaneous lupus erythematosus (SCLE) describes a photosensitive eruption that commonly forms annular lesions, but is associated with systemic disease only occasionally. Lesions of discoid lupus erythematosus vary greatly; however, they rarely are annular.
SCLE is characterized by the rapid appearance of small or large, erythematous to pink-colored plaques with raised borders, central clearing, and an easily detached scale.41,42 The eruption is extremely photosensitive and, thus, most commonly will present on the face, upper trunk, and the backs of the arms.41
In differentiating SCLE from other annular lesions, a history of sun exposure in correlation with the appropriate distribution supports the diagnosis. Patients often are Caucasian women aged 15 to 40 years.42
Because of the transient nature of the eruption, treatment is centered around sun protection.42 If medical therapy is preferred, topical corticosteroids or antimalarial agents, such as hydroxychloroquine, can be used.41
Sarcoidosis is an idiopathic systemic disease characterized by non-caseating granulomas in multiple organ systems — mainly the lungs, but also the skin, lymph nodes, eyes, and salivary glands.7,9 The disease is more common in women and typically begins between the ages of 20 and 40 years.9 Interestingly, in the United States, there is marked racial variation, with sarcoidosis affecting African Americans more often than Caucasians.9
Skin involvement is seen in up to one-third of those affected and may be the first and/or only clinical sign of disease.7,9 Lesion morphology varies, presenting as multiple round papules, patches, or plaques that favor the face, neck, and areas of prior injury such as tattoos and scars.7 Color ranges from red to purple to brown.7 Annular configurations may be present when multiple papules coalesce or when plaques clear centrally.7 Applying pressure to the firm lesions causes blanching, sometimes revealing a yellow-brown (apple-jelly) color.7 Lesions are almost always asymptomatic, although rarely may itch.9
Diagnosis may be straightforward in a patient with a known history of sarcoidosis; however, with no prior history, a biopsy of the lesion will reveal non-
caseating epithelioid granulomas.7 In newly diagnosed cases, a chest X-ray is warranted and, if abnormal, patients should be referred for pulmonary evaluation.9
Treating the underlying systemic disease often clears cutaneous lesions.9 Limited cutaneous eruptions can be treated with intralesional triamcinolone.9 Systemic corticosteroids are effective but generally are reserved for active pulmonary, ocular, cardiac, and central nervous system involvement or when skin disease is widespread.9
Seborrheic dermatitis is a common, chronic dermatosis present in up to 5% of the population.32 The pathogenesis has been linked to the overproduction of sebum and Malassezia yeasts. Therefore, eruptions occur in regions in which sebaceous glands are most active, such as the scalp, face, eyebrows, ears, and presternal area (see Figure 10), as well as large body folds such as the axillae and groin.36 Lesions are more common in men and are characterized by gradual onset of sharply demarcated patches or thin plaques that vary in color from red to orange to yellow. Flaky, visibly greasy, white to yellow scaling overlies affected areas.36 Most cases are pruritic, and symptoms generally intensify with sweat.32,36
Figure 10. Sharply Demarcated, Scaly Patch of Seborrheic Dermatitis Affecting the Presternal Area
Source: Karl Kellawan, MD
Seborrheic dermatitis may closely resemble tinea or psoriasis, especially in the groin. Distribution is helpful in distinguishing seborrheic dermatitis from tinea. When seborrheic dermatitis is present on the face, lesions are remarkably symmetric, mostly affecting the forehead, eyebrows, and retroauricular areas.36 When present in large folds, seborrheic dermatitis tends to be centered along the crease, whereas tinea is less often as symmetric.36 In addition, patches and plaques of seborrheic dermatitis typically are more numerous and appear greasier than lesions of tinea. Plaques of psoriasis are associated with a heavier scale that, unlike seborrheic dermatitis, bleeds when removed.32
Treatment consists of imidazoles, mainly ketoconazole, as a shampoo when present on the scalp or cream when present on the face and body.36 Topical steroids work quickly and are effective but should be limited because of the risk of steroid rosacea.32 Once cleared, daily maintenance therapy is important to prevent relapse.
Erythema multiforme (EM) is an acute and often recurrent eruption that commonly affects young adults.14 The reaction pattern represents an immune-mediated response to a variety of antigenic agents, most notably herpes simplex. Other triggers include drugs (penicillin, phenytoin, allopurinol, sulfonamides, barbiturates) and Mycoplasma infections.14 Erythema multiforme can be separated into EM minor and EM major, the more severe form with mucosal involvement. The minor variant is not associated with systemic symptoms, but EM major is accompanied by symptoms such as fevers and arthralgias.14
EM minor is characterized by distinctive “target-shaped” or “iris-shaped” lesions.14 Lesions evolve over several days, beginning as round, sharply demarcated erythematous macules that progress to raised, edematous papules.4 Mature lesions have three distinct zones — a dull red center, a pale outlining ring, and an encircling macular erythema.14 (See Figure 11.) Occasionally, atypical target lesions that are round, edematous, and composed of only two distinct zones are present.43 Lesions may sting, burn, and even blister at the center.43 Sites of predilection include the palms, dorsal hands, elbows, backs of the arms, knees, shins, dorsal feet, and soles.14,43
Figure 11. Target-shaped Lesions of Erythema Multiforme Affecting the Forearms Bilaterally
Source: Karl Kellawan, MD
EM major occurs primarily as a drug reaction. The eruption presents with the same target-shaped lesions seen in EM minor but is accompanied by systemic symptoms and mucosal involvement.14 Erosions and even ulcerations may involve the oral, genital, and ocular mucosa.14,43
EM often is confused with large urticarial lesions. To diagnose EM, several lesions must evolve into the classic, target-shaped ones described above.43 In addition, EM lesions remain fixed for multiple days, whereas individual urticarial lesions last less than 24 hours.
EM is self-limiting and usually resolves within weeks without complications.14 For limited cutaneous disease, symptomatic treatment with oral antihistamines or low-potency topical corticosteroids is sufficient.43 In recurrent cases precipitated by herpes simplex virus eruptions, chronic suppressive antiviral therapy with valacyclovir is effective.14 When oral lesions are present, topical corticosteroid gels and “swish and spit” rinses containing a mixture of lidocaine, diphenhydramine, and kaolin are helpful.14 In severely ill patients, systemic corticosteroids should be considered.43
Hansen’s disease, also known as leprosy, is a rare, chronic granulomatous disease caused by Mycobacterium leprae.44 Although mostly a disease of the developing world, cases in the United States occur in those who have resided in foreign countries or those living in southeastern states with exposure to armadillos, a natural host.1,45 In almost all new cases, a history of close contact with an untreated, infected individual is obtainable.45 Once a patient is infected, the disease has an insidious onset and an incubation period that ranges from three to 20 years.1 Hansen’s disease primarily presents in two forms, tuberculoid leprosy and lepromatous leprosy.45 In both forms, cooler areas of the body such as the skin, peripheral nerves, upper respiratory tract, and eyes are affected.1,45 Warmer areas such as the axilla, groin, and scalp usually are spared. Often, peripheral nerves are affected first, resulting in paresthesias and numbness of the infected area; however, symptoms may be mild and go undiagnosed until cutaneous lesions appear.45
The tuberculoid form represents a strong cell-mediated immune response.45 Patients present with localized disease, consisting of fewer than five asymmetrically distributed lesions characterized by large plaques with a raised, sharply defined border and an atrophic, depressed center.45 Typically, the borders are erythematous to purple in color while the centers often are hypopigmented. Lesions may be dry, scaly, and hairless, but most importantly, anesthetic.44,45 The superficial nerves supplying the area may be enlarged, tender, and palpable.1,45
The lepromatous form represents a poor cell-mediated immune response.45 Patients present with generalized disease, consisting of numerous, symmetrically distributed lesions characterized by small, poorly defined hypopigmented macules without associated anesthesia.45 Eventually, nodules and raised plaques of the face (leonine facies), ears, elbows, hands, and knees may appear.45 Nerve involvement can occur, but will present as a symmetric stocking-glove pattern neuropathy.45
Diagnosis of Hansen’s disease is made by identifying the infectious acid-fast bacilli in skin or nerve lesions with biopsy.45 In the United States, tuberculoid leprosy is treated with a combination of dapsone and rifampin for 12 months.45 Lepromatous leprosy is treated with a combination of dapsone, rifampin, and clofazimine for two years.45
Annular skin lesions are among the most common dermatologic presentations. Although tinea is often to blame, many other entities mimic these infections. Establishing a broad differential and focusing on key morphological characteristics will improve accuracy of diagnosis, limit unnecessary treatment, and lead to faster resolution of disease.
- Hsu S, Le EH, Khoshevis MR. Differential diagnosis of annular lesions. Am Fam Physician 2001;64:289-296.
- Elewski BE, et al. Fungal Diseases. In: Bolognia JL, Schaffer JV, Cerroni L. Dermatology. 4th ed. Elsevier Limited; 2018:1329-1363.
- Perkins J, Buckland M, Miller RA. Fungus among us? Dermatophyte infections, mimickers, and treatment options. Primary Care Reports 2017;23:77-87.
- James WD, Berger TG, Elston DM. Diseases Resulting From Fungi and Yeasts. In: James WD, Berger TG, Elston DM. Andrews’ Diseases of the Skin: Clinical Dermatology. 12th ed. Philadelphia: Elsevier; 2016:285-318.
- Kaushik N, Pujalte GG, Reese ST. Superficial fungal infections. Prim Care 2015;42:501-516.
- Moriarty B, Hay R, Morris-Jones R. The diagnosis and management of tinea. BMJ 2012;345:e4380.
- Rosenbach M, et al. Non-infectious Granulomas. In: Bolognia JL, Schaffer JV, Cerroni L. Dermatology. 4th ed. Elsevier Limited; 2018:1644-1663.
- Piette EW, Rosenbach M. Granuloma annulare: Pathogenesis, disease associations and triggers, and therapeutic options. J Am Acad Dermatol 2016;75:467-479.
- James WD, Berger TG, Elston DM. Macrophage/Monocyte Disorders. In: James WD, Berger TG, Elston DM. Andrews’ Diseases of the Skin: Clinical Dermatology. 12th ed. Philadelphia: Elsevier; 2016:699-725.
- Wood GS, Reizner GT. Other Papulosquamous Disorders. In: Bolognia JL, Schaffer JV, Cerroni L. Dermatology. 4th ed. Elsevier Limited; 2018:161-174.
- Eisman S, Sinclair R. Pityriasis rosea. BMJ 2015;351;h5233.
- James WD, Berger TG, Elston DM. Pityriasis Rosea, Pityriasis Rubra Pilaris, and Other Papulosquamous and Hyperkeratotic Diseases. In: James WD, Berger TG, Elston DM. Andrews’ Diseases of the Skin: Clinical Dermatology. 12th ed. Philadelphia: Elsevier; 2016:199-208.
- Drago F, Ciccarese G, Rebora A, et al. Pityriasis rosea: A comprehensive classification. Dermatology 2016;232:431-437.
- James WD, Berger TG, Elston DM. Erythema and Urticaria. In: James WD, Berger TG, Elston DM. Andrews’ Diseases of the Skin: Clinical Dermatology. 12th ed. Philadelphia: Elsevier; 2016:136-152.
- Mu EW, Sanchez M, Mir A, et al. Paraneoplastic erythema annulare centrifugum eruption (PEACE). Dermatol Online J 2015;21:pii: 13030/qt6053h29n.
- España A. Figurate Erythemas. In: Bolognia JL, Schaffer JV, Cerroni L. Dermatology. 4th ed. Elsevier Limited; 2018:320-331.
- Sommer LL, Reboli AC, Heymann WR. Bacterial Diseases. In: Bolognia JL, Schaffer JV, Cerroni L. Dermatology. 4th ed. Elsevier Limited; 2018:1259-1295.
- James WD, Berger TG, Elston DM. Bacterial Infections. In: James WD, Berger TG, Elston DM. Andrews’ Diseases of the Skin: Clinical Dermatology. 12th ed. Philadelphia: Elsevier; 2016:136-152.
- Nadelman RB. Erythema migrans. Infect Dis Clin North Am 2015;29:211-239.
- Peroni A, Colato C, Schena D, Girolomoni G. Urticarial lesions: If not urticaria, what else? The differential diagnosis of urticaria: Part I. J Am Acad Dermatol 2010;62:541-555.
- Grattan CE, Saini SS. Urticaria and Angioedema. In: Bolognia JL, Schaffer JV, Cerroni L. Dermatology. 4th ed. Elsevier Limited; 2018:304-319.
- Rudikoff D. Differential diagnosis of round or discoid lesions. Clin Dermatol 2011;29:489-497.
- Weston G, Payette M. Update of lichen planus and its clinical variants. Int J Womens Dermatol 2015;1:140-149.
- Shiohara T, Mizukawa Y. Lichen planus and lichenoid dermatoses. In: Bolognia JL, Schaffer JV, Cerroni L. Dermatology. 4th ed. Elsevier Limited; 2018:188-207.
- James WD, Berger TG, Elston DM. Lichen Planus and Related Conditions. In: James WD, Berger TG, Elston DM. Andrews’ Diseases of the Skin: Clinical Dermatology. 12th ed. Philadelphia: Elsevier; 2016:209-224.
- Feldmeier H, Schuster A. Mini review: Hookworm-related cutaneous larva migrans. Eur J Clin Microbiol Infect Dis 2012;31:915-918.
- Bravo FG. Protozoa and Worms. In: Bolognia JL, Schaffer JV, Cerroni L. Dermatology. 4th ed. Elsevier Limited; 2018:1470-1502.
- James WD, Berger TG, Elston DM. Parasitic Infestations, Stings, and Bites. In: James WD, Berger TG, Elston DM. Andrews’ Diseases of the Skin: Clinical Dermatology. 12th ed. Philadelphia: Elsevier; 2016:418-450.
- Ferreira FR, Santos LD, Tagliarini FA, Lira ML. Porokeratosis of Mibelli — literature review and a case report. An Bras Dermatol 2013;88(6 Suppl 1):179-182.
- Requena L, Requena C, Cockerell CJ. Benign Epidermal Tumors and Proliferations. In: Bolognia JL, Schaffer JV, Cerroni L. Dermatology. 4th ed. Elsevier Limited; 2018:1894-1916.
- James WD, Berger TG, Elston DM. Genodermatoses and Congenital Anomalies. In: James WD, Berger TG, Elston DM. Andrews’ Diseases of the Skin: Clinical Dermatology. 12th ed. Philadelphia: Elsevier; 2016:542-578.
- James WD, Berger TG, Elston DM. Seborrheic Dermatitis, Psoriasis, Recalcitrant, Palmoplantar Eruptions, Pustular Dermatitis, and Erythroderma. In: James WD, Berger TG, Elston DM. Andrews’ Diseases of the Skin: Clinical Dermatology. 12th ed. Philadelphia: Elsevier; 2016:185-198.
- van de Kerkhof PCM, Nestle FO. Psoriasis. In: Bolognia JL, Schaffer JV, Cerroni L. Dermatology. 4th ed. Elsevier Limited; 2018:138-160.
- Griffiths CE, Barker JN. Pathogenesis and clinical features of psoriasis. Lancet 2007;370:263-271.
- Naldi L, Gambini D. The clinical spectrum of psoriasis. Clin Dermatol 2007;25:510-518.
- Reider N, Fritsch PO. Other eczematous eruptions. In: Bolognia JL, Schaffer JV, Cerroni L. Dermatology. 4th ed. Elsevier Limited; 2018:228-241.
- Barrett M, Luu M. Differential diagnosis of atopic dermatitis. Immunol Allergy Clin North Am 2017;37:11-34.
- Silverberg NB. Typical and atypical clinical appearance of atopic dermatitis. Clin Dermatol 2017;35:354-359.
- Suh KS, Park JB, Yang MH, et al. Diagnostic usefulness of dermoscopy in differentiating lichen aureus from nummular eczema. J Dermatol 2017;44:533-537.
- James WD, Berger TG, Elston DM. Atopic Dermatitis, Eczema, and Noninfectious Immunodeficiency Disorders. In: James WD, Berger TG, Elston DM. Andrews’ Diseases of the Skin: Clinical Dermatology. 12th ed. Philadelphia: Elsevier; 2016:62-89.
- Lee LA, Werth VP. Lupus Erythematosus. In: Bolognia JL, Schaffer JV, Cerroni L. Dermatology. 4th ed. Elsevier Limited; 2018:662-680.
- James WD, Berger TG, Elston DM. Connective Tissue Diseases. In: James WD, Berger TG, Elston DM. Andrews’ Diseases of the Skin: Clinical Dermatology. 12th ed. Philadelphia: Elsevier; 2016:153-178.
- Hotzenecker W, Prins C, French LE. Erythema Multiforme, Stevens-Johnson Syndrome, and Toxic Epidermal Necrolysis. In: Bolognia JL, Schaffer JV, Cerroni L. Dermatology. 4th ed. Elsevier Limited; 2018:332-347.
- Ramos-e-Silva M, Ribeiro de Castro MC. Mycobacterial Infections. In: Bolognia JL, Schaffer JV, Cerroni L. Dermatology. 4th ed. Elsevier Limited; 2018:1296-1318.
- James WD, Berger TG, Elston DM. Hansen’s Disease. In: James WD, Berger TG, Elston DM. Andrews’ Diseases of the Skin: Clinical Dermatology. 12th ed. Philadelphia: Elsevier; 2016:331-342.
What can ringworm be mistaken for? ›
Ringworm is sometimes mistaken for forms of eczema and other skin conditions, like psoriasis. Unlike nummular eczema, the affected areas don't vary in color, and the patches don't burn and sometimes don't even itch.What looks like ringworm but isn't ringworm? ›
Other conditions that occasionally look like ringworm include seborrhea, psoriasis, pityriasis, contact dermatitis (such as poison oak), drug reactions, tinea versicolor, vitiligo, erythema migrans (a rash seen in Lyme disease), and even lupus.What causes a rash that looks like ringworm? ›
Other rashes can look like ringworm, including spider bites, nummular eczema, and Lyme disease, a more serious infection that produces a bull's-eye shaped rash. These require different treatments, so it's important to consult a medical professional.What virus looks like ringworm? ›
Pityriasis rosea will often appear with a so-called herald patch, a single, round or oval lesion that can develop on any part of the body but primarily the trunk. The circular shape of the lesion is often mistaken for ringworm.What is a rash that looks like rings? ›
Ringworm often causes a ring-shaped rash that is itchy, scaly and slightly raised. The rings usually start small and then expand outward. Ringworm of the body (tinea corporis) is a rash caused by a fungal infection. It's usually an itchy, circular rash with clearer skin in the middle.How to tell the difference between ringworm and pityriasis rosea? ›
Pityriasis Rosea Vs Ringworm
Both ringworm and Christmas tree rash cause pink, flaky patches on the skin. Pityriasis rosea can develop on multiple body parts, though it most commonly occurs on the chest or back. Ringworm, however, can occur anywhere on the body, including the scalp, fingernails, face, or legs.
Nummular eczema is a type of eczema that causes a similar rash to ringworm. It leads to coin-shaped or oval patches, which can easily be mistaken for the rash caused by ringworm.How can you tell the difference between ringworm and dermatitis? ›
Ringworm is a contagious skin infection caused by a fungus. Nummular dermatitis is a type of eczema rather than a fungal infection. Ringworm tends to appear as one or two patches on your skin, but nummular eczema often causes multiple patches.Can psoriasis look like ringworm? ›
At first glance, psoriasis and ringworm can appear similar. Both conditions cause red, scaly, and itchy plaques to form on the skin. While ringworm is a temporary rash caused by a fungus, psoriasis is an autoimmune condition that lasts for a lifetime, although the symptoms can be treated.Can ringworm just be bumps? ›
Ringworm on the skin starts as a red, scaly patch or bump. Over time, it may look like one or more rings with raised, bumpy, scaly borders (the center is often clear).
What can cause a circular rash? ›
A circular rash is typical of ringworm (a contagious fungal skin infection. But it may also occur due to other skin conditions such as Lyme disease, eczema, psoriasis, pityriasis rosea, or granuloma annulare. Contact your healthcare provider for a diagnosis of any circular rash that does not resolve quickly.What looks like ringworm but isn't contagious? ›
Eczema and many other skin conditions can resemble ringworm. Both ringworm and eczema cause itchy, red skin. Unlike ringworm, eczema isn't contagious and doesn't spread from one area to another on your body.Is the lupus rash raised? ›
It can affect the skin, joints, kidneys, brain, and other organs. The round or disk shaped (discoid) rash of lupus produces red, raised patches with scales. The pores (hair follicles) may be plugged. Scarring often occurs in older lesions.What does pityriasis look like? ›
A single pink or red oval patch of scaly skin, called the "herald patch", usually appears at least 2 days before a more widespread rash develops. The herald patch ranges in size from 2cm to 10cm. It can appear on your tummy, chest, back or neck, and less often on your face or scalp, or near your genitals.What is leukemia rash? ›
Leukemia cutis appears as red or purplish red, and it occasionally looks dark red or brown. It affects the outer skin layer, the inner skin layer, and the layer of tissue beneath the skin. The rash can involve flushed skin, plaques, and scaly lesions. It most commonly appears on the trunk, arms, and legs.What does a viral skin rash look like? ›
The characteristics of viral rashes can vary greatly. However, most look like splotchy red spots on lighter skin or purplish spots on darker skin. These spots might come on suddenly or appear gradually over several days. They can also appear in a small section or cover multiple areas.Is a circular rash always ringworm? ›
Causes of a red circle on the skin other than ringworm. Many conditions can cause flaky patches or “rings” on the skin that could be confused with ringworm. They include pityriasis rosea, Lyme disease, nummular eczema, and psoriasis. Ringworm is an itchy, round rash caused by a fungus called tinea .Which is an itchy rash that usually forms a ring pattern? ›
Ringworm is a common skin infection that is caused by a fungus. It's called “ringworm” because it can cause a circular rash (shaped like a ring) that is usually red and itchy. Anyone can get ringworm.Can contact dermatitis look like ringworm? ›
With its itchy, red rash, contact dermatitis might be confused with ringworm. Contact dermatitis occurs when your body reacts to a chemical, such as a skin care product or detergent. Other symptoms might include: dry, scaly, cracked skin.Can eczema or psoriasis look like ringworm? ›
But nummular, or “discoid,” eczema also produces a round, scaly rash that can look like ringworm. If you think you have ringworm, but over-the-counter remedies fail to work, it may be time to see your doctor. You may have eczema, psoriasis, or some other skin condition.
How do you describe syphilis rash? ›
The characteristic rash of secondary syphilis may appear as rough, red, or reddish brown spots both on the palms of the hands and the bottoms of the feet. However, rashes with a different appearance may occur on other parts of the body, sometimes resembling rashes caused by other diseases.What does a herald patch look like? ›
A herald patch is an erythematous, 2 to 10 centimeter, round to oval scaly patch or plaque with a depressed center and raised border that frequently presents days to weeks before an eruption of pityriasis rosea, a common, self-limiting papulosquamous disorder.What does Nummular dermatitis look like? ›
The most common and noticeable symptom of nummular eczema is a patch of coin-shaped lesions on the body. The lesions frequently develop on the arms or legs, but they may eventually spread to the torso and hands. They may be brown, pink, or red.How do I know if my rash is fungal or eczema? ›
Look for Visible Signs of Infection
Eczema is typically itchy, red and scaly. When it's flaring, the skin may even appear weepy, oozy or crusty from all the inflammation. Still, skin infections caused by bacteria usually present with a red, hot, swollen and tender rash that often is accompanied with pus.
The first sign of discoid eczema is usually a group of small red spots or bumps on the skin. These then quickly join up to form larger pink, red or brown patches that can range from a few millimetres to several centimetres in size.How do I know if my rash is fungal? ›
What are symptoms of a fungal rash? A fungal rash is often red and itches or burns. You may have red, swollen bumps like pimples or scaly, flaky patches.Can a dermatologist identify ringworm? ›
A dermatologist can often tell if you have ringworm by looking at the infected area. Your dermatologist may also examine other areas of your body. It's common to have athlete's foot and ringworm on one or both hands. Sometimes, the infection spreads to one or more nails.Is ringworm a seborrheic dermatitis? ›
It is usually spread through direct skin contact […] Scalp ringworm, or tinea capitis, is a fungal infection that is common in childhood, but can happen at any age. Unlike other scalp conditions, like dandruff or seborrheic dermatitis, it is contagious and can spread to others.What are round scaly patches on skin? ›
Actinic keratoses are scaly spots or patches on the top layer of skin. With time they may become hard with a wartlike surface. An actinic keratosis (ak-TIN-ik ker-uh-TOE-sis) is a rough, scaly patch on the skin that develops from years of sun exposure.What are red circular patches on skin? ›
Discoid eczema, also known as nummular or discoid dermatitis, is a long-term (chronic) skin condition that causes skin to become itchy, swollen and cracked in circular or oval patches. Without treatment, discoid eczema can last for weeks, months or even years.
Can stress trigger ringworm? ›
Yes, stress can be a cause of ringworm infection. Stress or alcohol acts as a trigger also, at times, causes a flare-up of the infection.Is ringworm smooth or bumpy? ›
A ringworm infection on the skin is indicated by roundish, flat patches that have a raised, scaly border.Can a bug bite look like ringworm? ›
Since spider bites, certain types of eczema, psoriasis, yeast infections and Lyme disease can look nearly identical to ringworm, it's important to see a doctor right away.How to tell the difference between nummular eczema and ringworm? ›
Nummular eczema typically causes coin-shaped patches, while ringworm often produces ring-shaped patches. Ringworm is a fungal infection that can spread between people. It is usually treatable with antifungal medications and should clear up within a couple of weeks. Nummular eczema is an inflammatory skin condition.What is a circle rash that doesn't itch? ›
Ringworm (dermatophytosis) is a temporary circular rash that appears red or pink on light skin tones and brown or gray on skin of color. The rash may or may not itch, and it may grow over time. It can also be transferred if your skin comes in contact with the skin of someone who has the fungal infection.What autoimmune diseases cause rash? ›
- Sjogren's syndrome.
- Hypothyroidism & myxedema.
- Celiac disease.
Stress can lead to a type of rash called hives. Hives are raised, itchy bumps that can be round or irregular in shape. Stress management and home remedies can help with the discomfort from stress hives.Is granuloma annulare a ringworm? ›
Granuloma annulare is often mistaken for ringworm. Ringworm, however, is usually scaly and itchy. Granuloma annulare is not. This rash can also be mistaken for bug bites or a rash caused by a tick with Lyme disease.What causes Nummular dermatitis? ›
Extremely dry skin is dehydrated skin
Researchers believe that skin dryness plays a role in causing nummular eczema. You can develop excessively dry skin during winter when the humidity in the air drops or when taking a medication that can dry out your skin.
The exact cause of granuloma annulare is unknown (idiopathic). Numerous theories exist linking the cause to trauma, sun exposure, thyroid disease, tuberculosis, and various viral infections. However, no definitive proof has been shown for any of these theories.
What does a blood disorder rash look like? ›
The rashes resemble patches of pinpoint red or purple spots, known as petechiae. These red spots may be raised or flat on the skin. They can appear anywhere on the body but are more common on the neck, arms, and legs. The petechial red spots do not typically cause any symptoms like pain or itching.What does SLE rash look like? ›
Many people with lupus experience a red or purplish rash that extends from the bridge of the nose over to the cheeks in a shape that resembles that of a butterfly. The rash may be smooth, or it may have a scaly or bumpy texture. It can look like a sunburn. The medical term for this type of rash is a malar rash.What is a malar rash? ›
Malar rash, also named a butterfly rash, is a common facial presentation of multiple disorders. It is characterized by an erythematous flat or raised rash across the bridge of the nose and cheeks, which usually spares nasolabial folds. It may be transient or progress to involve other areas of facial skin.How do I know if my rash is ringworm? ›
Check if it's ringworm
The main symptom of ringworm is a rash. It may look red, silver or darker than surrounding skin, depending on your skin tone. The rash may be scaly, dry, swollen or itchy. Ringworm can appear anywhere on the body, including the scalp (tinea capitis) and groin (jock itch).
Frequently Asked Questions : How can I tell the difference between ringworm and eczema? Ringworm is often round in shape, itchy, and has black dots at its center. Eczema symptoms include redness, dry skin, swelling of the affected area, oozing, and crusting if scratched.What does the beginning stage of ringworm look like? ›
The infection initially appears as discolored, often scaly patches on affected areas. These patches typically appear red on lighter skin or brown-gray on darker skin. Ringworm may spread from an affected area to other parts of the body, such as the: scalp.How do I know if my rash is fungal or bacterial? ›
Skin infections caused by viruses usually result in red welts or blisters that can be itchy and/or painful. Meanwhile, fungal infections usually present with a red, scaly and itchy rash with occasional pustules.What are 3 symptoms of ringworm? ›
- Itchy skin.
- Ring-shaped rash.
- Red, scaly, cracked skin.
- Hair loss.
How soon do symptoms appear? The incubation period is unknown for most of these agents, however ringworm of the scalp is usually seen 10 to 14 days after contact and ringworm of the body is seen 4 to 10 days after initial contact.Can ringworm disappear by itself? ›
Although ringworm can go away by itself, it's not common. While ringworm is present on your skin, you're still contagious to others.
Can pityriasis rosea be mistaken for ringworm? ›
Because of its shape, the first patch (herald patch) might be erroneously thought to be ringworm. The herald patch is usually followed by smaller spots and itching. Although the exact cause of pityriasis rosea hasn't been determined, it's thought to be triggered by a viral infection.