White Patches – Symptoms, Causes, Treatments

White patches are usually caused by one of two conditions: tinea versicolor or vitiligo. Less commonly, white patches on the skin can be caused a skin inflammation known as eczema.

Tinea versicolor is a type of fungal infection that leads to the development of white patches. The patches can appear anywhere on your body, depending on where the fungus grows. The white patches seen in vitiligo are the result of an autoimmune disorder. In vitiligo, the body’s immune system mistakenly targets melanocytes, the cells that produce your skin pigment, as a foreign substance. When these cells are destroyed, the lack of skin pigment causes white patches. Eczema is a condition where the skin is overly sensitive to common allergens and becomes scaly, itchy, and sometimes white.

Common causes of white patches

White patches may be caused by common conditions including:

• Tinea versicolor, a fungal infection of the skin

• Vitiligo, an autoimmune disorder that destroys the color-producing cells in your skin

Additional causes of white patches

White patches can also be caused by other conditions, including eczema. This is a common allergic skin condition, especially in children. It usually causes itching and scaling of the skin and, rarely, white patches. In adults small circular areas of pigment exhaustion may develop on areas of skin where there has been chronic sun exposure.

Serious or life-threatening causes of white patches

In some very rare cases, white patches may be a symptom of a serious or life-threatening condition that should be evaluated immediately by a healthcare provider. These cases include precancerous changes in the skin and skin cancers.

Questions for diagnosing the cause of white patches

To diagnose your condition, your doctor or licensed health care practitioner will ask you several questions related to your white patches including:

• When did you first notice the white patches?

• Did you start any new medications or try any new types of food immediately before the white patches formed?

• Do you have any other skin lesions?

• Do you have any other symptoms?

• Does the white patch itch or burn?

• Have the white patches changed in size, shape or color?

• Have you had similar lesions before?

• Have you tried any medications or other measures for your white patches?

• Do the white patches come and go with the seasons or with rainy or dry weather?

What are the potential complications of white patches?

White patches result of a variety of causes, but they are usually mild and not associated with complications. Once the underlying cause is diagnosed, it is important for you to follow the treatment plan that you and your health care professional design specifically for you to reduce the risk of potential complications including:

• Cosmetic disfigurement
• Further hypopigmentation (loss of color in the skin)
• Scarring
• Spread of cancer

Erythema Multiforme (for Parents) – Nemours KidsHealth

What Is Erythema Multiforme?

Erythema multiforme is an allergic reaction. It causes a rash of spots with dark centers and pale red rings that look like a target or “bulls-eye.” Some spots can have a small blister or scab in the middle.

What Are the Signs & Symptoms of Erythema Multiforme?

Erythema multiforme (air-uh-THEE-muh mul-teh-FOR-mee) starts with pink or red blotches. They grow over a few days into round spots that look like targets with red, pink, and pale rings.

Often, the rash starts on the arms, hands, legs, and feet, then appears on the face, neck, diaper area, and body. Some kids get a few spots in the mouth. If there are many spots on the lips or mouth, it is called erythema multiforme major.

The rash is most often on both sides of the body. It might not bother kids, but it can itch or burn.

As the rash goes away, the skin where the spots were can look dark for a few months, but won’t leave a scar.

The rash might be the only sign, but sometimes kids with erythema multiforme also:

• feel tired
• have a low fever
• have sore muscles and joints
• have puffy hands or feet

What Causes Erythema Multiforme?

Most cases of erythema multiforme happen because the body has an allergic reaction to an infection or a medicine. The most common trigger is the germ that causes cold sores. In kids, a germ that causes lung infections also can trigger erythema multiforme.

Less often a medicine causes it. Some medicines that can cause a reaction are:

• penicillin or sulfa-based antibiotics
• some anti-seizure medicines
• anesthesia 
• nonsteroidal anti-inflammatory drugs (NSAIDs), like ibuprofen

Is Erythema Multiforme Contagious?

No, the rash can’t spread from person to person. If an infection causes it, that infection can spread. But someone else who gets the infection may not get the rash too.

How Is Erythema Multiforme Diagnosed?

Doctors know it’s erythema multiforme by looking at it. To help figure out what caused it, the doctor will ask about any recent sickness the child had and any medicines he or she takes. Sometimes, the cause isn’t known.

How Is Erythema Multiforme Treated?

Erythema multiforme goes away on its own. If the cause is an infection, the doctor may treat that. If a medicine was the cause, the doctor will stop it and use a new one if a medicine is still needed.

If your child has erythema multiforme caused by the cold sore germ, the rash might come back when cold sores come back. If it keeps coming back, the doctor may give a medicine to fight the cold sore germ to keep the rash away.

Doctors might treat some severe cases with steroid medicines.

How Can Parents Help?

To help make kids feel better, doctors may suggest:

• putting cool packs on the rash
• taking a cool bath or shower
• using acetaminophen (like Tylenol or a store brand) for pain or fever
• using antihistamines (like Benadryl, Claritin, Zyrtec, or store brands) 
• putting creams on the skin to help with itchiness

These treatments won’t make the rash go away faster, but will make a child feel better until the rash is gone.

When Should I Call the Doctor?

Call the doctor if you think your child has erythema multiforme. Other rashes can look similar.

If your child is diagnosed with erythema multiforme, call the doctor if your child has any of these problems:

• a lot of spots in the mouth
• trouble drinking liquids
• pain that doesn’t get better with pain medicine
• spots around the eyes or the white part of the eyes look red
• peeling skin

What Else Should I Know?

The erythema multiforme rash often goes away in 1 to 2 weeks, but can last as long as 4 weeks. It doesn’t cause a scar, but in some kids might leave darker spots on the skin for a few months.

It can be hard to wait until the rash goes away. You can help your child by treating the itching and pain and calling the doctor if you think your child is getting worse.

Common childhood rashes | Pregnancy Birth and Baby

Meningitis rash

If you think your child might have meningitis rash, go to the nearest emergency department immediately. You can read more about serious childhood rashes here.

Rashes with no fever or itching

Milia (blocked oil glands)

Up to half of newborn babies develop small white spots called milia on their face, especially on the nose. These are just blocked pores, and they’re not itchy or contagious. They usually clear up without treatment within a few weeks.

Erythema toxicum

Many newborns develop a blotchy red skin reaction called erythema toxicum, which can appear between 2 days and 2 weeks after birth. Flat, red patches or small bumps often first appear on the face and spread to the body and limbs. The rash is harmless, not contagious, and will clear after a few days or a week.

Baby acne

Some babies get acne on their cheeks and nose in the first few months of life. These pimples normally clear up without any treatment, usually in a few months, but sometimes it can take a year.

Nappy rash

Nappy rash is an inflammation of the skin in the nappy area that looks red, sore and inflamed. Nappy rash is caused by a number of things, including urine or poo irritating the baby’s skin.

To avoid nappy rash, keep the nappy area clean and dry with frequent nappy changes and nappy-free time. You can help protect the skin by putting on a barrier cream such as zinc or soft white paraffin at each nappy change.

Persistent nappy rash can be treated with a medicated cream. Don’t use talcum powder or antiseptics to treat nappy rash. If your baby’s skin has developed a fungal infection, you’ll need to use an antifungal ointment. Ask your doctor or pharmacist for advice.

Erythema multiforme

Erythema multiforme is a rash triggered by an infection, medication or an illness. Red spots develop on the hands or feet before spreading across both sides of the body (over a day or so). The spots are not usually itchy, but might become raised or blistered.

Your baby might feel unwell or have a mild fever before the rash appears. Erythema multiforme is not contagious, and usually clears up without treatment in 3 to 6 weeks.

Keratosis pilaris (‘chicken skin’)

Keratosis pilaris is a harmless condition where the skin becomes rough and bumpy, as if permanently covered in goose pimples. These bumps most commonly occur on the upper arms and thighs. You can try several things to help the rash to clear up.

Rashes that might be itchy

Eczema

Eczema causes the skin to become itchy, red, dry and cracked, especially in the creases at the knees and elbows. It is usually treated with corticosteroid creams to reduce inflammation, and moisturisers to stop the skin from drying out.

Eczema is a long-term condition that can show up when babies are only a few months old. Certain triggers, such as viral infections, soap and pool chlorine, can cause symptoms to appear.

Ringworm (tinea)

Ringworm is a contagious, mild skin infection that causes a ring-like red rash with a clear centre. It can occur almost anywhere on the body, although the most common areas are the baby’s scalp, feet and groin.

Ringworm is caused by a fungus, not a worm, and is usually treated with over-the-counter antifungal creams. You should keep your child home from childcare or school until a day after you have started treatment to prevent spreading the infection.

Prickly heat (heat rash)

Heat rash might appear if your baby gets hot in a humid environment. The rash shows as tiny red bumps or blisters on the skin, which can be very itchy. Cooling your baby down and avoiding humidity is the best way to counteract heat rash, which usually clears within 2 to 3 days without treatment.

Impetigo (school sores)

Impetigo is a highly contagious bacterial infection of the skin. It causes red sores and blisters that form a yellow crust. It is very common in children aged 2 to 6, for whom it is not usually serious, but it can be dangerous for newborn babies. It is common in children who have scabies.

If your child has impetigo, you should see your doctor, who might prescribe an antibiotic cream, ointment or tablet. This should clear the infection within 7 to 10 days. You should keep your child home from childcare or school and away from young babies until the sores have dried up, usually a few days after treatment starts.

Hives (urticaria)

Hives is a raised, red, itchy rash that can appear on any part of the body at any time, but is common on the chest, stomach and back, as well as the throat and limbs. Hives usually disappears within a few days without any treatment. Your pharmacist can advise you about over-the-counter medications to treat hives. If the rash doesn’t go away, you should see your doctor.

Pityriasis rosea

Pityriasis rosea is a mild skin rash that sometimes appears after a sore throat, cold or fever. It usually affects only children over 10.

It begins with a single pink or tan patch on the chest or back. Oval red patches then appear on the chest or back and limbs over the next weeks. They might be itchy, and your child might feel tired and unwell.

The exact cause of pityriasis rosea is unclear, and experts believe it is probably not contagious. The rash usually clears up within a couple of months without treatment.

If you are pregnant, pityriasis rosea can in rare cases lead to complications. See your doctor if you are pregnant and come into contact with a child who has pityriasis rosea.

Molluscum contagiosum

Molluscum contagiosum is a viral skin infection that is spread by skin-to-skin contact or by sharing swimming pool water or towels.

Molluscum contagiosum spots look like pimples and grow into round pearly white lumps, usually 2 to 5 millimetres in size. They can be itchy. Usually they heal without treatment within 6 months, but it might take longer.

Rashes with fever

Slapped cheek disease (fifth disease)

Slapped cheek disease is a viral infection that mainly affects pre-school and school-age children. It typically causes a bright red rash on both cheeks that spreads as a ‘lacy’ rash on the body and limbs. Occasionally, it causes fever.

Slapped cheek disease is usually mild and clears up in a few days without treatment. The child is contagious before the rash appears, but not once it has appeared.

The virus can affect a pregnant woman, potentially causing a type of anaemia in her unborn baby. It can also cause miscarriage. If you suspect you or your child has slapped cheek disease, you should avoid contact with women who are, or might be, pregnant.

Hand, foot and mouth disease

Hand, foot and mouth disease is a mild but highly contagious viral illness that causes a rash on the palms of the hands and soles of the feet. It is not the same as the foot-and-mouth disease that affects farm animals.

The disease is common in childcare and kindergartens. Your child might feel unwell and have a fever and blisters on the hands and feet and in the mouth, and also in the nappy area, that last 7 to 10 days. Children with hand, foot and mouth disease should stay away from childcare or school until all the blisters have dried up.

Hand, foot and mouth disease usually resolves on its own without major problems but in rare cases it can be more serious especially in people whose immune system is not functioning normally or pregnant women. These rare problems include infections of the brain and heart muscle and miscarriage in pregnant women.

Roseola infantum

Roseola infantum is a contagious viral infection that can cause cold-like symptoms and a high fever. Kids with roseola infantum have raised pink spots that start on the chest, stomach and back and spread to the limbs. The child is contagious before the rash appears, but not after. The rash usually lasts 3 to 5 days.

The high fever may last for a few days. Roseola infantum can also cause some children to have a febrile convulsion. If your child has a convulsion (fit), call triple zero (000) immediately and ask for an ambulance. Febrile convulsions are scary to see but are generally not harmful.

When to seek help

Many babies develop a skin rash in their first days or weeks as their sensitive skin adapts to a new environment. Most rashes are harmless and go away on their own. But if your baby seems unwell, or if you’re worried, you should see your doctor. They can advise about the cause and whether treatment is necessary.

Whatever their age, you should take your child to the doctor if they have a rash and persistent high temperature, cold or cough symptoms or swollen neck glands.

Treatment of common childhood rashes

If you think your child might be contagious, they should stay at home. Keep them away from school, childcare and other children. You should also keep them away from women who are pregnant, or who might be pregnant, since some childhood infections can cause serious problems in unborn babies.

You can use paracetamol or ibuprofen (in babies aged over 3 months) to reduce fever — read the packet instructions carefully to ensure your child receives the right amount for their age and weight.

Your pharmacist can advise you on treating the symptoms of common rashes. For example, you can use over-the-counter creams to prevent itchiness.

If you are concerned about your child, call Pregnancy, Birth and Baby on 1800 882 436 to talk to a maternal child health nurse, or call Healthdirect on 1800 022 022 to talk to a registered nurse. Alternatively, contact your doctor.

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Diabetes Rash: Causes, Appearance and Prevention

What is a diabetes rash?

Diabetes affects various parts of your body, including your skin. An estimated 1 in 3 people with diabetes (Type 1 or Type 2) will develop a skin rash or other skin problem at some point.

When you have diabetes, your chances of having dry, itchy skin are higher than someone who doesn’t have the disease. You’re also more likely to get other diabetes-related skin conditions.

What causes a diabetes rash?

For people who don’t have diabetes, a skin rash may be the first sign of high blood sugar (hyperglycemia) or prediabetes. Your healthcare provider can help you take steps to prevent diabetes.

If you take medications for diabetes, a skin rash may indicate that you need to adjust treatments to lower your blood sugar (glucose) levels. Some other rashes result from reduced blood flow to your extremities (hands and feet).

What does a diabetes rash look like?

Diabetes rashes look different depending on the type and cause.

Some diabetes rashes only affect people with diabetes. They usually go away when blood sugar is under control. These rashes include:

• Blisters (bullosis diabeticorum): Painless blisters may form on the backs of hands and feet and on the legs and forearms. This rare condition most often affects people who have diabetic neuropathy.
• Diabetes dermopathy: Light-brown, round-shaped scaly patches, like age spots, appear on the shins. These harmless spots don’t need treatment.
• Digital sclerosis: Some people with Type 1 diabetes develop hardened, thick, waxy skin on the backs of their hands. The finger joints stiffen, making movement difficult. A related rash is scleredema adultorum of Bushke which is tightness, thickening, and hardening of the back, neck, shoulders and face. There are various treatments that dermatologists can provide for this.
• Necrobiosis lipoidica diabeticorum (NLD): This lower leg rash is more common in women. NLD causes raised, red, shiny patches with a yellow center. Blood vessels may be more noticeable. The rash may be itchy and painful. You should see a dermatologist for treatment options.
• Diabetes Foot Syndrome: These are ulcers that develop from trauma to the skin. The ulcers can take a long time to heal and there is an increased risk for infection.

Other conditions can affect anyone, but are particularly common among people with diabetes. These rash-causing conditions can also be a warning sign of pre-diabetes:

• Acanthosis nigricans (AN): This condition causes dark, velvet-looking bands of discolored skin. It commonly affects people who have overweight/obesity. Acanthosis nigricans can be a warning sign of high blood sugar or prediabetes.
• Disseminated granuloma annulare: Granuloma annulare often affects healthy children and young adults. In people with diabetes, disseminated granuloma annulare forms rings or arcs on the fingers, hands, feet and ears. The rash may be red, reddish-brown or skin tone. It doesn’t cause pain, but it may itch. Many times this will heal without therapy. For small areas of involvement, topical steroids can be useful in treatment.
• Eruptive xanthomatosis: Firm, yellow, pea-sized skin bumps may itch and be encircled in red. This rash most often affects the backs of the hands, feet, arms, legs and buttocks. Among people with Type 1 diabetes, it’s most common in men who have high cholesterol.
• Vitiligo: People with Type 1 diabetes are more prone to this skin condition. It causes skin to lose pigment, the substance that gives skin its color. Some people notice light or white patches of skin. Rarely, it itches or hurts. Treatments include corticosteroid creams, laser treatments and light therapy.
• Skin tags: These are small brown bumps on your skin, often on your eyelids, neck, armpits or groin. These usually don’t have any symptoms and no treatment is necessary.
• Lichen planus: A lichen planus rash is characterized by itchy purple bumps on the skin, sometimes with a white lacy pattern. This is usually on the ankles and wrists, but can sometimes be seen in the mouth. There are many therapies, both topical and pills that can be used to treat this.
• Acquired reactive perforating collagenosis (ARPC): This is usually seen in patients with kidney disease. The rash is usually red itchy bumps. Treatment can consist of topical steroids, steroid injections to the rash and other medications.

What other skin conditions affect people with diabetes?

People with diabetes can have any skin condition. But sometimes, people with diabetes have a rash or other skin irritation due to:

• Allergic reactions: People with diabetes may have an allergic reaction to oral diabetes medications or injectable insulin. You may develop a rash or hives and swelling (urticaria) at the injection site or elsewhere on your body. Contact your healthcare provider if you think you’re having an allergic reaction.
• Bacterial infections: Having diabetes increases the risk of bacterial skin infections. You may develop bacterial infections in eyelid glands (sty) or deep under the skin (boils and carbuncles). Infected skin may be swollen, hot, red and painful. You’ll need antibiotics to get rid of the infection.
• Dry, itchy skin: High blood sugar and certain skin conditions can cause dry, itchy skin. If you have poor blood circulation, your lower legs may itch the most. Moisturizers can help.
• Fungal infections: A yeast called Candida albicans causes most fungal infections in people with diabetes. You’ll have moist areas of tiny red blisters or scales that itch. Skin fungus tends to affect skin folds, including under the breast, between fingers and toes, around nailbeds, and in the armpits and groin. Common fungal infections include jock itch, athlete’s foot and ringworm. Antifungal medications can help.

How can I prevent diabetes-related skin problems?

The best thing you can do to prevent skin problems is to keep blood sugar levels within the range recommended by your healthcare provider. Proper skin care can lower your chances of getting a skin rash, infection or wound that’s difficult to heal.

Take these steps to prevent skin problems:

• Check your skin daily for signs of rashes, redness, infections or sores.
• Use warm (not hot) water and moisturizing soap in the shower. (Soaking in a tub dries out skin.)
• Pat skin dry with a towel (don’t rub), making sure to dry in between fingers, toes and skin folds.
• Apply fragrance-free moisturizers after showering while skin is still damp and soft. Look for creams and ointments (not lotions) with ceramide to help skin retain moisture.
• Apply creams containing 10% to 25% urea (an emollient) to cracked, dry heels at bedtime.
• Prevent dehydration and keep skin hydrated by drinking plenty of fluids.
• Treat cuts and wounds immediately with soap and water. Use antibiotic ointments only if your healthcare provider gives the OK. Bandage the wound daily. Call your provider if you notice signs of redness, pain, drainage or infection.
• Use a humidifier to add moisture to the air in your home.

A note from Cleveland Clinic

Having diabetes increases your risk for skin rashes and skin problems. It’s important to pay attention to your skin. Contact your healthcare provider as soon as you notice a rash or something that doesn’t look quite right. A rash may be a sign that you need to change medications or dosages to get blood sugar under control. A proper skin care routine can lower your risk of diabetes-related skin problems.

Pityriasis alba (dry white patches)

Author: A/Prof Amanda Oakley, Dermatologist, Hamilton, New Zealand, 1997. Updated January 2016. Revised September 2020.

What is pityriasis alba?

Pityriasis alba is a low-grade type of eczema/dermatitis mainly seen in children.

The name describes its appearance: pityriasis refers to the characteristic fine scale, and alba to its pale colour (hypopigmentation).

Who gets pityriasis alba?

Pityriasis alba is common worldwide with a prevalence in children of around 5%.

• Pityriasis alba mainly affects children and adolescents aged 3 to 16 years, but can occur in older and younger people.
• It affects boys and girls equally.
• The hypopigmentation of pityriasis alba is more prominent, and the condition perhaps more common, in dark skin compared to white skin.

What causes pityriasis alba?

The cause of pityriasis alba is unknown.

• Pityriasis alba often coexists with dry skin and atopic dermatitis.
• It often presents following sun exposure, perhaps because tanning of surrounding skin makes affected areas more prominent.

Researchers have not reached any conclusions about the relationship of pityriasis alba to the following:

• Ultraviolet radiation
• Excessive or inadequate bathing
• Low levels of serum copper and other trace elements
• Malassezia yeasts (which produce a metabolite, pityriacitrin, that inhibits tyrosinase thus causing hypopigmentation).

What are the clinical features of pityriasis alba?

Classic pityriasis alba usually presents with 1 to 20 patches or thin plaques.

• Most lesions occur on the face, especially on the cheeks and chin.
• Patches may also appear on the neck, shoulders, and upper arms and are uncommon elsewhere.
• Patch size varies from 0.5 to 5 cm in diameter.
• Patches are round, oval or irregular in shape.
• Pityriasis alba may have well-demarcated or, more usually, poorly defined edges.
• Itch is minimal or absent.
• Hypopigmentation is more noticeable in summer.
• Dryness and scaling is more noticeable in winter when environmental humidity tends to be lower.

Typically, a patch of pityriasis alba evolves through several stages.

1. Slightly scaly pink patch or plaque with a just palpable papular surface.
2. Hypopigmented patch or plaque with fine surface scale.
3. Then post-inflammatory hypopigmented macule without scale.
4. Resolution.

Pityriasis alba

See more images of pityriasis alba …

Dermoscopy of pityriasis alba

• Poorly defined pale area
• White structureless areas
• Faint pigment network
• Superficial white scale
• Normal hair colour

How is pityriasis alba diagnosed?

Pityriasis alba is usually a clinical diagnosis but may be confused with several other disorders that cause hypopigmentation.

To exclude these, investigations may include:

• Wood lamp examination: the hypopigmentation of pityriasis alba does not enhance, and there is no fluorescence
• Scrapings for mycology: microscopy and fungal culture are negative in pityriasis alba
• Skin biopsy: biopsy is rarely required, but may reveal mildly spongiotic dermatitis and reduction in melanin.

What is the treatment for pityriasis alba?

No treatment is necessary for asymptomatic pityriasis alba.

How can pityriasis alba be prevented?

The development or prominence of pityriasis alba can be reduced with sunscreen use to minimise sun tanning.

What is the outlook for pityriasis alba?

Pityriasis alba clears after an average of one year, with a range of a few months up to two or three years. The colour gradually returns completely to normal.

References:

• Al-Refu K. Dermoscopy is a new diagnostic tool in diagnosis of common hypopigmented macular disease: A descriptive study. Dermatol Reports. 2018;11(1):7916. doi:10.4081/dr.2018.7916. PubMed
• Miazek N, Michalek I, Pawlowska-Kisiel M, Olszewska M, Rudnicka L. Pityriasis alba–common disease, enigmatic entity: up-to-date review of the literature. Pediatr Dermatol. 2015;32(6):786-91. doi:10.1111/pde.12683. PubMed
• Karanfilian KM, Behbahani S, Lambert MW, et al. The pathophysiology of pityriasis alba: time-dependent histologic changes.  Clin Dermatol. 2020;38(3):354-6. doi:10.1016/j.clindermatol.2019.07.002. PubMed
• Jadotte YT, Janniger CK. Pityriasis alba revisited: perspectives on an enigmatic disorder of childhood. Cutis. 2011;87(2):66-72. PubMed
• Khafagy GM, Nada HR, Rashid LA, El-Samanoudy SI, Abd El-Sattar EM. Role of trace elements in pityriasis alba. J Trace Elem Med Biol. 2020;59:126422. doi:10.1016/j.jtemb.2019.126422. PubMed
• Ingram JR. Eczematous disorders. In: Griffiths C, Barker J, Bleiker T, Chalmers R, Creamer D (eds). Rook’s Textbook of Dermatology [4 volumes], 9th edn, Wiley Blackwell, 2016:39.25-6.

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Not All Round Rashes Are Ringworm: A Differential Diagnosis of Annular and Nummular Lesions | 2018-10-18 | Relias Media

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

Introduction

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.

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

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

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

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

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

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.

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

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

Urticaria

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

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

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.

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.

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

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

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.

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

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

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

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

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

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

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

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

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

Summary

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.

REFERENCES

1. Hsu S, Le EH, Khoshevis MR. Differential diagnosis of annular lesions. Am Fam Physician 2001;64:289-296.
2. Elewski BE, et al. Fungal Diseases. In: Bolognia JL, Schaffer JV, Cerroni L. Dermatology. 4th ed. Elsevier Limited; 2018:1329-1363.
3. Perkins J, Buckland M, Miller RA. Fungus among us? Dermatophyte infections, mimickers, and treatment options. Primary Care Reports 2017;23:77-87.
4. 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.
5. Kaushik N, Pujalte GG, Reese ST. Superficial fungal infections. Prim Care 2015;42:501-516.
6. Moriarty B, Hay R, Morris-Jones R. The diagnosis and management of tinea. BMJ 2012;345:e4380.
7. Rosenbach M, et al. Non-infectious Granulomas. In: Bolognia JL, Schaffer JV, Cerroni L. Dermatology. 4th ed. Elsevier Limited; 2018:1644-1663.
8. Piette EW, Rosenbach M. Granuloma annulare: Pathogenesis, disease associations and triggers, and therapeutic options. J Am Acad Dermatol 2016;75:467-479.
9. 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.
10. Wood GS, Reizner GT. Other Papulosquamous Disorders. In: Bolognia JL, Schaffer JV, Cerroni L. Dermatology. 4th ed. Elsevier Limited; 2018:161-174.
11. Eisman S, Sinclair R. Pityriasis rosea. BMJ 2015;351;h5233.
12. 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.
13. Drago F, Ciccarese G, Rebora A, et al. Pityriasis rosea: A comprehensive classification. Dermatology 2016;232:431-437.
14. 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.
15. Mu EW, Sanchez M, Mir A, et al. Paraneoplastic erythema annulare centrifugum eruption (PEACE). Dermatol Online J 2015;21:pii: 13030/qt6053h39n.
16. España A. Figurate Erythemas. In: Bolognia JL, Schaffer JV, Cerroni L. Dermatology. 4th ed. Elsevier Limited; 2018:320-331.
17. Sommer LL, Reboli AC, Heymann WR. Bacterial Diseases. In: Bolognia JL, Schaffer JV, Cerroni L. Dermatology. 4th ed. Elsevier Limited; 2018:1259-1295.
18. 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.
19. Nadelman RB. Erythema migrans. Infect Dis Clin North Am 2015;29:211-239.
20. 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.
21. Grattan CE, Saini SS. Urticaria and Angioedema. In: Bolognia JL, Schaffer JV, Cerroni L. Dermatology. 4th ed. Elsevier Limited; 2018:304-319.
22. Rudikoff D. Differential diagnosis of round or discoid lesions. Clin Dermatol 2011;29:489-497.
23. Weston G, Payette M. Update of lichen planus and its clinical variants. Int J Womens Dermatol 2015;1:140-149.
24. Shiohara T, Mizukawa Y. Lichen planus and lichenoid dermatoses. In: Bolognia JL, Schaffer JV, Cerroni L. Dermatology. 4th ed. Elsevier Limited; 2018:188-207.
25. 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.
26. Feldmeier H, Schuster A. Mini review: Hookworm-related cutaneous larva migrans. Eur J Clin Microbiol Infect Dis 2012;31:915-918.
27. Bravo FG. Protozoa and Worms. In: Bolognia JL, Schaffer JV, Cerroni L. Dermatology. 4th ed. Elsevier Limited; 2018:1470-1502.
28. 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.
29. 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.
30. 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.
31. 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.
32. 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.
33. van de Kerkhof PCM, Nestle FO. Psoriasis. In: Bolognia JL, Schaffer JV, Cerroni L. Dermatology. 4th ed. Elsevier Limited; 2018:138-160.
34. Griffiths CE, Barker JN. Pathogenesis and clinical features of psoriasis. Lancet 2007;370:263-271.
35. Naldi L, Gambini D. The clinical spectrum of psoriasis. Clin Dermatol 2007;25:510-518.
36. Reider N, Fritsch PO. Other eczematous eruptions. In: Bolognia JL, Schaffer JV, Cerroni L. Dermatology. 4th ed. Elsevier Limited; 2018:228-241.
37. Barrett M, Luu M. Differential diagnosis of atopic dermatitis. Immunol Allergy Clin North Am 2017;37:11-34.
38. Silverberg NB. Typical and atypical clinical appearance of atopic dermatitis. Clin Dermatol 2017;35:354-359.
39. 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.
40. 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.
41. Lee LA, Werth VP. Lupus Erythematosus. In: Bolognia JL, Schaffer JV, Cerroni L. Dermatology. 4th ed. Elsevier Limited; 2018:662-680.
42. 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.
43. 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.
44. 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.
45. 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.

White rash on the hands – Question to the dermatologist

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Good to know about ALLERGIES TO WHEAT FLOUR (hvete)

ALLERGY TO WHEAT FLOUR ( hvete )

Useful information on wheat flour allergy – Fact sheet of the Norwegian Asthmatics and Allergy Association

What is food allergy?

An allergic reaction to food occurs due to the fact that the body reacts to certain types of proteins contained in food.For some, this reaction can be very strong, even after eating a small amount of intolerable food. Others experience only unpleasant sensations that pass without dramatic consequences. Food allergies are more common in children than in adults. In most cases, food allergies disappear during preschool age. It is not uncommon to dislike several types of food. When avoiding foods that contain important nutrients, you should find good substitutes for them in order to maintain a healthy and varied diet.

What is wheat flour allergy?

When allergic to wheat flour, a person is allergic to proteins contained in wheat. Most wheat allergy sufferers should also avoid contact with related cereals such as rye, barley and spelled. The gluten-free diet is the same as for celiac disease patients.

Wheat allergy is most common in young children. Most of the children get rid of this allergy before they reach school age.Symptoms range from gastrointestinal symptoms, worsening eczema and rash, to allergic shock.

Wheat dust allergy

Some allergy sufferers react to wheat dust (for example, when baking), even though they tolerate the wheat contained in the food. A reaction to wheat dust can include asthma attacks, worsening eczema, or a runny nose. This type of allergy is most common among bakers. Treatment is to avoid flour dust.

Anaphylactic shock due to physical activity and associated with wheat

One of the rare forms of wheat allergy is a reaction to wheat only when physical activity follows the intake of wheat. These reactions usually first appear in adolescence or adulthood.

False positive test results

In the presence of the above forms of wheat allergy, positive results of Pirquet tests and blood tests for IgE antibodies usually appear. However, many people can show positive test results without showing allergy symptoms when they eat wheat. This applies, for example, to people who are allergic to grass pollen.This is why laboratory tests of wheat tolerance in combination with symptoms and known reactions to food should be considered.

Non-allergic reactions to wheat

It should also be noted that in some cases people can react to wheat without having a wheat allergy or celiac disease. This is especially true for vague gastrointestinal symptoms, the reduction of which is reported by many as a result of the elimination of wheat from the diet.These symptoms may be due to the high fiber (fructan) content in wheat (and rye). These types of fiber can lead to bloating and loose stools, especially in people with irritable bowels. Spelled flour is usually well tolerated in such cases, especially if the spelled contains gluten.

Where can wheat be kept?

Wheat is found in most Norwegian grain and bakery products. In addition, wheat flour is used in a number of complex foods such as sauces and soups.Wheat flour forms the basis of pasta, couscous, bulgur and semulia. Most allergy sufferers also react to rye and barley.

Because gluten-containing grains are found in a large number of foods, you should always check the ingredient list when shopping for multi-ingredient foods. According to the labeling regulation, all products containing wheat or other gluten-containing cereals must be properly labeled with the relevant cereals.

What can you eat if you are allergic to wheat flour?

Wheat protein is not found in foods made solely with milk, eggs, meat, fish, marine crustaceans, fruits, nuts, oil or vegetables. Be aware that pickles and spice mixes can sometimes contain wheat.

Cereals such as corn, rice, buckwheat, millet, quinoa, sorghum and millet are good substitutes for wheat, rye and barley. Many people tolerate gluten-free oats as well.

Special gluten-free foods can be eaten: flour mixes, pasta, biscuits, crispbread and breakfast cereals. Some of them contain wheat starch, but the amount of protein in it is so low that for most allergy sufferers this will not be a problem. Gluten-free foods can be found in a wide variety of stores and health food stores. Some bakeries sell gluten-free baked goods.

Ration

Since cereals are widely used and are an important source of nutrients in the Norwegian diet, it is necessary to ensure that the correct diagnosis is made in order to maintain the correct diet and avoid unnecessary bans.

Gluten-free prepared foods such as gluten-free bread and cereal mixes are often based on rice, corn, potato or wheat starch. These starch-based foods are low in fiber and nutrients compared to regular wholemeal breads. Relying solely on these types of grains increases the risk of constipation and nutritional deficiencies.

Natural gluten-free grains are rich in nutrient-rich varieties. Millet, buckwheat, quinoa, and millet are good examples of these grains. That is why, you should bake bread based on these products, adding fiber and grains to it to increase the amount of fiber taken.

The Norwegian Celiac Association can provide information on the disease and gluten-free diets.www.ncf.no

Herpes sore throat in children and adults – symptoms, treatment | HEXORAL®

15.11.2021

171 478

7 minutes

Contents:

Causes of herpangina
Symptoms of herpetic sore throat
Herpetic sore throat
Herpetic sore throat in children
Sore throat in children
Sore throat in children
Sore throat in children Herpetic sore throat is an acute infectious disease caused by enteroviruses. Herpangina is not related to the herpes virus. The name is due to the fact that a rash in the throat with illness is similar to herpetic vesicles ³ .

The peak incidence in Russia occurs in August-September. Seasonality is associated with swimming in reservoirs in the summer months and the opening of kindergartens and schools in early autumn ² .

Causes of herpangina

Herpetic sore throat can be caused by about 70 serotypes of enteroviruses. Most often these are Coxsackie B, Coxsackie A17 viruses and enterovirus 71 90 115 1 90 116.

Since the only vector of enteroviruses is humans, you can become infected by contact with a sick person or with a virus carrier who has no symptoms of the disease ¹ . According to the literature, the number of virus carriers can be up to 46% of people ² .

The virus is excreted into the external environment with feces and droplets of saliva. It is also contained in the vesicles that appear in the patient’s throat. Children suffer from enterovirus infections more often, although the disease also occurs in adults ⁵ .

A sick person or a virus carrier secretes viruses from the upper respiratory tract within 3 weeks after infection, and with feces – up to 8 weeks. In the first two weeks, herpetic sore throat is most contagious ¹ .

You can get infected in the following way ³ :

• through dirty hands, objects and food, if they get a virus;
• after drinking contaminated water from a reservoir;
• upon contact with a sick person or a virus carrier.

Herpes sore throat virus is also transmitted transplacentally – from mother to fetus ³ .

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Symptoms of herpetic sore throat

The disease begins acutely. From the moment of infection to the first symptoms, it takes from 2 to 14 days ³ . The temperature rises to 38-39 ° C. The patient feels weakness, headache, chills, less often nausea, vomiting and enlargement of the submandibular lymph nodes are possible, ^1.2.3 .

Herpangina goes through several stages ² :

• The day before the appearance of a rash in the throat, the patient feels a mild pain.On examination, reddening of the palatine arches and the posterior pharyngeal wall can be seen.
• Then on the mucous membrane of the soft palate, palatine arches, tonsils and uvula, rashes appear – small papules (nodules) up to 5 mm in diameter with a red corolla.
• The nodules turn into bubbles, which burst after 1-2 days.
• Painful erosions with a gray-white coating form in their place.

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Herpetic sore throat in children

Children are usually infected in school or kindergarten ^2.3 .Because of the pain and heat, they are restless, tearful, often refuse to eat and drink, because food irritates the erosion on the mucous membrane and causes discomfort. But children often become dehydrated because they refuse to drink water or juices. At the same time, the child’s tongue becomes dry, the elasticity of the skin decreases ¹ . Against the background of a high temperature, convulsions may occur ¹ .

Blistering rashes in children can appear not only on the mucous membrane of the throat, but also on the hands and feet, and even on the buttocks and forearms.This manifestation of enterovirus infection is called viral pemphigus of the oral cavity and extremities or mouth-hand-foot syndrome. The disease is contagious in 100% of cases, is more often mild, can affect nails ³ .

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The course of herpetic sore throat

The diagnosis of herpetic sore throat can be made by an otorhinolaryngologist, therapist or pediatrician by examining the patient and clarifying his complaints. To track the changes characteristic of a viral infection, the doctor may prescribe a general blood test, and to confirm enteroviral sore throat, a specialist can use a pharyngeal smear and a blood test for specific antibodies. You can also find the pathogen in the feces or inflammatory fluid that is secreted from the vesicles ^1.4 .

Manifestations of herpetic sore throat can go away on their own in less than 10 days. But in any case, at the first symptoms of the disease, you must definitely consult a doctor. Do not self-medicate ^2.3 .

In some cases, herpetic sore throat can cause complications from the nervous system. At the same time, ¹ appear:

• pronounced spasm of the occipital muscles, due to which the child cannot bend his head;
• limb muscle weakness;
• impaired consciousness.

Severe complication of herpetic sore throat – damage to the soft membranes of the brain, brain and spinal cord ^1.3 .

The highest risk of complications in newborns, therefore, they need careful treatment and care ³ . It is important to stay hydrated and give your child enough fluids ¹ .

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Treatment of herpetic sore throat

Patients with complications need hospitalization in an infectious diseases hospital and treatment under the supervision of narrow specialists – a neurologist and a cardiologist.If a doctor has recommended home treatment, the patient should be closely monitored ² .

The sick person should be isolated and kept in a clean, well-ventilated area so as not to infect other family members. Quarantine must be observed until symptoms subside ¹ .

With herpangina, ^1,3,4 :

• Wash hands as often as possible, including after feeding and changing a diaper to a sick child.
• Disinfect surfaces and objects with which the patient came into contact.
• Drink plenty of fluids to stay hydrated. At the same time, pay attention to the temperature of the drink: hot, warm drinks irritate the mucous membranes and cause additional discomfort. You can drink cool drinks.
• Eat food in liquid or gruel form. Spicy, salty, sour, including fresh fruit, even in the form of mashed potatoes, is not suitable for a patient with herpetic sore throat.
• Rinse your mouth with saline solution after every meal to maintain oral hygiene and avoid causing erosion by bacteria.
• Use a soft toothbrush to reduce trauma to the mucous membrane.

There is currently no proven antiviral drug to treat herpes sore throat by targeting its pathogen. Sometimes the doctor can prescribe funds that support the local immunity of the pharyngeal mucosa ¹ .Antibiotics for herpangine are not prescribed ⁶ .

The goal of treatment for herpangina is to relieve the symptoms of the disease ⁴ .

If body temperature exceeds 38.5 ° C, physical methods such as cold compresses and ice packs may be used. Your doctor may also recommend anti-inflammatory and antipyretic drugs ¹ . Local treatment includes anti-inflammatory, analgesic, enveloping and antiseptic agents ¹ .

For the symptomatic treatment of herpetic sore throat, the doctor may prescribe the drugs HEXORAL ^{® 7,8,9,10,11} . For irrigation of the pharyngeal mucosa, it is convenient to use the HEXORAL ^® spray. The active substance of the spray is hexetidine. It acts against the main bacteria found in the oral cavity and on the pharyngeal mucosa ⁸ . Also, the drug is active against some viruses and fungi of the genus Candida ⁸ . Due to the local anesthetic effect of hexetidine, HEXORAL ^® spray helps to reduce pain ⁸ .For rinsing, HEXORAL ^{® 7} solution is suitable. It is allowed to use the HEXORAL ^® spray and solution in children from 3 years old ^7.8 .

If herpetic sore throat causes severe pain and discomfort, HEXORAL ^® TABS EXTRA lozenges, which contain the anesthetic lidocaine ¹⁰ , can help adolescents over 12 years of age and adults. HEXORAL ^® TABS lozenges may be suitable for children over 4 years of age. The anesthetic benzocaine in their composition helps to relieve pain in the pharynx and mouth ⁹ .

All drugs for herpes sore throat should be used only after consulting a doctor. With pronounced erosion, the solution and spray HEXORAL ^® are contraindicated ^7.8 , and only a specialist can prescribe tablets for resorption after examining the pharynx ^9.10 .

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The information in this article is for reference only and does not replace professional medical advice. Consult a qualified professional for diagnosis and treatment.

Sources

1. Corsino CB, Ali R, Linklater DR. Herpangina. 2020 Jun 23. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2020 Jan–. PMID: 29939569.https: //www.ncbi.nlm.nih.gov/books/NBK507792/
2. Ter-Bagdasaryan L.V., Ratnikova L.I., Stenko E.A. Clinical and epidemiological aspects of enterovirus infection // Infectious diseases: news, opinions, training. 2020.Vol. 9, No. 1. S. 88-93. doi: 10.33029 / 2305-3496-2020-9-1-88-93 https: // infect-dis-journal.ru / ru / jarticles_infection / 672.html? SSr = 2601343bdb01ffffffff27c__07e4040b011a36-9772
3. Alacheva Z.A., Rybalka O.B, Kulichenko T.V. Or fear has big eyes. Questions of modern pediatrics. 2017; 16 (4): 286-290. doi: 10.15690 / vsp.v16i4.1774) https://vsp.spr-journal.ru/jour/article/viewFile/1787/713
4. Herpangina Brenda L. Tesini. University of Rochester School of Medicine and Dentistry // MSD Manual – 2019
   https://www.msdmanuals.com/ru/professional/infectious-diseases/enteroviruses/gerpangina
5. Kozlovskaya O.V., Katanakhova L.L., Kamka N.N., Evseeva A.N. Epidemiological, clinical and diagnostic features of enterovirus infection in children and adults Vestnik SURGU. Medicine. 2018; (2): 56-60. https://surgumed.elpub.ru/jour/article/view/140/141
6. Kuo KC, Yeh YC, Huang YH, Chen IL, Lee CH. Understanding physician antibiotic prescribing behavior for children with enterovirus infection. PLoS One. 2018 Sep 7; 13 (9): e0202316. doi: 10.1371 / journal.pone.0202316. PMID: 30192893; PMCID: PMC6128467.https://pubmed.ncbi.nlm.nih.gov/30192893/
7. Instructions for use of the drug HEXORAL ^® SOLUTION: https://www.hexoral.ru/preparaty/rastvor
8. Instructions for use of the drug HEXORAL ^® AEROSOL: https://www.hexoral.ru/preparaty/spray
9. Instructions for use of the drug HEXORAL ^® TABS: https://www.hexoral.ru/preparaty/tabs
10. Instructions for use of the drug HEXORAL ^® TABS EXTRA: https: //www.hexoral.ru / preparaty / tabs-extra

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Rash in the chest area

Redness, irritation, itching, peeling, soreness, as well as the appearance of inflammatory skin elements on the chest and décolleté in women (dermatitis, urticaria).

Reasons

A rash in the chest area can have the same causes as a rash on any other part of the body, or specific only to this area.

Specific causes of rashes (occurring only in the chest area):

Breast abscess

Inflammatory breast cancer

Ectasia of the ducts of the mammary glands,

Mastitis (an infection in the breast tissue that most often affects women who are breastfeeding),

Eczema of the nipple,

· Paget’s disease (breast cancer of the nipple).

Common causes of a rash include:

Atopic dermatitis (eczema),

Candidiasis (especially in the area under the breast),

Cellulite (skin infection),

Dermatitis,

Urticular rash and angioedema,

Psoriasis

Scabies,

· Seborrheic dermatitis,

· Shingles.

When should I see a doctor?

Emergency if you have:

Fever

· Strong pain,

Wounds that do not heal

Red streaks from a rash,

Yellow or green fluid from the elements of the rash,

As planned , if:

The rash periodically disappears and reappears;

· Symptoms of the rash get worse and cause discomfort.

Diagnostics and treatment

With a complaint of a rash in the absence of other symptoms, you should immediately consult a dermatologist. In Moscow, dermatologists see patients at the Moscow Scientific and Practical Center for Dermatovenereology and Cosmetology and in its branches located in all districts of the city.

Recording is conducted without a referral from a therapist, you can register yourself on the Center’s website

Read more – Moscow Scientific and Practical Center for Dermatovenereology and Cosmetology

Recommendations for self-care of your skin before your doctor’s appointment:

· Do not scratch, comb the rash, or injure your skin with any products or household tools.

· You can apply an unscented moisturizer to your skin.

Think and rule out all possible triggers that may have contributed to the rash (new clothes, new laundry detergent, cosmetics, exotic foods, etc.