Five common skin problems--and a string of pearls for managing them


The author reviews the presentation, diagnosis, and treatment of a handful (and they are a handful!) of dermatologic complaints: eczema, diaper rash, scabies, lice, and alopecia areata.


Focus: Skin disorders

Five common skin problems—and a string of pearls for managing them

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By Tor Shwayder, MD

The author reviews the presentation, diagnosis, and treatment of a handful (and they are a handful!) of dermatologic complaints: eczema, diaper rash, scabies, lice, and alopecia areata. The tips he offers along the way are gleaned from his experience.

Pattern recognition is the essence of dermatology, learned by careful observation interlaced with good history taking. The text below and the accompanying figures will help you build your own visual library for five common dermatologic problems. Treatment options are discussed at length, sprinkled with recommendations based on my two decades of clinical experience.


From the Greek "to boil over," eczema is a general term encompassing several phenotypes characterized by very itchy skin and a predictable distribution and age of onset. Most dermatologists use the terms atopic eczema and atopic dermatitis (AD) interchangeably. In the last decade, much has been discovered about the etiology of AD1 and what occurs along leukocyte and interleukin signal pathways. One such pathway follows the antigen-presenting cell from the skin surface down into the dermis. When this cell encounters a triggering antigen, antigen-presenting cells at the skin surface stimulate Th-2 cells to elaborate certain interleukins—chemical signals that cause Th-0 cells to become Th-2 cells. This revs up the inflammatory pathways.

A discourse on possible atopic pathways is beyond the scope of this article. A reasonable conclusion is the following: For eczema to occur, a patient must have the atopic gene(s) plus antigenic or environmental stimulation. This combination leads to biochemical aberrations, IgE dysregulation, and loss of balance of the immune response. Common antigen stimulants are dry surroundings, changes in weather (usually from warmer to cold), Staphylococcus aureus, and itchy clothing. Less common antigenic stimuli include house dust mites, certain foods, aeroallergens, and psychosomatic factors.2

Different types of eczema are labeled atopic, nummular, dyshidrotic, seborrheic, and xerotic. Atopic eczema is the type most commonly seen in pediatric practice. The morphology and distribution of atopic eczema can be divided by age.

The infantile phase (0 to 2 years) usually starts in the first few months of life. Although many mothers report that the eczema began "right at birth," skin needs to dry out and be exposed to antigens before eczema becomes evident. Average age of symptom onset is about 3 months, although some infants develop symptoms as early as a few weeks after birth. Red papulovesicles appear, followed by oozing and crust formation. The skin is very dry. The child often wiggles constantly, a way to "scratch" areas she or he cannot reach. For this reason, bald spots are noted over the occiput or erosions on the chin (Figure 1). Once coordinated movements begin, the child scratches almost continuously, leading to scratch marks and, often, to secondary infection with S aureus. The head and neck are invariably involved, and distribution is usually generalized to the trunk, arms, and legs. Lesions are patchy or confluent. The folds of the neck, antecubital fossa, and knee fossa are almost always spared. The diaper area is usually spared until the child is toilet trained; lesions can be found at the edges of the diaper but not in areas that are always wet and protected by the diaper (unless the child is able to get the diaper off and scratch).


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Childhood phase (2 to 12 years). As eczema waxes and wanes, the picture becomes polymorphous (that is, many different pictures present). Acute sites have excoriations, redness, papules, and bleeding. Chronic sites have lichenification—a characteristic skin thickening with infiltrated red plaques, accentuated skin folds, and postinflammatory hyperpigmentation (Figure 2).

The distribution of eczema changes between 18 and 24 months of age. Extremity extensor lesions become more flexural. The wrists and ankles become prime targets of scratching, and the face, less so. When the child stops wearing diapers, the buttocks become excoriated. The upper posterior thighs and the dorsum of the hands are frequently involved. These children continue to have dry skin. They also have hyperlinearity of palms and soles, pityriasis alba, infraorbital folds (Dennie-Morgan), and keratosis pilaris.

Adolescent phase (12 to 18 years). Localized acute eczema sometimes persists after the generalized form quiets down. Of special note is localized eczema affecting the eyelids, infra-auricular fold (where the earlobe touches the cheek), fingertips, convexities of the toes, cheilitis, nipple, and vulvar area. Antecubital fossa, neck folds, upper posterior thighs, knee folds, and ankles are often involved (Figure 3). Dry skin remains an underlying problem.

There are two dermatologic approaches to treating atopic dermatitis: wet and dry. Not a lot of hard data exist on these disparate methods. I have used the wet approach with success for the last 20 years (Table 1). I recommend the following:

  • Bathe the child twice a day in warm water.

  • Use mild soap to cleanse only the dirty areas.

  • After rinsing, leave the child very moist.

  • Apply a topical steroid, in the lowest therapeutic strength, to red or itchy areas on the moist skin.

  • Apply moisturizer on top of the steroid and to the rest of the body as well.


Treating atopic eczema

Keep the skin at a high, even level of humidity

Apply topical steroids bid as needed

Apply liberal amounts of a topical moisturizer many times a day

Use an antistaphylococcal antibiotic as needed

Use an oral antihistamine for its sedative effect

Sources: Bigby M: A thorough systematic review of treatments for atopic eczema. Arch Dermatol 2001;137:1635; Oranje AP, De Waard-Van Der Spek FB: Atopic dermatitis: Review 2000 to January 2001. Curr Opin Pediatr 2002;14:410


I prescribe 1% hydrocortisone for the face and diaper and groin area, and 0.05% desonide (Tridesilon) for other parts of the body. Both are nonfluorinated and unlikely to cause side effects. I usually choose preparations with an ointment base, especially in dry-weather months, and creams other times. (I do not recommend lotions because they are too thin to work as well.) If the patient cannot afford a brand-name moisturizer, simple petrolatum (Vaseline) works well.

If desonide ointment does not help, move up to 0.1% triamcinolone ointment. Because triamcinolone is fluorinated, avoid using it on the face, neck folds, axillary folds, and diaper area.

In the last three years, topical calcineurin inhibitors (tacrolimus and pimecrolimus), also known as topical immunomodulators, have been introduced. These compounds block interaction between the antigen-presenting cell and the Th-2 lymphocyte by interfering with calcium signaling. Both topical calcineurin inhibitors on the market work reasonably well and have been tested extensively in children as young as 2 months of age to assure their safety; to date, no adverse effects have been found when these medications are used as directed (twice a day prn for eczema). Because these medications are not steroid-based, they can be used anywhere on the body, including the face and skin folds.3 I use them as second-line therapy mainly because they are expensive, and partly because they are new and I am getting comfortable with their dose-response curve. Prescribing restrictions for age vary by country; I believe these medicines are safe and use them at whatever age eczema begins. (In the United States, tacrolimus and pimecrolimus are not approved for use in children younger than 2 years.)

I prescribe an antistaphylococcal antibiotic to minimize the S aureus population—not because the child has cellulitis or lymphangitis but because staphylococcus alone can trigger the immune cascade, causing more itching. To reduce the chance of selecting for resistant clones, use antibiotics (oral or topical) in short bursts of seven to 10 days rather than continuously. First- generation cephalosporins work well for this purpose, as does topical Bactroban, which should be applied to areas that are excoriated, open, or obviously infected.

Although eczema is not a histamine-mediated disease, an oral antihistamine can be given for its soporific effects. Because antihistamines induce tachyphylaxis, they should not be given continuously. Advise parents to give them to their child as needed, not prophylactically.


To promote use of the steroid only twice a day but use of the moisturizer many times daily, do not instruct the pharmacist to compound the steroid with the moisturizer.

Advise parents of patients who wear diapers to apply moisturizer at every diaper change. During wet-weather months, moisturizers can be applied less often, depending on the child's case.

The guiding principle for choosing a moisturizer should be: the thicker and greasier, the better. I prefer moisturizers that have to be scooped out of a jar with fingers rather than those in pump bottles or topical oils. Bath oils are of minimal help and make the child slippery.

A comment about food and aeroallergens: The dermatologist does a great job treating the skin but tends to ignore these two factors. The allergist, on the other hand, tends to overrate them and undertreat the skin. A balance needs to be struck. In my experience, food allergy and aeroallergens exacerbate eczema in only a minority of cases. I usually prefer to use the "soak, Rx, grease" method described above, and then wait and see. If this approach controls the eczema, the parents do not have to worry about diet, dust, dogs, and so on. If this method fails, I engage an allergist to help. Be aware that most parents are looking for the ONE EVIL FOOD, believing that eliminating it from the diet will solve their child's problem. This is, of course, false.

Similarly, most parents expect their child's eczema to be gone after one visit. In reality, treating eczema is like running a marathon. Most cases fizzle out between 2 and 6 years of age; the disease can, however, last many years to decades. If there is a strong history of atopy in the family, eczema may be lifelong.4

Home social issues may need to be considered. Mothers of children with eczema tend to sleep with their child so they can hold their child's wrists to prevent scratching. This sleep behavior can influence the family dynamic and should be addressed.

Although there is no "quick fix" for eczema, there are good support groups. I urge all my patients and their parents to join, learn, and share. More information can be obtained from the National Eczema Association for Science and Education (4460 Redwood Hwy., Ste. 16-D, San Rafael, CA 94903-1953, 800-818-7546; ).

Diaper rash

In Shakespeare's As You Like It, Jacques's "Seven Ages of Man" speech begins with " . . . the infant mewling and puking in the nurse's arms," and ends with "second childishness and mere oblivion, sans teeth, sans eyes, sans taste, sans everything." The playwright has aptly described the two populations affected by diaper dermatitis.5

For most of the 20th century, physicians blamed ammonia for diaper dermatitis. Not until the late 1970s was it shown that ammonia is not the cause. In the 1980s, investigators elucidated the fact that fecal enzymes (lipase and protease) become activated by the alkalinity of urine, causing skin damage.6 The key to curing diaper dermatitis, then, is to keep the perineum clean and dry, free of feces and urine.7 The take-home message? There's no such thing as an "ammoniacal" diaper dermatitis.

There are six main types of diaper rash:

  • In primary irritant diaper dermatitis, glazed red plaques tend to develop over the convex surfaces of the perineum. Erosions can occur (Figure 4).

  • Candida diaper rash is characterized by bright red scaly plaques, often with sharp margins. Small papules and pustules are found, and satellite lesions may be noted. The rash involves the folds as well as the convexities of the perineum. (Candida can also occur as a primary infection in the diaper area, rather than secondary to diaper dermatitis.)

  • Atopic diaper dermatitis is seen in conjunction with eczema elsewhere on the body. Excoriations are a hallmark, along with crusting and lichenification. Convex surfaces predominate.

  • Intertrigo diaper dermatitis is characterized by sharply demarcated red plaques in the folds, with little scale.

  • In seborrheic diaper dermatitis, the folds have salmon-colored scaly plaques with a slight yellowish scale. Usually, the scalp, ear folds, neck folds, axillary vaults, umbilical recess, and knee and arm folds display the same rash (Figure 5). Of great importance in differentiating seborrheic diaper rash from other types is that the child is asymptomatic, other than the rash.

  • Psoriatic diaper dermatitis is distinctive: A clearly delineated red plaque with slight scale looks like it was painted on the perineum in exact lines straight down the center (Figure 6). It usually stretches from just over the clitoral hood to the upper gluteal cleft in the midline. In boys, the base of the penis, inner folds, and gluteal cleft are involved. Psoriasis can involve other areas of the body as well.



When evaluating possible diaper rash, perform a thorough, full-body exam. If the skin is scaly, especially if there are pustules, do a KOH (potassium hydroxide) microscopic exam to rule out Candida or dermatophyte.

Treatment consists of keeping the child's bottom dry and clean (Table 2). Advise the parents to change the diaper frequently and to clean the perineum gently during each change. The efficacy and safety of baby wipes have been tested,8 and they are fine to use as long as the child does not react to the preservatives and the parents do not mind the cost and the smell.


Preventing and treating diaper rash

Keep the child's bottom clean and dry; change the diaper frequently

Clean the perineum gently when changing the diaper

If the skin is red, use 1% hydrocortisone cream bid

If Candida or intertrigo is present (or both), use an antifungal cream, such as clotrimazole, bid

Cover the cream and the diaper area with zinc oxide paste or Triple Paste ointment


If the diaper area is red, prescribe 1% hydrocortisone cream, bid. If Candida or intertrigo is present (or both), also prescribe an antifungal cream such as clotrimazole, bid. Cover the cream(s), as well as the entire diaper area, with zinc oxide paste or Triple Paste ointment.


Instruct parents to use the hydrocortisone and antifungal creams at different times, thereby necessitating at least a qid diaper change.

To clean off zinc oxide paste, advise parents to try mineral oil.

Baby powders reduce the coefficient of friction; most are talc derivatives. Because it is difficult to apply a powder and a cream at the same time, I recommend using powders only after the rash has healed. Cornstarch powder is fine; neither it nor talc powder supports Candida growth as once suspected. An important hazard with a powder, however, is that the child could grab the canister, believing it to be a bottle of milk, and inhale the powder, leading to aspiration pneumonia.

The use of cloth diapers has almost disappeared in the United States.9 There have been great advances in the absorbancy of synthetic diapers, and increased absorbancy, in and of itself, can reduce the incidence of diaper rash. Some of the more expensive brands incorporate various ointments into the inner lining of the diaper. Company studies have shown a reduction in the incidence of diaper rash with the use of these diapers.10–12


This arachnid is an eight-legged creature that infests many mammalian species, including farm animals, pets, and, of course, humans. The infestations are species-specific— for example, dog scabies (a cause of mange) will not infest man. Transmission is, for the most part, by skin-to-skin contact. Although it is possible to contract scabies by sleeping on contaminated sheets, the mite itself dries up and dies quickly once off the human body.

Scabies infests all races and ages. After coming in contact with skin, the mite exudes a keratinase and sinks down one or two cell layers into the epidermis. There, it moves slowly forward, parallel to the epidermal level (at a centimeter a day), passing its life cycle of about a month. It takes about three to four weeks for an infested human to begin itching. The infestation can be insidious and especially difficult to detect in clean people. (The act of scrubbing the skin removes the mite, and you are less likely to consider scabies in a well-groomed patient.) The adage to remember is: Not everyone who itches has scabies; not everyone who has scabies itches. Don't guess—do a scraping (detailed below) to make a firm diagnosis.

A clinical exam will reveal small red papules and tiny crusts. If you are lucky you will see a burrow—but don't count on it. In babies, you see a wide, scattered distribution of small red papules. Of note are red nodules in the axillae (Figure 7). In children, most cases involve the wrists (Figure 8), hands, face, buttocks, and instep of the foot or the ankle. In fact, one study showed 95% of infested cases had wrist and hand involvement.13 Women tend to get lesions around the nipples; men, on the glans penis (Figure 9). Consider red nodules on the glans penis to be scabies until proven otherwise.



Although some old textbooks say otherwise, scabies can infest the scalp and face. It can also be found under the nails (from scratching).

Diagnosis is made by identifying the mite or its feces or eggs under the microscope. Place a drop of mineral oil on the papules, crusts, or itchy area, scrape gently with a #15 scalpel blade, and place all the scrapings on a glass slide. Add more oil and a coverslip, then examine the slide under the microscope under low power (Figure 10).

Once the diagnosis is made, the index case should be treated with a scabicide (Table 3). Permethrin (a pyrethroid) cream and lindane lotion are the two scabicides readily available in the US. Other preparations, such as benzyl benzoate suspensions and malathion lotions, are used in other countries. The patient should apply the medicine head to toe, not overlooking the face, scalp, folds, recesses, and under the nails. I usually have the index case treated a second time a week later. Two treatments are sufficient.14


Getting rid of scabies

Confirm the diagnosis

Treat the patient head-to-toe with a topical scabicide; don't forget the face, scalp, folds, recesses, and under the nails

Repeat treatment in one week

Treat all skin-to-skin contacts once

Wash bedding, towels, and recently worn clothes; heat non-washable contact items in the dryer for 20 minutes

Prescribe a low-potency steroid cream for post-scabetic eczema


The Food and Drug Administration (FDA) recently issued a health advisory about lindane. The advisory announced the addition of warning labels that emphasize lindane's use as second-line, not first-line, therapy because of safety issues; neurotoxicity has been reported following not only misuse or overuse but also, in rare cases, following a single application according to directions. The labeling states that lindane should be used with caution in, among others, patients weighing less than 110 pounds, especially infants, and that it is contraindicated in premature infants. I have used lindane lotion for 20 years on hundreds (if not thousands) of patients without problems. In light of the FDA advisory, however, I recommend that permethrin cream be used first.

Recently, oral ivermectin has been shown to be very effective at treating scabies. A single dose of 200 µg/kg is sufficient,15 although some authors recommend giving a second dose.16 A 1% topical ivermectin solution has been used successfully in open clinical trials in South America.17

I usually treat all members of the same family under the same roof at the same time with a scabicide. This is because scabies can be subtle, and not everyone with active scabies infestation has symptoms to suggest it. I also treat anyone who has had skin-to-skin contact with the index case. (I use only one treatment for contacts and family members.) If there has been no skin-to-skin contact but other contact has occurred (such as at school or day care or among visiting relatives), or if it is unknown whether there has been skin-to-skin contact, I try to examine the person who may be affected to make a definitive diagnosis. This is a gray area and demands a rational approach. Regrettably, many physicians treat even the index patient without confirming the diagnosis. It is always best to "know," not "guess," especially because a diagnosis of scabies sends shock waves through the family. Upheavals are the norm and recriminations are frequent, for a variety of social and psychological reasons.

Bedding, towels, and recently worn clothes should be washed; soap and hot water do the job nicely. Those items that cannot be washed but can be heated should be placed in a dryer at high temperature for 20 minutes. Items that can be neither washed nor heated should be placed in a plastic bag for a week. Any mites will die within hours and any eggs will hatch and die in that time.

Norwegian scabies is a subtype of scabies in which the patient has thickly crusted lesions embedded with thousands of mites. It is seen in immunodeficient patients, such as those with AIDS, and in patients with Down syndrome. The condition is treated with repeated applications of a scabicide together with an agent to remove the scale. Oral ivermectin has recently been shown efficacious in treating Norwegian scabies.15


Most patients still itch after the mite dies, a condition called post-scabetic eczema. A prescription for 2.5% hydrocortisone cream or 0.05% desonide ointment bid with an oral antihistamine should lead to gradual resolution over two to four weeks.

Always check for and confirm active infestation before re-treating with the scabicide.

Be aware that there has not been a single documented case of scabies resistance in the world. Most reports that claim resistance are not well documented and include cases in which the health-care provider did not treat the whole body, did not treat family contacts, did not clean the environment, and, as a rule, did not confirm the infestation or the cure microscopically. (In clinical practice, it is not necessary to routinely confirm the cure if there is a clinical response, but such confirmation is necessary, in my opinion, to support claims of scabies resistance.)


Head lice are true insects, with three body parts and six legs (Figure 11). Unlike the scabies mite, lice are visible to the naked eye. You do, however, need a calm child, bright light, and magnification to see the lice or the nits along the hair shafts (Figures 12 and 13). Don't be fooled by dandruff flakes.



Several pediculocides are on the market: Lindane, permethrins, pyrethroids, and malathion are the most readily available, with malathion liquid having the best kill rate.18 The pediculocide should be applied as directed. Most important, the nits should be removed. Even with the best pediculocide, 5% to 35% of the nits will still hatch, which is why the patient should be treated a second time a week later.

A recent American Academy of Pediatrics clinical report on head lice states that manual removal of nits following treatment with a pediculicide is unnecessary to prevent spread.19 The report does note that none of the pediculicides is 100% ovicidal, however, and that manual removal of nits after treatment is therefore recommended by some (myself included) to prevent re-infestation. Many states have "no-nit" policies that prevent the child from returning to school if any nits are present. In fact, if no crawling lice have been noted for two weeks in children who have been treated, any nits that remain are, in all likelihood, empty cases or non-viable eggs. A balance needs to be maintained between excluding children unnecessarily from school and preventing infection of classmates.

Make sure no family members or playmates have lice. Clean combs, brushes, hats, scarves, and other personal items that have come in contact with hair.20,21 It is prudent (and, in some cases, required) for the physician or the patient's family to notify the child's school or day care of the infestation.

Other treatments have been reported anecdotally and have not been critically tested. These include cotrimoxazole in the same dosage given for otitis media, topical ivermectin shampoo (outside the US), and 5% permethrin cream applied to the scalp. The latter is prescribed to overcome the permethrin resistance of lice.22 Unlike scabies, resistant clones of lice can be noted in the laboratory and in real life. Anytime a new pediculocide is introduced in an area, resistant clones of lice develop over time. The medical response should be to rotate pediculocides regularly to try to keep one step ahead of the insects.

In contrast to head lice, body lice are rare, usually affecting only "street people." These lice live in clothing, not on the body, so throwing away infested clothes is the only "treatment" necessary. Pubic lice resemble marine crabs (hence their colloquial name, crab lice) and can infest the skin anywhere there is hair, including the eyelashes, eyebrows, axillary area, and scalp. The louse lives for four to six weeks, but dies after 12 hours if it does not get a blood meal. The nits hatch after six to eight days.

Patients and parents who prefer not to use a chemical treatment for lice have three options:

1. Pick and comb out the nits and lice daily. A fine comb should be used, and the hair should be cut short. Wetting the hair beforehand slows the lice so they don't move away from the comb.

2. Cut all the hair. A very close buzz cut will do. This is extreme but will work. Check the axillary and pubic areas to be sure no infection lurks there.

3. Cover the hair with grease or mayonnaise or a similar substance. The theory is that doing so asphyxiates the lice and nits, although there is no scientific proof that the technique works.

Alopecia areata

We are gaining a better understanding of the immunology of alopecia areata (AA), but it still remains one of the bigger dermatologic mysteries. Simply put, lymphocytes of a specific subclass are attracted to a definite antigen on the root sheath of the hair follicle. For an unknown reason, this antigen-antibody interaction causes the hair growth mechanism to shut down.23 I tell my patients that their condition is like a factory on strike: the machinery is all there, we just need to get the workers back to their jobs. It is also important to note that the condition is not a consequence of stress, diet, hair care products, vitamin deficiency, a poor or deficient immune system, or other popular misconceptions.24

AA presents as nonscarring, asymptomatic hair loss (Figure 14). The affected area is usually completely bald and coin shaped. The scalp is smooth and shows no change in color. Crusting, follicular plugging, and pustules are absent. At the margin of an active spot are "exclamation point hairs," short hairs 2 to 4 mm long with darker, thicker tops and thin, light bottoms. If you tug gently at the margins of the hair loss area a few hairs will painlessly come out. Often, multiple areas of hair loss coalesce into bald spots ringing the scalp above and behind the ears (called a tonsur). The same antigen-antibody interaction is responsible when all the scalp hair falls out (alopecia totalis) and when all scalp hair plus body hair falls out (alopecia universalis).



In as many as two thirds of patients, the nails develop small, uniform pits in an organized pattern or rows. Some or all nails may be affected. Nail dystrophy may proceed or follow hair loss and is probably due to a subtle cross-reactivity between the target keratin proteins on the hair root sheath and similar proteins in the nail keratins.

The differential diagnosis includes tinea capitis. A distinguishing feature is that tinea capitis shows black dots of hair protruding from the hair shafts just at the surface of the scalp, and not exclamation point hairs. Scale, pustules, and itch are usually present as well.

Telogen effluvium, hair loss resulting from a traumatic stimulus, shows diffuse hair loss that does not give clear coin-shaped areas. There are no broken off hairs or exclamation point hairs.

Trichotillomania, compulsive hair pulling, presents with irregular areas of hair loss, but the hairs are all of different lengths. Again, there is no clear area of baldness.

Treatment options for AA include intralesional steroid injection administered directly into the bald areas.25 Low potency (3 to 5 mg/kg) triamcinolone suspension works well injected into the dermis. This is repeated monthly until hair growth returns. Intralesional steroids are the only treatment that consistently makes the hair regrow in alopecia areata. However, it takes training and knowledge of the side effects to use them. They are painful, as all shots are. There are rare complications such as atrophy of the skin or, if you give too much steroid, systemic effects. I recommend that you refer the patient to the dermatologist if you do not have the training to perform these injections. A topical steroid is usually of minimal help in treating AA.

An alternate treatment is a topical irritant such as anthralin cream 0.1% to 1%, which is applied for a short period once daily and then washed off. Start with the lowest strength cream, and gradually increase the contact time—from 10 to 15 minutes a day initially, to 30 to 60 minutes a day—until redness and irritation are noted. The cream should be applied daily until growth appears; applications can be tapered slowly over the next month.

Topical agents that cause contact dermatitis, such as diphenylcyclopropenone, are applied in the same manner as anthralin cream. Little data exist on the use of topical calcineurin inhibitors—tacrolimus and pimecrolimus creams—for AA.

Other options are to ignore the hair loss and for the patient to wear a wig. AA waxes and wanes at irregular intervals, so a controlled study is necessary to "prove" a therapy works. Some such studies exist, but many treatments offered for AA are simply "experience based." It is difficult to assert that these treatments resolve the problem any faster than if the condition had been left to run its own course.

The bottom line: If the physician can reassure the parent that the child is otherwise well, no treatment is necessary (Table 4). If, however, the patient or parent prefers treatment rather than waiting, intralesional steroid injection is, in my experience, the best option. As noted, these injections require training and finesse on the part of the practitioner; if necessary, refer the child to a dermatologist.


Managing alopecia areata

Reassure the patient and parent that this is a local skin problem and not a sign of systemic trouble.

If the patient (or parent) wants treatment, intralesional steroid injections work best; refer to a dermatologist if you are unfamiliar with this procedure. Other treatments have a minimal or modest effect; weigh the side effects against the patient's (or parent's) desire for treatment before prescribing.

Suggest that the family contact the National Alopecia Areata Foundation ( ).

Alopecia totalis is difficult to treat—refer to a specialist.


Controversy exists regarding the incidence of autoimmune thyroid disease in patients with alopecia areata.26–29 Several articles point out that the probability of a thyroid abnormality mirrors the prevalence of the disease in the community. I have stopped screening for thyroid problems in patients with AA unless they, or an immediate blood relative, have a history of thyroid-related symptoms. Similarly, I believe there is no connection between AA and other autoimmune diseases that have been "linked" to AA in the past.


The prognosis is good if onset of AA occurs after puberty, the areas of hair loss are discrete, the patient does not have eczema, and there is no family history of AA.

The prognosis is poor if onset of AA is before puberty, hair loss is total and occurs in an ophiasis pattern (tonsur), the patient has eczema, and there is a family history of AA.

As long as a spot is regrowing hair, the prognosis is good.

When the hair loss is total, hair can regrow (albeit rarely), but the longer the area remains bald, the less likely this will happen.

Total hair loss occurs in a very small percentage of AA patients. Share this fact with parents, because many assume their child will lose all his or her hair.

I suggest that all my patients contact the National Alopecia Areata Foundation for information and support (NAAF, P.O. Box 150760, San Rafael, CA 94915-0760; 415-472-3780; ).



The author thanks Arnold Oranje, MD, Erasmus University, Sophia Children's Hospital, Rotterdam, Netherlands, for Figures 6 and 14.



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9. Baker L: Bottoming Out. Why are diaper services disappearing? Emagazine 1998(Sept-Oct);1(5):

10. Spraker MK: Update: Diapers and diaper dermatitis. Pediatr Dermatol 2000;17:75

11. Odio M, Friedlander SF: Diaper dermatitis and advances in diaper technology. Curr Opin Pediatr 2000;12:342

12. Odio MR, O'Connor RJ, Sarbaugh F, et al: Continuous topical administration of a petrolatum formulation by a novel disposable diaper. 2. Effect on skin condition. Dermatology 2000;200(3):238

13. Taplin D, Meinking TL, Chen JA, et al: Comparison of crotamiton 10% cream (Eurax) and permethrin 5% cream (Elimite) for the treatment of scabies in children. Pediatr Dermatol 1990;7:67

14. Bigby M: A systematic review of the treatment of scabies. Arch Dermatol 2000;136:387

15. Meinking TC, Taplin D, Herminda JL, et al: The treatment of scabies with ivermectin. N Engl J Med 1995;333:26

16. Burkhart CG, Burkhart CN: Optimal treatment for scabies remains undetermined. J Am Acad Dermatol 2001;45:637

17. Victoria J, Trujillo R: Topical ivermectin: A new successful treatment for scabies. Ped Dermatol 2001;18:63

18. Meinking TL, Entzel P, Villar ME, et al: Comparative efficacy of treatments for pediculosis capitis infections. Arch Dermatol 2001;137:287

19. Frankowski BL, Weiner LB: Head lice: American Academy of Pediatrics clinical report. Pediatrics 2002;110:638

20. Roos TC, Alam M, Roos S, et al: Pharmacotherapy of ectoparasitic infections. Drugs 2001;61:1067

21. Potts J: Eradication of ectoparasites in children. How to treat infestations of lice, scabies and chiggers. Postgrad Med 2001;110(1):57

22. Schachner L: Treatment resistant head lice: Alternative therapeutic approaches. Pediatr Dermatol 1997;14:409

23. Hordinsky MK: Alopecia areata: Pathophysiology and latest developments. J Cutan Med Surg 1999(Nov); 3:S28

24. Picardi A, Abeni D: Stressful life events and skin diseases: Disentangling evidence from myth. Psychother Psychosom 2001;70(3):118

25. Madani S, Shapiro J: Alopecia areata update. J Am Acad Dermatol 2000;42:549

26. Lutz G, Bauer R: [Autoimmunity in alopecia areata. An assessment in 100 patients.] (In German) Hautarzt 1988;39:5

27. Muller HK, Rook AJ, Kubba R: Immunohistology and autoantibody studies in alopecia areata. Br J Dermatol 1980;102:609

28. Shellow WV, Edwards JE, Koo JY: Profile of alopecia areata: A questionnaire analysis of patient and family. Int J Dermatol 1992;31:186

29. Lewinski A, Broniarczyk-Dyla G, Sewerynek E, et al: Abnormalities in structure and function of the thyroid gland in patients with alopecia areata. J Am Acad Dermatol 1990;23:768

DR. SHWAYDER is director, pediatric dermatology, Henry Ford Hospital, Detroit, Mich. He is a consultant with Ferndale Laboratories (maker of ELA-Max and Locoid), a member of the speaker's bureau with Novartis Pharmaceuticals (maker of Elidel [pimecrolimus]) and Fujisawa (maker of Protopic [tacrolimus]), and a recipient of a grant from Summers Lab (maker of Triple Paste diaper ointment).


Tor Shwayder. Five common skin problems--and a string of pearls for managing them. Contemporary Pediatrics July 2003;20:34.

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