Clinical Challenge: A Pruritic Scaly Rash on the Beard - MPR

Clinical Challenge: A Pruritic Scaly Rash on the Beard

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A 68-year-old male develops an itchy scaly rash in his beard. He admits that he dyed his beard several days prior to presentation.

This patient is allergic to paraphenylenediamine (PPD), a chemical commonly used in permanent hair dyes. PPD supplies the natural look of the dye and prevents the dye from losing color with shampooing. Unfortunately, PPD is recognized as a common cause...

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This patient is allergic to paraphenylenediamine (PPD), a chemical commonly used in permanent hair dyes. PPD supplies the natural look of the dye and prevents the dye from losing color with shampooing. Unfortunately, PPD is recognized as a common cause of allergic contact dermatitis (ACD).

PPD is found in its colorless non-oxidized state in hair dyes and requires another substance to oxidize with to produce color. Hair dyes with PPD come with two bottles — one with the hair dye containing non-oxidized PPD and the other containing the oxidizer.

The oxidation process produces a partially oxidized intermediate of PPD. This partially oxidized PPD is responsible for hair-dye induced acute contact dermatitis.

Once fully oxidized, PPD is no longer allergenic. Hence, patients who may be allergic to PPD from hair dye can usually wear dyed wigs or other dyed clothing without experiencing an allergic response.

In allergic patients whose hair has been dyed, sensitivity can manifest as itching, redness, and puffiness of the upper eyelids, tops of the ears, temples and back of the neck.

Classically, in mild cases, dermatitis is restricted to the upper eyelids or the rims of the ears. In more severe cases, involvement of the scalp and the face may be present. With a severe enough response, patients may even present with complete closure of the eyelids. If a patient has been coloring facial hair, eyelashes or beards, eyelid dermatitis may be present.

In terms of risk populations, PPD allergic contact dermatitis is typically found in individuals who dye hair, such as hairdressers, but may also affect those who handle the chemical in other professions. Chronic exposure classically affects hairdressers, but may also affect those who work in photography development or rubber vulcanization.

Patients who develop PPD may first develop eruptions on the backs of the hands, the wrists, the forearms, the eyelids and the nose. These lesions consist of an eczematous, erythematous and oozing dermatitis.

If the patient has chronic exposure, as seen in those who work with PPD, lichenification and scaling may be seen from repeat acute dermatitis and scratching. In rare cases, severe PPD allergy can result in contact urticaria and, rarely, anaphylaxis.

PPD has also been found in tattoo ink in higher concentrations than what is typically found in hair color products. Allergies that occur in those tattooed with ink containing high concentrations of PPD may present with an acute vesicular allergic reaction, which may eventually result in scarring and hyperpigmentation.

Patch testing to test for hypersensitivity is used to establish a PPD allergy diagnosis.

Treating PPD dermatitis from a hair dye allergy begins with a thorough washing of the hair and scalp with mild soap or a soap-less shampoo to remove any excess dye. For any residual partially oxidized PPD, a 2% hydrogen peroxide solution or compress of potassium permanganate in a 1:5000 dilution may complete the oxidation process.

Application of topical steroids or oral corticosteroids may be indicated. Management of PPD dermatitis on other parts of the body is treated like any acute dermatitis/eczema using topical corticosteroids and emollients.

Patients with PPD allergy may also show cross-reactivity to other frequently used cosmetic chemicals. They may have an allergic response to azo dyes, a chemical used in temporary hair dyes and also as a coloring agent in some foods and medication.

Benzocaine and procaine, a local anesthetic used by doctors and dentists, may also have cross-reactivity. Patients are thus encouraged to inform their doctors or dentists if they have a PPD allergy.

Finally para-aminobenzoic acid (PABA), an ingredient used in sunscreens and creams in over-the-counter preparations, may also cross-react. Because of this, patients with PPD allergy should only use sunscreens labeled PABA-free.

For those sensitive to PPD-containing hair dye, use of semi-permanent or temporary dyes may be the solution. In the case of sensitivity to either of these options, vegetable dye such as henna is another option. Metallic dyes often used by men will also not cross-react, but may contain other allergens such as nickel, cobalt or lead.

Other answer choices

Sesquiterpene lactone is the primary allergen in allergic contact dermatitis caused by the Asteraceae family of plants, the most classic of which is chrysanthemum.

Asteraceae dermatitis presents on areas of skin exposed to flowers or pollens. It is most commonly seen in florists and people working in other occupations that handle with flowers. Allergy can result from direct contact with the plant, its pollen or skin care products that use the plant extracts.

The most common presentation is dermatitis of the eyelids and hands of a florist. In severe cases, allergy to sesquiterpene lactone has been resulted in angioedema, urticarial and systemic contact dermatitis.  

Patch testing helps confirm a diagnosis of sesquiterpene lactone allergy. Concomitant allergy to balsam of Peru and rosin is common, both of which also originate from plants.

Urushiol is the predominant allergen in Toxicodendron genus of flowering plants in the sumac family, Anacardiaceae. Urushiol contact dermatitis typically occurs with exposure to poison ivy, and its related family members, including poison oak and poison sumac. Individuals previously sensitized to the plant initially present 48 hours after exposure.

The lesions typically begin on the backs of the fingers, in the interdigital spaces, on the wrists or eyelids, but may sometimes begin on the ankle or other exposed body part. The initial symptom is marked pruritus followed by inflammation, vesicles and bullae.

The most characteristic diagnostic feature is the linearity of the grouped vesicles. Eyelids may become puffy. Because the fingers may transfer the allergen to other body parts, including the forearms and genitalia, these areas are frequently affected.

Washing off the causative urushiol oil prevents further spread, and tapered systemic steroids are effective for severe responses. If the eruption is limited, local application of topical corticosteroids is preferred. Antihistaminic ointments may further sensitize the patient and should be avoided.

Diallyl disulfide is the main allergen found in the plant family Alliaceae. This family includes onions, garlic and chives. Diallyl disulfide allergic contact dermatitis classically presents as fingertip dermatitis in homemakers and those who cook, most commonly on the thumb, index and middle fingertips of the non-dominant hand where the garlic clove is held.

Diallyl disulfide dermatitis will often present as hyperkeratosis, desquamation and fissuring in an asymmetric pattern. In previously sensitized patients, inhalation of garlic dust can induce asthma, and garlic poultices can cause significant burns due to severe irritation.

For allergic patients who must continue handling plants from the family Alliaceae, reusable domestic rubber gloves are protective. Disposable gloves containing vinyl, latex and polyethylele and nitrile will not protect sensitized individuals who handle garlic or onions.

Christopher Chu, BS, is a medical student at Baylor College of Medicine.

Adam Rees, MD, is a graduate of the University of California Los Angeles School of Medicine and a resident in the Department of Dermatology at Baylor College of Medicine also in Houston.

References

  1. Bolognia J, Jorizzo JL and Rapini RP. “Chapter 14 – Allergic Contact Dermatitis.” Dermatology. St. Louis, Mo.: Mosby/Elsevier, 2008. Print.
  2. James WD, Berger TJ, Elston DM et al. “Chapter 6 – Contact Dermatitis and Drug Eruptions.” Andrews’ Diseases of the Skin: Clinical Dermatology. Philadelphia: Saunders Elsevier, 2006. Print.