What is a suncream allergy



So that´s why we´re allergic to sun creams

News: Oct 05,

What happens to sunscreens when they are exposed to sunlight? And how is the skin affected by the degradation products that form? This has been the subject of research at the University of Gothenburg and Chalmers University of Technology that will be presented at the upcoming dermatologist conference in Gothenburg.

A growing hole in the ozone layer and a change in sunbathing habits own brought an increase in the number of cases of skin cancer worldwide. One way of dealing with this has been to advocate sunscreens, though greater use of these products has triggered an increase in contact allergy and photocontact allergy to sun protection products.
“We know that sun creams pass through the skin into our bodies, but we don’t know what effects they own on us,” says Isabella Karlsson, doctoral student at the Department of Chemistry at the University of Gothenburg’s Faculty of Science.

“Many of them actually break below in the presence of sunlight. We therefore wanted to glance at what can happen to the chemical sun protection agents when exposed to UV rays, and how the degradation products that form affect the skin.”

In their study, the researchers own come up with an explanation of what happens during this process.
“Arylglyoxales, one of the degradation products, turned out to be highly allergenic,” says Karlsson. “Which could explain why some people are allergic to creams that contain dibenzoylmethanes, one of the UVA-absorbing substances in sun creams.”
This has made for a better understanding of the mechanism behind photocontact allergy, which could lead to a product that does not cause allergy, and could determine which sun creams people are most likely to be sensitive to.

But their discovery is already having an impact.

The healthcare system has endless found it hard to test patients with suspected photocontact allergy, but thanks to the study a new test is being developed.
“We’re just starting to work with various dermatology clinics on assessing the test,” explains Karlsson. “So more patients will be capable to discover out whether they own photocontact allergy, which could assist them in their everyday lives and reduce the burden on the healthcare system.”

PHOTOCONTACT ALLERGY AND CONTACT ALLERGY
A photocontact allergic reaction results from the chemical alteration of sunscreens by sunlight, with the body’s immune system then responding with an allergic reaction.

The reaction is unusual, and the cause of the condition is generally sunscreens. The symptoms are eczema-like rashes that can itch. The treatment is to avoid the substance that causes the allergy.

For more information, please contact:
Isabella Karlsson, PhD student at the Department of Chemistry at the Faculty of Science, tel. +46 31 91 08, e-mail:[email protected]
Anna Börje, researcher at the Department of Chemistry at the Faculty of Science, tel. +46 31 90 12, e-mail: [email protected]

Title of the study: Photodegradation of Dibenzoylmethanes: Potential Cause of Photocontact Allergy to Sunscreens
Authors: I.

Karlsson1, L. Hillerstrom1, A. Stenfeldt1, J. Mårtensson2, A. Borje1 1

Dermatochemistry and Skin Allergy, Department of Chemistry, University of Gothenburg, 2Organic Chemistry, Department of Chemical and Biological Engineering, Chalmers University of Technology

Time and date: pm on Saturday 9 October
Venue: Lecture room F07 at the Swedish Exhibition & Congress Centre, Gothenburg

Download the conference programme and other information from: thenburgorg

BY:
38 69, 24 82 70

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Skin Disorders

A.

What skin disorders do we assess with these listings?

We use these listings to assess skin disorders that may result from hereditary, congenital, or acquired pathological processes. The kinds of impairments covered by these listings are: Ichthyosis, bullous diseases, chronic infections of the skin or mucous membranes, dermatitis, hidradenitis suppurativa, genetic photosensitivity disorders, and burns.

B. What documentation do we need?

When we assess the existence and severity of your skin disorder, we generally need information about the onset, duration, frequency of flare-ups, and prognosis of your skin disorder; the location, size, and appearance of lesions; and, when applicable, history of exposure to toxins, allergens, or irritants, familial incidence, seasonal variation, stress factors, and your ability to function exterior of a highly protective environment.

To confirm the diagnosis, we may need laboratory findings (for example, results of a biopsy obtained independently of Social Security disability evaluation or blood tests) or evidence from other medically acceptable methods consistent with the prevailing state of medical knowledge and clinical practice.

C. How do we assess the severity of your skin disorder(s)?

We generally base our assessment of severity on the extent of your skin lesions, the frequency of flare-ups of your skin lesions, how your symptoms (including pain) limit you, the extent of your treatment, and how your treatment affects you.

1. Extensive skin lesions.

Extensive skin lesions are those that involve multiple body sites or critical body areas, and result in a extremely serious limitation. Examples of extensive skin lesions that result in a extremely serious limitation include but are not limited to:

a. Skin lesions that interfere with the motion of your joints and that extremely seriously limit your use of more than one extremity; that is, two upper extremities, two lower extremities, or one upper and one lower extremity.

b. Skin lesions on the palms of both hands that extremely seriously limit your ability to do fine and gross motor movements.

c. Skin lesions on the soles of both feet, the perineum, or both inguinal areas that extremely seriously limit your ability to ambulate.

2. Frequency of flare-ups.

If you own skin lesions, but they do not meet the requirements of any of the listings in this body system, you may still own an impairment that prevents you from doing any gainful activity when we consider your condition over time, especially if your flare-ups result in extensive skin lesions, as defined in C1 of this section.

Therefore, if you own frequent flare-ups, we may discover that your impairment(s) is medically equal to one of these listings even though you own some periods during which your condition is in remission. We will consider how frequent and serious your flare-ups are, how quickly they resolve, and how you function between flare-ups to determine whether you own been unable to do any gainful activity for a continuous period of at least 12 months or can be expected to be unable to do any gainful activity for a continuous period of at least 12 months. We will also consider the frequency of your flare-ups when we determine whether you own a severe impairment and when we need to assess your residual functional capacity.

3. Symptoms (including pain).

Symptoms (including pain) may be significant factors contributing to the severity of your skin disorder(s). We assess the impact of symptoms as explained in §§ , , , and of this chapter.

What is a suncream allergy

4. Treatment.

We assess the effects of medication, therapy, surgery, and any other form of treatment you get when we determine the severity and duration of your impairment(s). Skin disorders frequently reply to treatment; however, response to treatment can vary widely, with some impairments becoming resistant to treatment. Some treatments can own side effects that can in themselves result in limitations.

a. We assess the effects of continuing treatment as prescribed by determining if there is improvement in the symptoms, signs, and laboratory findings of your disorder, and if you experience side effects that result in functional limitations.

To assess the effects of your treatment, we may need information about:

i. The treatment you own been prescribed (for example, the type, dosage, method, and frequency of istration of medication or therapy);

ii. Your response to the treatment;

iii. Any adverse effects of the treatment; and

iv.

What is a suncream allergy

The expected duration of the treatment.

b. Because treatment itself or the effects of treatment may be temporary, in most cases sufficient time must elapse to permit us to assess the impact and expected duration of treatment and its side effects. Except under and , you must follow continuing treatment as prescribed for at least 3 months before your impairment can be sure to meet the requirements of a skin disorder listing.

(See H if you are not undergoing treatment or did not own treatment for 3 months.) We consider your specific response to treatment when we assess the overall severity of your impairment.

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D. How do we assess impairments that may affect the skin and other body systems?

When your impairment affects your skin and has effects in other body systems, we first assess the predominant feature of your impairment under the appropriate body system. Examples include, but are not limited to the following.

1. Tuberous sclerosis primarily affects the brain.

The predominant features are seizures, which we assess under the neurological listings in , and developmental delays or other mental disorders, which we assess under the mental disorders listings in

2. Malignant tumors of the skin (for example, malignant melanomas) are cancers, or neoplastic diseases, which we assess under the listings in

3. Autoimmune disorders and other immune system disorders (for example, systemic lupus erythematosus (SLE), scleroderma, human immunodeficiency virus (HIV) infection, and Sjögren’s syndrome) often involve more than one body system. We first assess these disorders under the immune system disorders listings in We assess SLE under , scleroderma under , Sjögren’s syndrome under , and HIV infection under

4.

Disfigurement or deformity resulting from skin lesions may result in loss of sight, hearing, lecture, and the ability to chew (mastication). We assess these impairments and their effects under the special senses and lecture listings in and the digestive system listings in Facial disfigurement or other physical deformities may also own effects we assess under the mental disorders listings in , such as when they affect mood or social functioning.

E. How do we assess genetic photosensitivity disorders?

1. Xeroderma pigmentosum (XP). When you own XP, your impairment meets the requirements of A if you own clinical and laboratory findings showing that you own the disorder.

(See E3.) People who own XP own a lifelong hypersensitivity to every forms of ultraviolet light and generally lead extremely restricted lives in highly protective environments in order to prevent skin cancers from developing. Some people with XP also experience problems with their eyes, neurological problems, mental disorders, and problems in other body systems.

2. Other genetic photosensitivity disorders.

Other genetic photosensitivity disorders may vary in their effects on diverse people, and may not result in an inability to engage in any gainful activity for a continuous period of at least 12 months.

Therefore, if you own a genetic photosensitivity disorder other than XP (established by clinical and laboratory findings as described in E3), you must show that you own either extensive skin lesions or an inability to function exterior of a highly protective environment to meet the requirements of B.

You must also show that your impairment meets the duration requirement. By inability to function exterior of a highly protective environment we mean that you must avoid exposure to ultraviolet light (including sunlight passing through windows and light from unshielded fluorescent bulbs), wear protective clothing and eyeglasses, and use opaque wide spectrum sunscreens in order to avoid skin cancer or other serious effects.

Some genetic photosensitivity disorders can own extremely serious effects in other body systems, especially special senses and lecture (), neurological (), mental (), and neoplastic (). We will assess the predominant feature of your impairment under the appropriate body system, as explained in D.

3. Clinical and laboratory findings.

a. General. We need documentation from an acceptable medical source to establish that you own a medically determinable impairment.

In general, we must own evidence of appropriate laboratory testing showing that you own XP or another genetic photosensitivity disorder. We will discover that you own XP or another genetic photosensitivity disorder based on a report from an acceptable medical source indicating that you own the impairment, supported by definitive genetic laboratory studies documenting appropriate chromosomal changes, including abnormal DNA repair or another DNA or genetic abnormality specific to your type of photosensitivity disorder.

b. What we will accept as medical evidence instead of the actual laboratory report. When we do not own the actual laboratory report, we need evidence from an acceptable medical source that includes appropriate clinical findings for your impairment and that is persuasive that a positive diagnosis has been confirmed by appropriate laboratory testing at some time prior to our evaluation. To be persuasive, the report must state that the appropriate definitive genetic laboratory study was conducted and that the results confirmed the diagnosis. The report must be consistent with other evidence in your case record.

F. How do we assess burns?

Electrical, chemical, or thermal burns frequently affect other body systems; for example, musculoskeletal, special senses and lecture, respiratory, cardiovascular, renal, neurological, or mental.

Consequently, we assess burns the way we assess other disorders that can affect the skin and other body systems, using the listing for the predominant feature of your impairment. For example, if your soft tissue injuries are under continuing surgical management (as defined in M), we will assess your impairment under However, if your burns do not meet the requirements of and you own extensive skin lesions that result in a extremely serious limitation (as defined in C1) that has lasted or can be expected to final for a continuous period of at least 12 months, we will assess them under

G. How do we determine if your skin disorder(s) will continue at a disabling level of severity in order to meet the duration requirement?

For every of these skin disorder listings except and , we will discover that your impairment meets the duration requirement if your skin disorder results in extensive skin lesions that persist for at least 3 months despite continuing treatment as prescribed. By persist, we mean that the longitudinal clinical record shows that, with few exceptions, your lesions own been at the level of severity specified in the listing. For A, we will presume that you meet the duration requirement. For B and , we will consider every of the relevant medical and other information in your case record to determine whether your skin disorder meets the duration requirement.

H. How do we assess your skin disorder(s) if your impairment does not meet the requirements of one of these listings?

1. These listings are only examples of common skin disorders that we consider severe enough to prevent you from engaging in any gainful activity. For most of these listings, if you do not own continuing treatment as prescribed, if your treatment has not lasted for at least 3 months, or if you do not own extensive skin lesions that own persisted for at least 3 months, your impairment cannot meet the requirements of these skin disorder listings. (This provision does not apply to and ) However, we may still discover that you are disabled because your impairment(s) meets the requirements of a listing in another body system or medically equals the severity of a listing.

(See §§ and of this chapter.) We may also discover you disabled at the final step of the sequential evaluation process.

2. If you own not received ongoing treatment or do not own an ongoing relationship with the medical community despite the existence of a severe impairment(s), or if your skin lesions own not persisted for at least 3 months but you are undergoing continuing treatment as prescribed, you may still own an impairment(s) that meets a listing in another body system or that medically equals a listing.

If you do not own an impairment(s) that meets or medically equals a listing, we will assess your residual functional capacity and proceed to the fourth and, if necessary, the fifth step of the sequential evaluation process in §§ and of this chapter.

What is a suncream allergy

When we decide whether you continue to be disabled, we use the rules in §§ and of this chapter.

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Category of Impairments, Skin Disorders

Ichthyosis, with extensive skin lesions that persist for at least 3 months despite continuing treatment as prescribed.

Bullous disease (for example, pemphigus, erythema multiforme bullosum, epidermolysis bullosa, bullous pemphigoid, dermatitis herpetiformis), with extensive skin lesions that persist for at least 3 months despite continuing treatment as prescribed.

.

Chronic infections of the skin or mucous membranes, with extensive fungating or extensive ulcerating skin lesions that persist for at least 3 months despite continuing treatment as prescribed.

Dermatitis (for example, psoriasis, dyshidrosis, atopic dermatitis, exfoliative dermatitis, allergic contact dermatitis), with extensive skin lesions that persist for at least 3 months despite continuing treatment as prescribed.

Hidradenitis suppurativa, with extensive skin lesions involving both axillae, both inguinal areas or the perineum that persist for at least 3 months despite continuing treatment as prescribed.

Genetic photosensitivity disorders, established as described in E.

A. Xeroderma pigmentosum. Consider the individual disabled from birth.

B. Other genetic photosensitivity disorders, with:

1. Extensive skin lesions that own lasted or can be expected to final for a continuous period of at least 12 months,

OR

2. Inability to function exterior of a highly protective environment for a continuous period of at least 12 months (see E2).

Burns, with extensive skin lesions that own lasted or can be expected to final for a continuous period of at least 12 months (see F).

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Treatment Options

Table 1.

Treatment options for eyelid dermatitis (T topical, S systemic)

Characteristic findings on physical examination

Atopic dermatitis is the most common cause of chronic eyelid dermatitis, which mimics changes seen in other chronic eczemas, with hyperpigmentation, lichenification, and diffuse scaling. Excessive chronic rubbing of the eyelids can cause eyelash and eyebrow hair loss. Dennie Morgan infraorbital folds, periorbital darkening (the “allergic shiner”), keratoconus, and anterior subcapsular cataracts are other clinical findings seen in chronic atopic eyelid dermatitis.

Full skin examination is significant and helpful in identifying other typical areas of involvement by atopic dermatitis (Figure 11, Figure 12).

What to be alert for in the history

Rosacea is a chronic inflammatory disorder mostly affecting fair skin individuals.

Patients are generally adult females in a to year-old age group. Typical facial rosacea presents with facial flushing (triggered by stress, spicy food, heat, or alcohol), redness, and acne-like lesions. Symptoms are nonspecific and encompass stinging, burning and itching of the areas involved. Numerous report skin sensitivity to a variety of topical products and sun.

Topical and intranasal steroids are a common trigger of a persistent rosacea flare. Ocular rosacea can be present in the absence of the characteristic rosacea features.

Variety of ocular and eyelid symptoms are reported: dry eyes, sensation of grittiness or foreign body, light-sensitivity and swelling, itching or scaling of the eyelids.

Characteristic findings on physical examination

As eyelid dermatitis can be an episodic occurrence, patients can present with relatively normal eyelid examination. In general, eyelid dermatitis appears as erythematous, often scaly, sometimes crusty and oozing plaques on either upper or lower eyelids or both, unilateral or bilateral.

Edema is often present, but not without erythema and scaling.

The palpebral and bulbar conjunctiva are generally spared, but can appear slightly erythematous as a reaction to the surrounding inflammation. Upper lid involvement is more associated with airborne contact allergens, whereas lower lid dermatitis is more commonly associated with contact dermatitis induced by eye drops. In a photodistributed dermatitis again lower eyelids will be involved, while upper eyelids, especially creases, will be spared.

Allergic or irritant dermatitis more often presents as acute eyelid dermatitis with intense pruritus, weeping, brightly erythematous and edematous papules and plaques.

Although vesicles are also a hallmark of acute contact dermatitis, they are less common periorbitally. Presence of vesicles should alert the clinician to consider a herpetic viral infection (herpes simplex or zoster; Figure 10). Yellow honey-color crusting can also indicate bacterial impetiginization.

Contact dermatitis is often bilateral. Unilateral involvement suggests an infectious cause such as herpes zoster or erysipelas. Hordeolum and chalazion generally localize to one eye as well.

If eyelids present with swelling (edema) in the absence of erythema, scaling or pruritus, other eyelid conditions need to be considered, such as angioedema or hypothyroidism-induced periorbital edema.

Expected results of diagnostic studies

Contact eyelid dermatitis is a clinical diagnosis in most cases, as history in combination with improvement when avoiding the allergen/irritant are enough to finalize diagnosis.

In more hard cases, patch testing to a number of contact allergens can assist distinguish a specific cause.

Patch testing is the gold standard for evaluation of ACD. Unfortunately a large number of allergens thought to cause ACD of the eyelids are not found on the only patch test material approved by the Food and Drug istration, the TRUE test, necessitating more extensive testing. Even once a relevant allergen has been identified, it can remain a challenge to eliminate contact with the substance or substances that cross-react with the allergen. For example “unscented” or “fragrance-free” formulations do not guarantee the elimination of perfume cross-reactors.

Useful databases own emerged that can assist identify products free of a patients known allergen.

The Contact Allergen Management Program (CAMP) is maintained by and accessible to clinician members of the American Contact Dermatitis Society.

When vesicles are present, the preparation of a Tzanck smear or a viral culture can assist law out a herpes outbreak. Bacterial culture helps to identify a cause of impetigo.

Contact dermatitis is not generally examined by biopsy and separating allergic from irritant contact dermatitis is impossible by histology.

The histology of both shows spongiotic dermatitis (intercellular edema) in early and subacute stages, sometimes with intra-epidermal eosinophils, and the thickened epidermis and papillary dermal fibrosis of lichen simplex chronicus with prolonged involvement.

ATOPIC DERMATITIS OF EYELIDS

What to be alert for in the history

Patients with eyelid dermatitis due to seborrhea report scaling as their main concern; where as level of pruritus is generally variable. In addition to eyelid involvement, most complain of redness and scaling in several other sebaceous-rich areas of skin, such as the scalp, eyebrows, retroauricular skin, nasolabial creases, central chest, axilla, groin, and inframammary folds.

Symptoms are often chronic with periods of exacerbation.

Table 1.
First Line treatment Second Line treatment
Severity of condition Mild Moderate-Severe Mild Moderate-Severe
Allergic/ irritant contact dermatitis Avoid allergen or irritant(T): low potency topical steroid twice a day up to 10 dayseg, hydrocortisone % ointment Avoid allergen or irritant(T): mid-potency steroid (eg, triamcinolone % ointment) twice a day up to 5 days, followed by topical calcineurin inhibitors (TCIs; tacrolimus % ointment or pimecrolimus 1% cream) twice a day until resolution of symptoms Avoid allergen or irritant(T): TCIs (tacrolimus % ointment or pimecrolimus 1% cream) twice a day until resolution of symptoms Avoid allergen or irritant(S): short course of corticosteroid (eg, prednisone 40 to 60mg orally daily for 1 to 3 weeks)
Atopic dermatitis (T): low-potency topical steroid twice a day up to 10 days (T): mid-potency steroid twice a day up to 5 days, followed by TCIs (tacrolimus % ointment or pimecrolimus 1% cream) twice a day until resolution of symptoms(S): sedating antihistamines (eg,: hydroxyzine 25 to 50mg every evening to treat pruritus (T): over-the-counter barrier creams or ointments as needed (eg, petrolatum) (T): TCIs (tacrolimus % ointment or pimecrolimus 1% cream) twice a day until resolution of symptoms
Seborrheic dermatitis (T): ketoconazole 2% cream twice a day until resolutionluke warm compresseswashing eyelashes with baby shampoo to work out the scales (T): low potency steroid twice a day up to 10 days (T): ketoconazole 1% to 2%, selenium sulfide %, or over-the-counter zinc pyrithione, or salicylic acid-containing shampoo diluted ; wash the areas daily until resolution (T): TCIs (tacrolimus % ointment or pimecrolimus 1% cream) twice a day until resolution of symptoms
Rosacea-induced eyelid dermatitis luke warm compresses to improve blepharitisartificial tears to assist with ocular irritation (S): tetracycline class antibiotics.

eg, minocycline mg orally twice a day or doxycycline mg orally twice a day for 6 weeks, then taper or stop

(T):metronidazole % to 1% cream, gel, lotion or sodium sulfacetamide 10% lotion , cleanser (T): extremely short course of low- potency steroids up to 5 to 7 dayseg, hydrocortisone % cream or desonide % lotion

Patient Management

FOLLOW-UP AND MONITORING

Regardless of the etiologies of eyelid dermatitis, if the patient has severe enough disease to warrant oral steroids or mid-potency topical steroids, the patient should be seen back in clinic in 2 to 4 weeks.

In cases of mild-to-moderate disease in which low-potency topical steroids are being used, then follow-up visits are still encouraged but can be postponed to every 2 to 3 months.

Signs of steroid overuse (atrophy, telangiectasias, striae), cataracts (corneal opacities), symptoms of glaucoma and infections should be monitored at every visit.

Patients with severe atopic eyelid dermatitis should be followed regularly by ophthalmology. The side effects of topical corticosteroids increase with the longer duration and higher potency steroids.

What is a suncream allergy

TCIs should be used if disease can not be cleared with a 7 to 10 days course of topical corticosteroids.

Patients with ocular rosacea should be followed every 3 months if they are on an oral medicaton for their disease. They should also be advised to see an ophthalmologist for periodic evaluation. Women of child-bearing age on tetracyclines should be appropriately counseled to stop the medication if they are planning on becoming pregnant, as it can lead to dental anomalies in a fetus. In patients taking minocycline, blue-gray pigmentary changes are possible 12 to 24 months into treatment, hence an alternative medication plan is needed after patient has taken minocycline for more than 1 year.

MAINTENANCE THERAPY

For long- term maintenance therapy of severe disease, it is significant to minimize the long-term use of higher potency topical steroids.

What is a suncream allergy

For severe disease, patients should include daily or twice daily use of TCIs. Sometimes use of topical steroids is also needed for maintenance therapy, but should be limited to twice a week use in such cases. Using low-potency topical steroids on the weekends and moisturizers or TCIs during the relax of the week can be a reasonable maintenance plan.

For moderate disease twice a week use of low-potency topical steroids with barrier replacement therapy (moisturization) on the other days is safe and efficatious.

For mild disease, barrier replacement therapy (moisturization with plain % petrolatum) is the mainstay. For diseases love atopic dermatitis, barrier replacement therapy is crucial to assist patients stay in remission longer.

Expected results of diagnostic studies

Diagnostic workup should include anti-nuclear antibody (ANA) screen as well as myositis-specific antibodies, muscle enzyme levels (creatine phosphokinase, aldolase), electromyography, and muscle biopsy (triceps most sensitive) or MRI.

The extent of workup for malignancy is debated but can be guided by family history, patient symptoms, general physical examination (including rectal, pelvic and breast), and every age-appropriate cancer screening. Skin biopsy can be helpful in demonstrating subtle vacuolar interface dermatitis on histology.

Characteristic findings on physical examination

Heliotrope rash is a violaceous or lilac discoloration of the periorbital eyelid skin, sometimes accompanied by significant edema or scaling (Figure 14). Other cutaneous signs of DM are erythematous to violaceous papules and plaques over the metacarpalphalangeal joints, also known as Gottrons papules; the “V” sign of the anterior neck and the “shawl sign” described as macular erythema and poikiloderma (telangiectasia, atrophy, hypo- and hyperpigmentation).

Characteristic findings on physical examination

Clinically, upper and lower eyelids can be erythematous, scaly and edematous, generally involving eyelash margin with greasy scaling.

Mild to severe conjunctival injection can be present. Chronic inflammation can lead to lid thickening.

The most helpful findings are clinical signs of facial rosacea. Diffuse erythema and prominent telangiectasias on the cheeks, forehead, nose, and chin. Inflammatory papules and little pustules without comedones are seen in acneiform rosacea in the same distribution. Sebaceous hyperplasia and tissue hypertrophy can be seen over the central forehead, nose (rhinophyma) or chin predominantly in male patients. If none of the cutaneous findings of rosacea are present, referring patient to an ophthalmologist is recommended to confirm diagnosis.

Immediate diagnosis of ocular rosacea is significant, as undiagnosed and untreated it carries the risk of corneal scarring.

Expected results of diagnostic studies

Ocular rosacea is also a clinical diagnosis, and biopsy is rarely needed.

DERMATOMYOSITIS, AS PERTAINS TO EYELID DERMATITIS

Dermatomyositis (DM) is an idiopathic inflammatory myopathy with characteristic skin findings, which often precede development of proximal muscle weakness by weeks to months. This is a rare condition that can overlap with other autoimmune rheumatic diseases.

DM carries a risk of systemic complications related to muscle weakness (respiratory failure, dysphagia, bowel dysmotility) and an increased relative risk of malignancy.

Pathophysiology of various causes of eyelid dermatitis

CONTACT DERMATITIS OF THE EYELIDS

The unique anatomy of the eyelid makes it a susceptible site for inflammation. With thickness about a fourth that of other facial skin (about mm) there is facile penetration of allergens or irritants.

Auto-inoculation from distant sites or even shut personal contacts is possible, and airborne exposures must be considered.

In allergic contact dermatitis the inflammation is mediated by a delayed (type IV) hypersensitivity reaction that occurs after sensitization. Commonly prescribed antihistamines used for type I IgE-mediated hypersensitivity are useful only for their soporific effects in type IV reactions.

Irritant dermatitis is mediated by direct toxic effect of a chemical whose physical properties such as hydrophobicity influence ability to penetrate the stratum corneum and cause cellular damage.

Pre-existing disruption of the skins barrier, as is common in disorders love atopic dermatitis, may enhance the penetration of these molecules. Thus individual skin condition alters the threshold at which a chemical becomes an irritant and efforts to maintain skin hydration and barrier become important.

ATOPIC DERMATITIS OF EYELIDS

Atopic dermatitis (AD) is a common and genetically predisposed skin condition with initial symptoms developing in infancy or childhood and varying clinical patterns at diverse stages of life.

The eyelids are a commonly involved site in AD owing to the thin nature of the area being easily traumatized by scratching. The associated condition icthyosis vulgaris is caused by faulty or absent fillagrin, a protein critical in maintaining a normal skin barrier. The loss of fillagrin results in a retention hyperkeratosis characterized by hyperlinear palms, keratosis pilaris (follicular rough bumps on the upper arms and thighs), and xerotic fine scales on the extensor surfaces.

It is thought that the disrupted skin barrier in AD leads to more facile penetration and presentation of allergens accounting for the increased frequency of allergies seen.

These patients are prone to secondary bacterial, fungal, and viral infections, own higher rates of staphylococcal colonization, often requiring antibiotic or antiviral therapy. This predispostion to infection is partially due to the impaired barrier function of the skin, but is also due to altered innate immunity, seen by decrease of endogenous antimicrobial peptides in atopic skin.

SEBORRHEIC DERMATITIS OF THE EYELIDS

The pathogenesis of seborrhea is debated but largely thought to be secondary to epidermal colonization by the lipophyilic and nonpathogenic yeasts of the Malassezia and Pityrosporum species.

An altered immune response is thought to be involved as evidenced by the more severe presentations found in the HIV/AIDS population. Severe seborrheic dermatitis is also often present in patients with Parkinsons disease (Figure 14).

OCULAR ROSACEA

Pathophysiology of rosacea is poorly understood. Multiple etiologies own been suggested, including environmental triggers, altered antimicrobial peptides melieu, presence of skin bacteria and possibly Demodex folliculorum connection. Vascular proliferation and dermal degeneration contribute to development of erythematotelangiectatic rosacea. For ocular rosacea, specifically meibomian gland dysfunction resulting in altered tear film and irritation, was proposed as a potential etiology.

Who is at Risk for Developing this Disease?

Risk factors for developing eyelid dermatitis are related to its varying etiologies; however, female patients are reported to comprise 90% of cases of eyelid dermatitis.

ACD is the most common cause of eyelid dermatitis, ranging from 50% to 76% of cases.

ICD is sometimes counted together with ACD, hence it is hard to estimate its prevalence.

Patients with a history of a primary dermatologic condition, such as AD, seborrhea, rosacea, psoriasis, are also at higher risk of developing contact (allergic or irritant) eyelid dermatitis due to already present alteration of skin barrier.

Characteristic findings on physical examination

Clinically, upper and lower eyelids protest poorly circumscribed erythematous thin plaques with greasy yellow or fine white scale. When eyelash margin alone is affected and no other cutaneous findings are identified, seborrheic dermatitis of the eyelids is the most likely diagnosis (Figure 13).

Skin examination of sebaceous-rich areas of the skin and their involvement by seborrheic dermatitis also helps to support the diagnosis.

Expected results of diagnostic studies

Seborrheic dermatitis is a clinical diagnosis. Rarely, tinea faciei can present with similar findings (Figure 14), and KOH examination can be helpful to law out this fungal infection. If seborheic dermatitis, including seborrhea of the eyelids, is extremely severe or acute in onset, an HIV test should be ordered. The histology of seborrheic dermatitis depends on the age of the lesion biopsied, showing acute, subacute, or chronic/psoriasiform spongiotic dermatitis.

OCULAR ROSACEA

What to be alert for in the history

Thirty to sixty percent of patients with DM own periorbital skin findings of DM, the heliotrope rash (Figure 15).

Although it is asymptomatic, signs of periorbital darkening, fine scaling and especially eyelid swelling can be the initial concerns that bring a patient into a physicians office. Patients with those findings should be asked about new photosensitivity, fatigue, muscle weakness, examples being difficulty with rising from a chair or brushing hair.

Unusual Clinical Scenarios to Consider in Patient Management

One specific conundrum that patients with eyelid dermatitis face is the development of an allergic contact dermatitis to the product that they are using to treat their condition. As alluded to earlier, a flare in previosly well controlled eyelid dermatitis or eyelid dermatitis that has suddenly became resistant to therapy should immediate evaluation for every topical contact exposures.

Examples include ACD to topical steroids, topical antibiotics, preservatives, or inactive ingredients within medications. Use of petrolatum/ointment base preparations can assist minimize such events, as even fragrances make their way into some topical steroid preparations. Repeat patch testing should be considered.

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Are You Confident of the Diagnosis?

Eyelid dermatitis is an umbrella term describing a group of inflammatory skin disorders that localize to the eyelids and resemble eczema. There are numerous causes of eyelid dermatitis, hence it is a vexing problem for patients and can represent a diagnostic and therapeutic dilemma.

Knowledge of the common causes and their key features can focus the history and physical examination and alert the clinician to more serious conditions.

Time course, patient age, symptoms, presence or absence of scale or edema, distribution (isolated lesion vs multiple, discreet vs diffuse, bilateral vs unilateral, lid margin vs crease) assist differentiate the diverse types of eyelid dermatitis. This chapter reviews the common periorbital dermatoses with emphasis on their distinguishing features.

Most common causes of eyelid dermatitis are

Contact dermatitis (allergic and irritant), 50% to 76% of cases

Atopic dermatitis, 12% to 17%

Seborrheic dermatitis 8% to 16%

Rosacea, less than 5%

There are other conditions of the eyelids that mimic eyelid dermatitis and are not to be missed, such as dermatomyositis.

The broader differential diagnosis includes other connective tissue diseases (discoid lupus erythematosus [Figure 1], Sjögrens, etc), psoriasis, contact urticaria, infections (viral, bacterial or fungal), and drug reactions. Neoplasms benign or malignant can also mimic dermatitis and can localize to an eyelid. Discussion of those conditions is beyond the scope of this chapter.

CONTACT DERMATITIS OF THE EYELIDS

Contact dermatitis is comprised of allergic contact dermatitis (ACD) and irritant contact dermatitis (ICD); these can be hard to differentiate and own overlapping characteristics.

Expected results of diagnostic studies

Again, atopic dermatitis (AD) of eyelids is a clinical diagnosis, rarely requiring any diagnostic studies.

As discussed with allergic and irritant contact dermatitis, swab cultures are sometimes necessary to assess for presence of a bacterial and/or viral infection that can complicate diagnosis.

Skin biopsy shows similar changes to contact and seborrheic dermatitis with acute or subacute spongiotic dermatitis early on, and psoriasiform spongiotic dermatitis or lichen simplex chronicus at later chronic stages. Laboratory testing of entire serum IgE can be elevated (but not diagnostic), and skin prick tests for type I sensitizations are frequently positive (food allergies, pollens, dust mites), but again are not diagnostic of AD.

SEBORRHEIC DERMATITIS OF THE EYELIDS

What to be alert for in the history

Patients presenting with eyelid dermatitis caused by atopic dermatitis (AD) often own a history of chronic eyelid itching, redness and scaling; plus they often own eczema diagnosis since early childhood.

Pruritus, sometimes unbearable, is often their main concern, as they become trapped in endless itch-scratch-itch cycles. Personal or family history of atopy (AD, or allergic rhinitis/hayfever or asthma) is typically present. AD is diagnosed on the basis of major criteria (family history of eczema, severe pruritus, facial and extensor distribution in infants, flexural distribution in adults) and numerous minor criteria. As nipple dermatitis is fairly specific for AD, asking about that symptom can confirm diagnosis.

What to be alert for in the history

A careful history of exposures is critical to the diagnosis of contact dermatitis.

These historical reviews can be fairly extensive and occasionally require a referral to a contact dermatitis specialist within dermatology for a comprehensive workup. A flare in previously well controlled atopic or seborrheic dermatitis may represent a new allergic contact dermatitis and should immediate re-evaluation of exposures. It is high yield to enquire the patient about occupation, hobbies, home and yard care responsibilities, and of course, cosmetics, skin care products, and prescription medications.

Irritant contact dermatitis (ICD) often presents with a history of burning or stinging skin, generally within minutes of application of offending product.

Pruritus is more common with an allergic contact dermatitis (ACD), and the rash onset is generally reported 1 to 2 days after exposure to an allergen. Exposures (and their associated allergens) that can cause eyelid dermatitis:

Eyelash curlers (nickel, rubber additives; Figure 2, Figure 3, Figure 4), chemicals contained in facial tissues (preservatives), make-up applicators (rubber additives), nail polish (tosylamide formaldehyde resin; Figure 5), artificial nails (acrylates; Figure 6), household cleaners (irritant reaction), ophthalmic solutions (preservatives, antibiotics, topical beta-blockers; Figure 7), shampoos (cocomidopropyl betaine; Figure 8, Figure 9), hair dye (paraphenylenediamine) and poison ivy/oak (urushiol).

Facial or hand moisturizers (preservatives, formaldehyde releasers, sunscreen chemicals, lanolin)

Various cosmetics including eyeliners, mascara, eyeshadow, lipstick (fragrances, formaldehyde releasers, shellac, sunscreen chemicals).

Mascara causes an irritant reaction more often than allergic.

Although nickel is not a common ingredient in cosmetic products, it has been hypothesized to contaminate products during manufacturing.

Jewelry, keys, coins (nickel and gold) can transfer to skin from the handling of those metal objects by hands.

Topical antibiotics (neomycin and bacitracin) are common over-the-counter self-remedies, which patients apply to inflamed skin in an attempt to treat it. Both are frequent causes of allergic contact dermatitis.

Airborne allergens (urushiol, fragrances, lichens, other various botanicals)

Systemic Implications and Complications

Systemic complications associated with eyelid dermatitis are rare.

CONTACT DERMATITIS OF EYELIDS

Systemic contact dermatitis may result from a systemic exposure (injection or oral, intranasal, intravenous istration) to a contact allergen (or one that cross-reacts) in a patient who is already sensitized.

Agents that own been reported to cause systemic allergic contact dermatitis include ethylenediamine, various antibiotics, corticosteroids, fragrances (balsam of Peru), propylene glycol, sorbic acids, metals, cashews, and mangos. Those patients will own extensive body dermatitis, not just eyelids.

Clinical features include a widespread eczematous eruption favoring the buttock and flexural areas, which may be accompanied by generalized systemic complaints including fever, malaise, nausea, and headaches.

The diagnosis can be made by detailed history and patch testing as described previously.

ATOPIC DERMATITIS OF EYELIDS

Atopic dermatitis is commonly associated with respiratory allergy, asthma, and less commonly food allergies. Patients with atopic dermatitis are more susceptible to bacterial (Staphylococcus aureus) and viral infections (molluscum contagiosum, warts and herpes virus) due to disrupted barrier function, defects in cellular immunity and decreased levels of antimicrobial peptides that are generally present in the skin.

Viral and bacterial cultures, Tzanck smears, or viral polymerase chain reaction asays (PCRs) can assist make the diagnosis.

If herpes virus infection is suspected and involves the periocular region, immediate evaluation by an ophthalmologist is warranted to check for corneal involvement (herpes keratitis), which can lead to blindness if left untreated.

Keratoconus (conical cornea) is associated with chronic atopic dermatitis, and numerous studies propose that excessive eyelid rubbing is the most causative factor in AD patients that develop keratoconus. Cataracts (subcapsular) own been described both as a manifestation of atopic dermatitis and as a complication of corticosteroid treatment.

Currently cataracts associated with atopic dermatitis and corticosteroid therapy are indistinguishable clinically. Ophthalmologic examination is recommended in patients with symptoms of decreased vision and severe chronic eyelid disease.

SEBORRHEIC DERMATITIS OF EYELIDS

Severe seborrheic dermatitis may be asociated with neurologic conditions, such as Parkinsons disease, epilepsy, and multiple sclerosis. Severe recalcitrant seborrheic dermatitis has also been observed in patients with human immunodeficiency virus (HIV), and may be the presenting sign prompting HIV-1/2 antibody screening.

OCULAR ROSACEA

Ocular complications of rosacea include blepharitis, conjunctivitis, meibomian impactions, hordeola, corneal neovascularization, corneal ulcerations and scarring.

Symptoms of recurrent blushing is common in patients with vascular rosacea. Rarely, the lymphatic vessels can be involved and can lead to persistant woody induration fo the central face, termed solid facial edema. Low grade fever, myalgias, leukocytosis and elevated erythrocyte sedimentation rate (ESR) can be seen in association with rosacea fulminans.

DERMATOMYOSITIS

In patients with dermatomyositis, associated systemic findings include progressive symmetric proximal muscle weakness.

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Rarely patients can develop cardiac myositis and interstitial lung disease. Muscle disease may present before, concurrently, or after cutaneous manifestations. In adult patients (usually >50 years of age), dermatomyositis may be the presenting manifestation of an underlying malignancy. Age appropriate or symptom-directed malignancy screening should happen every 6 months for 2 years after diagnosis.

Optimal Therapeutic Approach for this Disease

CONTACT DERMATITIS

When contact dermatitis is suspected, undergoing patch testing with a screening tray as well as patients personal products is often crucial to pinpoint a causative allergen or an irritant. If patch testing is not possible, then open application use test with a suspected topical product can be helpful.

Complete avoidance of the relevant allergen or irritant is paramount.

Patient education should be thorough and patients should get a printed list of the names and synonyms of every positive allergens. Suggestions for possible alternative to the allergenic products should be provided.

Treatment of acute disease should include the use of low-potency topical steroids in an ointment base twice daily for up to 10 days. Alternatively for more severe disease, mid-potency topical steroid in an ointment base can be used twice a day for 3 to 5 days, followed by the use of TCIs until the rash resolves. Although TCIs own minimal systemic absorption, black box warnings should still be discussed.

Not uncommonly TCIs can cause local side effects such as burning and stinging.

Use of these agents after several days of low- to mid-potency topical steroids (after much of the acute inflammation has resolved) can minimize the discomfort. In severe disease, a short course of oral corticosteroids may be necessary; however, this should be reserved for cases in which the allergen is known and the exposure was limited. Treatment with topical steroids should be used with caution, as the eyelids are extremely thin and are more prone to the adverse side effects such as atrophy, and in chronic use cases can lead to glaucoma and cataracts.

ATOPIC DERMATITIS

For acute flare-ups, aggressive treatment with medium strength topical steroids in an ointment base for 3 TO 5 days may be necessary, followed by use of TCIs until clear (or low-potency topical steroids for 5 to 7 more days).

application of cool compresses for 20 to 30 minutes prior to application of the topical steroid can be beneficial. However, cool compresses should be used with caution as it may lead to excessive dryness or irritation from repeated wet-to-dry cycling.

For chronic or persistent disease, daily to twice daily use of TCIs may be necessary. For mild disease, low-potency topical steroids twice daily up to 10 days are effective.

For maintenance, ample moisturization to restore the skin barrier is crucial. Examples of such agents include plain % white petrolatum, or thick over-the-counter moisturizing creams (eg, Cetaphil, Eucerin, Aquaphor, Aveeno).

Elimination of potential irritants is also significant in disease control.

Oral antihistamines such as diphenhydramine or hydroxyzine or doxepin can be used at bedtime to assist break the itch-scratch cycle during sleep. Patients should be warned about the sedative side effects of these medications.

SEBORRHEIC DERMATITIS

A variety of treatment options exists. The mainstay of eyelid and facial disease treatment is ketoconazole 2% cream.

Shampoos containing salicyclic acid, selenium sulfide, zinc pyrithione and ketoconazole are generally used to treat scalp disease. These agents can also be used to treat the eyelids but should be diluted to minimize irritancy. A short course of a low-potency non-fluorinated topical steroid can also be used to treat acute flares, however, the relapse rate is high. TCIs can be useful in severe cases or in those who fail to reply to low-potency topical steroids or are intolerant of ketoconazole cream.

ROSACEA

Oral tetracyclines are an effective treatment option for moderate-to-severe ocular rosacea. Treatment should start with a higher dosing regimen (doxycycline or minocycline to mg daily or tetracycline mg QID or mg BID) for 6 weeks, then tapering off completely or to a lower-dose maintenance regimen.

Potential side effects of this class of medications include but are not limited to gastrointestinal upset (nausea, vomiting, diarrhea), vaginal yeast infections, photosensitivity, and rarely hypersensitivity skin reactions. Low-dose doxycycline/minocycline (50mg daily) and extended release formulations of those medications can be used if higher doses can not be tolerated.

For milder disease, proper eyelid hygiene can assist reduce symptoms. This includes warm compresses for 5 to 10 minutes, accompanied by tender massage of the tarsal plate toward the lid margin.

This serves to turn over stale and stagnant lipid secretions from the meiobian glands. Artificial tears can also be helpful for dry eyes. Also topical antibiotics applied to the lid margins can be helpful in decreasing the bacterial flora.

What is a suncream allergy

Topical corticosteroids occasionally can be used to control severe flares, however, long-term use is discouraged, as it can lead to glaucoma and cataracts, as well as exacerbation of acneiform-type rosacea on the relax of the face.

DERMATOMYOSITIS

Systemic treatment of dermatomyositis often depends on the level of muscle inflammation or symptoms of weakness, as well as severity of skin involvement. Such treatments are beyond the scope of this chapter.

What is the Evidence?

Amin, KA, Belsito, DV. The aetiology of eyelid dermatitis: a year retrospective analysis.

Contact Dermatitis. vol. pp. (This retrospective study evaluated more than patch test patients, 8% of which had eyelid dermatitis. Allergic contact dermatitis was the most common cause, surpassed only by seborrheic dermatitis when the eyelids alone were affected.)

Goossens, A. Contact allergic reactions on the eyes and eyelids. Bull Soc Belge Ophthalmol.

What is a suncream allergy

vol. pp. (This large study examined more than patients with conjunctivitis or eyelid dermatitis and found allergic contact dermatitis in 56% of patients tested. The study reviews classes of allergens, their sources, and modes of exposure.)

Guin, JD. Eyelid dermatitis: experience in cases. J Am Acad Dermatol. vol. pp. (This article reviews cases of eyelid dermatitis. With patch testing and ancillary tests a relevant allergic contact dermatitis was found in 76% of patients.

Among the 12% of patients that had atopic dermatitis, 70% had a relevant allergen. Seborrheic dermatitis, psoriasis, and connective tissue disease each constituted less than 5% of cases.)

Papier, A, Tuttle, DJ, Mahar, TJ. Differential diagnosis of the swollen red eyelid. Am Fam Physician. vol. pp. (A useful overview for general practitioners who are likely to see a mixture of primary dermatologic conditions as well as trauma, infection, and malignancy.)

Peralejo, B, Beltrani, V, Bielory, L. Dermatologic and allergic conditions of the eyelid. Immunol Allergy Clin North Am.

vol. pp. (A wide literature review of eyelid dermatoses, their diagnosis, and treatment.)

Rietschel, RL, Warshaw, EM, Sasseville, D, Fowler, JF, DeLeo, VA, Belsito, DV. North American Contact Dermatitis Group. Common contact allergens associated with eyelid dermatitis: data from the North American Contact Dermatitis Group study period. Dermatitis. vol. pp. 7(Examining data on patients with exclusively eyelid dermatitis, patients screened by patch testing of 65 allergens had a relevant positive exposure 72% of the time. 65% of these positives could be attributed to a shorter list of only 26 allergens, a series proposed as a potential screening set for eyelid dermatitis.)

Zug, KA, Palay, DA, Rock, B.

Dermatologic diagnosis and treatment of itchy red eyelids. Surv Ophthalmol. vol. pp. (Asuccinct review focusing on the physical examination, history, and differential diagnosis of the inflamed eyelid.)

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We all know the importance of wearing sun cream — but these products can prove tricky for people with existing skin conditions.

‘If your skin is already inflamed or broken, for example, applying sun creams may aggravate it, so finding one that suits your skin type is essential,’ says Dr Justine Hextall, a consultant dermatologist and medical director of the Tarrant Highway Clinic in Arundel, Sussex.

As a general law, you should select sun protection that’s at least SPF 30 and with a three to five-star UVA , Dr Hextall picks her best buys for diverse skin issues

Sun wisdom: As a general law, you should select sun protection that’s at least SPF 30 and with a three to five-star UVA rating

ACNE

This is triggered by an over-production of oil in the skin’s sebaceous glands, which can then block pores.

Though the sun can be helpful for acne, it can also be problematic for patients using certain treatments that make the skin more sensitive, says Dr Hextall.

‘People using retinoid creams containing vitamin A, the oral treatment Roaccutane or laser treatments are at risk of hyperpigmentation [dark patches] or sunburn, so they need to apply sun cream more than most.’

However, numerous acne patients worry that oily sun creams will block their pores and make their spots worse.

Winner: This acclaimed product contains both chemical and mineral blocks

BEST BUY: Eau Thermale Avene Cleanance Sunscreen SPF50 (50ml, now £12, ).

Generally, creams that provide a physical sun block — using minerals to deflect the sun’s rays — are better for oily skin than chemical blocks, which work by absorbing light and releasing it as heat from the skin, says Dr Hextall, as they are less likely to cause a reaction.

This product contains both chemical and mineral blocks.

However, Dr Hextall says: ‘This is the first sun protection product I’ve come across which actively treats acne — it contains ingredients such as monolaurin, which inhibits oil production and has an antibacterial effect. And the thermal spring water used to make it is well-known for its anti-inflammatory qualities.’

ROSACEA

Winner: Designed for the face, this cream is lightly tinted and chemical-free

An inflammatory skin condition, this causes red flushing on the nose, cheeks, chin and forehead, and sometimes spider veins and thickened skin on the nose. Around 5 per cent of adults are affected by it.

‘Sunlight is one of the main triggers for a rosacea attack, then the skin becomes red and inflamed and more sensitive to sun products,’ says Dr Hextall.

‘If you own rosacea and sunscreens own irritated your skin in the past, select a physical rather than a chemical block, which may be less likely to cause irritation.’

BEST BUY: Bare Republic Mineral Sunscreen Tinted Face SPF30 (50ml, £17, ).

Designed for the face, this cream is lightly tinted and chemical-free.

‘It contains zinc and titanium oxide to provide a physical sun block, and is tinted to camouflage redness,’ says Dr Hextall. ‘It’s also fragrance-free, so less likely to cause irritation or dryness, and could be easily worn underneath make-up.’

Industry change: For numerous years, the range of suncreams wasn’t tailored to sensitivities

VITILIGO

DUE to a lack of the pigment melanin, people with vitiligo own pale white patches on their skin — and these are more vulnerable to sunburn, says Dr Hextall.

Another group of people who own to be particularly careful in the sun are those who own had skin cancer previously — including malignant melanomas and less dangerous forms, such as basal cell carcinoma — and those taking immunosuppressant medications (such as transplant patients).

‘UV rays can penetrate clouds, so people at risk still need to protect themselves every day whatever the weather, even if they’re not in the sun,’ says Dr Hextall.

Winner: This reduces sun-induced patches that can turn cancerous by 53 per cent

BEST BUY: Actinica Lotion (80g, £, ) has ‘broad spectrum UV protection’ specially for people at higher risk of skin cancer, according to the manufacturers.

It was found to reduce actinic keratosis lesions (sun-induced scaly patches that can turn cancerous) by 53 per cent within two years in people who’d had an organ transplant, according to a study published in the British Journal of Dermatology.

‘Other products may own the same effect, but this company is the only one that has done the research to prove it can prevent actinic keratosis,’ says Dr Hextall.

‘Though it’s not specifically marketed at vitiligo patients, I ponder it would be a excellent product for this condition because of the extremely high protection it offers.

‘It’s particularly useful for applying to the scalp if you’re bald — the area is prone to sun-induced lesions regardless of whether you’re immune-suppressed.’

ECZEMA

Winner: In a little study, 84 per cent of people said their skin condition had improved after using this product for two weeks

This condition affects one in five children and one in 12 adults. Skin is dry, itchy and inflamed and can crack and become infected.

Sunlight can either improve eczema symptoms or aggravate them.

‘Patients should glance for an emollient-based sun cream which will lock moisture in to the skin as well as protect it from UV rays,’ says Dr Hextall.

BEST BUY: Eucerin Additional Light Sun Lotion SPF 50 (ml, £, ). ‘This contains octocrylene, which has a hydrating effect, and glycerine, which attracts water into the skin,’ says Dr Hextall.

‘It also contains licorice extract, an antioxidant with an anti-inflammatory effect, and has a light texture that is easily absorbed with no greasy finish.’

In a little study, 84 per cent of people said their skin condition had improved after using this product for two weeks, she adds.

Safety: Every leading cancer charities stress the importance of wearing SPF-enhanced lotions 

POLLUTION DAMAGE

In addition to the sun’s rays, microparticles of pollutants — from traffic fumes and smoking, for example — can penetrate and further damage the skin.

A study published in the Journal of Investigative Dermatology comparing women living in urban and rural environments over 24 years found that those exposed to more pollution had more dark spots and wrinkles.

‘There’s evidence the sun and pollution work together, and the combination can accelerate skin damage and ageing,’ says Dr Hextall.

Winner: This contains iron oxide mineral blocks to protect against longer wave-length infra-red radiation from the sun

BEST BUY: Murad City Skin Age Defense Wide Spectrum SPF 50 (50ml, £45, ).

This contains lutein — a compound found in some vegetables — which the makers claim creates a barrier to pollutants.

‘There is some evidence from lab studies of lutein protecting cells against blue light [from phones and laptops], though I would love to see more,’ says Dr Hextall.

‘The product does contain iron oxide mineral blocks to protect against longer wave-length infra-red radiation from the sun.

Some scientists claim infra-red may alter collagen — the scaffolding structure in the skin — and lead to wrinkles and sagging skin.

‘But the cream is pricey and you could possibly get a similar effect by eating more antioxidant-rich foods and applying a vitamin C serum under a sun cream.’

PSORIASIS

Winner: Although not specifically-designed for psoriasis sufferers, it’s inexpensive and fragrance-free

AROUND million people are affected by psoriasis, which causes red, raised, scaly plaques of skin.

It occurs when the immune system becomes too athletic and speeds up the new skin replacement process.

‘Sunlight can improve psoriasis in some cases, but it’s still vital to protect the skin,’ says Dr Hextall.

‘Historically, most psoriasis creams own been fairly greasy, so patients tend to complain about having to apply oily sun creams on top. But newer treatments are more easily absorbed.’

BEST BUY: Soltan Sensitive Hypoallergenic Suncare Lotion SPF 30 (ml, £6, ).

‘Though this product isn’t specifically designed for psoriasis, it’s a excellent choice for the condition because it’s easily absorbed and moisturises to prevent dryness and reduce peeling,’ says Dr Hextall.

‘Because it’s reasonably priced, there’s more chance people will apply it in sufficient quantities.

It’s also fragrance-free, so less likely to cause irritation.’

Winner: It’s fragrance-free, non-greasy and contains moisturisers, tell experts 

SENSITIVE SKIN

People with generally sensitive skin can react to perfumes and chemicals, causing a rash.

BEST BUY: Solero Ultra-Sensitive Sun Lotion SPF 50 (ml, £7, lloyds ).

‘This is specially formulated for people prone to skin allergies and eczema,’ says Dr Hextall. It’s fragrance-free, non-greasy and contains moisturisers.

SUN ALLERGY

Up to 15 per cent of Britons suffer from polymorphic light eruption, a rash thought to happen when UV light triggers a reaction by the immune system.

It is sometimes described as a sun allergy.

‘It causes a pimply rash that tends to appear 24 to 48 hours after sun exposure,’ says Dr Hextall. It is often worse at the start of summer, when the skin hasn’t been exposed to much sun.

‘If skin becomes boiling and inflamed an oily sun cream can trap in the heat, making the rash worse.’

Winner: It contains the antioxidant alpha-glucosylrutin, which mops-up free radicals

BEST BUY: Eucerin Sun Allergy Protection Creme-Gel SPF 50 (ml, £19, ). It contains the antioxidant alpha-glucosylrutin (AGR), extracted from the pagoda tree.

‘AGR may offer protection against polymorphic light eruption by mopping up free radicals [harmful molecules produced by sunlight], and as such reducing the immune response which causes this reaction,’ says Dr Hextall.

‘Impressive research shows that this ingredient can significantly reduce the risk of developing sun allergy symptoms.’

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