Plants causing contact dermatitis: Overview, Allergic Contact Dermatitis due to Anacardiaceae Plants, Allergic Contact Dermatitis due to Asteraceae Plants and Others
Contact Dermatitis, Plants – Dermatology Advisor
Are You Confident of the Diagnosis?
What to be alert for in the history
IRRITANT CONTACT DERMATITIS
The most common history for those developing ICD to plants is direct exposure, often prolonged, with plants containing irritants. Often, fissuring or dermatitis will develop on fingertips/fingers as the hands are most commonly in contact. Dryness, fissures, scaling, and erythema chiefly affect the fingertips, hands, and forearms and are often accompanied by subungual hyperkeratosis.
ALLERGIC CONTACT DERMATITIS
There are two distinct exposure methods that should be taken into account for ACD to plants. The first is the most intuitive, direct exposure to allergenic plants leading to dermatitis often in a linear distribution. The second is much less intuitive – exposure to plant extracts in topical personal care products.
The most common causes of phototoxic reactions from plants are exposures to citrus (lime, lemon and orange). This may occur when citrus is used in an outdoor setting while preparing beverages. The phototoxic furocoumarin is in the citrus juice and when exposed to sunlight causes an exaggerated sunburn-like reaction. Other causes are figs and roots/grasses in the umbilliferae family.
Characteristic findings on physical examination
Some plants have allergens or potent irritants and are able to produce a dermatitis in a linear fashion on areas exposed for short periods of time, such as brushing up against a bruised or broken leaf/stem. The most typical presentation of ACD is linear, vesicular and pruritc dermatitis on exposed areas. Extensive exposure may lead to extensive dermatitis on widespread body surface areas. The primary lesions tend to be vesicular coalescing plaques of dermatitis. Irritant exposures may present with vesiculation and erythema. With chronic exposure for either type of dermatitis, a hyperkeratotic, fissuring, erythematous dermatitis may be present. A common finding is fingertip hyperkeratosis and fissuring.
Expected results of diagnostic studies
Diagnostic studies are often not needed for irritant contact and clear allergic contact exposures, though rarely a skin biopsy may be useful. Diagnosis is confirmed by taking an appropriate history and confirmatory skin examination. It is not possible to predict which of the many potential allergens is the cause of a dermatitis from a product. In most cases, personal care products contain multiple allergens including plant extracts both as active ingredients and/or as fragrances as well as many preservatives. For allergies to plant extracts used in personal care products, diagnostic patch testing is helpful.
Who is at Risk for Developing this Disease?
Nearly everyone is at risk for developing plant dermatitis of some sort during their lifetime. In the United States, the most ubiquitous cause of allergic contact dermatitis is the Anacardiaceae family of plants (poison oak, poison ivy and sumac). Approximately 70% of individuals living in endemic areas will develop ACD to this family during their lifetime. The risk for developing poison ivy is directly related to exposure. It is most commonly seen in individuals with outdoor exposures from 2 to 7 days before developing pruritic dermatitis on exposed areas. Phytophotodermatitis occurs in those exposed to furocoumarin-containing plants and subsequent UV/sunlight exposure.
What is the Cause of the Disease?
IRRITANT CONTACT DERMATITIS
All ICD is caused by caustic or irritant action, directly on the skin. It is not an immunologically mediated process; it is toxic only.
Oxalates: irritant crystals in the plant leaves, stems and/or roots
Furocoumarins: phototoxic chemical naturally produced. Requires sunlight for reaction.
Solanacaea: capsaicin in these plants cause stinging/burning
Onion/Garlic (Allium spp): diallyl disulfide causes both allergic and irritant reaction, often on fingertips
Brassicaceae family (including mustard and radish): thiocyanates present in all parts of the plant
Euphorbiaceae (florist’s croton and spurges): phorbol esters present in entire plant
Ranunculaceae (buttercup flowers): protoanemonin glycoside in damaged plants can produce vesiculation and linear streaks similar to phytophotodermatitis
ALLERGIC CONTACT DERMATITIS
ACD is a type IV delayed-type hypersensitivity reaction. These reactions require both an initial sensitization through epidermal exposure, Langerhans cell processing, presentation to T-cells in the regional lymph nodes thus producing memory T-cells. On subsequent re-exposure, dermatitis is produced through this Th3 dominant reaction.
The most common plant allergens/families are outlined here:
Anacardiaceae: Urushiol in this large family produces dermatitis. Common sources are poison oak/ivy. Less well known sources: cashew fruit/shells, mango skins, Japanese lacquerware made from the sap of the Japanese lacquer tree.
Compositae family: A large family of common plants. The most common cause of dermatitis is the chrysanthemums. Also includes echinacea, calendula, feverfew and chamomile.
Tulip and Peruvian Lilly (alstroemeria): common cause of hand dermatitis in florists.
Tea tree oil (Melaleuca alternifolia): Often used in “alternative” or “natural” preparations. Older, more oxidized tea tree oil is more allergenic.
Fragrances: The list of plants with potential fragrance cross-reactions is nearly endless. Common plant allergens include lavender, jasmine, rose, bergamot (also a phototoxin)
Onion/Garlic: Allergen is diallyl disulfide.
Systemic Implications and Complications
There are minimal systemic implications or complications of topical exposures to plant irritants and allergens in most cases. Ingestion of calcium oxalates can be both a bothersome or potentially life-threatening exposure. Chewing of leaves of oxalate-containing plants produces burning of the mouth and throat, choking and gagging.
Significant ingestions may lead to severe digestive upset, breathing difficulties and possibly coma and death. Permanent liver and kidney damage may also occur.
Topical therapy is adequate for mild cases. Fluocinolone 0.5% or Triamcinolone 0.1% applied to the involved sites in appropriate amounts will speed healing.
Oral therapy is rarely necessary. Over-the-counter diphenhydramine 12.5 or 25mg by mouth as necessary may be used if pruritus is bothersome.
MODERATE OR SEVERE DERMATITIS
Topical therapy: For localized, smaller area dermatitis with significant symptoms, clobetasol 0.05% used twice daily until symptoms/dermatitis resolves or for 3 weeks. Widespread dermatitis responds to triamcinolone 0.1% cream used twice daily. When dispensed in a 454g jar this will provide adequate amounts of medication for a large surface area. Over-the-counter oatmeal baths may be soothing.
Oral therapy: For widespread, symptomatic dermatitis in amenable individuals, oral prednisone will alleviate symptoms and speed recovery. One tapering dosage regimen is prednisone 10 mg tabs by mouth: 6 tabs daily for 4 days, then 4 tabs daily for 4 days, then 2 tabs daily for 4 days, finally 1 tab daily for 4 days. Oral antihistamine agents are useful for sedation when sleep is desired. Hydroxyzine 12.5 to 25mg by mouth, as necessary up to 4 times daily is often helpful for symptomatic relief, predominantly due to its sedating effects. Non-sedating antihistamines are unlikely to be helpful, as these outbreaks are not histamine driven.
Topical antipruritic agents containing diphenhydramine or pramoxine are not recommended due to the risk for development of type IV allergy.
Considering the self-limited nature of these conditions, in most cases, physical modalities such as phototherapy are not necessary. For longer duration, chronic dermatitis possibly caused by plant extracts in topical products, phototherapy may be useful in clearing dermatitis after an allergen has been identified. Surgical therapy for these conditions is not necessary or desired.
Optimal Therapeutic Approach for this Disease
For all severity of dermatitis from plants, topical therapy is preferable for first-line treatment. Topical corticosteroids are safe and effective with appropriate use for self-limited dermatitides such as plant allergic contact dermatitis. For mild disease, oral therapy is rarely warranted. For most, symptomatic relief (decreased pruritus) begins within 6 hours of application of an appropriate-strength topical corticosteroid. Often, full resolution of dermatitis will take 1 to 2 weeks.
Severe, widespread and symptomatic cases may require additional oral therapy with antipruritics and corticosteroids in addition to topical therapy. Some symptomatic relief with oral corticosteroids often begins within 6 hours of the first dose. Severe dermatitis may take longer to resolve, but many cases will be clear or nearly clear within 2 weeks. Oral corticosteroids should be carefully used in those with hypertension or diabetes.
These conditions are self-limited in most cases. For most, as-necessary follow-up is all that is necessary. For suspected plant extract dermatitis that you are not able to figure out clinically, consider referral for patch testing.
In general, barrier creams are ineffective in the prevention of ACD. The one exception to this generality is the commercially available product to prevent poison oak/ivy dermatitis caused by urushiol – Ivy Block. In clinical studies, Ivy Block (quaternium-18 bentonite) completely prevented or significantly decreased reactions to the urushiol. Tetrix is an oil-in-water emulsion that is useful for preventing ICD. It is unclear if it is useful in preventing ACD.
Management of those exposed to plants in an occupational setting is challenging. For many, the exposures are due to repetitive use of the hands/fingers to trim and arrange flowers, such as in a florist. Use of cotton gloves alone will not prevent allergen transfer from the plant to the fingers. Latex gloves provide more protection, but the allergens are able to diffuse through latex usually within several hours. Nitrile/plastic gloves provide better protection. Unfortunately, chronic use of gloves may lead to development or worsening of ICD due to the maceration and wet/dry cycles from sweating. The most successful treatment is avoidance of the offending plants(s). The most common causes are the Compositae plants, with the chrysanthemum being the most common cause of ACD in florists. Secondarily, Peruvian lilly/alstroemeria and tulips are causes of fingertip dermatitis.
In rare cases, a widespread dermatitis in non-exposed areas may develop. For example, poison ivy dermatitis develops on the legs 1 week following an exposure while hiking. This progresses in the typical pattern. Autoeczematization is a flare of pruritic morbilliform dermatitis, often generalized, which develops in non-allergen-exposed areas. Treatment is the same as with other allergic dermatitis.
What is the Evidence?
Chemical irritant dermatitis. In: McGovern , TW, Barkley , TM. “Botanical dermatology”. (Extensive review with tables of causes of plant ICD.)
Phytophotodermatitis. In: McGovern , TW, Barkley , TM. “Botanical dermatology”. (Extensive review of phytophotodermatitis.)
Allergic contact dermatitis. In: McGovern , TW, Barkley , TM. “Botanical dermatology”. (Broad, well written review of plants causing ACD.)
Marks , JG, Fowler , JFF, Sherertz , EF, Rietschel , RL. “Prevention of poison ivy and poison oak allergic contact dermatitis by quaternium-18”. J Am Acad Dermatol . vol. 33. 1995. pp. 212-6. (Study discussing effectiveness of quaternium-18 bentonite barrier cream.)
Schalock , PC, Zug , KA. “Protection from occupational allergens”. Curr Probl Dermatol . vol. 34. 2007. pp. 58-75. (Extensive review of barrier creams for preventing ACD.)
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Plant dermatitis | DermNet NZ
What is plant dermatitis?
Plant dermatitis (also called ‘phytodermatitis’) is a reaction to skin contact with certain plants.
It is not always obvious which plant is responsible for the dermatitis (also known as eczema). Sometimes a rash may develop without direct contact with the plant; the juices may be on clothing or the fingers. A plant cause for dermatitis is suspected when there is a linear or streaky pattern. It is nearly always asymmetrical.
The rash may take various forms. Some plants only cause a rash if the sun is shining on the skin at the same time. This is called photocontact dermatitis. Big blisters appear on exposed parts which have been in contact with the plant. Anyone can get this kind of plant dermatitis, which settles leaving pigmentated patches, which may last several months. When caused by perfume, it is known as ‘berloque dermatitis’.
Irritant contact dermatitis arises in those with sensitive skin, if they’ve handled the plants too much, or if the plants have prickles or barbs. Stinging nettles cause contact urticaria.
Other plants cause a rash only in certain people who have developed an allergy to them. This is called allergic contact dermatitis. A number of cases of very allergic contact dermatitis resulting in facial swelling and blistering of exposed parts are seen every year due to Rhus trees (Toxicodendron succedaneum), which are specimen trees with lovely autumn colours. Primula obconica and chrysanthemum can also cause allergic rashes. Not everyone is allergic to these plants, but those who are may even get rashes from pollen carried in the wind.
Allergic contact dermatitis to a plant is not contagious and the blister fluid does not spread the rash. The rash appears between four hours and 10 days after exposure to the plant, depending on individual sensitivity and the amount of contact. Sometimes more rash appears after treatment has begun due to bloodstream spread of the allergy to other areas (autoeczematisation).
Compositae dermatitis images supplied by Dr Shahbaz A. Janjua
What is the treatment for plant dermatitis?
Plant dermatitis is self-limiting. It clears up without treatment, as long as exposure to the plant is avoided. Topical steroids, and sometimes by oral steroids may be necessary to treat the rash. If there are blisters, compress the areas for 15 minutes twice daily with a mixture of a tablespoon of white vinegar in a litre of water. Ice packs or cold showers will temporarily relieve itching. Steroids are less effective when the skin is blistered. Avoid soap as it irritates.
The only way to prevent plant dermatitis is to avoid contact with the responsible plant when it has been identified. Your dermatologist may be able to organise allergy testing (patch tests). We do not test for reactions to the most strongly allergenic plants because the tests could themselves create a new allergy. Many plants also cause irritant dermatitis and so patch tests must be performed and interpreted by an expert.
Plant Dermatitis – an overview
DERMATITIS IN TRAVELERS
Dermatitis is a general term for superficial, cell-mediated inflammation of the skin. Dermatitis is classified according to etiology and clinical features. Common types include atopic dermatitis, contact dermatitis, nummular dermatitis, seborrheic dermatitis, and hand (so-called dyshidrotic) dermatitis. A tropical climate may exacerbate a pre-existing dermatitis, though higher ambient humidity and UV light often help dermatitis.
Newly acquired dermatitis in travelers usually represents contact dermatitis. Contact dermatitis is further divided into irritant contact dermatitis and allergic contact dermatitis. Irritant contact dermatitis occurs on contact with an agent capable of causing injury and inflammation in most, if not all, persons (e.g., strong alkaline solutions). Allergic contact dermatitis occurs in sensitized individuals on contact with a specific antigen that does not cause dermatitis in non-sensitized individuals (e.g., poison ivy or oak).
Irritant contact dermatitis is caused by soaps, solvents, detergents, cleansers, cutting oils, and acid or alkaline solutions. ‘Dishpan hands’ is an example of chronic irritant contact dermatitis caused by soaps and frequent wetting of the skin. Individual susceptibility to any irritant varies greatly. Most occupational dermatitis is irritant contact dermatitis.
Allergic contact dermatitis can result from exposure to an enormous array of chemical compounds but requires specific sensitization. The most common sensitizers include nickel, chromates, rubber, formaldehyde, paraphenylenediamine, ethylenediamine, thimerosal, and neomycin. It is important to remember that many products sold for use on the skin contain sensitizers such as neomycin, benzocaine, ethylenediamine, fragrances, and lanolin.
Some topical agents can act in concert with UV light to produce photocontact dermatitis. Musk ambrette, a common ingredient in fragrances and cosmetics, and, ironically, sunscreen agents, such as PABA and oxybenzone, can cause photoallergic contact dermatitis.
Plant dermatitis (phytodermatitis) is a subset of contact dermatitis of particular importance to those traveling to rural areas. Many plants in a number of different families produce sensitizing chemicals. Poison ivy, poison oak, and poison sumac are members of the family Anacardiaceae and produce a resin containing 3-pentadecyl catechol, a potent sensitizer capable of sensitizing 70% of the population. Related plants containing cross-reacting chemicals include the Japanese lacquer tree (Rhus verniciflua), the India marking nut tree, raw cashew shells (Apacardium occidentale), mango rind (Mangifera indica), and the fruit of the ginkgo (Ginkgo biloba). Causes of plant dermatitis depend on the local flora. Mango dermatitis is the most common plant dermatitis in Hawaii. Philodendron is the most common cause in India. Primrose is a frequent sensitizer in Europe.
Phytophotodermatitis is a sun-induced plant dermatitis. Celery, limes, lemons, parsley, figs, and others contain natural psoralens that can incite a phototoxic reaction when contact with these plants is followed by sun exposure. Cases of systemic phototoxicity after ingestion of these plants followed by UV exposure are reported.
The primary lesions of dermatitis are erythematous papules and vesicles. In severe cases, bullae form and papules coalesce into plaques. Chronic lesions show scale, secondary changes of lichenification, and sometimes bacterial superinfection. Pruritus is a constant feature of dermatitis. Contact dermatitis is distributed in sites of contact, often giving a bizarre or artifactual appearance. The thicker skin of the palm and soles is more resistant to irritants and is often not involved. Allergic contact may be spread with the hands to other sites of the body such as the face, eyelids, and genitals. Plant dermatitis classically shows linear vesicles or bullae where the skin brushed against the causative plant.
Dermatitis is usually diagnosed clinically by the typical morphology of the rash. Biopsy may be useful in doubtful cases, but it does not identify the cause of the dermatitis. Establishing the cause of contact dermatitis requires careful questioning on exposure to plants, soaps, chemicals, topical medications, and the activities associated with the dermatitis. Patch testing is invaluable in the diagnosis of allergic contact dermatitis.
Differential diagnosis of dermatitis includes scabies, insect bites, certain drug eruptions, swimmer’s itch (cercarial dermatitis), psoriasis, and onchocerciasis.
Dermatitis of any etiology is treated in a similar manner. In the case of contact dermatitis, avoidance of the offending agent is most important. Protective clothing or gloves may be helpful when the person must continue the activities associated with the dermatitis. Excessive washing is irritating and impairs the barrier function of the skin. Similarly, mildly inflamed skin often improves with emollient alone.
Mild cases of papular or vesicular dermatitis are treated with topical steroids appropriate for the body area affected. Weeping or exudative lesions should be compressed with tap water or Burow’s solution for 15–30 min, four times a day, followed by topical steroids.
Severe contact dermatitis is best treated with prednisone 40–60 mg/day (adult dose), tapering the dose over 2–3 weeks. In allergic contact dermatitis, stopping the prednisone too soon often results in recurrence of the eruption. If a sensitized person contacts a known allergen, the skin should be promptly washed with soap and water to remove all possible allergen.
If secondary bacterial infection is present, it should be treated with antibiotics effective for Staphylococcus and Streptococcus sp.
A survey of plants responsible for causing allergic contact dermatitis in the Amathole District, Eastern Cape, South Africa
Open Archive in partnership with SAAB
We documented plants responsible for allergic contact dermatitis (ACD).
Twenty four plant species in 11 families were reported as causative agents of ACD.
The Asteraceae was probably the most important allergenic plant family.
67% of the allergenic plants are principally used as food.
Health care practitioners need to be aware of possible occupational causes for all cases of ACD.
An inventory of allergenic plants can enable vulnerable individuals to discover the source of their dermatitis and thus prevent re-exposure. However, because of the relatively little data available in the scientific literature with regard to the adverse effects of plant, the aim of this study was to document the plants responsible for allergic contact dermatitis (ACD) in the Eastern Cape. Interview questions targeted the local names of plants that cause allergies when in direct contact with the skin.
Twenty four plant species in 11 families were reported as causative agents of ACD. The Asteraceae was probably the most important allergenic plant family, represented by commonly used medicinal plants such as Artemisia afra, vegetables such as Lactuca sativa and weeds such as Conyza bonariensis. Sub-acute eczematous lesions of the face and the exposed areas of the upper limbs were characteristic of Asteraceae allergies. Out of the 24 plants mentioned for causing ACD, 67% are principally used as food.
A high burden of occupational skin disease in the food industry will definitely translate into large costs in terms of days lost from work and adjustments necessary in the workplace. Therefore, health care practitioners need to be aware of possible occupational causes for all cases of ACD.
Allergic contact dermatitis
Eastern Cape, South Africa
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Copyright © 2015 South African Association of Botanists. Published by Elsevier B.V. All rights reserved.
Plants That Can Cause Skin Irritations
Some plants can cause itchy rashes when touched. Poison ivy may come to mind, but many common garden plants can also be skin irritants for sensitive people. Sometimes it is just a certain part of the plant that irritates, like the sap of Euphorbia or the roots of hyacinth. Although, for some extremely sensitive people, any part of a plant they are affected by can cause irritation.
Types of Plant Irritation
There are three general ways plants become skin irritants:
- Chemical irritation: In the common case of poison ivy, the irritating chemical compound, urushiol, is absorbed right into the skin. Some people remain unaffected while others can have an extreme reaction. Unfortunately, just because you’ve been immune to urushiol in the past does not mean you will never be affected by it, so everyone should use caution around poison ivy plants. Irritating chemicals also can be transmitted to your skin in the winter when a plant looks dormant.
- Light sensitivity: Some plants are irritants only when they are exposed to sunlight, which also happens to be when most people are in their gardens. This is the case for plants in the carrot family, like parsnips and Queen Anne’s Lace.
- Mechanical injury: Plants such as nettles have sharp edges or thorns that can break the skin and introduce their toxins through the wound.
What to Do if Exposed to One of the Plants
You may notice your skin becoming itchy, even before any visible irritation appears. At the first sign of irritation, wash the area with soap and water and gently blot dry. Avoid touching your eyes or mouth area. An over-the-counter cream may be all you need for relief, but call your doctor if the rash worsens or if you develop blisters.
Here are 36 plants of varying toxicity, and the health problems and conditions they cause.
Contact dermatitis – Australasian Society of Clinical Immunology and Allergy (ASCIA)
ASCIA PCC Contact dermatitis 201951.1 KB
Allergic contact dermatitis is a common skin condition that results in an itchy and weeping rash, usually a few days after direct skin contact. Common causes include nickel, chemicals, plants, cosmetics, perfumes and ointments.
Allergic contact dermatitis is common
Allergic contact dermatitis is a common skin condition which causes an itchy and weeping rash localised to the area in contact with the allergic trigger (allergen). It usually develops two or more days after contact with the allergen. It lasts as long as contact continues and for a short time afterwards, typically one to two weeks.
Nickel metal is the most common cause of allergic contact dermatitis
Approximately 8% of the population is allergic to nickel, and the prevalence is higher among females than males. Nickel may be found in the metal of costume jewellery, watch straps, bra clips and jeans studs. The ears are often affected by wearing of non-gold earrings. The usual precipitant is piercing of the ears. Two days after contact with the metal, an itchy rash develops which may blister and weep. This rash will continue for several days or longer, if further contact with the metal continues.
Plants may also cause allergic contact dermatitis
Some plants can trigger allergic contact dermatitis. Rashes often appear on exposed areas of the body after being oudoors. Allergic rashes may be triggered by direct contact with the plant, or a combination of sunlight plus contact, so called “photo-contact dermatitis”. Examples of plants in Australia that may cause contact dermatitis are chrysanthemums, primula, tomato plants, grevillea, english ivy and occasionally rhus trees. Lantana or vegetables such as parsnip or celery may cause photo-contact dermatitis.
Other causes include chemicals, creams and ointments
Other common causes of allergic contact dermatitis include chemicals in rubber, leather and dyes. Contact dermatitis to shoes is common, and any one of these chemicals could be the cause. Creams and ointments used on the skin may also cause allergic contact dermatitis.
The cause may be the base ingredient (such as lanolin), or the active agent (such as neomycin, an antibiotic). The first time the cream or ointment is applied, the rash will generally not appear for 10 to 14 days. If it is applied again, it will usually take only two days to develop. Perfumes, either on their own, or in cosmetics, can also cause allergic contact dermatitis. Even sunscreens can cause problems.
Patch testing can identify the cause of allergic contact dermatitis
There are many causes of allergic contact dermatitis, particularly where individuals are working in industry and in contact with chemicals. If the cause of allergic contact dermatitis is not obvious, patch testing can be helpful. This is usually performed by a medical specialist (dermatologist or clinical Immunology/allergy specialist), and involves placing a sample of the substance on the back, and seeing if a reaction occurs after a few days. While it is not always easy to find the cause of contact allergy, intensive patch testing usually provides an answer.
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ASCIA resources are based on published literature and expert review, however, they are not intended to replace medical advice. The content of ASCIA resources is not influenced by any commercial organisations.
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Updated May 2019
Allergic Contact Dermatitis to Plants: Understanding the Chemistry will Help our Diagnostic Approach
The α-methylene-γ-butyrolactones are part of a large and varied group of bioactive natural products widely present in plants. Their high chemical reactivity arises because of an α,β-unsaturated carbonyl system which allows the formation of covalent adducts with nucleophilic residues on diverse biomolecules. Most of these chemicals are of the sesquiterpene type (15-carbon-atom molecule) with an α-methylene group directed exocyclically to the γ-lactone ring. They are classified into 6 main groups of sesquiterpene lactone (SQL) structures: guaianolide, pseudoguaianolide, xanthonolide, ermophilanolide, eudesmanolide, and germacranolide (Fig. 1). They are the predominant allergens in the Compositae family as well as in other related plant families such as Jubulaceae, Magnoliaceae, Winteraceae, and Lauraceae.1 The α-methylene-γ-butyrolactones can also be found as more simple structures in the Liliaceae (tulipaline A) and Alstroemeraceae families.
Asteraceae or Compositae Family
The Asteraceae/Compositae family—also referred to as the aster, daisy, or sunflower family—comprises the second largest family of flowering plants in the world. It includes more than 22750 currently accepted species, spread across 1620 genera and 12 subfamilies. Over 200 species are important causes of contact dermatitis worldwide.2,3 This family presents a variety of edible plants, such as lettuce, chicory, dandelion, salsify, sunflower, scorzonera, artichoke and yacon. Many members are decorative flowers, such as chrysanthemums, gerbera, calendula, dendranthema, dahlias, and heleniums while many others are considered as common weeds. Species such as arnica, chamomile or feverfew are also used medicinally. Asteraceae/Compositae can be recognized by its inflorescence, consisting of many tiny flowers clustered to form a flower head and subtended by an involucre.
SQLs are the predominant allergens although other compounds such as epoxythymol-diesters and polyacetylenes may also be involved.4 SQLs are usually lipophilic, and are often located in the liquid-soluble part (oleoresin fraction) of the leaf, stem flower, and possibly in polen.2,4,5 Although the mechanism of sensitization is unknown, several possibilities have been proposed: pollen or dry debris airborne transportation, direct and/or indirect contact with parts of the plant, and allergen inhalation or ingestion.4,6
Some peculiar cutaneous eruptions caused by the Asteraceae/Compositae family have been described. The pseudophotodermatitis pattern occurs almost exclusively in middle-aged men with a history of outdoor exposure but is rare in children and women, although some studies have suggested an equal sex distribution.6,7 Exposed areas of the face, V of the neck, hands, and forearms are typically involved. In addition, areas not clearly exposed to sunlight such as retroauricular regions (Wilkinson triangle), eyelids, nasolabial folds, and the area beneath the chin are also involved, allowing its differentiation from a true photo-related dermatitis.7 In hot regions, during summer months dry dead plant material contributes to this airborne pattern of dermatitis. In the US, many Compositae weeds, including ragweed (Ambrosia species), induce this clinical pattern often called ragweed dermatitis8 or weed dermatitis in regions where other composite weeds predominate, such as Ambrosia, Artemisia, Helenium, and Iva species.9,10 A similar pattern was described in Australia where it is known as bush dermatitis because it is caused by species such as Arctotheca, Cassini, Conyza, Cynara, and Dittrichi11,12 and also in India where it is called parthenium dermatitis, where the culprit plant is Parthenium hysterophorus L13,14 Although these environmental conditions are not normally encountered in the temperate regions of Europe, some isolated reports of airborne dermatitis (ragweed dermatitis) induced by feverfew (Tanacetum parthenium [L] Sch. Bip.), chicory and lettuce, liverworts of the genus Frullania, and chrysanthemums1,6,9 have exceptionally been reported.
A second special clinical pattern has been described as atopic eczema-like eruption. Compositae allergy may be manifested as a generalized eczematous eruption with primarily flexural involvement. Although it most commonly occurs in elderly men in rural areas, cases in children have also been reported.4,15 An erythrodermic exfoliative pattern classically induced by the weed Parthenium hysterophorus L was also described. This plant was accidentally introduced to the west coast of India in contaminated seed wheat. Several thousands of cases of allergic contact dermatitis occurred, some of them fatal.16
Hand eczema is more frequent in women working in gardening after contact with weeds. A palmar distribution often predominates.17 Hand dermatitis is also associated with handling lettuce.18,19 Dermatitis confined to one or more localized areas such as facial dermatitis secondary to steaming chamomile tea or hand and arm dermatitis from herbal compresses20 has rarely been reported. Oral swelling, perianal pruritus and dermatitis of the trunk and arms were described in a sensitized patient who drank chamomile tea.20 Stomatitis and throat swelling have occurred in some patients after eating lettuce and endivia.21 In one single patient erythema multiforme was reported to develop after patch testing.22
A rare chronic and disabling eccematous photodermatosis known as chronic actinic dermatitis (CAD), photosensitive dermatitis, or actinic reticuloid, has been linked to the ACD to compositae. A high incidence of ACD to one or more allergens has been found among patients with CAD,23 and sesquiterpene lactones are commonly identified as allergens. It is thought that about 20% to 75% of patients sensitized to Asteracea (Compositae) have some degree of photosensitivity. Thus, the progression of ACD to sesquiterpene lactones to CAD has been postulated, but its origin is still unknown.
No ideal patch testing material to study Compositae-induced dermatitis exists. The Compositae family includes more than 1350 SQLs and almost 50% of them are potential contact allergens.2 SQLs with slight differences in molecular structure, may cause true cross-reactions, while identical SQLs from different species may be responsible of false cross-reactions. SQLs are not exclusive to the Compositae family and frequently show cross-reactivity with other plant families. Because the concentration of SQLs shows seasonal and geographic variations and as cross-reactions between different species are not complete, when a patient is not tested with the relevant plants, the diagnosis may be easily overlooked.
Fresh plants or plant extracts should not be used for patch testing because they may cause severe contact reactions and can also elicit active sensitization. False positive irritant reactions or false negative results caused by low content of allergens (degradation products) can also occur.
In 1986, Benezra and Epstein developed the sesquiterpene lactone mix (SL mix) a nonsensitizing and seldom irritant mixture of 3 of the 6 main structural groups of sesquiterpene lactones (alantolactone, costunolide and dehydrocostuslactone of eremophilanolide, germacranolide, and guaianolide group) (Fig. 2). This mixture can enable identification of about 60% of SQL sensitization cases24 and was included in the European baseline series.17 Other studies19,25–27 reported different percentages, which can partly be explained by phytogeographical variations and the diversity of SQL structures.28 An alternative preparation, the Compositae mix, based on a mixture of plant extracts (arnica, yarrow, tansy, German chamomile, and feverfew), detects a higher proportion of the cases; however, it may be irritant and cause patch test sensitization.29
Dandelion and feverfew extracts, together or individually, also appear to be more useful than the SL mix.30,31 Other blends have been proposed, such as a mixture of Achillea millefolium L, Chamaemelum nobile All, Helianthus anuus L, Tagetes minuta L, and Tanacetum vulgare L as well as extracts mixtures of arnica, German chamomile, feverfew, tansy, and yarrow.27
Jubulaceae Family (Liverworts)
Liverworts are nonvascular plants with a bryophyte life cycle. They comprise 4 genera: Frullania accounts for nearly 800 species and Jubula for 15, whereas Steerea and Neohattoria are both montypic. These plants are often epiphytes growing on trunks and branches of trees or shrubs. They are found throughout the world and are common in tropical and subtropical regions but rare in frigid climates. They are often resistant to desiccation and direct light. Jubula species are largely confined to damp shaded rock surfaces.
At least 11 species of Frullania have been described as responsible for allergic contact dermatitis.32Frullania dilatata (L) Dum and Frulanina tamarisci (L) Dum have been frequently implicated in Europe. Cases of allergic contact dermatitis were also described in British Columbia (Canada), the Pacific North-West of the United States, and in the South-West of France.
The most important allergen is frullanolide,33–35 an α-methylene-γ-butyrolactone sesquiterpene from the eudesmanolide structural group. Other α-methylene-γ-butyrolactones have been reported as sensitizers such as oxyfrullanolide 5, cis-b-cycloscotunolide 6, and eremofrullanolide 7.35–37Frullania dilatata (L) Dum contains exclusively the d- or (+)-enantiomer of frullanolide while Frullania tamarisci (L) Dum exclusively yields the l- or (−)-enantiomer.36 Both enantiomers are sensitizers, and in guinea pigs the stereospecificity of sensitization to one enantiomer has been demonstrated36,37 (Fig. 3).
Sensitization to Frullania can occur by direct handling of trees or by airborne contact through volatilization of its small particles, especially during warm weather or by the action of chainsaws.34,35 Forest workers often suffer from woodcutter’s eczema and domestic allergy can present in individuals who use lobe-leaved trees as firewood. Exposed areas of skin are typically affected, with an airborne pattern on the face and the V of the neck. This clinical pattern can mimic a photosensitivity pattern but it involves areas with little photoexposure such as the eyelids and nasolabial folds. The hands may become edematous, with involvement of finger webs but often sparing of the palms. Exceptional involvement of the genitalia and intertriginous folds has also been reported.38
Testing the patient with small pieces of Frullania is associated with a high risk of active sensitization. The SQL mix only detects about 1% of allergic reactions to Frullania. The frullanolide mix, a racemic mixture of (+)- and (−)-frullanolide at 0.01%, 0.033% and 0.1% in petrolatum39 is a safe and nonsensitizing test, but only shows 0.35% of positive reactions.
Although testing the patient with small pieces of Frullania is associated with a high risk of active sensitization, it could be used if there is high clinical suspicion. Frullanolide mix, a racemic mixture of (+)- and (−)-frullanolide at 0.01%, 0.033% and 0.1% in petrolatum39 has been used in several clinical trials proving to be a safe and nonsensitizing test, but with a lower sensitivity than the SQL mix. Therefore the allergen of choice in these cases is SQL mix, even though it only detects 1% of the allergic reactions to Frullania.
Cross-reactions with botanically unrelated plants that contain similar allergens, eg Laurus nobilis L,35Magnolia grandiflora L,40 and several Compositae may also occur.32,41,42
The tulip genus which comprises 109 species of showy flowers is the most important genus of the Liliaceae family. A number of species and many hybrid cultivars are grown in gardens, used as pot plants, or displayed as freshly cut flowers. Most cultivars of tulip are derived from Tulipa gesneriana. Professional bulb growers, bulb collectors, sorters, and packers are particularly at risk of contact dermatitis.
Tulip bulbs contain several glucosides including tuliposides A and B, which are weakly allergenic but are rapidly hydrolysed to tulipalin A and B. Tulipalin A appears to be the main sensitizer in clinical practice43 although tulipalin B also causes sensitization in guinea pigs44 (Fig. 4). Flowers, leaves and stems possess higher concentrations of tuliposide A than the bulbs; but sensitivity can develop from contact with any portion of the plant, although most of the cases occur in bulb growers who are continuously handling the bulbs. Contact with airborne allergens, although infrequent has also been reported.45
The most common presentation is a combined allergic and irritant hand dermatitis known as tulip fingers. It is characterized by painful, subungual and periungual erythematosquamous, sometimes erosive lesions involving the fingertips, particularly the first and second fingers of the dominant hand.46 There may be fissures, suppuration, and hyperkeratosis. The dermatitis may extend to the adjacent skin and rarely may involve distant areas or even give rise to a diffuse dermatitis.45,47 The dust in tulip sheds may induce conjunctivitis, rhinitis and asthma. Reaginic responses to tulip antigens can also occur.47
These species have a cluster of tuberous roots and produce leafy stems, bearing one to several brightly colored flowers. Several species are found in special collections and only 2 species are widely distributed and produced: Alstroemeria aurantiaca D Don, with orange flowers, which grows as a border plant, particularly in cottage gardens, and Alstroemeria ligtu (Peruvian lilies) which give rise to numerous colors, mostly in shades of lilac and pink, with darker veins and mottling on the petals (Fig. 5). They grow in Holland, South America, USA and Australia. Tulipalin A, the same allergen of the Liliaceae family, is the main responsible sensitizer and is found mainly in the petals and stem. The rate of sensitization for tulipalin A can exceed 50% in workers on Alstroemeria plantations.48
Dermatitis most commonly affects florist who strip off the leaves manually and are therefore exposed to the broken plant with a high risk of allergic contact dermatitis. The lesions, in contrast to tulip finger dermatitis, can be more severe and tend to involve the fingertips of all digits of both hands. Occasionally, the clinical pattern can be very similar to that produced by the garlic clove (but in a bilateral and symmetric distribution).49 Workers who cut the flowers often show palm eczema.50–55 Airborne dermatitis56 and post-inflammatory depigmentation have rarely been reported.57 False positive responses due to a primary irritant reactions may also occur.58
|Full name||Position||Qualification category||Certificate||Education|
|Eltsova Natalya Vladimirovna|| Chief Physician
|Higher, 1998 Nizhny Novgorod State Medical Academy|
|Hamitsaeva Irina Romanovna|| Head of department
|Higher, Moscow State University of Medicine and Dentistry, 2000.|
|Borisova Tatiana Timofeevna||Doctor of clinical laboratory diagnostics|| Higher
Clinical lab. diagnostics
| Clinical laboratory diagnostics
|Higher, 1998 Moscow Medical Academy named after I.M. Sechenov|
|Bogatova Elena Yurievna|| Head of laboratory
Clinical laboratory diagnostics doctor
| Clinical laboratory diagnostics
06/16/2016 No. 0377180538858
|Higher, 1985 Khabarovsk State Medical Institute|
|Prokopenko Svetlana Alexandrovna||Dermatovenereologist||Dermatovenereology|| Dermatovenereology 09/02/2019
|Higher, State Budgetary Educational Institution of Higher Professional Education “Russian National Research Medical University named after N.I. Pirogov “Ministry of Health of the Russian Federation, 2013.|
|Kozlova Evgeniya Yurievna||Dermatovenereologist|| Higher
|Higher, 1997 Moscow Medical Dental Institute|
|Kirillova Natalya Ivanovna||Dermatovenereologist|| Higher
|Higher, 19832nd Moscow State Medical Institute named after I.I. N.I. Pirogov|
|Klimontova Tatiana Vladimirovna||Doctor-laboratory assistant|| Higher
Clinical lab. diagnostics
| Clinical laboratory diagnostics 12/16/2019
|Higher, 1994 Kemerovo State University|
|Lyamina Elena Vladimirovna||Dermatovenereologist, Candidate of Medical Sciences|| Higher
|Higher, 1996 Tver State Medical Academy|
|Samokhvalova Elena Viktorovna (parental leave)||Dermatovenereologist||b / k|| Dermatovenereology 09/01/2017
|Higher, State Budgetary Educational Institution of Higher Professional Education “Russian National Research Medical University named after N.I. Pirogov “MH RF 2015.|
|Sityukov Yuri Pavlovich||Dermatovenereologist|| Higher
|Higher, 1st Moscow Medical Institute named after I.M. Sechenov, 1989|
|Staforova Ksenia Nikolaevna||Dermatovenereologist||b / k|| Dermatovenereology
|Higher, Moscow State University of Medicine and Dentistry. A.I. Evdokimova, 2013|
|Silakova Tatiana Alexandrovna||Dermatovenereologist||b / k|| Dermatovenereology
|Higher, 2011 SBEE HPE “Kursk State Medical University” MH and SR RF|
|Zaitsev Maxim Eduardovich||Dermatovenereologist||b / k|| Dermatovenereology
| Higher, 2016
GBOU VPO “First Moscow State Medical University named after THEM. Sechenov “MH RF
|Perevalova Maria Andreevna||Dermatovenereologist||b / k|| Dermatovenereology 03.07.2020
|Higher, 2018 FSBEI HPE “Perm State Medical University named after Ak. E.A. Wagner “|
|Udalova Irina Valerievna||Dermatovenereologist|| Second
|Higher, GOU VPO Saratov State Medical University named after IN AND. Razumovsky|
|Filatenkova Viktoria Petrovna||Doctor-laboratory assistant|| Higher
Clinical laboratory diagnostics
|Clinical laboratory diagnostics 15.03.2019 0177241849270||Higher, Siberian Order of the Red Banner of Labor Medical University, 1993.|
Dermatovenerology: Contact dermatitis – diagnostics and treatment in St. Petersburg, price
Contact dermatitis is an acute or chronic inflammation of the skin caused by direct contact with an irritating chemical (irritant) or allergen.
Features of the disease
- previous sensitization to the substance causing dermatitis,
- the presence of a latent period between exposure to a damaging agent and the development of dermatitis (24-48 hours),
- activation after this exposure of the inflammatory process on all areas of the skin ever sensitized by this allergen,
- allergy resistant for many years.
There are several types of dermatitis
- Atopic dermatitis is often associated with hereditary predisposition (passed down from generation to generation) and other allergic diseases such as asthma and hay fever.
- Contact dermatitis (CD) occurs after a predisposed person’s skin comes in contact with a certain substance that causes inflammation. There are two main types of contact dermatitis: allergic and irritant (irritable).
- Allergic CD is a type of dermatitis that is caused by exposure to an allergen. An allergen is a substance that leads to the development of a pathological “wrong” reaction of the immune system (normally, the immune system fights against diseases and infections). At the first contact with an allergen, the patient becomes sensitive to it (sensitized). With repeated contact with a substance, such a person has a reaction.
- Irritant CD – inflammation of the skin resulting from direct skin contact with any irritating substance (irritant).An irritant is a substance that damages the skin, causing it to become inflamed. This type of dermatitis can occur in most people with long enough exposure to irritants. Both types of dermatitis can lead to redness, dryness, cracked skin, and blisters, blisters, and other breakouts.
Sometimes, the same person can develop both irritant and allergic CD at the same time.
Irritant CD is more common than allergic CD.About 80% of CD cases are caused by irritants (irritants). About 75% of all cases of CD occur in the area of the hands. More common in women. About 20% of women develop symptoms of CD during their lifetime. CD can develop at any age. Elderly people may be more sensitive to drugs, while women may be more sensitive to cosmetics.
Contact dermatitis symptoms
Both allergic and irritant CD can lead to the following skin changes: redness, inflammation, blistering and blistering, dryness, thickening, cracking.The most commonly affected areas of the skin are the hands and face. Often, in addition to the skin in the area of contact with the allergen, the reaction spreads to other areas of the skin where there was no such contact. In contrast to allergic irritant CD, only the skin in the contact area is affected.
Possible causes of allergic contact dermatitis
- metals – nickel, cobalt, others,
- cosmetics – perfume, hair dye, nail polish,
- rubber – latex,
- textiles – paints, rubber, rosin,
- adhesives and binders – epoxy and others,
- some plants – chrysanthemums, tulips, primroses and others,
- some medicinal creams – steroid and others.
Possible causes of irritant contact dermatitis
- detergents and soaps,
- preservatives and perfumes,
- acids and alkalis,
- cement powder,
- water (especially hard, limestone or highly chlorinated),
- some plants – anemone, mustard and others.
Often contact with irritants is part of the job, so these workers are at risk of developing irritant CD. This type of work includes: cooking, house cleaning, hairdressing, agriculture and fishing, engineering, repair and construction, medicine, dentistry and veterinary medicine, painting.
Diagnosis of contact dermatitis
If contact factors can be identified from the patient’s medical history, then in the future it is necessary to take maximum measures to eliminate them and reduce contact.
Patch testing (applications of “patch tests”) – the main method for diagnosing irritants or allergens is to use. During testing, small amounts of several substances are added to the patient’s skin. The substances are attached to the patient’s back using a special hypoallergenic adhesive plate. After 24-48 hours, tests are removed and it is assessed whether there is a skin reaction to the diagnosed substances. In some cases, it is necessary to go to the doctor 1-2 more times after a few days to assess possible delayed reactions.
Contact dermatitis treatment
With the help of drugs, you can effectively eliminate the symptoms of contact dermatitis. On the background of therapy, in some patients the symptoms disappear completely, in others there is an improvement of varying degrees of severity. Identifying and eliminating contact with potential allergens or irritants is an important part of treating contact dermatitis. If the patient can successfully avoid such contact, then he will not develop any symptoms.If it is impossible to achieve complete elimination of contact, the doctor will help to minimize it.
In case of professional contact with allergens and irritants, protective equipment (clothing, gloves) must be worn. Emollients are substances that soften and moisturize the skin. They are especially useful for contact dermatitis because with this disease, dry and cracked skin often occurs. The type of emollient is chosen by the doctor depending on: the severity of dryness, skin area, individual preferences. You will also need different emollients at different stages of the disease: in the acute stage – one, in the chronic – the other, etc.
Topical (topical) corticosteroids. In the acute stage of the disease, when there is redness, inflammation, rashes, pain on the skin, the doctor may prescribe a topical glucocorticosteroid (CGC). This type of medication is used to quickly reduce skin inflammation. It is applied precisely to the area of contact and skin lesions.
Prevention of contact dermatitis
The best way to prevent contact dermatitis is to avoid contact with allergens and irritants that cause symptoms.If this is not possible, it is necessary: to clean, wash off the causative factor from the skin after contact with water, use protective equipment (masks, clothing, gloves), check all products, read labels to identify the possible content of causal factors.
Approaches to the treatment of allergic contact dermatitis uMEDp
One of the most common skin diseases is allergic contact dermatitis, which is diagnosed in 4–7% of patients visiting dermatological hospitals .The incidence of allergic contact dermatitis is significantly higher in industrialized countries, where there is a high concentration of allergens in the environment. More often the disease occurs in women 20–40 years old, with age the risk of its occurrence decreases . Allergic contact dermatitis is a delayed-type immunological reaction and develops in individuals with a hereditary predisposition as a result of sensitization mainly to low molecular weight chemical compounds.
The list of substances that can cause allergic contact dermatitis is constantly expanding, more than 3000 such substances and compounds are currently known . The disease most often develops upon contact with metals and their salts, plants, compounds containing rubber, medicines (Table 1). Certain allergens that cause allergic contact dermatitis are characteristic of different regions of the planet. The most common household allergen around the world is nickel, which is found in the coating of watches, zippers, jewelry, buttons, buckles, eyeglass frames, etc.[four]. Positive skin tests for nickel sulfate are observed in 16.7% of patients with allergic contact dermatitis . A significant role in the development of allergic contact dermatitis is played by the components of decorative cosmetics (lanolin, fragrances, quaternium-15, paraphenyldiamine, rosin, Peruvian balsam, etc.) [6–8]. As a rule, allergic reactions develop after contact with hair bleaching products, hair dyes, nail polish, powder, lipstick, dry perfume, etc.Positive reactions to Peruvian balsam, fragrances, quaternium-15 were observed in 11.6%, 10.4% and 9.3% of patients with allergic contact dermatitis, respectively. Often, the disease is provoked by detergents and detergents, shampoos, cosmetic preparations, which include formaldehyde . In 10.2% of patients with allergic contact dermatitis, a positive reaction to thimerosal (a mixture of thiosalicylic and ethyl mercuric acid) is detected, which is used as a preservative in vaccines, solutions for contact lenses, antiseptics and cosmetic products [5, 9, 10].The list of major allergens identified by the North American Contact Dermatitis Group includes two drugs – topical antibiotics neomycin sulfate and bacitracin. Most often they are used in combination with each other and topical steroids in ophthalmic creams, antibacterial ointments. Positive tests for neomycin sulfate and bacitracin were observed in 11.6 and 7.9% of patients with allergic contact dermatitis, respectively; cases of anaphylaxis and urticaria have been described [11-13].With the development of occupational allergic contact dermatitis, sensitization to compounds of chromium, nickel, cobalt, petroleum hydrocarbons, coal, synthetic resins, drugs, formaldehyde, formalin-containing polymers, acids, alkalis, etc. is most often detected [1, 5].
Topical corticosteroids are widely used in the treatment of diseases. However, it should be remembered that in 0.2–6% of patients, they caused the development of allergic contact dermatitis [14, 15].Depending on the chemical structure, corticosteroids are divided into four groups, within which cross-reactions are noted (Table 2) . A report from the North American Contact Dermatitis Research Group 2001-2002 reported positive patch tests in 3% of cases for tixocortol-21-pivalate, 1.1% for butenoside, and 0.5% for hydrocortisone -17-butyrate . Among 2,000 patients in a German clinic with allergic contact dermatitis, less than 1% had a positive skin test for topical corticosteroids.Moderate risk of allergy development has been determined for hydrocortisone-17-butyrate, amcinonide, butenoside; low risk – for clobetasol propionate, triamcinolone acetonide; low risk – for prednisolone, hydrocortisone, betamethasone, dexamethasone . The minimum risk of developing allergic reactions has been shown for mometasone furoate . Only one of 15 patients sensitized to topical corticosteroids experienced a cross-reaction with mometasone furoate. The results of this study made it possible to recommend mometasone furoate as an alternative therapeutic agent for patients sensitized with corticosteroids.
Allergic contact dermatitis develops as a result of epicutaneous introduction of an allergen. Moreover, after a latency period, which can range from 4-10 days to 6 months and even 1-5 years, acute allergic inflammation develops. Lesions appear in areas exposed to the allergen, however, clinical manifestations may go beyond the areas of exposure to allergenic agents. Against the background of erythema, accompanied by a sensation of itching, burning, heat, papules, vesicles, erosion, crusts, scales are observed.There is a true mild rash polymorphism. Erythematous, papular or vesicular elements are predominantly observed. Upon termination of contact with the allergen that caused the skin lesion, the phenomena of allergic contact dermatitis completely regress, repeated contact with the allergen causes relapses of the disease. With the development of allergic contact dermatitis, monovalent sensitization is usually noted. However, with chronic allergenic stimulation of the body, certain changes in the activity of the nervous, endocrine, immunological systems, sometimes with irrational therapy, the disease can be transformed into true eczema, accompanied by the development of polyvalent sensitization.
Diagnosis of allergic contact dermatitis is based on history, clinical presentation, physical examination, and skin patch tests. Application tests help to identify the allergen that causes allergic contact dermatitis, to confirm the clinical diagnosis, and to select substances that are safe for a particular patient. Research is not conducted in patients receiving systemic corticosteroids or immunosuppressive drugs. A relative contraindication is acute dermatitis of any localization.Application tests are recommended to be carried out no earlier than a month after the onset of acute contact dermatitis, when the stage of regression or remission occurs.
For different regions, standard test kits have been developed containing allergens used for application tests. The advantages of standardized test kits are the choice of allergens motivated for a given geographic region, a reasonable concentration of hapten at which the number of positive results is maximum and the number of irritation reactions is minimal, as well as the possibility of obtaining comparable results .Standard test kits are proposed: North American Contact Dermatitis Research Group – relevant for the North American region, European Environmental and Contact Dermatitis Research Group (EECDRG) (Table 3) [19, 20]. In addition, a number of countries use standard tests proposed by national contact dermatitis research groups . Since it is impossible to include all existing allergens in the standard series, the etiological factor of allergic contact dermatitis is not found in all patients.This is also facilitated by the development of false positive and false negative reactions. If negative results are obtained, studies are continued with more specialized series or with substances and products brought by the patient. Subject to all the rules of setting, application tests are informative in 80% of cases.
Treatment of allergic contact dermatitis begins with the elimination of the cause of the disease. It is necessary to eliminate the allergen from the skin surface, and also to exclude the patient’s repeated contact with this agent.Often it is difficult to eliminate the allergen due to possible cross-reactions with other agents that are part of the surrounding household items. With pronounced common clinical manifestations, general treatment with desensitizing agents, antihistamines, sorbents, vitamins is recommended . In some cases, one of the methods of choice is the systemic use of corticosteroids . Local treatment is carried out taking into account the severity of the inflammatory process and the predominance of certain elements in the clinical picture of the disease.With limited processes, to achieve regression of clinical manifestations, it is sufficient to use only external drugs.
The anti-inflammatory, antiallergic, immunosuppressive effects of glucocorticoids in various tissues and organs, including the skin, are realized through several mechanisms: a decrease in the synthesis of inflammatory mediators; reducing the number of antigen-presenting and mast cells; activation of histaminase and a decrease in the content of histamine in the focus of inflammation; a decrease in the activity of hyaluronidase and lysosomal enzymes, which leads to a decrease in the permeability of the vascular walls and the severity of edema; reducing the formation of free oxygen radicals; inhibition of the synthesis of mucopolysaccharides and nucleic acids .In addition to anti-inflammatory and immunosuppressive activity, glucocorticoids exhibit antimitotic and vasoconstrictor effects. The antimitotic effect is due to inhibition of protein synthesis, and the vasoconstrictor effect is due to the inhibition of the activity of natural vasodilators (histamine, bradykinin, prostaglandins) .
Currently, considerable experience has been accumulated in the use of mometasone furoate (Elokom) for various allergic dermatoses . The drug is obtained by introducing two chlorine atoms and a double furanylcarboxylic acid ester into the structure of methylprednisolone.The chemical structure of mometasone furoate provides sufficient anti-inflammatory and antiallergic efficacy, which is realized due to the suppression of the production of IL-1, 4-6, tumor necrosis factor α, inhibition of the expression of adhesive molecules (VCAM-1) [25, 26]. In terms of the strength of the anti-inflammatory activity of mometasone, furoate surpasses a number of fluorinated glucocorticosteroids, however, unlike the latter, the drug has a high safety profile: in the treatment of 22 653 patients with various chronic dermatoses, side effects were noted only in 0.4% of cases .Due to its pronounced lipophilicity, it easily penetrates through the epidermis into the deep layers of the skin, while the systemic absorption of the substance is low. When the drug is applied under an occlusive dressing for 8 hours, no more than 0.7% of the drug is absorbed into the systemic circulation . The high efficacy of mometasone furoate and the rapidity of the onset of the effect are largely due to the predominantly extragenomic mechanism of action of mometasone furoate, which distinguishes it from other topical glucocorticosteroids. Mometasone, forming a glucocorticoid-glucocorticoid receptor complex, can bind directly to transcription factors that are activated under the influence of inflammatory mediators .The binding of transcription factors can rapidly reduce the production of proinflammatory cytokines. Since the effect on the genome is minimal, mometasone furoate is not characterized by the development of side effects associated with this process. The high safety profile of the drug allows us to recommend Elokom cream and ointment for the treatment of patients without age restrictions, including children under 2 years of age.
Long-term interaction with receptors provides a long-term therapeutic effect, due to which it is sufficient to use mometasone furoate once a day.The advantage of the drug is also the presence of several dosage forms (ointment, cream, lotion), which are prescribed depending on the severity of allergic inflammation and the localization of the process. For chronic infiltrative processes, it is recommended to use an ointment. Due to the hygroscopic base of the cream, it is prescribed for acute inflammation, and the alcohol base of the lotion allows it to be used in areas of wetness, exudation, and when the process is localized on the scalp. It is also important to take into account that the base of Elokom ointment and cream has a number of therapeutic properties – moisturizing, antioxidant, antibacterial, which contribute to an increase in the effectiveness of treatment .The substances included in its composition give the base moisturizing, antioxidant, antibacterial properties. In addition, components with photoprotective properties are included in the Elokom cream, which makes it possible to choose this particular topical steroid for application to areas of the skin exposed to insolation.
We have used Elokom cream and lotion as an external therapy in the treatment of allergic contact dermatitis. The study included 54 patients (36 women and 18 men) aged 19 to 87 years.The development of allergic contact dermatitis was noted after contact with various substances (Table 4). In 19 cases, allergic contact dermatitis re-developed. In 24 patients, the process was widespread and localized on the skin of the trunk, upper and lower extremities, and face. Limited rashes in 3 cases were localized on the skin of the face, in 3 patients – the auricles, in 9 patients – on the neck and chest, in 5 – in the forearms, in 4 – in the axillary areas, in 6 – on the skin of the abdomen. There were lesions with clear boundaries; against an edematous hyperemic background, there were multiple vesicles, papules, erosion, oozing areas, scales, crusts (photo 1).In 8 patients, large blisters were observed on a hyperemic background. In all cases, the rash was accompanied by severe itching and burning. All patients clearly indicated the provoking factor, after contact with which the disease developed, therefore, they were recommended, first of all, to exclude contact with these substances. 30 patients with limited rashes received monotherapy with Elok cream and lotion once a day. A significant reduction in itching and burning was noted after the first application, clinical recovery was achieved on the 3-5th day of treatment.24 patients with a widespread process received general therapy with desensitizing agents, antihistamines, 3 patients with multiple bullous elements were once prescribed Diprospan 1.0 IM. Local therapy consisted of using Elokom cream and lotion once a day. On the 2-3rd day of treatment, all patients noted a significant improvement (reduction or cessation of itching and burning, partial regression of rashes). The resolution of the pathological process was noted on the 8-14th day of treatment.All patients noted the good tolerance of Elokom cream and lotion. There were no side effects or complications noted.
Clinical example. Patient T., 19 years old, complains of a rash on the skin of the abdomen, severe itching. The first rashes on the skin of the abdomen after contact with a metal buckle appeared 10 years ago. From time to time, after contact with metal buttons and buckles, an aggravation of the process was noted. The rash resolved after cessation of contact with the provoking factor and the use of topical corticosteroids.A real aggravation is observed within 3 weeks, when, after contact with a metal button on jeans, rashes appeared on the skin of the abdomen, accompanied by itching. As a remedy, the patient independently used a tincture of calendula, the use of which led to the spread of the process. On examination: the process is localized on the skin of the middle and lower abdomen (photo 2). There is a lesion with clear boundaries measuring 10.0 x 6.0 cm; against the background of congestive hyperemia, there are papules, pinpoint erosion, and crusts.Single papules of red color and excoriation go beyond the boundaries of the main focus. Subjectively – severe itching. Treatment was carried out: 1) elimination of contact with the provoking factor; 2) antihistamines; 3) Elokom cream once a day. On the 2-3rd day of treatment, itching resolved, regression of the rash was noted on the 8-10th day of treatment.
Our experience proves the high efficiency of Elokom cream and lotion in the treatment of allergic contact dermatitis. Due to the pronounced anti-inflammatory and antipruritic activity, a significant improvement in the pathological process and regression of subjective sensations are noted after the first applications of the drug.With limited lesion, monotherapy with Elokom is sufficient to achieve clinical remission. With common allergic contact dermatitis, it is advisable to use Elokom in complex treatment. The hygroscopic base of the cream and the alcohol base of the lotion effectively eliminate the phenomenon of wetting, have a drying effect, which contributes to the rapid achievement of the best therapeutic results. The minimal risk of developing an allergy to mometasone furoate makes the drug especially attractive in the treatment of allergic contact dermatitis.
Allergic contact dermatitis | Allergology
Allergic contact dermatitis is a type of dermatitis that develops after contact with an allergen. But for a sensitization reaction (allergy), a certain period of time must pass, sometimes up to several weeks. And already at the next contact with the allergen, dermatitis will immediately manifest itself.
Dermatitis can be either acquired or inherited at the genetic level. Plants, foods, cosmetics, or medications can cause the disease.
Symptoms and Diagnosis
The area of the allergic reaction is not limited to the place of contact with the allergen. Once on the skin, it is captured by the epidermis and, after a series of transformations, penetrates the lymph. There it is attacked by cells of the immune system (T-lymphocytes), after which the entire skin becomes sensitive to the allergen.
- bright redness of the skin;
- swelling and blistering;
- itching and burning in the affected area is possible.
The disease is diagnosed at a personal appointment with an allergist during a visual examination. Additionally, the patient is referred for skin tests. Test strips are made with different allergens and in case of redness of some of them, it is possible to identify what the patient is allergic to.
When treating allergic contact dermatitis, the first step is to eliminate the irritant causing the rash. An individual diet is being developed, and the intake of sorbing agents is prescribed.Antihistamines given by mouth or intramuscularly can help relieve rashes and itching. Additionally, it is necessary to apply corticosteroid, disinfectant and epithelial ointments. Hospitalization in a hospital is indicated only in severe cases.
Treatment of allergic contact dermatitis in Lipetsk is carried out in the Andromeda clinic. By making an appointment with our allergist, you can quickly identify the cause of the rash and eliminate the allergen that causes them from your life. The doctor will suggest optimal therapy, recommend topical preparations to relieve itching and antihistamines to help eliminate rashes.
LLC CDC Good Doctor – Dermatitis
The group of dermatitis combines various inflammatory skin diseases. Dermatitis is classified depending on the causes and localization of the lesion. Healthy human skin has protective functions, but with prolonged exposure to aggressive substances or with a decrease in immunity, the protective properties of the skin decrease, as a result of which dermatitis occurs.Contact dermatitis can be caused by contact with any irritant: physical, chemical, biological and mechanical. As a result of severe irritation, an inflammatory reaction of the skin occurs, proceeding as an allergy or mechanically caused inflammation. The degree of clinical manifestations depends on the type of irritant, the time of exposure to the skin and on its characteristics. That is, dermatitis can manifest itself as a slight reddening of the skin, and deep ulcerative lesions.
Allergic contact dermatitis usually occurs in allergic individuals from contact with sensitizing substances.When contact with antigens occurs, a delayed-type response develops, the allergen interacts with the cells of the dermis and antigen-antibody complexes are produced, that is, the body’s immune system becomes hypersensitive to this irritant and upon repeated contact with the antigen, an inflammatory reaction of the skin or dermatitis is observed. With the allergic nature of dermatitis, a response may occur immediately after contact with an irritant, at a subsequent meeting, or after 5-7 days; the speed of the immune response and the intensity of manifestations depend on the concentration of antibodies in the human blood.In the development of allergic dermatitis, a hereditary predisposition and a history of allergic diseases (hay fever, bronchial asthma) are of great importance.
In women, with long-term therapy of acne vulgaris and rosacea with corticosteroids, the skin becomes thinner, its structure and the chemical composition of sebum change, which leads to perioral and periorbital dermatitis, since the skin in the mouth and around the eyes is most sensitive. Perioral dermatitis occurs in children with increased salivation and during teething.Provocative moments in the development of perioral dermatitis are chronic diseases of the digestive system, hormonal dysfunction, the presence of foci of chronic infection in the body. In people suffering from bulimia or neurological disorders, dermatitis can be observed in the perioral region due to frequent contact with the acidic contents of the stomach, due to the provocation of vomiting.
Atopic dermatitis occurs in young and middle-aged children with a burdened allergic history and poor nutrition.Atopic dermatitis is chronic, even if only one episode has been diagnosed; in adults, under unfavorable conditions, atopic dermatitis may recur.
Manifestations of dermatitis
The symptomatology of dermatitis depends on the severity of the disease. So, with simple contact dermatitis, there is a slight reddening of the skin, a local increase in temperature and a slight infiltration, in some patients itching and tingling sensations are possible in the affected area.But with prolonged contact with an irritant, dermatitis can manifest itself in the form of ulcerative-necrotic lesions, weeping blisters, after opening which it is possible to attach a secondary infection. Although in the history of the disease the triggering factor is still contact with the irritant, which distinguishes complicated forms of dermatitis from pyoderma. An important clinical point for diagnosis is a clear limitation of the affected area, contact dermatitis appears only at the site of exposure to an irritating factor, this is necessary to differentiate it from allergic dermatitis.
In allergic dermatitis, the course of the disease is more acute, swelling and redness are more pronounced, itching joins; an important symptom in the development of allergic dermatitis is the spread of clinical manifestations to areas of the skin that has not been in contact with an allergenic irritant.
Perioral dermatitis manifests as small nodules and pustules that are localized around the mouth, on the cheeks, in the nasal folds and on the bridge of the nose. The presence of a narrow band of healthy skin around the red border of the lips is an important diagnostic sign.The course of such dermatitis is long, rashes appear gradually, itching, peeling, dryness and a feeling of tightness of the skin are noted. For women, especially young women, cosmetic defects add a sense of psychological discomfort.
Atopic dermatitis is characterized by erythematous eruptions with a tendency to exudate and form vesicles; elements are localized in the knee-elbow folds, on the buttocks and on the face. In adults, with relapses of atopic dermatitis, rashes are also noted in places of folds, but papular infiltration develops on flaky dry skin with a tendency to dermographism.
Causes of dermatitis
The pathogenesis of dermatitis is based on the influence of exogenous and endogenous factors. External causes are referred to as exogenous, and internal ones are referred to as endogenous.
External causes are mechanical influences such as friction and prolonged squeezing, resulting in cracks, abrasions and puffiness. Physical exposure to high and low temperatures, ultraviolet, radioactive and X-ray radiation are also factors provoking dermatitis.The cause of dermatitis due to contact with chemicals are salts of heavy metals, acids, alkalis, household chemicals, chemical warfare agents. Some plants, fungi, bacteria and viruses also cause local inflammation of the dermis, most often primroses, plants of the buttercup family, hogweed and ash.
Endogenous factors that reduce the protective functions of the skin are hypo- and avitaminosis, metabolic disorders, endocrine disorders such as Addison’s disease and scleroderma.Taking drugs of the group of antibiotics, sulfonamides and the use of novocaine-containing drugs most often provokes drug dermatitis. Dermatitis of an allergic nature can occur as a result of a violation of the diet (strawberries, chocolate, coffee abuse). Diseases in which autointoxication is noted are often complicated by dermatitis, which are characterized by dryness, peeling and severe itching of the skin.
Perioral dermatitis occurs due to the abuse of cosmetics, inappropriate local treatment with hormonal drugs, sometimes the cause of such dermatitis is medicinal toothpastes that contain fluoride.Lack of vitamins A and E causes dry skin, which can provoke the appearance of perioral dermatitis.
The main causes of atopic dermatitis are malnutrition in infancy, malnutrition in pregnant women, a history of allergic diseases, and neuropsychiatric disorders. Statistical data on the incidence of atopic dermatitis in adults confirm that people of asthenic constitution with mental disorders of the type of anxiety-depressive states and with chronic diseases of the gastrointestinal tract caused by low enzymatic activity, dyskinesias and dysbacteriosis are at risk.
Diagnosis of dermatitis
Clinical manifestations and a history of exposure to irritants are usually sufficient to diagnose dermatitis. From laboratory tests to confirm the diagnosis, a clinical blood test (eosinophilia is noted in the blood), determination of the concentration of immunoglobulins and skin allergic tests. In allergic dermatitis, skin tests can help identify the allergen or group of allergens that are causing the dermatitis.To diagnose diseases associated with dermatitis, it may be necessary to consult a gastroenterologist, therapist, allergist and other specialists.
Basic principles of dermatitis treatment
First of all, it is necessary to eliminate the effect of the irritant factor in order to prevent further damage to the skin. A hypoallergenic diet improves skin condition, both for allergic and other types of dermatitis. To eliminate itching, reduce infiltration and swelling, antihistamines are prescribed, such as clemastine, loratadine, fexofenadine.At the same time, antihistamines of the latest generation do not cause drowsiness and disturbances in attention, which makes it possible for patients with dermatitis to lead a normal life.
If necessary, detoxification therapy is prescribed – activated charcoal, hydrolysis lignin, intravenous injections of sodium thiosulfate. But with intravenous detoxification therapy, especially if dermatitis is of an allergic nature, it is necessary to first test for drug sensitivity. Calcium-containing drugs reduce the sensitization of the body, but if you have a history of bronchial asthma, it is better to refuse such drugs.
Local treatment of dermatitis consists in the use of hormonal ointments. If the dermatitis is weeping, with the presence of vesicles, then treatment with antiseptics and infusions of chamomile, oak bark have a drying effect, wet-drying dressings with antiseptics and ointments give a good result in the treatment of weeping contact dermatitis.
If the course of dermatitis is complicated by the formation of vesicles and pustules, then the bubbles are opened in compliance with the rules of asepsis and antiseptics, and the surface is treated with aniline dyes.The use of iodine solutions on the affected areas is prohibited, they can only be treated with the edges of the wound in order to prevent the spread of infection.
Since itching and unpleasant sensations in dermatitis cause neurological disorders that prevent a speedy cure, the appointment of mild herbal sedatives is indicated for all patients. These are tinctures of motherwort, valerian, peony. Glycine and combined herbal remedies also have a good sedative effect.
If pancreatic dysfunction is the main cause of dermatitis, enzyme replacement therapy is necessary. In this case, taking pancreatin preparations is necessary after each meal. With dysbacteriosis, it is advisable to include fermented milk products in the diet, prebiotic therapy. As soon as the normal intestinal microflora is restored, the symptoms of dermatitis usually fade away.
Prevention of dermatitis
Rational nutrition, adherence to personal hygiene and sanitary and hygienic standards in the organization of work are fundamental to the prevention of dermatitis.It is necessary to exclude citrus fruits, chocolate, nuts, fish and fish dishes from the diet. Coffee, cocoa, hot spices and sauces, vinegar and mayonnaise are also not recommended for dermatitis. Eggplants, mushrooms, eggs, whole milk, strawberries, strawberries, baked goods, smoked meats, fried and baked dishes during the treatment of dermatitis should not be present on the menu. And the use of low-fat dairy products, green vegetables and light soups make drug therapy for dermatitis more productive.
Dermatitis – ProMedicina Ufa
Dermatitis is a syndrome that is an inflammatory response of the skin to various irritants.
Irritants causing dermatitis can be of a physical, chemical or biological nature.
There are so-called obligate irritants that cause simple dermatitis in every person. These include: friction, pressure, radiation and temperature effects, acids and alkalis, some plants (for example, nettle).Symptoms of simple contact dermatitis appear immediately or shortly after the first contact with an irritant, and the area of the lesion corresponds to the area of contact. Sometimes a chronic course of dermatitis is possible, with prolonged exposure to the irritant.
Optional irritants cause skin inflammation only in persons who are hypersensitive to them. These are diseases such as allergic contact dermatitis and atopic dermatitis. The number of facultative stimuli (sensitizers) is enormous and constantly increasing.
Allergic contact dermatitis, unlike simple contact dermatitis, does not develop immediately after contact with an irritant, and not at the first contact. In order for an allergic reaction (sensitization) to form, it takes up to several weeks from the first contact. Then, with repeated contact, dermatitis develops. The inflammatory response of the skin clearly does not correspond to the intensity of the stimulus, which will not cause any changes in people without allergies. The area of changes on the skin may go beyond the contact.
Atopic dermatitis is a very complex disease, a chronic inflammatory skin lesion of an allergic nature. It can be caused by several or even a lot of factors – allergens, and at the same time not only contact, but also coming in by inhalation (pollen, dust) or food (food allergy). Atopic diseases also include bronchial asthma, allergic rhinitis, etc. The predisposition to atopy is transmitted genetically. Atopic dermatitis usually develops in early childhood.Often, with age, the manifestations of this disease subside or disappear altogether.
Mandatory symptoms are typical for most dermatitis, regardless of the causes: itching, redness, peeling of the skin, in acute forms, exudative inflammation with abundant discharge is possible.
Additional symptoms, which are important in the differential diagnosis of specific dermatitis, are identified during interrogation, examination, laboratory studies, and functional tests.
Diagnostics and treatment
If dermatitis develops, it is better to see a doctor rather than self-medicate.In the treatment of simple contact dermatitis, the main thing is the cessation of the action of the irritant. Often patients, understanding the cause of the disease, cope with it themselves. However, there are cases (for example, severe chemical and thermal burns, frostbite) when the intervention of a doctor is simply necessary.
A dermatologist and allergist can help you with the treatment of dermatitis. If necessary, you may be referred to a gastroenterologist and other specialists.
Treatment of allergic contact dermatitis is prescribed by a dermatologist and is reduced primarily to identifying the allergen.You will be asked in detail about your lifestyle, occupational hazards, cosmetics that you use, etc. When the allergen is eliminated, the symptoms of contact dermatitis usually disappear.
The treatment of atopic dermatitis is much more difficult. This condition should be treated by a qualified allergist. Antihistamines are used (both for oral administration and in the form of ointments), glucocorticoid drugs, allergen-specific immunotherapy.
Contact dermatitis in a child – symptoms, methods of prevention and treatment
Contact dermatitis is a specific skin disease that develops directly at the site of exposure to an irritant.
Skin exposure to an irritant (antimicrobial drugs, chemicals, plants, insects, heat or cold, new clothing). The presence of burns, abrasions and scratches on the skin.
- Redness on the skin in places of contact with an obvious irritant
- Symmetrical eruptions with pronounced puffiness
- Severe itching
- Blisters on the surface of the skin, which subsequently break open, leaving behind weeping erosive areas
- Tearfulness, deterioration of normal sleep
It should be noted that contact dermatitis has two types of course – acute and chronic.The acute phase manifests itself almost immediately after contact with a possible stimulus and passes after its termination. The chronic type of the disease, as a rule, develops after several repeated contacts with the allergen, and its development is characterized by constant exacerbations.
In children, this disease has an extremely favorable outcome if the parents manage to stop it in time. That is, it does not require special or special treatment, and, as a rule, passes on its own, provided that the original stimulus is completely eliminated from the child’s life.
- Avoid skin contact with substances that cause an allergic reaction.
- In case of accidental contact with the skin of a known irritant – wash the skin thoroughly under running water and soap.
- Use of special hypoallergenic products for allergies to household chemicals (washing powders, home care products).
- Natural materials when choosing clothes, especially underwear.