•  Detergents

•  Solvents

•  Metal working fluids

-          Common allergens causing contact dermatitis

•       Nickel

•       Fragrance

•       Rubber

•       Medications including topical corticosteroids, lanolin, neomycin

•       Chromate

•       Formaldehyde and other biocides

•       Epoxyresin

•       Plant allergens

•       Hair-dressing chemicals

•       Director air borne contact may occur

•       Cosmetics (4)

6.    Mechanism of development:

-          When skin sensitizers penetrate the epidermis, they are taken up by Langerhans’ cells—bone marrow-derived members of the macrophage family that function as “professional antigen presenting cells.” The Langerhans’ cells leave the epidermis and migrate to the regional lymph nodes, where they enter the paracortical areas, the home of naive T lymphocytes. Probably while en route to the lymph node, the Langerhans’ cells process the sensitizer so it is physically associated with the HLA-DR molecules on the cell surface. In the node, the Langerhans’ cells “present” the sensitizer to T lymphocytes of the immune system. If T cells with the appropriate specific receptor recognize the complex of sensitizer and HLA-DR, they proliferate to establish “immunological memory.” The memory T cells that mediate allergic contact eczema are of the Th1 subtype, characterized by the production of interleukin 2 and interferon gamma. The induction of sensitization and establishment of immunological memory takes 8-14 days. Should re-exposure to the sensitizer occur, Langerhans’ cells carry it down into the dermis, where they present it to memory T cells travelling through the tissues and These are activated to release cytokines (including interferon gamma) that attract other cells and activate vascular responses, resulting in the characteristic inflammation of contact eczema.(9)

7.    Clinical features:

-          Contact dermatitis: contact dermatitis is an inflammatory skin process caused by an exogenous agents or agents that directly or indirectly injure the skin. Contact eczema develops as result of contact with injurious materials. These materials may injure by direct toxins actions (irritants) or may induce immunological reaction of delayed hypersensitivity reaction (allergens).

-          Irritant contact dermatitis: Any physical or chemical agent that is capable of producing, if applied for sufficient time and in sufficient concentration can lead to irritant dermatitis. Dermatitis occurs when the repair capacity of the skin is exhausted or when the penetration of chemicals excites an inflammatory response. This type of dermatitis occurs due to contact with irritants like detergents, acids, alkaline chemicals, oils, organic solvents, oxidants, and reducing agents. The intensity of the inflammation is related to the concentration of irritant and the exposure time. Mild irritants cause dryness, fissuring and erythema (cumulative irritant dermatitis; wear and tear dermatitis) and strong irritants may produce an immediate reaction characterized by burning, erythema, edema, blistering, and possibly ulceration of skin Housewife‘s eczema, diaper dermatitis and industrial dermatitis are common examples of cumulative irritant contact dermatitis. Housewife‘s dermatitis and industrial/occupational dermatitis commonly affect the hands. Treatment of acute irritant dermatitis requires washing quickly with water or a weak neutralizing solution or frequent wet compresses, followed by the application of a bland or antibacterial with mid-potency steroid cream. For chronic cases, removal of all adverse chemical and physical factors and the use of bland barrier cream and mid potency topical steroids are necessary along with protective gloves. (5)

-          Allergic Contact Dermatitis: ACD is a manifestation of delayed type hypersensitivity mediated by memory T lymphocytes in the skin. Prior exposure to the offending agent is necessary to develop the hypersensitivity reaction, which may take as little as 12 h or as long as 72 h to develop. The most common cause of ACD is exposure to plants, especially to members of the family Anacardiaceae, including the genus Toxicodendron. Poison ivy, poison oak, and poison sumac are members of this genus and cause an allergic reaction marked by erythema, vesiculation, and severe pruritus. The eruption is often linear or angular, corresponding to areas where plants have touched the skin. (6)

-          Parthenium dermatitis is the most common and severe type of allergic contact dermatitis seen in India. It is caused by a weed Parthenium hysterophorus which grows wild along roads, railway tracks and in the fields. It commonly manifests as air-borne contact dermatitis affecting mainly the face including the eyelids, neck, flexures of the extremities, and sometimes the whole body surface may be involved. Distribution of lesions on sun-exposed areas is not uncommon. There is worsening during summer and rainy season while the lesions undergo partial or complete remission during winter.

-          Nickel sensitivity is quite common and manifests as dermatitis due to ear rings, bangles, necklace, zips, metal buttons, and safety pins. Occupational nickel sensitivity affects the hands. Chromium allergy is also quite common and is usually due to leather footwear, cement etc.

Leather is the most common causes. Topical medicament dermatitis is commonly due to nitrofurazone and neomycin. Neomycin sensitivity is quite often superimposed on varicose and footwear eczema, and remains undetected due to its use with topical steroids.Hair dye dermatitis are also not uncommon and it’s becoming common due to high concentrations of paraphenylenediamine (PPD) in Kali Mehndi (black henna). Other types of allergic contact dermatitis peculiar in our country are bindi dermatitis. Black henna dermatitis and tooth powder dermatitis. The common allergens in India are metals (nickel, chromium), rubber chemicals (mercaptobenzothiazole), Parthenium (a weed), medicaments (nitrofurazone, neomycin) and hair dye (PPD). (4)

7.    INVESTIGATIONS: Although clinical examination is quite sufficient to suggest the diagnosis of eczema, as a general rule it is advisable to treat acute eczemas without investigations. On the other hand, chronic and recurrent eczemas should be investigated thoroughly to find the cause of eczema.

-          Patch Testing: It is the only scientific method available to confirm the diagnosis of allergic contact dermatitis but is not useful for irritant contact dermatitis as it detects the allergens responsible for type IV allergy only. It should be performed after the acute stage subsides. A series of allergens in adequate concentration are applied on the back with adhesive tape and left on for 2 days. The readings are taken on day 2 and day 4. The offending allergens will produce erythema and papulovesicles at the site of application. A good patch test should indicate contact sensitization and produce no false positive reactions.

-          Photopatch Testing: These tests are performed to find the cause of photo allergic contact dermatitis. It should be performed in photo distributed dermatitis. In photopatch testing also, the patches of chemicals are applied as for ordinary patch testing, except that they are applied in duplicate and after 24 hours one set of patches is removed and the under lying skin is irradiated with ultraviolet light. After irradiation, the patch sites are covered again and evaluated at day 2 and day 4.

-          Prick Testing: These are performed to detect the type I hypersensitivity reactions. Relevance of positive prick tests in establishing the cause of the eczema is questionable.

-          Serological Testing: Estimation of total serum IgE and IgE antibodies specific to certain antigens are useful diagnostic criteria for atopic dermatitis. Radio-allergosorbent test (RAST) is helpful to detect specific dietary environmental allergens, which could be aggravating the dermatitis.

-          Skin Biopsy: A skin biopsy is rarely required to diagnose the eczema and  histopathological  findings  will  depend  upon  the  stage.  (4)

8.    TREATMENT: Successful management of dermatitis requires a multipronged approach. Apart from the specific therapy, appropriate general measures are very helpful in treating the eczemas.

-          GENERAL MEASURES: Identification of any offending allergen, irritant or triggering factor is very important. Adequate measures to avoid the offenders may help in treating the dermatitis. Eczemas like atopic dermatitis and Asteatotic dermatitis are associated with dry skin and hence increased susceptibility to irritants. Maintaining proper hydration of the skin is important in treating dry eczema.

-          Topical Treatment: Wet compresses with a solution of either potassium permanganate (0.01%/light pink color) or aluminum sulphate (0.65%) followed by application of steroid lotion cream is best in the oozing stage of eczema. These compresses help by suppressing inflammation, removal of crusts, have antibacterial action and cause drying of the lesions. In the sub acute stage, wet compresses should be discontinued and only mid-potency topical steroid cream can be prescribed. Chronic eczema requires potent steroid in ointment base for topical application. In lichenified lesions, a topical steroid can be combined with keratolytic agents like salicylic acid or urea. For secondary bacterial infection a topical antibiotic can be combined with a steroid.

-          Systemic Treatment A short course of systemic steroids may be needed for extensive lesions and when an irritant dermatitis eruption (spread of an acute inflammatory dermatitis to distant sites is termed irritant dermatitis eruption or autosensitisation) develops in acute eczema. Systemic antibiotics are required for infected lesions. Oral antihistamines may be prescribed, as and when required, but may not be helpful in contact dermatitis. Steroid sparing agents like methotrexate in small weekly doses, azathioprine, and even cyclosporine may be required in recalcitrant cases like atopic dermatitis, Parthenium dermatitis, etc. (4)

9.    Homeopathic Approach: Some of homoeopathic remedy which are much important for treatment of exogenous eczema from source book like. Homoeopathic Therapeutics by Dr. Samuel Lilienthal and Boericke’s New Manual of Homoeopathic Materia Medica and Allen’s keynotes are as under.

1.      Mezereum: Eczema intolerable itching, chillyness with pruritus, worse in bed, eruptions ulcerated and form thick scabs under purulent matter exudates (7) eczema and itching eruptions after vaccination, eruptions moist, itching worse at night (8) eruptions with itching and pustules, followed by desquamation (9)

2.      Graphites: Rough, hard, persistent dryness of skin unaffected by eczema, eruptions oozing out sticky exudation (7) unhealthy skin,

Eruptions moist and fissured, upon eras between fingers and toes, oozes Watery, transplant and sticky fluids (8)

3.      Sulphur: skin itching voluptuous; scratching > feels good to scratch but causing burning, scratching << from eat of bed (8) skin affections after local medication, itching, burning worse scratching and washing (7) sequel of suppressed eruptions, itching with soreness after scratching (9)

4.      Petroleum: eczema of ears , serous or purulent discharge of fetid odor

(9) moist eruptions obstinate and dry eruptions on genitals and perineum

(8) eczema; thick greenish crust burning and itching, cracks bleed easily (7)

5.      Antimonium crudum: eczema with gastric derangements, vesicles and pustules, thick hard honey colored scabs (7) suppressed eruptions, disposition to abnormal growth of skin (8) eczema of nostril, sub acute eczema about mouth, eruptions burning and itching worse at night (10)

6.      Clematis: red, burning, vesicular, eruptions worse washing on cold water, worse face, hand, around occiput (7) eruption; itching and tingling which are moist during increasing moon and dry during waning moon (9)

7.      Arsenicum iodum: eczema of beard, watery, oozing, itching worse washing ,marked exfoliation of skin large scales , dry, scaly itching eruptions (7) eruption on face and extremities, with corrosive discharge (9)

8.      Cistus Canadensis: skin of hands hard, thick, dry, fissured; deep cracks (7) itching all over body, vesicular erysipelas of face (10)

9.      Thuja occidentalis: itching vesicles, with shooting pains, burning violently after scratching, scaly eruption on hands extending to temples, eyebrows, ears and neck (9) eruptions only on covered parts, painful sensitiveness of skin, smelling like a old cheese (10)

10. Sepia officinalis: dry and itching eruptions like scabies, bad effects where itch has been suppressed by mercury, excoriation esp. in joints

(10) dry offensive eruptions on vertex, back of hands, pruritus with vesicles on acrid base all over the part of the body (9)

11. Oleander : vesicular eruption about head of children, with smooth shinning surface, with drops of serum standing out here and there, humid scaly eruptions on the back part of the head, skin gets raw by rubbing of the clothing (9) gnawing itching, which compels scratching, sometimes when undressing (10)

8     BIBLIOGRAPHY: