Contact eczema

Environment and health-related problems Water-soluble chrome(VI) compounds in the wet cement or mortar have a highly sensitising effect and are up to 90% the cause of allergic cement dermatitis (cement eczema, bricklayer s itch ). The high alkalinity (pH = 13) of cement aids the development of this contact eczema. Bricklayer s itch is one of the most frequent professional diseases in the construction industry. 

Caution. This preparation should be performed in a good hood. Contact of all solutions with the skin should be avoided not only because haloarsines have a vesicant action but also because many organoarsenicals can produce allergic contact eczema if contact is frequent. 

Grangsjo, A. et al., Different pathways in irritant contact eczema Early differences in the epidermal elemental content and expression of cytokines after application of 2 different irritants, Contact Dermatitis, 35, 355, 1996. 

M13. Malten, K. E., Flare reaction due to vitamin B12 in a patient with psoriasis and contact eczema. Contact Dermatitis 1, 325-326 (1975). 

Croton is also the name given to Codiaeum variegatum, a highly decorative potted plant. Handhng this plant over a period of 6 months produced contact eczema of the hands in a nursery gardener. Patch tests with croton leaves were positive (5). 

The increased frequency of contact eczema due to cloxacillin and bacampicillin may be because they are intensely irritant and lipophilic (130). 

Mechanisms of non-immediate reactions are unclear but may be immunological and non-immunological. Delayed reactions of the IgE type are known (131). Aminopenicillins seem to be an important cause of non-immediate reactions (132-134). The morbilliform rash that begins 1-10 days after amoxicillin can be caused by a delayed cell-mediated immune reaction (135) as can fixed drug eruptions (136,137), toxic epidermal necrolysis (138-140), bullous erythroderma (141), and contact eczema (142). Investigation of these disorders should include delayed readings of skin tests (135). In patients with chronic urticaria, penicillin allergy was demonstrated by cutaneous tests. 

Suss R, Lehmann P. Haematogenes Kontaktekzem durch pflanzliche Medikamente am Beispiel des Kavawurzel-extraktes. [Hematogenous contact eczema cause by phyto-genic drugs exemplified by kava root extract.) Hautarzt 1996 47(6) 459-61. 

Lanolin alcohol Allergic contact eczema (SEDA-21, 501)... 

Nava et al. (19) have reported a case of eczematous dermatitis from TDI. Karol ejt al. (23) reported finding tolyl-specific antibodies in serum of two persons who displayed skin reactions when exposed to TDI. Rothe (25) described 12 cases of contact eczema in workers exposed to MDI or partially polymerized MDI and four similar cases in workers exposed to IPDI. 

Exposure Routes, Symptoms, Target Organs (see Table 5) ER Inh, Ing, Con SY Contact eczema in animals methemo, liver changes TO Skin, liver, blood First Aid (see Table 6) Eye Irr immed Skin Soap wash immed Breath Resp support Swallow Medical attention immed ... 

KP Peters, A Heese, OP Homstein. IgE-mediated contact eczema from latex. AUer-gologie 9 369-373, 1995. 

Simple molecular substances, as for example metal ions, amines, and epoxy monomers, primarily sensitize through skin contact. The reaction of these allergens to the body s own proteins leads to the formation of specific sensitized immune cells. Repeated skin contact can lead to an allergic contact eczema with a time delay. The sensitization is dependent on the intensity of the contact and the sensitizing potency of the substance. In the case of existing sensitization, mostly very small amounts of the corresponding substances can activate these skin reactions. 

Pirker, C., T. Moslinger, D.Y. Koller, M. Gotz, and R. Jarisch. 1992. Cross-reactivity with Tagetes in Arnica contact eczema. Contact Dermat. 26(4) 217-219. 

A systematic review of herbal medicines for lower back pain identified two trials of topical cayenne monopreparations and reported that adverse events in cayenne treatment groups were inflammatory contact eczema, urticaria, minute hemorrhagic spots, and vesiculation or dermatitis. In one trial, 15 adverse events were reported in the cayenne group and 9 in the placebo group (Gagnier et al. 2007). In a clinical trial of a topical capsicum plaster or placebo, localized adverse drug reactions were found in 7.5% of the patients on capsicum and 3.1% on placebo (Frerick et al. 2003). 

Sertoli, A., P. Campolmi, P. Fabbri, N. Gelsomini, and E. Panconesi. 1985. Contact eczema caused by Chrysanthemum morifolium Ramat. G. /to/. Dermatol. Venereol. 120(5) 365-370. Sharma, S.C., and S. Kaur. 1989. Airborne contact dermatitis from Compositae plants in northern India. Contact Dermat. 21(l) l-5. Sharma, S.C., R.C. Tanwar, and S. Kaur. 1989. Contact dermatitis from chrysanthemums in India. Contact Dermat. 21(2) 69-71. 

Jirasek, L., and M. Skach. 1962. Perioral contact eczema with eczematous stomatitis after the use of bay leaves (Laurus nobilis L.) in food. Cesk. Dermatol. 37 18-21. 

Pfutzner, W., A. Niedermeier, P. Thomas, and B. Przybilla. 2003. [Systemic contact eczema against balsam of Peru.] /. Dtsch. Dermatol. Ges. 1(9) 719-721. 

Frequent skin contact with paints and coating materials can cause skin disorders, particularly on the hands, in painters and coaters. The lipid-solubilizing properties of the organic solvents may cause or at least promote contact eczema. In particular, paints based on reactive resins (e.g., epoxy and polyester resins) may cause allergic skin disorders. Skin-sensitizing substances include residual monomers and reactive diluents (e.g., acrylates and epoxides) and paint additives (e.g., acid anhydrides. 

Rashes which evolve from contact dermatitis or which arise when patients already sensitized by exogenous contact ingest the allergen or receive it parenterally (hematogenous contact eczema) display special features. There is a dense eruption of papulovesicular lesions side by side with superficial eczematous changes. 

III) The symptoms correspond to a well-known allergic reaction to the specific drug, e.g., maculopapular rash, allergic contact eczema... 

Smeenk G (1973) Contact allergy to bufexamac. Dermatologica 147 334-337 Smeenk G, Prins FJ (1972) Allergic contact eczema due to chloracetamide. Dermatologica 144 108-114... 

Van Ketel WG (1975) Allergic contact eczema by Hexomedine . Contact Dermatitis 1 332 Van Ketel WG (1976 a) Allergic contact dermatitis from propellants in deodorant sprays in combination with allergy to ethyl chloride. Contact Dermatitis 2 115-119 Van Ketel WG (1975b) Immediate and delayed type allergy to erythromycin. Contact Dermatitis 2 363-364... 

Industrial exposure to alprenolol causing contact eczema was reported by Eken-VALL and Forsbeck (1978). Positive patch test reactions were demonstrated in 14 out of 32 patients with suspected contact dermatitis to alprenolol. 

Generalized urticaria Anaphylactic shock Anaphylactoid symptoms Serum-like disease Angioneurotic edema Generalized exanthema Contact eczema Blood dyscrasias Pruritus Local reactions Asthma Others... 

In Ippen s (1978) case of contact eczema, the epicutaneous test, with isoniazid as substance or as pulverized tablets (from several manufacturers), showed in all instances definite eczema reactions which exceeded the test areas and required local treatment with corticosteroids. Wang and Schmeo (1974) report the case of a patient with occupational allergy to isoniazid. Beside the allergic reaction of the immediate type (asthma bronchiale) there was a latent sensitization of the delayed reaction type (eczema reaction). This latent sensitization was manifested in a circumscribed area by the epicutaneous test. Reexposure to the allergen led to an asthmatic spasm of the bronchi and to recrudescence of the eczematous cutaneous efflorescences when it was inhaled. 

Workers in the paint manufacturing industry and painters have experienced occupational diseases, especially dermatosis affecting the hands and arms. Whereas several paint components have been shown to cause non-allergic and allergic contact eczema, organic solvents were shown to provoke mainly non-allergic contact eczema and some solvents cause only irritation (e.g., some ketones and esters). 

The first observations on experimental eczema date back to the end of the last century, thus opening the chapter of contact eczema. 

Indeed, in 1896, J. Jadassohn, after applying a mercurial plaster to the arm of a patient, observed for the first time a local reaction. He thus produced experimentally a bullous lesion and he was able to affirm that the eczematous lesions presented by this patient were caused by a hypersensitivity to mercury. This first experiment permitted the separation of contact eczema from the large group of eczemas of indeterminate origin. 

Since that time the studies concerning experimental eczema of man and animals have greatly increased. Their orientations are different histological, histo-chemical and immunological, but they all contribute to the elucidation of the mechanism of contact eczema. 

In order to demonstrate a general sensitization, most of the experiments on the guinea pig that we have described up to now were performed on animals whose sensitization was effected at a determined place (the neck) and in whom triggering of the eczema (a single application) took place at a location never previously in contact with the eczematogenic substance (flank or nipple). However, contact eczema in man is most often due to repeated contact of the eczematogenic substance on the same site. 

In man we know of the contact eczema due to azo dyes (see among others Mayer, 1928 and 1929 Dobkevitch and Baer, 1947). 

According to a great many investigators, superficial radiotherapy can be very beneficial for eczema in man, especially in severe and chronic cases. However, Sulzberger and Rostenberg (1939) have insisted that the true value of radiotherapy has not been established by critical methods. In 1954 Kemp and Kligman observed no effect of X-Rays on contact eczema in man. 

Heat urticaria, polymorphous light reaction, photo-allergic contact eczema, phototoxic contact eczema, SLE and porphyria must be differentiated from solar urticaria by history, appearance of the lesions, skin testing and laboratory examinations. Reactions on exposure to infrared light should be classified as heat urticaria. 

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