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Biomedical subjects

A I Lauerma

Publications and source records attributed to A I Lauerma.

43 records · Page 3Linked to original sources
PubMed1989

Patch test reactions to inhalant allergens in atopic dermatitis.

To study whether inhalant allergens could induce eczematous reactions on normal skin of atopic patients we applied birch pollen and house dust mite antigens at 500 times the concentration used for prick testing as epicutaneous tests. Six out of 17 patients with atopic dermatitis in remission had positive delayed type reactions to birch pollen and three to house dust mite. Only one out of 13 atopic patients without history of atopic dermatitis but with seasonal allergic rhinitis had a positive patch test reaction to birch pollen and no patient had positive test reactions to house dust mite. No positive patch test reactions to birch pollen or house dust mite were seen in the ten healthy control subjects. In patients with positive test reactions biopsies from the test sites revealed epidermal spongiosis and vesiculation. Immunostaining of the epidermis revealed keratinocytes displaying both CD1 and HLA-DR. The present study suggests that inhalant allergens can exacerbate atopic dermatitis.

Administration, Inhalation↗
PubMed1987

Cellular kinetics of delayed hypersensitivity test reactions to topical glucocorticosteroids.

The phenotypes of the infiltrating cells in 13 patients with delayed hypersensitivity to topical glucocorticosteroids (GCS) were studied from sequential biopsies of positive epicutaneous test reactions by using the avidin-biotin-complex (ABC) technique. Monoclonal antibodies were used to identify the cells with the following phenotypes: T3, T4/T4a, T6, T8, T9, T11, M1, Ia1 (HLA-DR), interleukin-2 receptor/T26a, and dendritic reticular cell. The cellular kinetics of GCS hypersensitivity reactions were compared with delayed hypersensitivity reactions caused by allergens not related to GCS. In both GCS and non-GCS reactions the epidermal dendritic T6+ cells were more numerous than dendritic Ia1+ cells. There was a decrease in the number of both cell types during these reactions; in GCS reactions the decrease in the number of T6+ cells was seen later than in non-GCS reactions. Ia1+ keratinocytes were seen at sites near dermal infiltrates. Compared with the non-GCS delayed hypersensitivity reaction, there were fewer pan T (T11+/T3+) in the GCS reaction. The relative numbers of M1+ monocytes and the T4/T8 ratio were substantially lower in the latter; these findings can be explained as a GCS effect which modulates the delayed type hypersensitivity reaction.

Administration, Cutaneous↗
PubMed1986

Delayed hypersensitivity to topical corticosteroids.

Topical hypersensitivity to corticosteroids was studied by epicutaneous testing using the Finn Chamber technic. The steroids were tested in both ethanol and white petrolatum and, in certain cases, in dimethyl sulfoxide. Additionally, commercial preparations were tested. Three groups of patients were studied: (1) patients with a history of hypersensitivity to at least two topical preparations (five of ten patients studied showed a positive patch test reaction for corticosteroids), (2) patients in whom topical corticosteroid hypersensitivity was suspected because of treatment-resistant eczema (seven of twenty-five patients showed a positive patch test reaction), and (3) dermatologic inpatients and outpatients undergoing epicutaneous testing for suspected topical hypersensitivity. Hydrocortisone-17-butyrate (H-17-B) was included in the standard patch test series; of 450 patients tested, two showed a positive patch test reaction. All the patients with corticosteroid hypersensitivity had a positive reaction to H-17-B. In six patients, additional hypersensitivities to one or several other steroid preparations were seen. Use testing was performed as an open test, with 0.1% or 1% H-17-B in ethanol on normal skin of the flexor side of the upper extremities. A positive test reaction was seen in only one of nine patients. Results of use testing with the commercial 0.1% H-17-B (Locoid) ointment were always negative. Our study suggests that the sensitivity of patch tests for corticosteroid hypersensitivity can be increased by using ethanol as vehicle.

Administration, Topical↗
PubMedDate not supplied

Trimellitic anhydride-sensitive mouse as an animal model for contact urticaria.

The respiratory allergen trimellitic anhydride (TMA) has been shown to induce IgE production and immediate ear swelling in mice sensitized to it. We studied whether TMA sensitivity could be used as an animal model for immunological contact urticaria. BALB/C mice were sensitized to TMA by topical applications. Groups of animals were pretreated on the ears with the glucocorticosteroid (GCS) betamethasone-17,21-dipropionate, the antihistamine (AH) diphenhydramine hydrochloride, the non-steroidal anti-inflammatory drug (NSAID) indomethacin or vehicle (VEH). Ears were challenged with TMA and ear thickness was measured at baseline and 1, 2, 4, 8 and 24 h after challenge. Trimellitic anhydride caused a significant biphasic ear swelling response with an early peak at 1-2 h, a plateau at 4 h and a late peak at 24 h. However, there was also an early swelling by TMA in non-sensitized mice, suggesting that non-immunological as well as immunological mechanisms contribute to early swelling by TMA. Glucocorticosteroid suppressed significantly the early and to some extent the late TMA responses, while AH suppressed only early and NSAID only late TMA responses. Ear swelling in TMA-sensitive BALB/C mice may represent a combination of immunological and non-immunological contact urticaria and allergic contact dermatitis. Mice sensitive to TMA may be helpful in defining pharmacological agents affecting contact urticaria and the model is perhaps suitable for identification of some immunologically mediated contact urticants.

Administration, Topical↗