Allergic nickel and chromate hand dermatitis induced by orthopaedic metal implant.
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Biomedical subjects
Publications and source records attributed to L Förström.
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BACKGROUND: Adapalene is a new chemical entity that exhibits tretinoin-like activities in the terminal differentiation process. OBJECTIVE: We evaluated a dose range effect of two concentrations of adapalene gel as acne treatment and compared adapalene 0.1% gel with tretinoin 0.025% gel in the treatment of acne patients in two large multicenter studies. METHODS: Multicenter, investigator-masked, parallel group studies including 89 acne patients in the dose range study and 591 patients in the concurrent controlled studies were conducted. RESULTS: Adapalene gel 0.1% was significantly more effective in treating acne lesions than 0.03% adapalene gel. Adapalene gel 0.1% was significantly more effective than 0.025% or tretinoin gel in one study and of the same effectiveness in the other study. Adapalene gel was always better tolerated than tretinoin gel. CONCLUSION: Adapalene 0.1% gel is a safe and effective treatment of acne vulgaris.
It is known from experimental studies that antigenic potency and the concentration of antigen determine whether exposure to an antigen will result in sensitization. A single accidental exposure to concentrated antigen may therefore induce primary sensitization. The purpose of this report was to collect clinical cases in which a single exposure had resulted in contact dermatitis suspected to be allergic. Only patients without previous relevant skin symptoms were included. Patch testing was used to demonstrate sensitization. 6 patients developed occupational allergic contact dermatitis from accidental exposure. Patch testing revealed allergy to diglycidylether of bisphenol A epoxy resin, polyfunctional aziridine hardener, methyl acrylate, phenol-formaldehyde resin, and methylchloroisothiazolinone/methylisothiazolinone (Kathon LX), respectively. Furthermore, 2 patients developed allergic contact dermatitis from their first exposure to tear gas chemicals, namely omega-chloroacetophenone and ortho-chlorobenzylidene malonitrile. A single exposure can therefore induce both sensitization and subsequent allergic contact dermatitis without further exposure. The allergens described must be considered strong allergens. The skin should immediately be cleaned if an accidental splash with such an allergen has taken place.
In 15 months, we detected allergic patch test reactions to tioconazole in 14 patients. 9 of the 14 patients were allergic to additional imidazole derivatives used as antifungal agents. The positive patch test reactions to tioconazole may have been caused either by simultaneous sensitization or more probably by cross-reactivity between the various commercially used imidazole derivatives with a similar chemical structure. The abundant use of tioconazole in concentrated (up to 28%) topical formulations in Finland could be the major cause of the apparent increase in allergic reactions.
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Alpha-fluoromethylhistidine (alpha-FMH), a new irreversible inhibitor of mammalian histidine decarboxylase, was tested in the treatment of idiopathic cold urticaria in 11 patients. In the initial trial with 50 mg b.i.d., a significant decrease (about 30%) in the total blood histamine level was found after 3 weeks of treatment but clinically there was no improvement in the symptoms of ten cold urticaria patients nor in the responses to the ice-cube test. In the second trial with three patients suffering from severe idiopathic cold urticaria, a higher dose of up to 500 mg b.i.d. of alpha-FMH for 3 weeks resulted in a marked decrease in the total blood histamine level as well as in an apparent inhibition of histamine synthesis in the skin previously exposed several times to cold water. The symptoms of cold urticaria and the responses in the ice-cube tests also decreased simultaneously. No clinical side effects nor changes in laboratory analysis were seen during the treatment with alpha-FMH. These results suggest that alpha-FMH may be useful in the treatment of severe cold urticaria especially in combination with histamine exhaustion of mast cells using cold water.
To determine whether patients with familial benign chronic pemphigus have an increased risk for the development of contact allergies to topical therapy, we performed epicutaneous tests in 15 patients with this disease. Nine had positive patch test reactions of which seven were allergic to compounds used in local treatments. Allergic reactions in more than one patient were seen to neomycin sulfate (three patients), bacitracin (two), and hydrocortisone-17-butyrate and betamethasone-17-valerate (two). Although no comparable control group was similarly studied, the frequency of sensitization appears to be increased in patients with familial benign chronic pemphigus.
We showed earlier that most patients with contact dermatitis due to corticosteroids show cross-reactions when patch tested with hydrocortisone-17-butyrate (H-17-B). To test whether H-17-B could be used for detecting topical corticosteroid allergy, we screened patients undergoing routine patch testing with H-17-B. Patients with clearly allergic or doubtful/mildly irritant patch test reactions to H-17-B, and with a history suggesting topical corticosteroid allergy, were further tested with a large panel of steroid preparations. 20 out of 4039 patients (0.5%) showed definite allergic test reactions to corticosteroids. A further 165 patients with clinically suspected corticosteroid allergy were directly tested with a panel of steroid preparations; 14 patients showed positive patch test reactions. Altogether, 33 out of 34 patients with corticosteroid allergy had positive test reactions to H-17-B. Inclusion of 1.0% H-17-B in ethanol in the standard patch test series improves the diagnosis of topical corticosteroid hypersensitivity.
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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.
Twelve patients with oral lichen planus (OLP) suspected of dental restorative metal allergy were examined. All patients were patch tested with several metals including six different mercury compounds. One (8%) patient showed a positive patch test to two mercury compounds whereas no mercury allergy was found in a reference group of 17 patients suspected of dental restorative material allergy but without OLP lesions. The mercury allergic OLP patient was further tested on palatal mucosa but no reactions developed. Moreover, the energy dispersive X-ray microanalysis failed to show any contaminating metals in his OLP lesion. Mucosal biopsies were taken in close contact with amalgam fillings from nine OLP patients but these disclosed no evidence of lichenoid or dysplastic alterations. In OLP lesions, the immunofluorescence findings showed fibrinogen deposition, altered basement membrane and elastic fiber staining and intense Ulex europeaus I lectin fluorescence through all epithelial cell layers. Therefore, the present patch tests did not reveal increased frequency of mercury or other metal allergy in OLP patients and the mucosal biopsies failed to show any histologic or immunofluorescence alterations deviating from idiopathic OLP lesions.
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.
The Mantoux test and a chamber tuberculin test applied to the surface of the skin in 4 concentrations were performed on 229 children and 516 adults. The results were recorded at 72 hours. There was a significant correlation between the two tests. The chamber tuberculin test is technically easy, painless and atraumatic. It gives an opportunity of using a full range of concentrations of tuberculin resulting in a quantitative measurement of sensitivity in one and the same test procedure.
A series of 43 patients with therapy-resistant viral warts of long-duration were treated with dinitrochlorbenzene (DNCB). Of the 37 patients, who completed the treatment, 19 were cured, including five of seven patients with hyperkeratotic tumor-like warts. The majority of the patients showed a depressed cell-mediated immune response. 25 patients were reexamined 5 years later and 8 additional patients answered on inquiry. Six (18%) of these patients had warts. Eight of the 21 primarily tuberculin-negative patients had developed immunity to tuberculin, and none of them had warts. Five of the 6 patients with warts were still tuberculin-negative. The reaction to DNCB had reverted to negative in 17 (68%) out of 25 tested patients and in the majority of the remaining cases a weak reaction only was seen. The study does not tell if the cure is a consequence of the DNCB treatment or a function of time. However, it shows that cure is associated with normalization of the cell-mediated immune response. The DNCB hypersensitivity seemed to disappear with time and late complications were not documented.
Monoclonal antibodies used in the avidin-biotin-peroxidase complex (ABC) method and a histochemical azo-dye method for acid alpha-naphthyl acetate esterase (ANAE) were used to identify T lymphocytes and their functional subpopulations, B cells, and mononuclear phagocytes in tuberculin-test reactions. At 6 and 24 hr up to 52% of all dermal inflammatory cells in situ were T6+, whereas at 72 hr no T6+ cells were observed in the dermis. This suggests that in the initial phases of tuberculin reactions the epidermal Langerhans cells are mobilized to the perivascular spaces in the dermis. At 6, 24, and 48 hr T3+ T lymphocytes usually formed the main inflammatory cell type in situ. The high proportion of Ia+ T lymphocytes and the variations in the local proportion and numbers of T4+ and T8+ cells suggest that T cells play an active role in the generation of a positive tuberculin reaction. At 72 hr T-pattern ANAE+ lymphocytes accounted for 64 +/- 9 and 35 +/- 10% of all cells in situ in epicutaneous and intradermal tuberculin reactions, respectively (P less than 0.05). The corresponding values for M-pattern ANAE+ macrophages were 27 +/- 9 and 53 +/- 10% (P less than 0.10). This indicates that the recruitment of mononuclear phagocytes is delayed if tuberculin is applied epicutaneously rather than injected intradermally.
Inflammatory cells in situ in Kveim reaction papules were identified in 15 patients with avidin-biotin-peroxidase complex and biotin-avidin-peroxidase methods for surface epitopes and with a simultaneously capturing azo dye method for cytoplasmic acid alpha-naphthyl acetate esterase (ANAE). The spatial relationship of cells in granulomas indicates a concentric arrangement. Endogenous peroxidase-negative, ANAE+, but OKIa-negative immunoincompetent epithelioid cells were in the center. T3+, ANAE+ T lymphocytes formed 60-80% of all cells in the lymphocyte mantle surrounding the epithelioid core. T4/T8 was 2:1. Equal proportions (5-15%) of Ia+ lymphocytes and M pattern ANAE+, endogenous peroxidase-positive mononuclear phagocytes on the one hand and T3+ and T pattern ANAE+ cells on the other in individual patients indicate that the proportion of activated T blasts in situ was less than 15%. The close contacts between different immunocompetent cells in the periphery indicates this as the site for cellular interactions.