PubMed Health⌕ Search

Biomedical subjects

T van Joost

Publications and source records attributed to T van Joost.

At least 19 recordsLinked to original sources
PubMed1992

Burning mouth syndrome: a possible etiologic role for local contact hypersensitivity.

BACKGROUND: The pathogenesis of the burning mouth syndrome (BMS) is not yet understood. Apart from psychologic factors, several etiologic "somatic" factors have been reported. OBJECTIVE: In 22 patients (19 women, 3 men, mean age 56 years) classified with BMS, clinical and laboratory investigations were performed, with particular emphasis on the role of contact hypersensitivity. Twenty of the 22 patients wore a complete or partial denture. METHODS: Besides clinical and laboratory investigations patch testing was performed with a standard routine series and a standardized denture-dental (acrylate and metal) series. RESULTS: Folate, iron, pyridoxine deficiency, and Candida infections were found, but correction of the deficiency or treatment of the infection was of no benefit. Contact allergy to allergens used in the production of acrylate-based dentures was observed in six (27%) of the cases (all wore a denture); positive reactions were seen to N,N,-dimethyl-4-toluidine (3 cases), to 4-tolyldiethanolamine (2 cases), to benzoylperoxide (2 cases), and to oligotriacrylate (1 case). In six cases (27%) a possible relevant sensitization was seen to dental metals and in particular to gold chloride (four cases). CONCLUSION: The possible role of local hypersensitivity reactions to denture or dental components as etiologic factors in BMS must be considered.

Adult↗
PubMed1992

Sensitization to azo dyes: negative patch tests to yellow and red azo dyes in printed paper.

An over 2 x fold increase in para-aminoazobenzene allergy was observed in patients with allergic contact dermatitis during the years 1990-1991. Presuming that an increase in colour-printed newspapers might be a new unrecognized source of clinical allergy to azo dyes, patch tests were performed in 32 patients with an established p-aminoazobenzene allergy using a series of important azo dyes used in offset printing ink (Pigment Yellow 12, Pigment Yellow 13, Pigment Red 53, Pigment Red 57), as well as with dye-containing inks and specimens of colour-printed newspaper containing these azo dyes. In 25 out of the 32 patients (78%), positive patch tests were seen to textile azo dyes, in particular to Disperse Orange 3 (24 patients). In none of the 32 patients were reactions observed to the azo dyes used in printing ink, to the inks used or to the colour-printed paper specimens, indicating that these products were apparently not a cause of contact dermatitis in our group of patients with azo dye sensitization.

Adult↗
PubMed1992

Cyclosporine in atopic dermatitis. Modulation in the expression of immunologic markers in lesional skin.

BACKGROUND: In previous studies, oral cyclosporine was highly effective in the treatment of patients with severe atopic dermatitis. In this study seven patients with severe and therapy-resistant atopic dermatitis underwent therapy with cyclosporine, 5 mg/kg/day, for 6 weeks. OBJECTIVE: The effect of cyclosporine on the expression of cytokines, which probably play a role in this disease, was examined. METHODS: The study was performed with a panel of antibodies as markers of inflammatory cells, adhesion molecules, and cytokines (interferon-gamma [IFN-gamma], tumor necrosis factor-alpha [TNF-alpha] and interleukins 1 alpha, 1 beta, and 8 [IL-1 alpha, IL-1 beta, and IL-8, respectively]). They were visualized by indirect immunoperoxidase techniques. RESULTS: After 2 weeks of cyclosporine therapy, a reduction of 60% in the disease (severity and extent) was observed. This reduction was 89% after 4 weeks and 90% after 6 weeks of therapy. Results of indirect immunoperoxidase stains performed on lesional skin sections after 2 weeks of treatment showed statistically significant reduced numbers of CD14+, CD25 (IL-2R+) and IL-8+ inflammatory cells in the dermis and CD36(OKM5)+ cells in both the epidermis and dermis. The number of cells expressing IFN-gamma and TNF-alpha, assumed to be the products of the helper T-cell (TH)1 subset, was unaltered despite the impressive clinical benefit observed. Keratinocytes in lesional atopic skin did not express intercellular adhesion molecule type 1 (ICAM-1). The expression of the adhesion molecules ICAM-1, lymphocyte function-associated (LFA) type 1, and LFA-3 on inflammatory cells also remained unaffected by cyclosporine treatment. CONCLUSION: A statistically significant reduction in the number of activated T cells and in the number of cells expressing the IL-2 receptor (CD25) paralleled a marked improvement in the disease and supports the view that atopic dermatitis is based on a T-cell-mediated immune inflammation.

Administration, Oral↗
PubMed1991

The autologous mixed epidermal cell-T lymphocyte reaction is elevated in psoriasis: a crucial role for epidermal HLA-DR+/CD1a- antigen-presenting cells.

The objective of this study was to determine whether epidermal cells (EC) from psoriasis lesions and uninvolved skin could stimulate autologous T lymphocytes in the in vitro autologous mixed epidermal cell-T lymphocyte reaction (autologous MECLR). The functional role of antigen-presenting cell (APC) subsets was concurrently determined in this reaction. Mononuclear cells and purified T lymphocytes from peripheral blood of psoriasis patients showed a clear proliferative response to autologous unpurified epidermal cells from involved as well as uninvolved skin. The autologous mixed leukocyte reaction (MLR) was not elevated in psoriasis patients. In healthy controls and contact allergy patients, T-lymphocyte proliferation was not observed either in the autologous MECLR or in the autologous MLR. The level of proliferation in the autologous MECLR from psoriasis patients correlated to the number of epidermal cells that were added. To exclude the possibility that the observed proliferation in the autologous MECLR in psoriasis was due to the presence of epidermal T lymphocytes that were being stimulated and expanded in vitro, the stimulator EC were gamma irradiated (30 Gy) in some experiments. Preincubation of EC with cyclosporin A (CsA) significantly inhibited the autologous MECLR. The CsA-induced inhibition could be neutralized by the addition of fresh untreated EC to these cultures. This indicated that one of the modes of action of CsA in resolving psoriasis is, as some investigators have already shown, via inhibition of epidermal accessory cell function. In the autologous MECLR, APC from psoriasis skin could initiate this reaction, whereas APC from peripheral blood could not. This occurred in an MHC class II restricted fashion. Depletion experiments showed that Langerhans cells (HLA-DR+/CD1a+) were not the principal stimulators of autologous T lymphocytes in the MECLR. These results indicated that mainly HLA-DR+/CD1a- epidermal cells from psoriasis patients could stimulate autologous peripheral blood T lymphocytes in an MHC class II-restricted fashion.

Adult↗
PubMed1991

Differential role of lymphocyte function-associated antigens in the activation of nickel-specific peripheral blood T lymphocytes.

The possible role(s) of the adhesion molecules LFA-1 alpha (CD11a), LFA-1 beta(CD18), ICAM-1 (CD54), CD2 (T11, LFA-2), and LFA-3 (CD58) in the in vitro activation of nickel-specific peripheral blood (PB) T lymphocytes was studied. For this purpose, monoclonal antibodies (MoAb) to these markers were used. Both LFA-2 and LFA-3 appeared to be consistently involved, whereas LFA-1 was inconsistently involved. In studies using antigen-presenting cells (APC) isolated from peripheral blood to present nickel, anti-LFA-1 alpha and/or LFA-1 beta MoAb partially inhibited the in vitro activation of nickel-specific T lymphocytes in nine of 42 patients allergic to nickel. In the other 33 patients variable results, ranging from a slight increase or inhibition of proliferation to no inhibition at all, was observed, in particular when different anti-LFA-1 alpha MoAb were added to the cultures. In those patients who showed no inhibition when anti-LFA-1 (alpha and beta) MoAb were added, no inhibition was also observed when a mixture of anti-LFA-1 (alpha and beta) and ICAM-1 MoAb were added to the cultures. Similar results were also obtained using epidermal APC. In control experiments the various anti-LFA-1 (alpha and beta) MoAb effectively inhibited the tetanus toxoid and Con-A induced T-lymphocyte proliferation as well as the spontaneous aggregation of the JY cell line. Anti-CD2 and anti-LFA-3 MoAb strongly inhibited the proliferative responses of nickel-specific peripheral blood T lymphocytes from all 42 patients. These results indicated that the receptor-ligand interaction between CD2 and LFA-3 is essential for in vitro activation of nickel-specific peripheral blood T lymphocytes. This activation, however, does not regularly involve LFA-1 molecules on T lymphocytes. The involvement of LFA-1 in the activation of nickel-specific T lymphocytes correlated positively with high patch test scores to nickel and the disease activity in contact dermatitis patients.

Adolescent↗
PubMed1991

Bullous pemphigoid in children. Report of three cases with special emphasis on therapy.

Three children aged 4 months, 7 years, and 12 years, had bullous pemphigoid (BP). Two children suffered from disseminated BP and one (12 years) from vulvar localized BP. This last form has been described only once before in a girl. The various forms of pemphigoid in childhood are rare and reported in only about 40 instances. Bullous pemphigoid in childhood does not differ clearly from the adult counterpart, although lesions of the mucous membranes seem more common in childhood.

Adolescent↗