Biomedical subjects
Publications and source records attributed to J Ring.
We report on a female patient suffering from tuberculosis cutis colliquativa. The skin lesions were caused by hematogenic dissemination of mycobacteria tuberculosis spreading from the affected urogenital tract. The diagnosis was confirmed by culturing. Combined treatment with tuberculostatic agents for 5 months resulted in complete remission of the tuberculosis.
A 84-year-old female patient suffering from atypical fibroxanthoma is presented. A diagnosis of malignant melanoma or a cutaneous metastasis from an unknown primary tumor was suspected. The final diagnosis was established by immunohistological studies showing a strongly positive reaction to vimentin and a negative reaction to S-100 protein and cytokeratin.
Explore the source record for details and available documents.
The oral or parenteral application of certain contact allergens may elicit eczematous skin reactions "from the inside" in sensitized individuals; this phenomenon has been called "systemically induced eczema" or "hematogenous contact eczema". Both the clinical morphology and dermatopathology are very similar to classical allergic contact eczema. The distribution of skin lesions is mostly symmetrical and may affect the face or the anogenital area. The pathophysiology involves T-lymphocytes and probably secretion of cytokines similar to the well-known phenomenon of "flare-up". The most important contact allergens known to elicit systemically induced contact eczema are metal salts, drugs, phytoallergens and balsam of Peru. After careful diagnosis, a specific allergen avoidance is the basis of prophylaxis and therapy.
As a contributing factor, certain foods can provoke skin lesions in some patients with atopic eczema. In newborns with an increased risk of atopy, exclusive breastfeeding during the first months of life and delayed introduction of solid food seem to inhibit or to retard the manifestation of atopic disease. The pathomechanism of provocation of eczema by food has not yet been elucidated. The frequent finding of specific immunoglobulin E (IgE) antibodies to the offending food items suggests that immediate type allergic reactions may be involved. Furthermore, other allergic or nonimmunologic (pseudo-allergic) mechanisms have to be considered. History taking, skin tests, and radioallergosorbent test (RAST) may provide some information with regard to eliciting food, but these procedures usually are not sufficient to obtain a conclusive diagnosis. Oral challenge tests have to be performed in a controlled manner in order to identify food items that are not tolerated and thus have to be avoided. As most of the patients react only to one or two food items and as these often differ from one patient to another, undirected exclusion diet regimens are unnecessary and unethical. Furthermore, such diets bear the risk of malnutrition and of anaphylactic reactions after reintroduction of allergenic food. Dietary recommendations in atopic eczema have to be based on a careful allergological workup of the individual patient.
Human rIL-4 and human rIFN-gamma are able to induce the expression of the low affinity receptor for IgE (Fc epsilon R2/CD23) on normal human epidermal Langerhans cells, whereas IL-2 and PMA have no effect. A synergistic effect is observed when both cytokines are combined. These receptors are synthesized de novo by the LC since cycloheximide completely inhibits the appearance of Fc epsilon R2/CD23. Fc epsilon R2/CD23+ LC may have a major role in the pathogenesis of atopic eczema, as well as in the regulation of IgE synthesis.
A series of permanent IL-3-dependent cell lines have been established from normal BALB/c or C3H bone marrow using alpha-thioglycerol-supplemented culture medium and PWM-stimulated spleen cell-conditioned medium as a source of IL-3. The cell lines and derivatives cloned in agar resembled "mucosal type" mast cells with respect to phenotypic and functional properties. In this report we demonstrate that in vitro growth of these mast cell lines was not only dependent on IL-3 and synergistically enhanced by IL-4, but in addition regulated by alpha-thioglycerol which could be replaced by 2-ME or cysteamine. We show that these thiol-sensitive mast cell lines respond to a mast cell growth enhancing activity (MEA) present in spleen cell-conditioned medium and acting in concert with IL-3. Partially purified MEA was not able to stimulate the growth of IL-3-dependent 32Dcl.23 cells, IL-2-dependent CTLL-2 cells or the mouse T cell line F4/4K.6 (L3T4+) adapted to grow in purified IL-4. Moreover, 11B11 hybridoma-derived anti-IL-4 mAb specifically neutralizing mouse Il-4 were unable to abolish the bioactivity of MEA. PWM, CSF-1, GM-CSF, IL-1, IL-2, IL-5, IL-6, IL-7, IFN-gamma, TGF-alpha, TNF-alpha, NGF, or EPO did not substitute for MEA in our standard proliferation assay.
The symptomatology of allergic diseases may be imitated by non-immunological, so-called "pseudo-allergic" reactions. Phenocopies of any type of allergic reaction may occur. Pseudo-allergic drug reactions may be caused by the active components as well as by additives. Anaphylactoid pseudo-allergic reactions are of special clinical interest. Their pathomechanism has not been conclusively elucidated yet. Based on clinical and experimental data, we discuss some hypothetical mechanisms of a few compounds, always keeping in mind the possibility of allergic mechanisms not yet identified. For the diagnosis of pseudo-allergic drug reactions we need provocation tests, as skin tests are not possible, and routine in-vitro assays are not available.
Explore the source record for details and available documents.
To evaluate the reproducibility of patch test results, duplicate patch test series comprising 12 allergens were simultaneously applied to either side of the back in 63 patients by the use of a newly developed patch test system, TRUE Test. When a positive test result occurred on only one side of the back, it was regarded as nonreproducible. For evaluation of the concordance of test reactions between the TRUE Test and the Finn Chamber test, the same 12 allergens mixed in petrolatum were also applied to the upper back according to the Finn Chamber technique. The reproducibility of TRUE Test results was compared with the reproducibility of the Finn Chamber test in 76 other patients. The concordance of positive reactions between the two tests was 57%, somewhat lower than in recently published studies. The percentage of nonreproducible positive results was more than twice as high with Finn Chambers, (22 of 58 positive reactions, or 37.9%) as with the TRUE Test (5 of 28 reactions, or 17.9%). However, this difference in reproducibility in the two test systems was not significant as determined by the chi 2 test (p less than 0.05).
Patch tests with a series of 39 substances were performed in 41 patients on one side of the upper aspect of the back. Testing was repeated on the contralateral side of the back 1 week later (sequential testing). In 35 other patients, duplicate patch test series were simultaneously applied on both sides of the back (concomitant testing). If a positive reaction to a test substance was obtained at only one side of the back, the result was regarded as nonreproducible. Of all positive reactions, 40.0% were nonreproducible at sequential testing and 43.8% were nonreproducible at concomitant testing. Weakly positive reactions were far more often nonreproducible than stronger reactions.
Explore the source record for details and available documents.
Uninvolved and lesional skin of untreated and treated patients with atopic eczema has been investigated immunohistochemically to determine the conditions in which IgE-bearing CD1a+ Langerhans cells/indeterminate cells (LC/IC) occur in this disease. IgE-bearing epidermal dendritic cells were present in patients with elevated IgE serum level (greater than 300 UI/ml) and the staining pattern was stronger in lesional skin. On double immunostaining, a subpopulation of CD1a+ LC/IC was found not to bear IgE molecules as determined by the ratio IgE+/CD1a+ cells on serial sections as well. The ratio IgE+/CD1a+ cells decreased in patients who underwent a local therapy with glucocorticosteroids. These results suggest that the expression of IgE receptors and/or binding of IgE molecules on epidermal LC/IC in atopic eczema may be controlled by a complex network of mediators from the epidermis or the inflammatory infiltrate, or both, and that this phenomenon could be down regulated by glucocorticosteroids.
Apparently normal, and lesional skin from patients with atopic eczema were investigated immunohistochemically with anti-HLA-DR, -CD1a and -IgE antisera. A CD1a+ intercellular pattern was observed in uninvolved skin in the majority of the patients whereas an HLA-DR+/CD1a+ network, mostly localized in basal and supra-basal areas, was shown in lesional skin of virtually all of them. Moreover, an HLA-DR+/CD1a+IgE+ intercellular pattern was observed in some of the patients only and was predominantly localized in those areas characterized by lymphocyte exocytosis, spongiosis or vesicle formation. Whether keratinocytes are able to synthesize CD1a antigen and Fc epsilon R or if these molecules are only produced and shed by CD1a+/IgE+ epidermal dendritic cells remains unclear.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Irradiation of human peripheral leukocytes with ultraviolet A (UVA) induced a significant and dose-dependent reduction of anti-IgE or Ca-ionophore-stimulated histamine release without consistent influence upon C5a-induced release reactions. This effect was equally demonstrable in atopics and controls. In the presence of the radical scavenger superoxide dismutase, the UVA-induced inhibition of anti-IgE-induced histamine release was abolished. Under the conditions used, UVB exposure did not result in relevant changes of in vitro histamine release.
Explore the source record for details and available documents.