Severe phototoxic burn following celery ingestion.
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Biomedical subjects
Publications and source records attributed to J W Dijkstra.
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A 26-year-old white woman had reticulate nonmelanocytic hyperpigmentation anomaly characterized by partially blanching red-brown papules and macules and a histologic picture of digitate epithelial budding proliferation with lightly pigmented rete ridges. Except for the classically described hyperpigmentation at the rete ridge tips, the patient has Dowling-Degos disease. This case of a reticulate nonmelanocytic hyperpigmentation anomaly is probably a variant of Dowling-Degos disease.
PUVA is an acronym for psoralen plus ultraviolet-A radiation. This form of photochemical therapy is commonly used in the treatment of psoriasis and vitiligo, but it is also beneficial in other dermatologic diseases. An understanding of psoralen's mechanism of action and the unique properties of the various psoralen preparations is important in ensuring optimal results with this therapy.
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The recent identification of a T-cell-derived antigen-binding molecule (TABM), Trichinella spiralis factor (Tric-F), isolated from culture supernatants of lymphoid cells from mice infected with the intestinal helminth T. spiralis, has led to investigation of the ability of Tric-F to induce a T-cell-dependent feedback circuit that ultimately suppresses the production of other TABMs with similar (isotype-like) features. This form of regulation that has been identified in contact hypersensitivity and in delayed-type hypersensitivity (DTH) responses to tumor cells, was shown not to be antigen-specific but to be DTH-specific. Injection of mice with the TABM called picryl chloride factor (PCl-F) induced suppression of the production of DTH-initiating TABMs of other antigenic specificities. In this study, we report that intravenous injection of mice with Tric-F or PCl-F, 8 days before an oral infection with T. spiralis, induced suppressor cells that inhibited the T-cell-dependent influx into the gut of inflammatory cells, comprising mast cells and eosinophils. Similar results were obtained when the mice were skin sensitized with PCl 8 days prior to a T. spiralis infection, i.e. in a system where TABMs are known to be produced. The phenotype of these suppressor cells was Lyt-1-2+. This suppression preferentially affected the parasite-induced DTH-like response in the gut. In contrast, increased levels of IgA plasma cells in the gut, and worm expulsion were not affected by these treatments. In reciprocal experiments, intravenous injection of Tric-F, or PCl-F, or an oral infection with T. spiralis (that results in the production of TABMs) given 8 days before contact sensitizing mice with PCl, resulted in a suppression of elicitation of cutaneous DTH, as measured by ear swelling. In contrast, pretreatment with anti-dinitrophenyl IgE antibody did not interfere with intestinal inflammation to T. spiralis nor with DTH to PCl. Our results suggest that similar to cutaneous DTH, T. spiralis-specific T-cell factors are involved in the initiation and regulation of the DTH-like mast cell and eosinophil-rich intestinal inflammation that accompanies T. spiralis infections in the gut. Since both Tric-F and PCl-F induce suppression of cellular immune responses in vivo, independent of antigen specificity, it is concluded that Tric-F belongs to the same isotype of TABMs as PCl-F that therefore can be regulated by a non-antigen-specific, isotype-like, T-cell-dependent feedback mechanism.
Immunochemical and biological characterization was performed of an antigen-binding factor derived from culture supernatants of T cells from mice infected 4 days previously with the intestinal helminth Trichinella spiralis. Affinity chromatography with T. spiralis antigen resulted in the purification of a protein, provisionally designated Trichinella factor (Tric-F), that shared antigenic and other properties with a known T-cell-derived antigen-binding factor of different antigenic specificity, picryl chloride factor, which mediates an early 2-hour component of contact sensitivity. Tric-F lacked determinants of immunoglobulins and possessed determinants shared by other antigen-specific T cell factors, as determined by ELISA and antibody affinity chromatography. Biological activity of Tric-F was assayed in vivo and in vitro. Mice injected intravenously with Tric-F developed an antigen-specific early 2-hour ear swelling response following local challenge with T. spiralis antigen. These results corresponded to delayed-type hypersensitivity responses in the ears of T. spiralis-infected mice that comprised early 2-hour and late classical 24-hour responses. In vitro, Tric-F induced serotonin release by mast cells in the presence of T. spiralis antigen. Mast cells sensitized with Tric-F formed rosettes with antigen-coated sheep erythrocytes. It is suggested that Tric-F, an antigen-binding molecule that is T-cell-derived, mediates the early 2-hour component of delayed-type hypersensitivity and is involved in the initiation and regulation of T-cell-mediated intestinal inflammation during a T. spiralis infection in mice.
Astemizole is a new, long-acting H1 receptor antagonist that has proven effective in controlling the signs and symptoms of chronic idiopathic urticaria, without the sedative and anticholinergic side effects that typify use of many antihistamines. In an eight-week open study of 20 patients, astemizole significantly decreased the signs and symptoms of urticaria, as well as the severity of urticaria by anatomic location. Five patients reported complete clearing. Modest weight gain while on chronic therapy appears to be a significant side effect.
Histoplasmosis is caused by Histoplasma capsulatum, a dimorphic fungus. Because histoplasmosis is usually a self-limited disease in the majority of cases, treatment often is not needed in the normal host. However, severe cases of acute pulmonary histoplasmosis require therapy. Amphotericin B is considered the treatment of choice.
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A newcomer in the cosmetic market, the tan accelerator, has stimulated much publicity in recent months. We studied the effects of two brands of this product, used according to package instructions, in eighteen healthy volunteers. Readings at 24, 72, 96 hours, and 1 week failed to show augmented tanning. Our study contradicts the companies' claims of efficacy.
Two patients with the clinical and histopathologic findings of eosinophilic cellulitis are presented. In one patient there was a definite relationship between upper respiratory tract infection and flare-ups of eosinophilic cellulitis. This patient's condition was superimposed on a long history of chronic urticaria. In the other patient a relationship to recurrent sinusitis was possible but not definite. There were no other contributory underlying skin diseases in either patient. Eosinophilic cellulitis is not likely a disease entity as such but, instead, represents a severe urticarial hypersensitivity reaction to various stimuli. Collagen alteration by eosinophil granules results in flame figure formation and a granulomatous response, which may explain the prolonged persistence of the lesions.
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Transesophageal echocardiography (TEE) was performed within 24 hours after cardiac catheterization in 45 patients for assessment of native mitral valvular regurgitation. Color flow mapping was used in evaluating systolic regurgitant jet sizes. A jet demonstrated by TEE was 96% sensitive and 44% specific for angiographic mitral regurgitation. The presence of angiographic mitral regurgitation was best predicted by (single measurement) (1) a holosystolic jet, (2) a jet length greater than 2.5 cm, and (3) a jet area greater than 2 cm2. Severe angiographic mitral regurgitation (grades 3 and 4) was best predicted by (single measurement) (1) a jet area greater than 5 cm2, and (2) a jet length greater than 4 cm. It is concluded that the assessment of angiographic mitral regurgitation by TEE is improved by the measurement of these jet parameters, which have a high sensitivity and higher specificity than the presence of a jet alone. Furthermore, with TEE one is able to differentiate severe (grades 3 and 4) from absent or mild mitral regurgitation (grades 0, 1, and 2).