Fine-needle aspiration biopsy, curettage, and swab samples in bacteriologic analysis of leg ulcers.
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Biomedical subjects
Publications and source records attributed to I Helander.
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Irritant contact dermatitis caused by occupational contact with nitroglycerin has been known since the end of the last century. Nitroglycerin is an allergen, and the transdermal drug delivery systems for nitroglycerin recently used to treat angina pectoris have sensitized. 4 patients with allergic contact dermatitis caused by nitroglycerin from explosives are described, and 1 patient who was sensitized by transdermal nitroplaster. On patch testing, dynamite and/or the explosive components nitroglycerin, ethylene glycol dinitrate and dinitrotoluene gave allergic reactions. The following concentrations and vehicles are suggested for patch testing: nitroglycerin 0.5-2% pet., dinitrotoluene and ethylene glycol dinitrate 0.1-0.5% pet. Persons exposed to nitroglycerin at work should try to avoid skin contact by using protective gloves. It is advisable that those who have become allergic to nitroglycerin should wear disposable protective gloves when handling explosives.
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We present two patients, a 20-year-old female and an 18-year-old male, who suffered from persistent solid facial edema as a complication of acne vulgaris. They were treated with isotretinoin with moderate response and thereafter with lymph massage with further response. The female patient also received clofazimine with good response.
The immunological status of seven patients with disseminated melanoma during BCG scarification was followed. As parameters, the total peripheral blood leukocyte and lymphocyte counts, serum immunoglobulin levels, natural ABO blood group antibodies, lymphocyte responses in vitro to PHA and PPD, and skin reactivity against PPD and candidin were followed during a period of 2--36 months. The EAC-rosette-forming cells increased and the E-rosette-forming cells decreased during prolonged BCG therapy. The skin reactions and lymphocyte responses showed in most patients conversion from negative to positive or augmentation at the start of the therapy. Later on, however, the values in most patients dropped before disseminated disease became clinically apparent. In the only surviving patient the values first increased, remained high, and after 100 weeks treatment decreased. After 140 weeks' treatment immunological parameters are similar to pre-treatment levels. The possibility that prolonged intensive BCG treatment might eventually suppress the immune system, and thus result in an enhanced risk of dissemination of the disease, is discussed.
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Dapsone proved to be effective treatment in a patient who suffered from erthema elevatum diutinum. Serious neurological side effects, however, appeared. The basic mechanism appeared to be a distal axonal degeneration of the motor neurons. Sensory conduction studies were normal in five consecutive EMG examinations. A diagnosis of anemia pernicosa was also made bu the blood values returned to normal after starting B12-vitamin therapy. Penicous anemia seemed not be an etiological factor in the polyneuropathy of our patient because we were not able toshow any damage to the sensory axons.
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A 36-year-old healthy man with atypical necrobiosis lipoidica of the face is described. The lesions were annular with a raised erythematous palpable border. The centres were slightly depigmented and atrophic, without telangiectasia or hair loss. Histopathological changes revealed prominent giant cells in small groups without clear granuloma formation. They were located at all levels of the drmis between the collagen bundles.
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Extracts were prepared from lichen planus lesions and from healthy epidermis of normal controls. Their effect on the migration and lymphocyte transformation of autologous leukocytes was studied. On the whole, the ranges of variation and mean values of the autologous leukocyte migration indices obtained in the presence of LP skin extract or sediment from 10 LP patients did not significantly differ from those recorded in the presence of similar extracts prepared from the epidermis of 12 normal controls. Two assays with LP skin sediment antigen and one assay with LP supernatant antigen, however, fell within the range of significant changes in migration. Lymphocyte transformation, as indicated by increased thymidine uptake, was significantly stimulated by LP epidermis in 1 case of 5 LP patients. Extracts from normal epidermis did not affect the transformation of autologous lymphocytes. The phytohemagglutinin response of lymphocytes from LP patients was the same as that of normal controls. The results do not indicate that cell-mediated immunity toward epidermal antigens play any significant role in the etiopathogenesis of lichen planus.
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Homogenates of irradiated and non-irradiated skin from 16 patients with chronic polymorphous light eruptions (CPLE) were examined to detect possible light-induced antigen to cell-mediated immunity. The leukocyte migration agarose tests which were performed disclosed no evidence of migration inhibition in either type of skin. These findings do not support the theory of CPLE being a delayed hypersensitivity reaction against an antigen formed in the skin by actinic radiation.