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At least 181 records · Page 10Linked to original sources
PubMed2004

Treatment of irritant and allergic contact dermatitis.

The treatment of contact dermatitis lies principally in the avoidance of the offending agent. In certain circumstances, avoidance protocols are insurmountable, and therapy is rendered to assuage the inflammatory component and its consequent objective and subjective findings. However, the options thereafter vary, as some patients will require continuous symptomatic therapy despite avoidance of the purported offending agent. This manuscript will review established treatment options for contact dermatitis, such as corticosteroids and dietary manipulation, as well as discuss some promising new therapies from the last decade, such as the immunomodulatory and anti-inflammatory agents.

Adrenal Cortex Hormones↗
PubMed1990

Studies on contact dermatitis in stomatological staff.

84 patients with contact dermatitis (38 dentists, 18 dental nurses and 28 dental technicians) were studied. All were patch tested with standard patch test series of the CMEA countries and with some professional allergens. 31 (36.9%) of them had allergic occupational contact dermatitis and 39 (46.2%) had irrtiant contact dermatitis. The highest prevalence of irritant contact dermatitis was found among dental surgeons. The percentage of atopics in the group of patients with irritant contact dermatitis was twice greater compared to that in the group of patients with allergic contact dermatitis. The contact allergens most frequently encountered were acrylic compounds, disinfectants (eugenol, thymol, trioxymethylene) mercury compunds and anesthetics.

Adult↗
PubMed1987

Collaborative multidisciplinary approach to investigation of chemical-induced contact dermatitis.

Immune-mediated contact dermatitis induced by chemicals is a complex biologic process, the pathogenesis of which is not completely understood. Some immuno-dermatotoxins also induce direct dermatotoxicity. This pathogenic complexity presents a serious problem if one wishes to screen chemicals for dermatotoxic effect and investigate their pathogenic mechanism. Rapid toxicologic assays such as the mouse ear swelling test are excellent for detecting chemicals that cause contact dermatitis, but are limited for pathogenic investigations. Morphologic pathology is important for determining which pathologic reactions are involved, but is a relatively crude method for investigating immunobiologic mechanisms. Immunobiologic studies are being used for mechanistic investigations, but the relevance of many measured end points to assessment of immunotoxicity is still unclear. A collaborative multidisciplinary approach involving investigators conducting rapid toxicologic screen tests, morphologic pathology and immunobiology studies is proposed as a solution. This approach is based on complementary integration of the disciplines, and considers the advantages and limitations of each specialty.

Animals↗
PubMed1990

Occupational allergic contact dermatitis to airborne nitrofurazone.

Allergic contact dermatitis to nitrofurazone has been reported from Europe and elsewhere from the use of eyedrops and topical ointments, and the drug in some livestock feeds and veterinary medications has caused a few cases of allergic contact dermatitis in humans. The authors report what appears to be the first case of contact dermatitis from airborne nitrofurazone secondary to a powdered aquarium water additive.

Air Pollutants, Occupational↗
PubMed1990

The use of human T-lymphocyte clones to study T-cell function in allergic contact dermatitis to urushiol.

Allergic contact dermatitis to poison ivy (Toxicodendron radicans) is believed to be mediated by T lymphocytes specific for the hapten urushiol. Activated T lymphocytes may produce pathology by a variety of mechanisms including direct cytotoxicity, production of lymphokines, recruitment of non-specific effector cells, non-specific cytotoxicity, and possibly autologous DR reactivity. The regulation and pathogenesis of this condition was studied by cloning and characterizing urushiol-specific T cells from the peripheral blood of patients with poison ivy dermatitis. Multiple CD8+ (T8+) urushiol-specific clones were derived. All clones that proliferated in response to a crude extract of T. radicans also proliferated in response to purified urushiol. Thus, urushiol appears to be the single immunogenic component of T. radicans resin. Pentadecylcatechol (PDC), which differs from urushiol only in the lack of unsaturated bonds in its lipophilic tail, stimulated only one of seven clones tested. This suggests that the double bonds in the C15 lipophilic tail of urushiol are required for antigenicity. Several of the CD8+ urushiol-specific clone suppressed pokeweed mitogen-induced IgG production in the presence of urushiol. Suppression was triggered specifically by urushiol and required MHC compatibility both for the antigen-presenting cells and the responding B cells. These suppressor clones were isolated from convalescent blood and may represent a mechanism for the termination of an allergic contact dermatitis.

Antigens↗
PubMed1999

Contact dermatitis for primary care providers.

Contact dermatitis is an eczematous dermatitis developing at a site where the skin has been in direct contact with the cutaneous irritant or allergen from the environment. Irritant contact dermatitis (ICD) is the most common form. Allergic contact dermatitis (ACD) is inflammation of the skin caused by an antigen that elicits a type IV hypersensitivity reaction. Clinical evaluation and judgment are a critical part of the process. Patch testing in an objective method to aid in differentiating ACD from ICD and of verifying responsible allergens.

Algorithms↗
PubMed1986

Immunopathological and ultrastructural findings in human allergic and irritant contact dermatitis.

The histopathological features of allergic contact dermatitis were compared with those of irritant contact dermatitis in a group of 17 subjects. Each patient received simultaneous patch tests of a known allergen and a standardized irritant (benzalkonium chloride). The cellular changes occurring between 3 h and 7 days after patch test application were studied by light and electron microscopy and immunocytochemistry. No differences were observed between the induced allergic contact dermatitis (ACD) and the irritant contact dermatitis (ICD), either in the responding cell types or the sequence of cellular events. Both reactions showed a predominantly T lymphocyte infiltrate with no polymorphonuclear leukocyte involvement. Apposition of Langerhans cells to lymphocytes in the epidermis was seen in both types of response. Considerable variability in the intensity of reaction to irritant and allergen occurred within individuals. There was no statistically significant difference between the intensity of the reactions to the irritant and the allergen.

Adult↗
PubMed1989

Protein contact dermatitis in slaughterhouse workers.

Protein contact dermatitis, described as "gut eczema" or "fat eczema" by slaughterhouse workers, was first described a decade ago and presents as an itching, vescular eczema on the hands and fingers, a few hours after contact with animal material, especially gut material. In a cross-sectional study of 144 slaughterhouse workers, a cumulative prevalence of current and anamnestic cases of protein contact dermatitis of 22% was found, with the highest prevalence in workers eviscerating and cleansing gut. The scratch patch test was the only skin test showing positive results in workers with protein contact dermatitis, positive reactions being found, however, in less than half the cases.

Abattoirs↗
PubMed1982

Occupational contact dermatitis among rubber workers.

The occurrence of occupational contact dermatitis among workers in a rubber factory from 1976 to 1980 was studied. Insurance compensation was paid to 50 workers with dermatitis. 21 of the cases were allergic and 27 toxic contact dermatitis, giving a contact dermatitis frequency of 5.6/1000 workers. Paraphenylenediamine compounds were the main cause of allergic contact dermatitis and solvents the main cause of toxic contact dermatitis.

Dermatitis, Contact↗
PubMed1991

Occupational allergic contact dermatitis caused by nitroglycerin.

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.

Adult↗
PubMed1992

[Allergic contact dermatitis in the Negev].

Allergic contact dermatitis can be acute or chronic and is caused by delayed hypersensitivity to allergens in the surroundings. This retrospective study, the first of its kind in the Negev district, included 150 patients with allergic contact dermatitis. Nickel was the most frequent allergen causing contact dermatitis in both females and males, while chrome was second in frequency. Most of those with positive reactions to patch tests, were females. In females it appeared relatively early, in the 3rd and 4th decades, while in males it tended to appear later. The first lesions most frequently appeared on the dorsal aspect of the hands.

Adolescent↗
PubMed2004

Contact dermatitis: diagnosis and management.

Contact dermatitis accounts for 85-90% of all occupational skin diseases and, as a frequent cause of hand dermatitis, it can lead to unemployment and permanent disability. This article examines the two main types of contact dermatitis, their diagnosis and treatment.

Allergens↗