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PubMedDate not supplied

Antihistamines in the treatment of dermatitis.

BACKGROUND: Atopic dermatitis (AD) is an inflammatory skin disorder that is exceedingly challenging to treat. A prominent feature of AD is chronic pruritus. Early evidence suggested that pruritus in AD was partially due to mast cell release of histamines. Conversely, recent studies do not validate the role of histamine in the pathogenesis of pruritus. Conventional management continues to include the wide use of antihistamines to treat the persistent itch, however, there is an urgent need for therapy which will reduce the severity of pruritus for these patients. OBJECTIVE: To review the evidence in the literature for the use of antihistamines in the treatment of atopic dermatitis. METHODS: A MEDLINE search (1966-2002) was performed to obtain studies examining the use of antihistamines in the treatment of atopic dermatitis. Search terms included: atopic dermatitis; eczema; antihistamines; azatadine; brompheniramine; cetirizine; chlorpheniramine; clemastine; cyclizine; cyproheptadine; desloratadine; diphenhydramine; fexofenadine; hydroxyzine; loratadine; meclizine; promethazine; trimeprazine. Further references were gathered from these publications. RESULTS: Historically, antihistamines have been used in the treatment of AD. However, this review shows that the evidence for its use is inconclusive. At present, several antihistamines continue to provide relief of pruritus by central sedation, and they can also be used therapeutically for concomitant allergic conditions associated with AD. More clinical trials examining the therapeutic efficacy of antihistamines, especially with the newer nonsedating antihistamines, are necessary to elucidate their role in the treatment of AD. CONCLUSION: Dermatologists require additional evidence regarding the efficacy of antihistamines and their mechanism of action in the treatment of AD to enhance patient care.

Dermatitis, Atopic↗
PubMed2002

The relationship between HIV infection and atopic dermatitis.

Patients with HIV infection exhibit a wide range of skin pathology, including bacterial, fungal, and viral infections, skin tumors, inflammatory and eczematous eruptions, and drug rashes. HIV-infected adults commonly develop a condition that strongly resembles atopic dermatitis and is sometimes called "atopic-like dermatitis"; moreover, atopic dermatitis and other atopic disorders have been described as common manifestations of pediatric HIV infection. Conditions such as sinusitis, asthma, and hyper-IgE syndrome, and laboratory abnormalities, eg, elevated IgE levels, eosinophilia, and possible Th1-Th2 imbalances, suggest a predilection for atopic disorders in these patients. It is of interest to examine the immune perturbations intrinsic to HIV infection, and their possible role in triggering atopic dermatitis, and to consider whether other abnormalities, such as xerosis, bacterial or viral superantigens, or epidermal barrier disruption with altered presentation of cutaneous aeroallergens, might play a significant role.

Adrenal Cortex Hormones↗
PubMed2002

Ciclopiroxolamine cream for treating seborrheic dermatitis: a double-blind parallel group comparison.

BACKGROUND: The aim of this study was to compare the efficacy and tolerability of topically applied ciclopiroxolamine cream with that of the corresponding vehicle in patients with seborrheic dermatitis of the face. PATIENTS AND METHODS: The study was conducted as a multicenter prospective, randomized, double-blind parallel group comparison at 14 centers in Australia and New Zealand. 189 patients with clinically diagnosed seborrheic dermatitis participated in the study. Each patient applied ciclopiroxolamine 1% cream or the corresponding vehicle twice daily as a thin film to the affected skin areas and to clinically unaffected skin areas surrounding the lesions for 29 days. RESULTS: The rate of treatment success was significantly higher with ciclopiroxolamine than with vehicle (73.9 vs 53.6%; p = 0.003). Treatment with ciclopiroxolamine reduced the sum score of the clinical signs of seborrheic dermatitis to a greater extent than the vehicle (p </= 0.001). CONCLUSION: This study confirms that topical treatment with ciclopiroxolamine is effective and well tolerated in patients with seborrheic dermatitis.

Adult↗
PubMed1986

Avidity of antigliadin IgA and IgG antibodies in gluten-sensitive enteropathy and dermatitis herpetiformis.

Antigliadin antibodies (AGA) of IgG and IgA class were assayed with a modified enzymeimmunoassay in serum samples of 18 patients with gluten-sensitive enteropathy and 30 patients with dermatitis herpetiformis. No difference between antibody amount or avidity of the two groups of patients was observed. Avidity and total amount of AGA were also compared in 15 patients with a recent diagnosis of dermatitis herpetiformis and in 15 patients with a disease history of several years without a proper gluten-free diet. No difference in IgG antibodies was found but the amount of high avidity IgA antibodies was significantly higher in patients with several years' experience of dermatitis herpetiformis than in those with a recent diagnosis. The results indicate that in dermatitis herpetiformis, maturation of IgA response occurs. Further, clinically, maturation of anti-gliadin IgA response during the disease can increase the sensitivity of the patient against diet-derived gliadin.

Antibody Affinity↗
PubMed1983

Increased leukocyte histamine release with elevated cyclic AMP-phosphodiesterase activity in atopic dermatitis.

Maximal leukocyte histamine release in response to concanavalin A was significantly higher in a group of 16 adult patients with moderate to severe atopic dermatitis when compared to 13 adult nonatopic, normal subjects. In a further four atopic dermatitis patients, histamine release was similar to that in the normal group suggesting the existence of "high-releaser" and "low-releaser" subsets within the atopic dermatitis group. Leukocyte cAMP phosphodiesterase activity was significantly higher in the high-releaser group than in the low-releaser and normal groups. High and low histamine release responses showed strong correlations with high and low phosphodiesterase activities. Pretreatment with the experimental cAMP phosphodiesterase inhibitor Ro-20-1724 in high releasers reduced the histamine release to normal levels. These findings suggest that increased histamine "releasability" in atopic dermatitis is related to abnormalities in cyclic nucleotide regulation. Basophil percentages within the leukocyte preparation and the histamine content per basophil were not significantly different between the atopics and normals. Histamine release did not correlate significantly with serum IgE levels.

3',5'-Cyclic-AMP Phosphodiesterases↗
PubMed1993

Patients with severe atopic dermatitis have activated circulating basophils.

BACKGROUND: The purpose of this study was to define the potential role of the basophil in the pathogenesis of atopic dermatitis by comparing basophil releasibility in patients with food allergy and either mild or severe atopic dermatitis. METHODS: A clinical scoring system was used to differentiate patients into either a low clinical score (LCS) group, 10 patients, or a high clinical score (HCS) group, 14 patients. Basophil histamine release was measured with a radioenzymatic assay, and leukotriene C4 (LTC4) was determined with a radioimmunoassay. Histamine and LTC4 released from basophils spontaneously or after incubation with deuterium oxide, an IgE-dependent histamine-releasing factor, anti-IgE, and C5a were measured. RESULTS: Basophils from the HCS group released more histamine than those from the LCS group when stimulated with deuterium oxide (median percent total release: 85% vs 68%, p < 0.05), with 10 and 100 ng/ml of anti-IgE (58% vs 26% and 62.5% vs 37%, both p < 0.05) and 5 and 50 ng/ml of C5a (50.5% vs 11.5, p < 0.05; 49% vs 11%, p < 0.01, respectively). The spontaneous release of LTC4 from basophils was greater in the HCS group (median release: 34 vs 3.5 pg/0.1 ml, p < 0.05). Basophils stimulated with deuterium oxide, with 100 ng/ml anti-IgE, and 50 ng/ml C5a released more LTC4 in the HCS group (111.5 vs 39 pg/0.1 ml, p < 0.05; 64.5 vs 10 pg/0.1 ml, p < 0.01; 80 vs 1 pg/0.1 ml, p < 0.05, respectively). CONCLUSIONS: These data indicate that patients with more severe atopic dermatitis have "activated" circulating basophils in vivo and increased basophil releasibility, in particular in response to C5a. These studies may serve as markers for more severe atopic dermatitis.

Adolescent↗
PubMed1990

Infective dermatitis of Jamaican children: a marker for HTLV-I infection.

In Jamaican children infective dermatitis is a chronic eczema associated with refractory nonvirulent Staphylococcus aureus or beta-haemolytic streptococcus infection of the skin and nasal vestibule. 14 children between the ages of 2 and 17 years with typical infective dermatitis, attending the dermatology clinic at the University Hospital of the West Indies in Jamaica, were tested for antibody to human T-lymphotropic virus type 1 (HTLV-1). All were seropositive, whereas 11 children of similar age with atopic eczema were all negative. In 2 of 2 cases of infective dermatitis, the biological mother was HTLV-1 seropositive. None of the 14 patients showed signs of adult T-cell leukaemia/lymphoma, though experience with previous cases of infective dermatitis indicates the possibility of such progression.

Acute Disease↗
PubMed1991

Double-blind, controlled, crossover study of cyclosporin in adults with severe refractory atopic dermatitis.

A few patients remain severely affected by atopic dermatitis into adult life despite treatment with systemic steroids, azathioprine, and photochemotherapy. 33 patients took part in a double-blind, placebo-controlled, crossover study to assess the efficacy and safety of cyclosporin (5 mg/kg per day) in adults with severe refractory atopic dermatitis. Treatments were given for eight weeks each with one group (n = 16) receiving placebo followed by cyclosporin and another (n = 17) receiving cyclosporin and then placebo. Disease activity, extent of disease, sleep and itch, topical steroid use, and adverse events were assessed every two weeks. Both extent and activity of dermatitis were significantly improved (p less than 0.001) as were subjective measures of disease. 20 patients receiving cyclosporin reported adverse events compared with 8 taking placebo, although no patient required withdrawal from the study. Cyclosporin therapy led to an increase in the mean serum urea, creatinine, and bilirubin concentrations, although only the rise in bilirubin was significant (p = 0.001). Our results confirm that cyclosporin is a safe and effective short-term treatment for severe, refractory atopic dermatitis.

Adolescent↗
PubMed1993

Placebo-controlled trial of essential fatty acid supplementation in atopic dermatitis.

Treatment of atopic dermatitis with essential fatty acids remains controversial. A double-blind, placebo-controlled, parallel-group study was done to investigate the response of patients with atopic dermatitis to essential fatty acid supplements. Patients with atopic dermatitis were randomised to receive evening primrose oil, evening primrose oil and fish oil, or placebo for 16 weeks. Disease activity was monitored by clinical severity scores recorded by the investigator, topical steroid requirement, and symptom scores recorded by subjects. Of 123 subjects recruited, 102 completed the treatment period. No improvement with active treatment was demonstrated. Our study, which avoided the methodological and analytical problems of previous studies, found no effect of essential fatty acid supplementation in atopic dermatitis.

Adult↗
PubMed1991

Atopic dermatitis: new therapeutic considerations.

Atopic dermatitis is a genetically determined inflammatory condition in which the primary defect is expressed in one or more hematopoietic cells that infiltrate the skin. It is a multifactorial disease with inflammation triggered by a variety of factors. Among these, atopic dermatitis has been experimentally induced and reproduced by emotional-stress interviews and food challenges only. The inflammatory events of atopic dermatitis appear to initiated by mast cells, but eosinophils, monocytes, and T lymphocytes (predominantly CD4) also are present in lesions. The secondary effects of inflammation are a dry, brittle stratum corneum and pruritus, causing excoriation and a lichenified epidermal layer resulting from chronic rubbing. Therapeutic approaches to atopic dermatitis may be directed at several points in the evolution of the disease. Agents including emollients are needed to preserve and restore the stratum corneum barrier, and effective antipruritics are required to reduce the self-inflicted damage to the involved skin. Various other agents may be needed to antagonize mediators or cytokines and to inhibit cytokine expression and release from lesional, immune-effector cells. Likewise, new phosphodiesterase inhibitors, calcium-active agents, and antiallergic drugs may be used to reduce the quantity and pathologic functioning of inflammatory infiltrating cells in the skin.

Dermatitis, Atopic↗
PubMed1992

A double-blind, placebo-controlled, multicenter trial of lithium succinate ointment in the treatment of seborrheic dermatitis. Efalith Multicenter Trial Group.

BACKGROUND: Seborrheic dermatitis, an inflammatory dermatosis that principally affects sebaceous areas, may be related to the presence of the yeast Pityrosporum ovale. Topical therapy with corticosteroids, although in general effective, may be associated with several unwanted effects. The development of alternative non-steroid-based therapies may enable patients to avoid the use of topical steroids and help elucidate the pathogenesis of the disease. OBJECTIVE: This study aimed to assess the efficacy and safety of an ointment containing 8% lithium succinate in the treatment of seborrheic dermatitis. METHODS: The study consisted of a multicenter placebo-controlled clinical trial in 227 adult patients. RESULTS: Lithium succinate ointment was significantly more effective than placebo in treating all the symptoms of seborrheic dermatitis. No specific unwanted effects were associated with its use. Relapse was slow when treatment was stopped. CONCLUSION: The effectiveness of lithium succinate ointment in the treatment of seborrheic dermatitis adds to the evidence implicating P. ovale in the pathogenesis of that condition.

Adolescent↗
PubMed1992

The site of blister formation in dermatitis herpetiformis is within the lamina lucida.

BACKGROUND: Because the initial neutrophilic infiltrate in dermatitis herpetiformis is within the dermal papillae, most investigators have assumed the vesicles occur in this same area. This was supported by electron microscopy studies. In 1983 Klein et al. refuted this concept, suggesting that vesicle formation was within the lamina lucida above the lamina densa. Despite this study, current literature continues to state that blister formation is below the lamina densa. OBJECTIVE: Our purpose was to determine the ultrastructural site of blister formation in early and late vesicles of dermatitis herpetiformis. METHODS: We evaluated eight biopsy specimens from four patients by immunomapping with antibodies to bullous pemphigoid antigen, laminin, type IV collagen, and epidermolysis bullosa acquisita antigen. RESULTS: In both early and late vesicles blister formation was found to be above the lamina densa in the lamina lucida. CONCLUSION: These findings are contrary to the commonly held concept that the blister in dermatitis herpetiformis is below the lamina densa and confirm the findings of Klein et al. that the site of blister formation in dermatitis herpetiformis is above the lamina densa within the lamina lucida.

Basement Membrane↗
PubMed1990

Flare factors and atopic dermatitis: the role of allergy.

Atopic dermatitis is a genetically determined eczematous skin disease strongly influenced by environmental conditions called flare factors. Allergic reactions are one such flare factor. These reactions include contact urticaria, allergic contact dermatitis, and late phase reactions. Contact urticaria could induce eczema by eliciting scratching. A late phase reaction may be involved in eczema produced by prolonged epicutaneous applications of antigens in individuals with immediate sensitivity to these antigens. Mechanisms of allergic contact dermatitis might also elicit dermatitis. Environmental allergens may include mold, dust, mite, pollens, foods, danders and bacteria.

Allergens↗
PubMed1994

Serum soluble IL-2 receptor (sIL-2R) and eosinophil cationic protein (ECP) levels in atopic dermatitis.

We examined the serum soluble IL-2 receptor and eosinophil cationic protein levels in patients with atopic dermatitis (n = 21), patients with urticaria (n = 12), and normal healthy individuals (n = 14). We found that both soluble IL-2 receptor levels and eosinophil cationic protein levels were significantly higher in atopic dermatitis than in urticaria or normal controls. Although both soluble IL-2 receptor levels and eosinophil cationic protein levels were significantly correlated with clinical severity scores in atopic dermatitis, the correlation between eosinophil cationic protein levels and clinical severity scores was higher than that between soluble IL-2 receptor levels and clinical severity scores. However, soluble IL-2 receptor levels, eosinophil cationic protein levels and clinical severity scores were not significantly correlated with IgE levels. The chronological changes of soluble IL-2 receptor and eosinophil cationic protein levels differ from patient to patient. However, levels of soluble IL-2 receptor and eosinophil cationic protein seem to parallel to each other in 65% of patients with AD. Measurement of serum eosinophil cationic protein or soluble IL-2 receptor levels may be a useful tool to monitor the short-term or long-term disease activity of atopic dermatitis in conjunction with clinical severity scores.

Adolescent↗
PubMed1996

Role of staphylococcal enterotoxins in pathogenesis of atopic dermatitis: growth and expression of T cell receptor V beta of peripheral blood mononuclear cells stimulated by enterotoxins A and B.

In order to investigate the role of staphylococcal enterotoxins in the pathogenesis of dermatitis in atopic patients, the growth and expression of T cell receptor V beta in peripheral blood mononuclear cells (PBMCs) from atopic dermatitis patients induced by stimulation with staphylococcal enterotoxin A (SEA) or staphylococcal enterotoxin B (SEB) were examined. Lymphocyte stimulation tests (LST) using SEA or SEB were performed in atopic dermatitis (AD) patients (n = 10) and normal controls (n = 5). PBMCs from AD patients displayed significantly stronger responses to SEA or SEB than those from the controls. To ascertain further whether SEA acts as a superantigen in atopic dermatitis, the expression of 22 genes in the variable region of the beta chain (V beta) of T cell receptors (TcR) was examined before and after stimulation with SEA by a reverse transcriptase-polymerase chain reaction (RT-PCR). Before stimulation, only weak expression of V beta was observed, and the expression of the various V beta segments was uniform in the normal controls (n = 3). In the AD patients (n = 3), the expression of V beta was enhanced, but was not uniform in 2 out of 3 patients and the pattern of expression was characteristic in each individual. This suggests that V beta expression varies in individual AD patients and displays restricted heterogeneity, reflecting the diversity of the etiology of the disease. After culture of the SEA-stimulated cells, no difference was observed in the expression of TcR V beta segments in the 3 normal controls as compared with that prior to stimulation, but particular V beta segments were intensely expressed in 3 AD patients, displaying distinct patterns (case I: V beta 9, V beta 10, V beta 18; case 2: V beta 6.1-3; case 3: V beta 6.1-3, V beta 18). Many of these V beta segments corresponded with those known to be induced by SEA. These results suggest oligoclonal proliferation of T cells in the peripheral blood of AD patients and high responsiveness in each clone, and since the expression of V beta segment after SEA stimulation was restricted, the actions of staphylococcal enterotoxins as superantigens were suggested.

Adolescent↗
PubMed2005

Expression of IL-31 gene transcripts in NC/Nga mice with atopic dermatitis.

To search for the pruritogen of atopic dermatitis, a characteristic symptom in atopic dermatitis patients, we examined interleukin-31 (IL-31) mRNA expression in NC/Nga mice as an animal model of atopic dermatitis. The expression of IL-31 mRNA in the skin of NC/Nga mice with scratching behavior was significantly higher than that in NC/Nga mice without scratching behavior. Our findings suggest that IL-31 may participate in the cause of itch sensation and promote scratching behavior in NC/Nga mice with atopic dermatitis.

Animals↗
PubMed2006

Effects of TS-022, a newly developed prostanoid DP1 receptor agonist, on experimental pruritus, cutaneous barrier disruptions and atopic dermatitis in mice.

TS-022, {4-[(1R, 2S, 3R, 5R)-5-Chloro-2-((S)-3-cyclohexyl-3-hydroxyprop-1-ynyl)-3-hydroxycyclopentyl] butylthio} acetic acid monohydrate, inhibits ADP-induced platelet aggregation, an effect significantly antagonized, as in the case of prostaglandin D(2) by the prostanoid DP(1) receptor antagonist (BW A868C). TS-022 is a prostanoid DP(1) receptor agonist, originally developed as a novel anti-pruritic drug for patients with atopic dermatitis. We examined the effects of TS-022 on experimental pruritus, cutaneous barrier disruption, and atopic dermatitis and in in vitro immune function tests. Topically applied TS-022 significantly suppressed scratching in skin-lesioned NC/Nga mice from a concentration of 2.5 nM, and this scratch-suppressive activity was significantly antagonized by BW A868C. Tacrolimus (FK-506) and dexamethasone, used as reference drugs for atopic dermatitis, also exhibited suppressive effects against scratching, but only at concentrations of 125 and 25,000 microM. TS-022 applied topically, once a day for 2 days, significantly accelerated repair of the cutaneous barrier disruption caused by mechanical scratching, from concentrations of 2.5 nM. This acceleration of repair of the disrupted cutaneous barrier by this drug was also significantly antagonized by BW A868C. FK-506 and dexamethasone showed no beneficial effects on the repair of the disrupted cutaneous barrier. Repeated topical application of 2.5 microM of TS-022 and 12.5 microM of FK-506 once a day for 6 weeks significantly improved the skin inflammation scores in the NC/Nga mice. In regard to the effects of TS-022 in vitro, the inhibitory activity of TS-022 against concanavalin A-induced cytokine production by splenocytes was marginal as compared with that of FK-506 or dexamethasone. These results suggest that the beneficial therapeutic effects of TS-022 in NC/Nga mice with atopic dermatitis are mediated by its suppressive effect on scratching and its effect of accelerating repair of the disrupted cutaneous barrier, both effects being attributable to its prostanoid DP(1) receptor agonistic activity.

Acetates↗
PubMed2004

Photoallergic contact dermatitis from ketoprofen induced by drug-contaminated personal objects.

BACKGROUND: Photoallergic contact dermatitis from ketoprofen has been recognized since the mid-1980s. Skin reactions have been reported to continue weeks after discontinuation of ketoprofen. One reason for this could be residual ketoprofen in the skin, which has been shown in a skin biopsy specimen. OBJECTIVE: We sought to report on 3 cases of photoallergic contact dermatitis from ketoprofen in topical anti-inflammatory gels and on relapses of dermatitis appearing after use of ketoprofen-contaminated objects. METHODS: We patch and photopatch tested, with standard series, the anti-inflammatory gel, ketoprofen, and its ingredients in serial dilutions and extracts of personal objects. We performed chemical investigations of personal objects with thin-layer chromatography, high-pressure liquid chromatography, and gas chromatography-mass spectrometry. RESULTS: Photoallergy was demonstrated to ketoprofen, which was detected in personal objects. CONCLUSION: Relapses of photoallergic contact dermatitis in patients photoallergic to ketoprofen can be induced by ketoprofen-contaminated objects such as bandages and slippers.

Administration, Topical↗