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PubMed1983

Early diagnosis of infantile seborrhoeic dermatitis and atopic dermatitis--clinical features.

In a prospective study of thirty-seven infants presenting with dermatitis in infancy it was found that pruritus, a positive family history of atopy, and the age of onset of skin lesions were of little value in distinguishing atopic dermatitis from infantile seborrhoeic dermatitis. The most useful distinguishing features were the increased incidence of lesions on the forearms and shins in atopic dermatitis, and in the axillae in infantile seborrhoeic dermatitis. The onset of skin lesions solely in the napkin area favoured a diagnosis of infantile seborrhoeic dermatitis, but when more than one site was involved the distinction was less clear. Infantile seborrhoeic dermatitis carried a much better prognosis than atopic dermatitis. In thirty-six out of thirty-seven infants the definitive diagnosis could be made with confidence on clinical grounds by the age of I year, but was often difficult at first presentation in early infancy.

Dermatitis, Atopic↗
PubMed2005

Analysis of T cell receptor (TCR) BV-gene clonotypes in NC/Nga mice developing dermatitis resembling human atopic dermatitis.

BACKGROUND: Our previous study showed that T cells in skin lesions of human atopic dermatitis (AD) had oligoclonal accumulation, indicating the involvement of antigen-specific immune reactions at those sites. Recently, NC/Nga mice, which develop skin lesions similar to AD, have been proposed as a model for that disease. OBJECTIVE: To clarify whether NC/Nga mice are suitable as a model for human AD from the viewpoint of their antigen-specific immune responses. METHODS: Reverse transcription-polymerase chain reaction (RT-PCR) and single strand conformation polymorphism (SSCP) analyses were conducted to detect TCR BV genes of clonally expanded T cells derived from NC/Nga mice at an early phase of the AD-like dermatitis, at a late phase of the dermatitis, and with no AD-like dermatitis. RESULTS: (1) T cells with TCR BV 7, 10 and 17 reside in the skin of NC/Nga mice without the AD-like dermatitis. (2) T cells with these BV genes contain oligoclonal accumulations, however, expanded T cell clonotypes are also detected in the spleen and exist constantly during the course of the AD-like dermatitis. (3) Development of the AD-like dermatitis is associated with additional oligoclonal expansion/accumulation of T cells with TCR BV 2, 4 and 6 genes. (4) Progression of the AD-like dermatitis is associated with further oligoclonal expansion/accumulation of T cells with the TCR BV 14 gene. (5) Some of the expanded TCR clonotypes are common between the individual mice and between early and late phases. CONCLUSIONS: Taking these data together with the previous human AD studies, NC/Nga mice seem to be an appropriate model for human AD.

Animals↗
PubMed2003

Administration of anti-interleukin 18 antibody fails to inhibit development of dermatitis in atopic dermatitis-model mice NC/Nga.

BACKGROUND: Interleukin (IL)-18 has been shown to activate basophils to produce histamine and IL-4 and to induce naive T cells to differentiate into T-helper (Th) 2 cells. However, when expressed together with IL-12, IL-18 induces Th1 cell development and inhibits IgE synthesis. Previously we reported that serum IL-18 levels were elevated in the sera from atopic dermatitis-model mice NC/Nga, prior to the onset and during the development of dermatitis. OBJECTIVES: We studied whether neutralization of IL-18 activity might affect dermatitis in NC/Nga mice, to investigate the role of IL-18 on dermatitis. METHODS: NC/Nga mice were given weekly anti-IL-18 antibody starting at 5 weeks of age to 13 weeks and development of dermatitis, scratching behaviour and serum IgE concentrations were evaluated. RESULTS: Continuous injections of anti-IL-18 antibody failed to inhibit the onset and development of dermatitis and IgE elevation. The treatment, rather, tended to lead to an exacerbation of dermatitis and scratching behaviour. In addition, the administration of anti-IL-18 antibody did not ameliorate the responsiveness of lymphocytes to IL-4, which was previously demonstrated as an immunological abnormality in the mouse. CONCLUSION: This study demonstrates that, at least in NC/Nga mice, IL-18, although excessively expressed before the onset of dermatitis, shows antiallergic actions.

Animals↗
PubMed1991

Lack of efficacy of topical cyclosporin A in atopic dermatitis and allergic contact dermatitis.

Since oral cyclosporin A (CsA) has demonstrated its effectiveness in psoriasis and atopic dermatitis, efforts have been made to develop a topical CsA formulation, thus avoiding systemic adverse events. A limited number of publications are available on the use of topical CsA in allergic contact dermatitis and atopic dermatitis. Moreover the response rate of humans to topical CsA is about 50% or less. We now report our results with three new topical CsA formulations on allergic contact dermatitis and atopic dermatitis. No significant improvement was found in 16 atopic dermatitis patients and 7 allergic contact dermatitis (nickel sulphate) patients.

Administration, Cutaneous↗
PubMed2004

Fewer melanocytic nevi found in children with active atopic dermatitis than in children without dermatitis.

OBJECTIVE: To investigate the effects of atopic diseases on nevus development during childhood. DESIGN: A descriptive survey of nevi in a cohort of 8- and 9-year-old children combining a skin examination and a validated questionnaire regarding atopic dermatitis, allergic rhinoconjunctivitis, and bronchial asthma. SETTING: Fifty-one primary schools in Sweden. PARTICIPANTS: A total of 788 children born in 1992 participated in 1999 in a prevalence study of allergic diseases. The present study was restricted to the 545 children from that study who were still living in the community, and 515 (94%) of them participated. The cumulative incidence of atopic dermatitis, allergic rhinoconjunctivitis, and bronchial asthma was 24%, 12%, and 13%, respectively, from birth to age 7 years as reported by questionnaire; 3% reported all 3 diagnoses. RESULTS: Children with reported atopic dermatitis and findings of active dermatitis on examination had fewer nevi (median, 4; mean, 7.4) than children with no reported atopic disease and no active dermatitis found on examination (median, 9; mean, 11.2) (P<.001). Children who developed active atopic dermatitis after the questionnaire was filled out (ie, during the last 2 years) had fewer nevi than children with no atopic disease (median, 3; mean, 5.3) (P<.001). There was no difference in nevus number between the children with bronchial asthma or allergic rhinoconjunctivitis and children with no atopic disease. CONCLUSION: Children with atopic dermatitis had few melanocytic nevi, which suggests that the proinflammatory cytokine network in the atopic skin might inhibit melanocyte growth and/or progression to nevi.

Asthma↗
PubMed1994

The U.K. Working Party's Diagnostic Criteria for Atopic Dermatitis. II. Observer variation of clinical diagnosis and signs of atopic dermatitis.

The level of agreement between 14 physicians as to what constitutes a case of atopic dermatitis was tested on 15 selected patients with a range of diagnoses. Between-observer agreement was good, with a mean pair agreement index (P0) of 0.94, and a chance corrected index (kappa) of 0.78. Between-observer agreement in the recording of 18 separate physical signs of atopic dermatitis was then tested by asking the 14 physicians to note the presence or absence of each sign in a different group of patients to those seen in the first part of the exercise. Substantial between-observer agreement (kappa > 0.61) was only present for truncal dermatitis. Most signs showed only fair to moderate agreement (kappa 0.21-0.60), and some signs, such as keratosis pilaris, xerosis, orbital pigmentation, fine hair, and extensor dermatitis, showed poor agreement (kappa 0.01-0.20). The findings were similar when the responses of two independent observers from the national study outlined in Paper I were compared for each sign. Within-observer variation for the recording of physical signs was substantially better than between-observer variation. Physicians interested in atopic dermatitis agree reasonably well on what constitutes a typical case of atopic dermatitis. Between-observer variation with regard to some physical signs of atopic dermatitis is of a magnitude which argues against their continued use in clinical and epidemiological studies.

Dermatitis, Atopic↗
PubMed2005

The hypomagnesic rat model: dermatitis-prone hairless rats with mild magnesium depletion fed a diet low in lipids did not develop pruritic dermatitis.

BACKGROUND/PURPOSE: In the hypomagnesic dermatosis of rats, low-dietary magnesium leads to lowered serum Mg2+, universal dermatitis and scratching. The model is postulated to work better if the diet also has a low content of lipids. Pruritus is seen in patients suffering from anorexia nervosa and resolves on weight restoration. Lipid depletion of the diet and/or lowered body weight may therefore be important in developing pruritus. The purpose of the present study was to investigate whether a diet low in lipids can induce pruritus in dermatitis prone rats because of mild magnesium depletion thereby focusing on the role of lipids in the hypomagnesic dermatosis rat model. METHODS: Fourteen male hairless rats, 3 weeks of age, were fed a diet deficient in lipids and with a lower content of magnesium for a 4-week period and compared with 11 controls fed a normal diet. The skin was inspected daily and transepidermal water loss (TEWL), serum Mg2+ and scratching activity were measured. At the end, skin biopsies were taken from the flank and ears. RESULTS: Serum Mg2+ was significantly lowered in the diet group (P<0.001) but the rats developed no dermatitis or increased TEWL compared with 11 rats in a control group. Biopsies were normal with no sign of inflammation. Rats in the diet group had inferior weight gain, were less active and spent more time asleep than control rats (P<0.01). Furthermore, scratching activity monitored in the last week of the study as the number of scratch-sequences per awake minute was reduced in the diet group (P<0.001). CONCLUSION: The lipid-deficient diet was not able to induce pruritic dermatitis despite the fact that the rats were dermatitis prone because of mild magnesium depletion. It is not confirmed that dietary lipid depletion plays any significant role in the hypomagnesic dermatitis rat model. The dermatitis and the model appear to be strictly dependent on efficient magnesium depletion manufactured with very low magnesium levels.

Animals↗
PubMed1997

Elevated serum levels of soluble CD30 are associated with atopic dermatitis, but not with respiratory atopic disorders and allergic contact dermatitis.

Type 2 helper T-cell immune responses can be demonstrated in the human atopic disorders atopic dermatitis and allergic asthma/rhinoconjunctivitis. The CD30 (Ki-1) antigen, originally described on Hodgkin and Reed-Sternberg cells, has recently been proposed as a marker of T cells with potent B-cell helper activity producing IL-5 and gamma-IFN, as well as on CD4+ and CD8+ T cells with a Th2 cytokine profile. As a soluble form of CD30 (sCD30) is released by CD30+ cells in vivo, we studied its clinical significance in atopic disorders compared with allergic contact dermatitis and healthy controls. Elevated sCD 30 levels were associated with atopic dermatitis (P < 0.0001), but not with respiratory atopic disorders or allergic contact dermatitis. sCD30 levels in patients with atopic-dermatitis were independent of serum IgE. The particular occurrence of serum sCD30 in patients with atopic dermatitis indicates a special regulatory function of CD30+ cells in this disease.

Adolescent↗
PubMed2000

Identification of Malassezia species isolated from patients with seborrhoeic dermatitis, atopic dermatitis, pityriasis versicolor and normal subjects.

We identified Malassezia species isolated from 42 patients with seborrhoeic dermatitis, 17 patients with atopic dermatitis, 22 patients with pityriasis versicolor, 35 normal subjects and 73 healthy medical students. Regarding the prevalence of Malassezia species in the 35 normal subjects, the frequency of isolation of Malassezia globosa was 22%, M. sympodialis 10% and M. furfur 3%. M. slooffiae, M. pachydermatis, M. restricta and M. obtusa were infrequently isolated from normal skin. Two different species were isolated coincidentally from seven samples. In the patients with atopic dermatitis, M. furfur was isolated more frequently from lesional skin (21%) than non-lesional skin (11%). However, there was no statistical significance. Therefore, this result, by itself, is insufficient to prove that M. furfur should be considered to be an exacerbating factor of atopic dermatitis. In seborrhoeic dermatitis, M. furfur (35%) and M. globosa (22%) were isolated from lesional skin on the face at significantly high rates in comparison with the normal subjects. Therefore, M. furfur and/or M. globosa may be pathogens of seborrhoeic dermatitis. M. globosa was isolated at a frequency of 55% from lesional skin of pityriasis versicolor, while all other species were below 10%. These data suggest that the pathogenic species of pityriasis versicolor is M. globosa.

Adolescent↗
PubMed2000

Pilot study of IFN-gamma-induced specific hyposensitization for house dust mites in atopic dermatitis: IFN-gamma-induced immune deviation as a new therapeutic concept for atopic dermatitis.

IFN-gamma/IL-4 imbalance is a central immunologic defect which is responsible for increased IgE antibody response in atopic dermatitis. Effects of hyposensitization were controversial in atopic dermatitis. Reversed IFN-gamma/IL-4 balance was induced using IFN-gamma in atopic dermatitis and specific hyposensitization with house dust mites (HDM) was tried in the status of IFN-gamma-induced immune deviation. A total of 58 atopic dermatitis patients who had obvious allergy to HDM were selected in this study. IFN-gamma-induced hyposensitization for HDM was tried in 10 patients. Twenty-two patients received IFN-gamma therapy and six were treated by simple hyposensitization. Twenty were enrolled as control subjects. The clinical severity scores decreased effectively only by IFN-gamma-induced hyposensitization for HDM. Specific hyposensitization for HDM in the status of IFN-gamma-induced immune deviation successfully improved atopic dermatitis. HDM might play a pathogenic role in subpopulation of atopic dermatitis.

Adolescent↗
PubMed2006

Induction of scratching behaviour and dermatitis in various strains of mice cohabiting with NC/Nga mice with chronic dermatitis.

BACKGROUND: NC/Nga (NC) mice with similar pathological and behavioural features as seen in human atopic dermatitis are used as a model of the disease. Under normal circumstances, spontaneous and persistent scratching occurs in NC mice and this can lead to the onset of skin inflammation. OBJECTIVES: We examined the induction of scratching behaviour in NC, BALB/c, ICR and C3H/HeN mice, and of dermatitis in NC and BALB/c mice, by cohabitation with mice with dermatitis. METHODS: NC, BALB/c, ICR and C3H/HeN mice were kept together with NC mice with chronic dermatitis (CNV-NC) for 2 weeks, and the numbers of scratching episodes were counted. NC and BALB/c mice were also kept together with CNV-NC mice for 24 weeks and the skin severity score was assessed. The score was assessed for a further 8 weeks after separation of these mice. RESULTS: The number of scratching episodes in NC, BALB/c, ICR and C3H/HeN mice was increased by cohabitation with CNV-NC mice. Cohabitation with CNV-NC mice led to dermatitis in both NC and BALB/c mice. The number of scratching episodes and the skin severity score in BALB/c mice were about half of those in NC mice. When cohabitation with CNV-NC mice stopped, the number of scratching episodes and the skin severity score decreased in BALB/c mice, but not in NC mice. Changes in the histopathological data of BALB/c mice supported the severity of skin inflammation. CONCLUSIONS: Our study demonstrates that scratching behaviour and dermatitis can be induced in various strains of mice by cohabitation with CNV-NC mice, and that cessation of cohabitation leads to a recovery in BALB/c mice but not in NC mice.

Animals↗
PubMed2004

Establishment of allergic dermatitis in NC/Nga mice as a model for severe atopic dermatitis.

Mite antigen has been suggested to play important roles in the onset and/or development of atopic dermatitis, and mite antigen-induced dermatitis models appear beneficial for the basic study of atopic dermatitis. In the present study therefore, we attempted to establish an allergic dermatitis model in mice using Dermatophagoides farinae crude extract as an antigen. Mite antigen solution at a concentration of 1 or 10 mg/ml was painted 5 times repeatedly at an interval of 7 d onto the ear of NC/Nga or BALB/c mice with or without simultaneous tape-stripping. Apparent biphasic ear swelling was observed after the 4th and 5th antigen applications in both strains of mice treated with 10 mg/ml of antigen solution. Thickening of the epidermis, fibrosis of the dermis, and the accumulation of inflammatory cells were also observed after the 5th application. The inflammatory changes were more evident in NC/Nga mice than in BALB/c mice and potentiated by tape-stripping. The ear swelling was accompanied by increased serum IgE, increased expression of interleukin-4 mRNA and decreased expression of interferon-gamma mRNA in cervical lymph nodes and ears. These results indicate that ear swelling caused by repeated mite antigen application with simultaneous tape-stripping has a Th2-dominant background and that the inflammatory responses are expressed more potently in NC/Nga mice than in BALB/c mice. The dermatitis caused by mite antigen in NC/Nga mice appears to be a useful model for the basic study of atopic dermatitis.

Animals↗
PubMed2001

[Induction of atopic dermatitis-like skin lesion in NC/Nga mice--the influence of the skin barrier destroying solution to the induction of dermatitis].

NC/Nga mouse is well known as a mouse model for atopic dermatitis. In general, when NC/Nga mouse are raised under specific pathogen free (SPF) conditions no skin lesions are detected, but when under non-filtrated (conventional) condition, atopic dermatitis like skin lesions appear spontaneously. However, this dermatitis develops in 70-90% of mice (not 100%), which makes it difficult to perform reproducible experiments every time. This study was performed under SPF conditions, using the four solutions (2% SDS, 4% SDS, ethanol, acetone/ether) to destroy the skin barrier function, and thereafter, applying the extracted solution of mite: Dermatophagoides pteronyssinus, which is a very popular antigen in pathogenesis of human atopic dermatitis. The extracted solution of mite was applied repeatedly on the NC/Nga mice with a pretreatment of barrier destroying solution and after 8 weeks the mice developed severe dermatitis (clinical skin condition score of 7-10.2 points) with marked elevation of plasma IgE level, whereas mice coated only with the barrier destroying solution showed weak skin lesion with no elevation of plasma IgE level. BALB/c mice, which are employed as control, showed weak skin lesion (clinical skin condition score of 0-3.8 points) and slight elevation of plasma IgE level after repeated application of the extracted solution of mite with a pretreatment of the barrier destroying solution, whereas mice coated only with the barrier destroying solution showed weak skin lesion and the no elevation of plasma IgE level was observed. In this study, using several solutions to disturb the skin barrier function before applying the antigen, we have found a suitable condition and types of solutions in inducing dermatitis in NC/Nga mice.

Acetone↗
PubMed2002

Occupational allergic contact dermatitis is more prevalent than irritant contact dermatitis: a 5-year study.

BACKGROUND: Irritant contact dermatitis is thought to be the leading cause of occupational skin disease in the United States. Recent reports suggest otherwise. OBJECTIVES: The purposes of this study were to determine the prevalence of allergic and irritant forms of occupational contact dermatitis in the population seen at a Midwestern dermatologic referral clinic, report professions commonly affected by occupational skin disease, and indicate which substances are frequent allergens. METHODS: A retrospective analysis of patch test data collected at the University of Kansas between 1994 and 1999 was performed. RESULTS: Of 537 patients who underwent patch testing, 135 (25%) had occupational skin disease. Allergic contact dermatitis affected 81 (60%) patients, and irritant contact dermatitis was found in 46 (34%). Health care professionals, machinists, and construction workers accounted for nearly half of all patients with occupational skin disease. Nickel sulfate, glutaraldehyde, and thiuram mix were the most common allergens. CONCLUSION: Patch tests with a wider array of allergens than those currently available in the United States are needed to prevent misdiagnosis of occupational contact dermatitis.

Adult↗
PubMed1980

Increased "in vivo" lymphocyte blastogenesis in the peripheral blood of patients with atopic dermatitis and allergic contact dermatitis.

The spontaneous 3H-thymidine (3HT) labelling of some lymphocyte subpopulations has been studied in the peripheral blood of five patients with atopic dermatitis and five with widespread allergic contact dermatitis and compared with that in 10 healthy subjects. One hour after addition of 3HT to heparinized blood, lymphocytes were separated and processed with two different rosetting techniques (E-rosette test and Active E-rosette test). The cell suspensions were cytocentrifugated and autoradiography undertaken. An increased number of 3HT labelled lymphocytes was observed in the peripheral blood of patients with dermatitis as compared to controls. These labelled lymphocytes were E-rosette-forming cells (T cells) and E-non-rosette-forming cells (non-rosette-forming T cells and non-T cells). The ratio between the labelling index (LI) of E-rosette- to the LI of non-E-rosette-forming cells was in favour of T cells in allergic contact dermatitis (ratio = 3.09) whereas in atopic dermatitis (ratio = 0.93) the DNA synthesis was relatively greater in the non-rosette-forming cells. It is suggested that this increased LI of peripheral blood lymphocytes could be related to the increased derman mononuclear cell 3HT-labelling that has been reported previously in these inflammatory skin diseases.

Adolescent↗
PubMed2005

[A common and insidious side-effect: allergic contact dermatitis caused by bufexamac used in the treatment of dermatitis. Results from the Information Network of Departments of Dermatology (IDVK)].

BACKGROUND AND OBJECTIVE: Bufexamac is a non-steroidal, anti-inflammatory drug used in the topical treatment of atopic dermatitis, stasis dermatitis and perianal eczema. The substance is known to cause severe allergic contact dermatitis (ACD) as an adverse effect (AE), which may be indistinguishable from the eczema which is to be treated. Hence the diagnosis of this AE is often considerably delayed. In order to estimate the quantitative importance of ACD to bufexamac, data of the Information Network of (German) Departments of Dermatology (IVDK) from July 1999 to December 2004 were analysed. PATIENTS AND METHODS: During the study period, 39,392 unselected patients from 40 German departments of the IVDK were patch tested with bufexamac (5 % pet). The results of the reading after 72 hours were analysed. The dichotomized patch test result was further assessed for possible risk factors from the patients' history and clinical diagnosis by Poisson regression analysis. RESULTS: In 560 of 39,392 patients contact allergy to bufexamac was diagnosed, i. e. 1.4 % (95 % confidence interval: 1.3 - 1.5), standardized for sex and age. The Poisson regression analysis revealed a significantly increased risk associated with the following factors: multiple sensitization, perianal eczema, underlying atopic dermatitis, leg dermatitis, female gender and residence in areas of Germany other than Eastern Germany. The latter observation can be explained by low prescription rates in Eastern Germany. CONCLUSION: Bufexamac is an important allergen. Extrapolating the frequency of 1.4 % in our data to the whole German population by the CE-DUR approach yields an estimate of about 6000 cases per year. In view of the high frequency of sensitization, the pitfalls in diagnosis, the severity of the course of disease and the lack of efficacy of this drug, the risk to benefit ratio is obviously critical.

Administration, Topical↗
PubMed2001

Targeting keratinocyte apoptosis in the treatment of atopic dermatitis and allergic contact dermatitis.

BACKGROUND: Activation and skin-selective homing of T cells and effector functions in the skin represent sequential events in the pathogenesis of atopic dermatitis and allergic contact dermatitis. OBJECTIVE: T cell-mediated keratinocyte apoptosis plays a key pathogenetic role in the formation of eczematous dermatitis. IFN-gamma released from activated T cells upregulates Fas on ke-ratinocytes, which renders them susceptible to apoptosis. The lethal hit is given to keratinocytes by means of Fas ligand expressed on the T-cell surface or released to the inflammatory microenvironment. We sought to investigate whether drugs used for the treatment of eczematous disorders interfere with this pathogenic pathway. METHODS: T cell-mediated, Fas-induced keratinocyte apoptosis in a keratinocyte-T cell coculture system serves as an in vitro model of eczematous dermatitis. We tested, in this model, whether immunomodulatory agents (dexamethasone, cyclosporine A, rapamycine, tacrolimus/FK506, intravenous immunoglobulin [IVIG], and theophylline) are able to inhibit apoptosis of keratinocytes. Additionally, skin biopsy specimens from patients with untreated and successfully treated eczematous dermatitis were evaluated for keratinocyte apoptosis. RESULTS: Dexamethasone, cyclosporine A, FK506, rapamycine, and IVIG are inhibitors of keratinocyte apoptosis induced by activated T cells. This effect is mediated by 2 major mechanisms directed on T cells or keratinocytes. T-cell activation was mainly inhibited by dexamethasone, FK506, cyclosporine A, and rapamycine. Interestingly, high-dose dexamethasone and IVIG directly inhibited Fas-mediated keratinocyte apoptosis. In vivo keratinocyte apoptosis was significantly reduced after successful topical treatment of eczematous lesions. CONCLUSION: These results demonstrate mechanisms of action of current treatment approaches and provide a future for more focused therapeutic applications.

Acute Disease↗
PubMed1981

Chronic pruritic dermatitis in asthmatic monkeys: a subhuman primate analogue of atopic dermatitis?

In a group of adult normal rhesus monkeys and monkeys with IgE-mediated asthma observed over a period of 15 years, 2 of the latter group were found to have chronic, generalized pruritus and dermatitis. The skin lesions were recurrent and located on the flexural surfaces of the forearms leading to the thickened, scaling, lichenified dermatitis in that area in the skin of 1 monkey. The pruritus and skin lesions subsided following therapy with depot methylprednisolone but recurred after this therapy was discontinued. Both animals had recurrent severe cutaneous infections in excoriated lesions following scratching without infections in other organs. The cutaneous infections responded to penicillin therapy but recurred with scratching. No deficiencies in immunoglobulin levels, or lymphocyte responses to phytohemagglutinin were found in these 2 monkeys. The 2 animals differed from normal animals by their high titers of immediate skin reactivity to ascaris antigen, persistent and severe asthmatic responses to ascaris antigen, high IgG antibody levels to ascaris antigen but all of the latter findings were also present in asthmatic monkeys without dermatitis. Cutaneous biopsies of lesions were nonspecific but provided no evidence for other explanations for the dermatitis which appears to be an analogue of human atopic dermatitis.

Adrenal Cortex Hormones↗