Narrowband ultraviolet B treatment improves vitamin D balance and alters antimicrobial peptide expression in skin lesions of psoriasis and atopic dermatitis

Background Narrowband ultraviolet B (NB‐UVB) is a routine treatment for psoriasis and atopic dermatitis (AD) but its effect on vitamin D balance is not well studied. Objectives To examine whether NB‐UVB treatment in winter improves vitamin D balance in psoriasis and AD, and to study the effects of NB‐UVB on antimicrobial peptide and cytokine expression in the skin. Methods Eighteen adult patients with psoriasis, 18 with AD and 15 healthy subjects received a total of 15 NB‐UVB exposures on the whole body, given three times a week. Serum calcidiol (25‐hydroxyvitamin D) was measured by radioimmunoassay. Antimicrobial peptide and cytokine expression in skin lesions was examined by real‐time quantitative polymerase chain reaction. Results At onset 16 (89%) patients with psoriasis, 17 (94%) patients with AD and eight (53%) healthy subjects had vitamin D insufficiency (calcidiol < 50 nmol L^?1). NB‐UVB treatment significantly increased (P < 0·001) serum calcidiol. The increase was 59·9 nmol L^?1 (95% confidence interval, CI 53·5–66·9) in psoriasis, 68·2 nmol L^?1 (95% CI 55·4–80·1) in AD and 90·7 nmol L^?1 (95% CI 63·8–123·4) in healthy subjects. Psoriasis Area and Severity Index and SCORAD improved significantly (P < 0·001) but no correlation to the increase of serum calcidiol was found. Cathelicidin and human β‐defensin 2 (HBD2) expression was high in skin lesions of psoriasis. After six NB‐UVB treatments cathelicidin increased further while HBD2 expression decreased. A similar trend was observed in AD lesions. NB‐UVB caused a marked but nonsignificant decrease of interleukin (IL)‐1β and IL‐17 in psoriasis lesions. Conclusions The present study shows that in addition to a significant improvement of psoriasis and AD, NB‐UVB treatment effectively corrects vitamin D insufficiency. It also increases cathelicidin and decreases HBD2 levels in healing skin lesions of psoriasis and AD. This effect might be mediated by improved vitamin D balance and the local cytokine network.     

Microanalysis of an antimicrobial peptide, beta-defensin-2, in the stratum corneum from patients with atopic dermatitis

Background  Antimicrobial peptides, such as defensin and cathelicidin, have recently been reported to play important roles in host defence and in cutaneous innate immunity. Although β-defensin-2 has been reported to be downregulated in the skin of patients with atopic dermatitis (AD), little is known about its role in the colonization of Staphylococcus aureus in the stratum corneum of patients with AD. A precise evaluation of these peptides in the stratum corneum as an antimicrobial barrier against S. aureus colonization has not yet been performed.
Objectives  To compare β-defensin-2 levels in the skin of patients with AD and healthy controls.
Methods  We developed a microanalytical technique to measure β-defensin-2 in the stratum corneum using a combination of immunoprecipitation and Western blotting.
Results  β-Defensin-2 in the stratum corneum was significantly higher in AD lesional skin compared with healthy control skin. The β-defensin-2 content in AD lesional skin also increased in proportion to the severity of the disease. Counting bacterial colonies revealed higher populations of S. aureus on lesional and nonlesional skin surfaces of patients with AD compared with healthy controls. Comparison of S. aureus colony numbers and β-defensin-2 levels demonstrated a positive correlation ( r  =   0·342, P  =   0·004, n  =   67) between both factors.
Conclusions  Collectively, these findings suggest that β-defensin-2 is induced in response to bacteria, injury or inflammatory stimuli and is not associated with vulnerability to S. aureus colonization in the skin of patients with AD.     

Structural and functional alterations in the beta2-adrenoceptor are caused by a point mutation in patients with atopic eczema

The density of beta2-adrenoceptors is significantly decreased in both keratinocytes and peripheral blood lymphocytes from patients with atopic eczema. Furthermore both cell types showed a sixfold increase in the K(D) for the specific binding of the non-specific antagonists (-)-[(3)H]CGP 12177 and [(125) I]CYP to keratinocytes and lymphocytes respectively compared with healthy controls. Based on these results polymorphism in the beta2-adrenoceptor gene was suspected. Consequently the entire intronless beta2-adrenoceptor gene was isolated from whole blood and by RT-PCR from keratinocyte extracts of nine patients with atopic eczema and four healthy controls. DNA sequence analysis of nine atopic eczema patients confirmed a substitution in codon (1618) GCC (Ala(119)) to GAC (Asp(119)). This point mutation is expressed on the third transmembrane helix only 13A away from the established agonist/antagonist binding site at Asp(113). Computer modelling of this third transmembrane helix revealed substantial structural changes in the mutant compared with the wild type. Epidermal keratinocytes were established from one patient with atopic eczema (homozygote), the mother (heterozygote) and one age-matched healthy control. Cells were grown in media containing different concentrations of l-phenylalanine and receptor densities were determined. The results showed that cells with atopic eczema showed an increased sensitivity to l-phenylalanine concentrations with a narrow homeostasis compared with healthy controls. The heterozygous mother was only 50% as sensitive as the child. In summary, the results indicate that atopic eczema is associated with a single point mutation in the beta2-adrenoceptor gene leading to an impaired adrenergic response in the epidermis of these patients.     

Changes in collagen I and collagen III metabolism in patients with generalized atopic eczema undergoing medium-dose ultraviolet A1 phototherapy

Fourteen patients suffering from acute, exacerbated atopic eczema were screened for changes in collagen I and collagen III metabolism in serum (n = 11), urine (n = 11) and skin biopsies (n = 9) before and after medium-dose ultraviolet (UV) A1 phototherapy (15 exposures of 50 J/cm2 over a 3-week period, total dose 750 J/cm2). Mature collagen I and, to a lesser extent, mature collagen III were found to be decreased after the therapy in skin samples from the irradiated patients. As markers of collagen I degradation, the cross-links pyridoline and deoxypyridoline were analysed in urine using high-performance liquid chromatography. Both cross-links were found to be mildly increased after UVA1 phototherapy, without reaching statistical significance. As markers of de novo collagen synthesis we screened for the procollagen I-carboxyterminal peptide (PICP) and procollagen III-aminoterminal peptide (PIIINP) levels in serum and skin. The ratio of PICP to PIIINP in serum dropped significantly after the UVA1 phototherapy, suggesting a different impact of UVA1 on the two collagens. These findings were paralleled by a diminished ratio of PICP to PIIINP in tissue samples. Staining for matrix metalloproteinase 1 (MMP-1) and its specific counterpart, tissue inhibitor of MMP-1 (TIMP-1), showed slight increases for both proteins by therapeutic UVA1; this was also seen in serum for TIMP-1 but not MMP-1. In our study, high-energy UVA1 doses induced changes of the skin collagens in patients with atopic eczema which are measurable by their metabolites in serum and urine.     

Differential suppression of epidermal antimicrobial protein expression in atopic dermatitis and in EFAD mice by pimecrolimus compared to corticosteroids

It has been suggested that the increased rate of bacterial infection in atopic dermatitis (AD) may be caused by reduced antimicrobial protein (AMP) expression. We were interested whether common treatments in AD affect antimicrobial defense. We investigated the effects of topically applied corticosteroids betamethasone valerate (BV) and triamacinolone acetonide (TA) and those of the calcineurin inhibitor pimecrolimus for 3 weeks on AMP expression in AD. BV and TA treatment in AD led to a significant reduction in AMP expression; protein expression of human beta-defensins (hBD)-2 and hBD-3, psoriasin, RNase 7 and cathelicidin LL-37 was below the level in skin of healthy controls. After pimecrolimus treatment, AMP expression was also reduced but less compared to BV and TA; the expression levels of hBD-2, psoriasin and RNase 7 still remained above the control levels. In essential fatty acid-deficient (EFAD) mice, a model of chronic skin barrier disease with inflammation, expression of the mouse beta-defensins mBD-1, mBD-3 and mBD-14 (orthologues for hBD-1, hBD-2 and hBD-3, respectively), was reduced by both treatments, again more pronounced by BV compared to pimecrolimus. In summary, we found that treatment for AD with corticosteroids in human skin and EFAD mice caused a strong reduction in AMPs; reduction was less with pimecrolimus. This result may explain the clinical observation that prolonged treatment with topical corticosteroids sometimes leads to bacterial infection.     

Treatment of atopic eczema with oral mycophenolate mofetil

BACKGROUND: Activated T and B lymphocytes are the predominant inflammatory cells in atopic eczema (AE) lesions. Mycophenolic acid, the active form of mycophenolate mofetil (MMF), blocks the proliferative responses of T and B lymphocytes. OBJECTIVES: In this pilot study, we examined the efficacy of MMF (CellCept(R), Hoffman La Roche, Grenzach-Wyhlen, Germany) in severe AE. METHODS: Ten patients with severe AE (severity index > 50) according to the Severity Scoring of Atopic Dermatitis (SCORAD) index were treated with oral MMF at an initial dose of 1 g daily during the first week and 2 g daily for a further 11 weeks. Laboratory examination including full blood count, lymphocyte subset analysis, serum immunoglobulins (IgE, IgG, IgM, IgA), total bilirubin, alkaline phosphatase, aminotransferases, lactate dehydrogenase and creatinine was performed every 2 weeks. Additionally, interleukin (IL)-10 and interferon (IFN)-gamma in serum were measured. RESULTS: None of the 10 patients who received MMF discontinued the trial because of lack of efficacy or adverse events. Compared with the baseline, the median scores for disease severity (SCORAD index) improved by 68% during treatment with MMF. The median serum IgE level decreased significantly, from 10,300 kU L-1 before treatment to 7830 kU L-1 after 12 weeks. MMF induced a significant increase in the T-helper (Th)-1-related cytokine IFN-gamma and a significant decrease in IL-10, mainly produced by Th2 cells. CONCLUSIONS: The present study demonstrates that oral MMF at a dose of 2 g daily is an effective, safe and well-tolerated immunosuppressive therapy for severe AE in adults.     

A comparison between criteria for diagnosing atopic eczema in infants

BACKGROUND: Epidemiological studies have shown different estimates of the frequency of atopic eczema (AE) in children. This may be explained by several factors including variations in the definition of AE, study design, age of study group, and the possibility of a changed perception of atopic diseases. The role of IgE sensitization in AE is a matter of debate. OBJECTIVES: To determine the prevalence and cumulative incidence of AE in a group of unselected infants followed prospectively from birth to 18 months of age using different diagnostic criteria; to evaluate the agreement between criteria; and to describe the association between atopic heredity and postnatal sensitization, respectively, and the development of AE according to the different diagnostic criteria. METHODS: During a 1-year period a consecutive series of 1095 newborns and their parents were approached at the maternity ward at the Odense University Hospital, Denmark and a cohort of 562 newborns was established. Infants were examined and followed prospectively from birth and at 3, 6, 9, 12 and 18 months of age. AE was diagnosed using four different criteria, the Hanifin and Rajka criteria, the Schultz-Larsen criteria, the Danish Allergy Research Centre (DARC) criteria developed for this study and doctor-diagnosed visible eczema with typical morphology and atopic distribution. Additionally, the U.K. diagnostic criteria based on a questionnaire were used at 1 year of age. Agreement between the four criteria was analysed at each time point and over time, and agreement between the four criteria and the U.K. questionnaire criteria was analysed. RESULTS: The cumulative 1-year prevalence of AE using the Hanifin and Rajka criteria was 9.8% (95% confidence interval, CI 7-13%), for the Schultz-Larsen criteria it was 7.5% (95% CI 5-10%), for the DARC criteria 8.2% (95% CI 6-11%), for visible eczema 12.2% (95% CI 9-16%) and for the U.K. criteria 7.5% (95% CI 5-10%). The pairwise agreement between criteria showed good agreement, with rates varying between 93% and 97% and kappa scores between 0.6 and 0.8. Agreement analysis of diagnoses between the four criteria demonstrated that cumulative incidences showed better agreement than point prevalence values. CONCLUSIONS: Agreement between different criteria for diagnosing AE was acceptable, but the mild cases constituted a diagnostic problem, although they were in the minority. Repeated examinations gave better agreement between diagnostic criteria than just one examination. Atopic heredity was less predictive for AE than sensitization to common food and inhalant allergens in early childhood.     

Factors influencing the occurrence of hand eczema in adults with a history of atopic dermatitis in childhood

A series of 955 persons aged 24-44 years, with atopic dermatitis in childhood, were interviewed in order to identify factors which increase the risk of developing hand eczema in adult life, or aggravate already existing hand eczema. Endogenous (constitutional) factors were in general of greater importance than exogenous factors, viz. chemicals, water, soil and wear (friction). Eczematous involvement of the hands in childhood was of predominant importance. In individuals without such involvement, severe (widespread) dermatitis in childhood was a dominant factor. Other factors, each of them significantly more important than the exogenous ones, were persistent eczema on other parts of the body and dry/itchy skin. The factors female sex, family history of atopic dermatitis and simultaneous bronchial asthma/allergic rhinitis were associated with increased risk of developing hand eczema in adult life, but were of limited importance compared with the other endogenous and the exogenous factors.     

Doxepin affects acetylcholine induced cutaneous reactions in atopic eczema

BACKGROUND: Atopic eczema (AE) is a chronic inflammatory skin disease with strong itching as the prominent symptom. The pathology of itch is still in discussion, but acetylcholine (ACH) seems to be a relevant pruritogenic mediator in AE. Since efficient benefit on pruritus and excoriations has been demonstrated with tricyclic agents, we investigated how the topical treatment with doxepin (5%, Boehringer Standard, Mannheim, Germany), a tricyclic compound with anticholinergic properties, may influence ACH induced itch and cutaneous sensations (erythema, wheal, axonreflex flare). METHODS: Eleven patients with AE were included in this double blind study. For 3 days we applied doxepin cream to a defined area on the volar forearm and basic ointment to the other side 4 times daily. On day 4, ACH and sodium chloride were i.c. injected into the pretreated arms. Vasoreactions and cutaneous sensations were measured similar to studies described in previous publications from our group. RESULTS: Doxepin treatment over 3 days reduced ACH provoked flare size more than 53% (P<0.005) and wheal size about 48% (P<0.005) whereas the maximal antipruritic effect was similiar to the basic therapy. The itch intensity, which is expressed as the mean AUC value, was rated at 6.12 arbitrary units after the neutral cream application and 5.9 arbitrary units after doxepin. CONCLUSIONS: The clinical and experimental effectiveness of doxepin as an antipruritic drug has been known for years. However, studies focusing on ACH as a pruritogenic mediator have not been performed. The duration of the doxepin application in our study seems to be appropriate since flare and wheal development were diminished. The reason why doxepin did not develop more antipruritic action compared to the vehicle cream may be due to the fact that the doxepin free cream already possessed an antipruritic action in this experimental study design. This is probably caused by rehydrating and moisturizing effects.     

Efficacy of naltrexone on acetylcholine-induced alloknesis in atopic eczema

Atopic eczema (AE) is a chronically pruritic inflammatory skin disease. Although the mediators and exact mechanisms eliciting and sustaining pruritus are not completely known, AE patients in clinical trials have been shown to benefit under treatment with morphine antagonists. Naltrexone (NAL) is a relatively pure morphine antagonist that blocks the effects of opioids twice as much as naloxone. NAL exhibits minimal pharmacological activity and displaces endorphines at mu- and kappa-receptors without its own intrinsic activity. NAL's excellent oral bioavailability and linear increases in the area under plasma concentration-time curve make it ideal for use in experimental studies. We designed our present experiments similar to former experiments evaluating both peripheral cutaneous sensations and central itch procession in order to gain more information about the possible distribution of opioid receptors and their involvement in the pathophysiology of pruritus. Eleven AE patients participated in our double-blind study. Either 25 mg of NAL (Nemexin) or a placebo (PLA) was given to the participants 60 min prior to the acetylcholine (ACH) injection [intracutaneous (i.c.) injection of 0.02 ml of 0.55 M]. A PLA stimulus with buffered saline served as control on the opposite forearm. We used laser Doppler flowmetry to measure the vasomotoric changes after ACH injection and recorded the duration and intensity of itch with a visual analogue scale (VAS). Following the evaluation of wheal and flare sensation, we obtained the area of itchy skin around the injection site (alloknesis) by gently stroking the surrounding skin with a brush in the centripetal direction towards the injection site. The results were planimetrically evaluated. Oral NAL reduced the perifocal itch significantly (P < 0.009). In four of our observations the area of alloknesis completely disappeared. Itch duration was reduced by 20 s and the intensity of itch was diminished, yet not significantly. NAL had no significant effects on cholinergic vasoreactions measured by the laser Doppler (P > 0.50) and especially failed to decrease the initial flux response, which is a typical sign of an altered vascular reaction (P > 0.25). The decrease of wheal (P = 0.008) and flare (P = 0.01) extension indicates an appropriate dosage of our treatment for this experiment. The most significant effects of NAL were observed in parameters of itch processing such as alloknesis (P = 0.009) and flare extension (P = 0.01). Therefore we favour the concept that NAL might have a stronger impact on central nervous mechanisms than on peripheral nociceptive structures.     

An exploratory prospective observational study of environmental factors exacerbating atopic eczema in children

BACKGROUND: Possible exacerbating factors are a major concern of parents of children with atopic eczema (AE). However, there is minimal evidence for their direct role in leading to disease flares. OBJECTIVES: To assess the association between 'trigger factors' and disease flares in AE. METHODS: Twenty-five children with AE were recruited. Participants completed diaries, recording severity and exposure to potential exacerbating factors (18 variables) over 28 days. Severity was assessed at baseline and study completion. The relationship between severity and exposures was assessed. RESULTS: At episode level, on the day of exposure (lag 0), hot weather correlated to increased scratch scores (P=0.043). At a lag of 2 days after exposure, damp weather was associated with raised scratch scores (P=0.027). At lag 3 days, elevated scratch scores were associated with sweating and stress (P=0.029 and 0.019, respectively). Outside damp was associated with elevated scores (P=0.001) at lag 4. Multivariate analysis of all significant variables showed that only damp at lag 4 was significantly associated with flares (P=0.039). CONCLUSIONS: This study suggests association between stress, damp and heat and disease flares. These findings need to be studied over a longer period, using objective exposure measures.     

Administration of acetylcholine and vasoactive intestinal polypeptide to atopic eczema patients

Responses to acetylcholine (ACh) and vasoactive intestinal polypeptide (VIP) were investigated in atopic eczema (AE) patients. To elucidate the involvement of histamine to ACh-provoked vasoreactions and sensations, we applied a selective H1-antagonist (cetirizine) 3 h prior to the ACh-administration. Solutions of acetylcholine (ACh, 0.55 M) and vasoactive intestinal polypeptide (VIP, 1.5x 10(-5) M) were injected (10 microl) intracutaneously into the volar forearm of 14 healthy subjects and 14 atopic eczema (AE) patients. The substances were applied as single stimulus as well as in combination. Sensations evoked by the stimulation were recorded using 2 visual analog scales (VAS). Vasoreactions were analyzed with the new technique of computer assisted video image analysis. With this method we measured the dynamics of the flare development and the extension of the final flare size independent of the observer's assessment. In control subjects the development and extension of the final flare size was almost similar, regardless whether ACh and VIP were applied in combination or separately. Compared to healthy controls, after injection of ACh, VIP and the combination of VIP and ACh smaller flare sizes were recorded in AE patients. After VIP was given, the control subjects reported pruritus, which was significantly augmented compared to AE patients. In contrast, controls reported a burning pain after the injection of ACh, whereas AE patients felt predominantly pruritus. Itch sensation after the combined application of VIP and ACh was significantly elevated in AE patients. Consequently, we assume that mediators of sudomotor neurons, i.e., VIP and ACh meet in AE patients apparently sensitized nociceptive primary afferents and induce exaggerated itch, pain and flare responses. When pretreated with the selective H1-antagonist cetirizine before ACh was injected, pain and erythema due to ACh was diminished in healthy controls. In contrast, cetirizine did not influence the size of erythema and the magnitude of sensation in AE patients. We conclude, that the release of histamine is not involved in ACh-induced erythema and pruritus in AE. These data provide evidence that pruritus can be elicited in atopic eczema by a cholinergic, histamine independent mechanism.     

Bath psoralen-ultraviolet A therapy in atopic eczema

AIMS: To evaluate the efficacy of bath psoralen-ultraviolet A (PUVA) therapy in severe cases of atopic dermatitis (AD) in adults using the extended Six Area, Six Sign Atopic Dermatitis (SASSAD) score. METHODS: Thirty-five adult subjects with severe AD underwent bath PUVA therapy for a maximum of 30 sessions ranging from one to three times a week. The only other treatment allowed during the study was topical application of hydrocortisone. RESULTS: There were a total of six drop-outs, three due to aggravation of symptoms. After the maximum 30 sessions the remaining 29 subjects showed 82.1% improvement in the severity of lesions, 75.2% reduction in extension of lesions, 74% improvement in itching and 79% improvement in night-time rest. Patient evaluations gave an overall score of 8.8 on a scale of 0-10.     

Efficacy of oral naltrexone on pruritus in atopic eczema: a double-blind, placebo-controlled study

Aim  The intent of our study was to determine the efficacy of oral naltrexone, an opiod antagonist, in the treatment of pruritus in patients with chronic eczema.
Methods  This double-blind, placebo-controlled study recruited 38 patients with eczema complaining from pruritus. Pruritus scores were evaluated. Patients were given placebo ( n  = 20) or naltrexone 50 mg ( n  = 18) for 2 weeks period. During the study, pruritus scores based on visual analogue scale system (VAS) were assessed three times: at the start of study, after 1 week, and after 2 weeks.
Results  In both groups, decreased VAS scores were observed, but naltrexone showed to be significantly more effective than placebo in decreasing VAS score after 1 week ( P <  0.005) and 2 weeks ( P <  0.001).
Conclusion  Naltrexone is more effective than placebo in the treatment of pruritus in patient with eczema. Naltrexone might be considered as an adjunct treatment in the treatment of pruritus. However, further studies in this aspect are highly fostered.

Conflicts of interest

This study and the authors were not supported by any company with a vested interest in the product being studied and the project was funded by Skin Research Center.     

Assessment of atopic eczema: clinical scoring and noninvasive measurements

BACKGROUND: Clinical scoring systems are widely used in clinical trials of atopic eczema (AE), while noninvasive methods are more often used for research purposes. Positive correlations between the two types of methods may be used in support of the validity of both in a clinical context. Few studies are available of the association between clinical scores and instrumental assessment of disease severity obtained with noninvasive instruments. OBJECTIVES: To compare clinical scores in AE with biometric data in AE. METHODS: Transepidermal water loss, stratum corneum hydration, erythema, scaling and subepidermal oedema were measured. 'Scoring of Atopic Dermatitis (SCORAD)', 'Eczema Area and Severity Index (EASI)' and 'Atopic Dermatitis Severity Index (ADSI)' were used for clinical scores. Two assessments at 6-month intervals at the antecubital fossa, dorsal forearm and popliteal fossa in 101 patients with AE and 30 controls were carried out. RESULTS: Significant correlations were found within the clinical scores (P < 0.0001 and r = 0.85-0.91) and between instruments and clinical scores (P < 0.0001 and r = 0.61-0.79). CONCLUSIONS: The various instruments and clinical scores showed internal agreement and noninvasive methods correlated significantly with the three different clinical scorings systems. This observation suggests that both methods provide data of clinical (scores) and biological (instrumental measures) relevance, and may be useful in future studies of AE. It is speculated that combined measures including scores and selected instruments may be particularly useful.     

Medium-dose ultraviolet (UV) A1 vs. narrowband UVB phototherapy in atopic eczema: a randomized crossover study

Background Ultraviolet (UV) A1 and narrowband (NB)‐UVB have been reported to be effective treatments for atopic eczema (AE). Objectives We aimed to compare the efficacy of medium‐dose UVA1 and NB‐UVB mono‐phototherapy in patients with AE. Methods A randomized double‐blind controlled crossover trial (ClinicalTrials.gov Identifier: NCT00419406) was conducted in which patients with AE received a 6‐week course of both medium‐dose UVA1 and NB‐UVB. Clinical efficacy was assessed using the Six Area, Six Sign, Atopic Dermatitis (SASSAD) score and a visual analogue scale for pruritus. Assessment of health‐related quality of life was performed using the Skindex‐29. Total immunoglobulin E (IgE) and eosinophilic cationic protein (ECP) were evaluated at baseline and after each phototherapy course. Results Twenty‐eight patients who completed both UVA1 and NB‐UVB phototherapy courses on an intention‐to‐treat basis were analysed according to the crossover design. Both interventions were associated with significant clinical improvement but there was no significant difference between treatments with respect to the mean ± SD relative reduction (RR) of the clinical scores (SASSAD, 43·7 ± 31·4% vs. 39·4 ± 24·1%, P = 0·5; pruritus score, 16 ± 61·8% vs. 25·2 ± 30·5%, P = 0·5, respectively). There was no significant difference in the mean ± SD RR of the Skindex‐29 after UVA1 and NB‐UVB phototherapy (12·7 ± 18·8% vs. 16·5 ± 17·6%, P = 0·1). Changes in the total IgE and ECP levels following UVA1 and NB‐UVB did not differ significantly (P = 0·3 and P = 0·9, respectively). Conclusions A 6‐week course of NB‐UVB and UVA1 phototherapy of AE resulted in significant clinical improvement. With regard to efficacy and tolerability, both phototherapeutic modalities may be considered comparably good.