Ulcerated Infantile Hemangioma: Novel Treatment with Topical Brimonidine‐Timolol

We report a 2‐month‐old boy with a painful ulcerated hemangioma on the lower mucosal lip extending to the vermillion border that caused feeding difficulty. It was successfully treated with topical brimonidine 0.2% and timolol 0.5%, a combination selective α₂‐adrenergic agonist and nonselective β‐blocker. After 6 weeks of treatment, the lesion reepithelialized and the patient's symptoms and functional complications resolved. Brimonidine 0.2% timolol 0.5% ophthalmic solution is an emerging alternative treatment for hemangiomas, offering the potential to target hemangioma growth through two synergistic mechanisms (β‐inhibition and α₂‐agonism) that may be especially effective for ulcerated lesions, the most common complication of infantile hemangiomas.     

α1‐AR agonist induced piloerection protects against the development of traction alopecia

Traction alopecia is hair loss that occurs after persistent pulling (e.g., during cosmetic procedures) on the roots of hair over time. Unlike plucking, which is painful, persistent pulling may go unnoticed until a patient presents with either bald spots or diffuse telogen shedding. Each hair follicle in the scalp contains an arrector pili muscle that, when contracted, erects the hair. The smooth muscle in the arrector pili expresses α₁ adrenergic receptors (α₁‐AR). As such, we hypothesized that contraction of the arrector pili muscle via an α₁‐AR agonist would increase the threshold of force required to pluck hair during cosmetic procedures. Female subjects, ages 18–40, were recruited to study the effect of topically applied phenylephrine, a selective α₁‐AR agonist, on epilation force and hair shedding during cosmetic procedures. In our blinded study, 80% of subjects demonstrated reduced shedding on days using phenylephrine compared to days using a placebo solution. The average reduction in hair loss was approximately 42%. In addition, the force threshold required for epilation increased by approximately 172% following topical phenylephrine application. To our knowledge this is the first study demonstrating the utility of α₁‐AR agonists in the treatment of traction alopecia and hair shedding during cosmetic procedures.     

Inhibition of mast cell infiltration in an LL‐37‐induced rosacea mouse model using topical brimonidine tartrate 0.33% gel

Brimonidine is a highly selective α2‐adrenergic receptor agonist approved by the FDA for the treatment of rosacea. Rosacea is a major clinical disease with vasodilatation and rash on the centre of the face, and that brimonidine as a vasoconstrictor can act as a remedy for rosacea. However, there is no study of how brimonidine has an effect on rosacea‐related immune cells or mechanisms in the skin to improve rosacea. In this study, we observed that clinical features of rosacea induced by LL‐37 in Balb/c mice were improved after the application of brimonidine gel, and we also showed a marked decrease in the number of inflammatory cells, especially mast cells (MCs) histologically. Furthermore, we confirmed that mRNA levels of MC enzymes increased by LL‐37 were reduced by brimonidine gel. To our knowledge, we first found that brimonidine has a mechanism of treating rosacea by reducing the number and mRNA levels of MC‐specific enzymes, an important immune cell in the pathogenesis of rosacea.     

Innervation and receptor profiles of the human apocrine (epitrichial) sweat gland: routes for intervention in bromhidrosis

Background Human apocrine (epitrichial) sweat glands secrete in response to local or systemic administration of catecholamines and cholinergic agonists. As the process of secretion in human apocrine glands is not fully understood and no literature detailing the expression of adrenergic, cholinergic and purinergic receptors is available, there is a need to know the receptor types. Such data could provide new approaches for the treatment of axillary bromhidrosis. Objectives To investigate the localization of nerve fibres, adrenergic, cholinergic and purinergic receptors in human axillary apocrine sweat glands by immunohistochemistry. Methods Human axillary apocrine sweat glands were investigated by serial sectioning of paraffin wax‐embedded skin samples from volunteers. Sections were examined by light microscopy and immunohistochemistry, using antibodies against neurofilament, α‐ and β‐adrenoceptors, P2Y₁, P2Y₂ and P2Y₄ purinoceptors, and M₃ cholinoceptors. Results Neurofilaments were found near the eccrine but not the apocrine gland. Apocrine glands demonstrated the presence of β‐2 and β‐3 adrenoceptors in the secretory coil of the gland, but not α‐1, β‐1 or M₃ receptors. Glandular purinergic staining (P2Y₁, P2Y₂ and P2Y₄) was found in what looked like myoepithelial cells, while P2Y₁ and P2Y₂ staining was found on apical membranes and diffusely throughout secretory cells. Eccrine gland staining acted as internal positive controls. Conclusions No nerve fibres were found near the apocrine gland, suggesting that any catecholamine influence is through humoral effects and that glands could be influenced by β‐adrenoceptor subtypes and purinoceptors. Blockage of both these types of receptors offers a route to controlling apocrine secretion from axillary glands and reducing the opportunity for the development of bromhidrosis.     

Ultraviolet B irradiation of the mouse eye induces pigmentation of the skin more strongly than does stress loading,by increasing the levels of prohormone convertase 2 and α‐melanocyte‐stimulating hormone

Background. In previous studies, we made the unexpected finding that in mice, ultraviolet (UV)B irradiation of the eye increased the concentration of α‐melanocyte‐stimulating hormone (α‐MSH) in plasma, and systemically stimulated epidermal melanocytes. Aims. To compare the extent of the pigmentation induced by social and restraint stress (which activate the hippocampus–pituitary system) with that induced by UVB irradiation. Methods. DBA/2 and sham‐operated or hypophysectomized DBA/2 mice were subjected to local UVB exposure using a sunlamp directed at the eye, and two types of stress (social and restraint) were imposed. Results. UVB irradiation of the eye or exposure to stress loading both increased the number of Dopa‐positive melanocytes in the epidermis, and hypophysectomy strongly inhibited the UVB‐induced and stress‐induced stimulation of melanocytes. Irradiation of the eye caused a much greater increase in dopamine than did the stress load. Both UVB eye irradiation and stress increased the blood levels of α‐MSH and adrenocorticotropic hormone (ACTH). In addition, the increase in plasma α‐MSH was greater in animals subjected to UVB eye irradiation than in those subjected to stress loading, whereas the reverse occurred for plasma ACTH. UVB irradiation to the eye and stress loading increased the expression of prohormone convertase (PC)1/3 and PC2 in the pituitary gland. The increase in expression of pituitary PC2 was greater in animals subjected to UVB eye irradiation than to stress, whereas no difference was seen between the two groups for the increase in PC1/3. Conclusions. UVB eye irradiation exerts a stronger effect on pigmentation than stress loading, and is related to increased levels of α‐MSH and PC2.     

Toll‐like receptor 2 mediates a cutaneous reaction induced by repetitive ultraviolet B irradiation in C57/BL6 mice in vivo

Toll‐like receptors (TLRs) mediate not only innate immunity against infection and but also sterile inflammation triggered by endogenous molecules. We conducted a comparative study of the different inflammatory responses induced by repetitive ultraviolet (UV) B irradiation in wild‐type (WT) and TLR2 knockout (KO) mice, to provide in vivo evidence of the role of TLRs in mediating UVB‐induced responses. UVB‐induced inflammatory responses were less severe in TLR2 KO mice than in WT mice after 6 weeks of repeated UVB irradiation. UVB‐treated TLR2 KO mice displayed less prominent erythema and scaling, and histopathology showed significantly thinner skin and less inflammatory cell infiltration than that in WT mice. UVB‐induced expression of heat‐shock protein 70 (an endogenous ligand of TLR2) was lower in TLR2 KO mice. Quantitative RT‐PCR revealed significantly lower gene expression levels of UVB‐induced interleukin (IL)‐1β, IL‐6 and matrix metalloproteinase (MMP)‐13 in TLR2 KO mice. TLR2 KO mice also showed significantly lower protein level expression of UVB‐induced IL‐1β in ELISA and MMP‐13 in Western blots. Our study demonstrated that TLR2 was associated with inflammatory responses to repetitive UVB irradiation in C57/BL6 mice. Moreover, it suggests that the role of TLR2 in the cutaneous response of UV irradiation and in developing new agents for modulating the effects of UV irradiation should be considered.     

Tropisetron via α7 nicotinic acetylcholine receptor suppresses tumor necrosis factor‐α‐mediated cell responses of human keratinocytes

Tropisetron is a serotonin receptor (5‐HT‐R)‐modulating agent and approved as an antiemetic for patients undergoing chemotherapy. In the gut, it acts via specific serotonin receptors, 5‐HT₃‐R, to elicit its beneficial effects against nausea. We investigated whether tropisetron can affect inflammatory cell responses of human primary epidermal keratinocytes (NHK) which are key cells in the regulation of skin homoeostasis. Tropisetron significantly and dose‐dependently suppressed tumor necrosis factor (TNF)‐α‐mediated mRNA expression and protein secretion of interleukin (IL)‐6 and IL‐8 in these cells. This effect of tropisetron was independent of p65/NF‐κB as shown by various NF‐κB signal transduction read‐outs. Importantly, the anti‐inflammatory tropisetron effect on NHK was neither mediated by 5‐HT₃‐R nor 5‐HT₄‐R since these receptors were absent in NHK. In contrast, NHK expressed α7 nicotinic acetylcholine receptors (α7nAchR) which previously were found to bind tropisetron. The α7nAchR antagonist α‐bungarotoxin neutralized, whereas AR‐R17779, a specific α7nAchR agonist, mimicked the suppressive effect of tropisetron on TNF‐α‐mediated IL‐6 and IL‐8 expression in NHK. Our findings suggest that tropisetron and probably other α7nAchR‐activating agents could be useful for the future therapy of inflammatory skin diseases.     

Die Anwendung des Excimerlasers 308 nm zur Psoriasis‐Behandlung

Background and Objective: Standard phototherapy for psoriasis (311 nm UVB or photochemotherapy) exposes the non‐affected skin to potentially damaging irradiation. The use of 308 nm XeCl excimer laser allows the selective irradiation of psoriatic lesions. We evaluated its therapeutic effectiveness. Patients/Methods: 28 patients with plaque stage psoriasis were involved in the study, 26 of them could be evaluated. In each patient a single plaque was chosen and then exposed to the laser irradiation thrice weekly. The initial dose was twice the MED (minimal erythema dose); the dosage was increased by one MED every second treatment. The usual dosages were 2 – 5 MED, while the cumulative UVB dosage was 3.6 – 15.2 J/cm². 17 Patients were treated 6 times, while 11 were treated 10 times. The Psoriasis Severity Index (PSI) was calculated for the individual plaque in order to assess the effectiveness of the therapy. The patients were followed regularly for 3 months following treatment, and then checked again at 1 year. Results: Most patients showed clear improvement. In 90 % the PSI at the end of treatment was reduced by at least 50 %; in 72 % it was only 33 % of the pre‐treatment value. The results between the patients receiving 6 and 10 treatments were similar. In 6 patients, the psoriatic lesion was still absent after 1 year, while in an additional 7, there had been long term improvement. The most common side effects were erythema and pruritus (100 %), blisters (35 %) and post‐inflammatory hyperpigmentation (80 %). Conclusion: The use of the 308 nm excimer laser is effective for chronic localized psoriasis and may lead to long‐lasting remissions.     

Comparing performance of Chromameter®, Mexameter® and full‐field laser perfusion imaging for measurement of ultraviolet B light‐induced erythema

Erythema induced by ultraviolet (UV)B light is a common skin reaction. Currently, three techniques, the Chromameter^® CR‐400, the Mexameter^® MX16 and full‐field laser perfusion imaging (FLPI), are widely used for dermatological evaluation of UVB‐induced erythema. However, there is little known about the comparative performance of these three techniques. This study was therefore designed to evaluate the effectiveness of the three techniques. Our findings showed that the performance of Chromameter and Mexameter for measurement of UVB‐induced erythema was very similar, while FLPI indicated acute erythema at D1 with the greatest fold change. Further studies of UVB dose‐dependence need to be carried out.     

Prostaglandin D2 production in FM55 melanoma cells is regulated by α‐melanocyte‐stimulating hormone and is not related to melanin production

Please cite this paper as: Prostaglandin D₂ production in FM55 melanoma cells is regulated by α‐melanocyte‐stimulating hormone and is not related to melanin production. Experimental Dermatology 2010; 19 : 751–753. Abstract: This study shows that prostaglandins in human FM55 melanoma cells and epidermal melanocytes are produced by COX‐1. Prostaglandin production in FM55 melanoma cells was unrelated to that of melanin suggesting that the two processes can occur independently. α‐Melanocyte‐stimulating hormone, which had no effect on melanin production in FM55 cells, stimulated PGD₂ production in these cells without affecting PGE₂. While cAMP pathways may be involved in regulating PGD₂ production, our results suggest that α‐MSH acts independently of cAMP, possibly by regulating the activity of lipocalin‐type PGD synthase. This α‐MSH‐mediated effect may be associated with its role as an immune modulator.     

Loss of INK4a/Arf gene enhances ultraviolet radiation‐induced cutaneous tumor development

The CDKN2A locus encodes for tumor suppressor genes p16^INK4a and p14^Arf which are frequently inactivated in human skin tumors. The purpose of this study was to determine the relationship between loss of INK4a/Arf activity and inflammation in the development of ultraviolet (UV) radiation‐induced skin tumors. Panels of INK4a/Arf^‐/? mice and wild‐type (WT) mice were treated with a single dose of UVB (200 mJ/cm²). For long‐term studies, these mice were irradiated with UVB (200 mJ/cm²) three times weekly for 30 weeks. At the end of the experiment, tissues were harvested from mice and assayed for inflammatory biomarkers and cytokines. A single dose of UVB resulted in a significant increase in reactive oxygen species (ROS) and 8‐dihydroxyguanosine (8‐oxo‐dG) lesions in INK4a/Arf^?/? mice compared to WT mice. When subjected to chronic UVB, we found that 100% of INK4a/Arf^?/‐ mice had tumors, whereas there were no tumors in WT controls after 24 weeks of UVB exposure. The increase in tumor development correlated with a significant increase in nuclear factor (NF)‐κB, cyclooxygenase‐2 (COX‐2), prostaglandin E₂ (PGE₂) and its receptors both in UVB‐exposed skin and in the tumors. A significant increase was seen in inflammatory cytokines in skin samples of INK4a/Arf^‐/‐ mice following treatment with chronic UVB radiation. Furthermore, significantly more CD11b⁺Gr1⁺ myeloid cells were present in UVB‐exposed INK4a/Arf^‐/‐ mice compared to WT mice. Our data indicate that by targeting UVB‐induced inflammation, it may be possible to prevent UVB‐induced skin tumors in individuals that carry CDKN2A mutation.     

Integrin αE(CD103) is induced but plays no pathogenic role in psoriasiform skin lesions of TGFβ1 transgenic mice

T‐cells expressing α_E(CD103), an integrin induced by TGFβ on T‐cells in vitro, accumulate within epithelia in inflammatory disorders, including psoriasis. However, it is unclear, if and how α_E(CD103) contributes to skin inflammation. Using two complementary approaches, we have investigated α_E(CD103) in psoriasis‐like skin inflammation of mice with transgenic epidermal expression of human TGFβ1: α_E(CD103) was inhibited by function‐blocking antibodies in vivo, and double‐mutants with additional α_E(CD103)‐depletion were generated in two different genetic backgrounds. Epidermal hTGFβ1 expression was associated with prominent expression of α_E(CD103) on infiltrating cells. However, neither treatment with α_E(CD103)‐blocking antibodies nor deficiency of α_E(CD103) in double‐mutant mice altered the psoriasis‐like phenotype. In addition, histopathological and flow cytometric analyses revealed similar pathological skin alterations and lymphocyte subgroups in the different mouse strains. Thus, while α_E(CD103) expression is indeed associated with hTGFβ1 in vivo, it has little, if any, influence on the course of the psoriasis‐like phenotype in K5.hTGFβ1 transgenic mice.     

Photosensitivity of murine skin greatly depends on the genetic background: clinically relevant dose as a new measure to replace minimal erythema dose in mouse studies

Artificial UV irradiation of murine skin is a frequently used method for testing photosensitivity, study carcinogenesis and photoprotective effects of different compounds. However, doses of UV radiation and mouse strains used in experiments vary greatly. The genetic background of mice may influence the photosensitivity as melanin content, pigmentation and hair cycle parameters are dissimilar. Doses of UV are often expressed in relation to the minimal erythema dose (MED) that was not necessarily determined for the given strain. We set out to standardize the method of measuring photosensitivity in three commonly used mouse strains, C57BL/6N, Balb/c and SKH‐1. We found that MED may not be determined for some strains as erythema development in mice with diverse genotypes differs greatly. We measured the oedema response in vivo and ex vivo by using OCT. Given the strain‐specific variability of erythema, we introduced Clinically Relevant Dose (CRD) as a new term to replace MED in experiments, to describe the lowest dose that triggers a perceptible skin reaction in mice. Not only the CRD but the proportion of erythema and oedema were different in strains examined. C57BL/6N mice display skin reactions at the lowest UVB dose, while SKH‐1 hairless mice show changes, mostly oedema, after higher doses of UVB. The cellular composition and skin thickness were examined by histopathology. IL‐1beta and IL‐6 levels in skin correlated with the increasing doses of UVB. Despite the variations in the degree of erythema and oedema, no major differences in cytokine expressions were seen among various strains of mice.     

Styling without shedding: Novel topical formula reduces hair shedding by contracting the arrector pili muscle

Approximately 40% of women experience excessive hair shedding during styling (e.g., hair brushing). Previously, we demonstrated that topically applied phenylephrine, a potent α₁ adrenergic receptor agonist, can be used to contract the arrector pili muscle of the follicular unit; thus, increasing the force required to pluck hair and reducing shedding during brushing. While demonstrating efficacy, phenylephrine has several drawbacks when applied to the scalp, including the possibility cardiovascular events. We hypothesized that a high concentration of a weak α₁ agonist would allow for: (a) rapid penetration through the stratum corneum eliciting a quick response; (b) a low probability of cardiac adverse events owing to the low receptor binding affinity; and (c) an efficacy of the weak α₁ agonist similar to that of phenylephrine at the local site of application. Accordingly, we developed a novel topical solution, AB‐102, containing a high concentration of a weak α₁ agonist. Several studies were conducted to test the safety and efficacy of AB‐102. In a dose escalating safety study, utilizing a wearable holter monitor, we observed no cardiac or hemodynamic adverse events. In addition, in a controlled efficacy study, AB‐102 reduced the number of hairs shed during brushing by up to 77% (average of 38%).     

In vitro and in vivo evidence of tyrosinase inhibitory activity of a synthesized (Z)‐5‐(3‐hydroxy‐4‐methoxybenzylidene)‐2‐thioxothiazolidin‐4‐one (5‐HMT)

Tyrosinase is a key enzyme that catalyses the initial rate‐limiting steps of melanin synthesis. Due to its critical role in melanogenesis, various attempts were made to find potent tyrosinase inhibitors although many were not safe and effective in vivo. We evaluated tyrosinase inhibitory activity of six compounds. Among them, (Z)‐5‐(3‐hydroxy‐4‐methoxybenzylidene)‐2‐thioxothiazolidin‐4‐one (5‐HMT) had the greatest inhibitory effect and potency as the IC₅₀ value of 5‐HMT was lower than that of kojic acid, widely‐known tyrosinase inhibitor. Based on in silico docking simulation, 5‐HMT had a greater binding affinity than kojic acid with a different binding conformation in the tyrosinase catalytic site. Furthermore, its skin depigmentation effect was confirmed in vivo as 5‐HMT topical treatment significantly reduced UVB‐induced melanogenesis in HRM2 hairless mice. In conclusion, our study demonstrated that 5‐HMT has a greater binding affinity and inhibitory effect on tyrosinase and may be a potential candidate for a therapeutic agent for preventing melanogenesis.     

Skin pigmentation after NB‐UVB and three analogues of prostaglandin F2α in guinea pigs: a comparative study

Background Ultraviolet B (UVB) is a well‐known modality in increasing skin pigmentation through a variety of proposed mechanisms. Prostaglandin release is one of these mechanisms. Prostaglandin F_2α (PGF_2α) analogues, which are used to control ocular hypertension, were reported to induce periocular skin hyperpigmentation. Objectives This study aims to evaluate the local effect of three prostaglandin F_2α analogues, namely Latanoprost, Bimatoprost and Travoprost on skin pigmentation. Assessment of the role of combination with narrow band UVB (NB‐UVB) to each of these drugs is evaluated as well. Methods This study involved 18 female adult wild guinea pigs with patchy white and red/brown fur. The hair was shaved from four red/brown areas on the dorsal skin of each animal. In two areas of each animal, one of the above‐mentioned drugs was applied alone and in conjunction with NB‐UVB. In the other two areas, the vehicle was applied alone and in conjunction with NB‐UVB exposure. Skin biopsies from each area were done at the start of the study and 4 weeks after, and stained with haematoxylin and eosin (H&E) and Masson‐Fontana (MF) stains. Clinical and histopathological changes were evaluated. Results Increased pigmentation was found in all areas with PGF_2α analogues with and without NB‐UVB. However, the former group had more effect both clinically and histopathologically. Conclusion PGF_2α analogues are promising drugs in inducing skin pigmentation. This effect can be enhanced with NB‐UVB exposure.     

P38 and JNK signal pathways are involved in the regulation of phlorizin against UVB‐induced skin damage

Phlorizin is well known to inhibit sodium/glucose cotransporters in the kidney and intestine for the treatment of diabetes, obesity and stress hyperglycaemia. However, the effects of phlorizin against ultraviolet B (UVB) irradiation and its molecular mechanism are still unknown. We examined the effects of phlorizin on skin keratinocyte apoptosis, reactive oxygen species (ROS) production, pro‐inflammatory responses after UVB irradiation and the changes of some signal molecules by in vitro and in vivo assay. We observed that phlorizin pretreatments inhibited HaCaT cell apoptosis and overproduction of ROS induced by UVB. Phlorizin also decreased the expression of UVB‐induced pro‐inflammatory cytokines, such as interleukin‐1 beta (IL‐1β), interleukin‐6 (IL‐6) and interleukin‐8 (IL‐8) at the mRNA level. Topical application of phlorizin on UVB‐exposed skin of nude mice prevented the formation of scaly skin and erythema, inhibited the increase of epidermal thickness and reduced acute inflammation infiltration in skin. Additionally, PCR, Western blot and immunohistochemical data showed that phlorizin reversed the overexpression of cyclooxygenase‐2 (Cox‐2) induced by UVB irradiation both in vitro and in vivo. The activation of p38 and JNK mitogen‐activated protein kinases (MAPK) after UVB irradiation was also inhibited by phlorizin. These findings suggest that phlorizin is effective in protecting skin against UVB‐induced skin damage by decreasing ROS overproduction, Cox‐2 expression and the subsequent excessive inflammation reactions. It seemed that p38 and JNK MAPK signal pathways are involved in the regulation of the protective function of phlorizin.     

Benefits and safety of Oxymetazoline cream 1% on rosacea-associated erythema: A systematic review and analysis of clinical evidence

Background

Facial persistent erythema is recognized as difficult feature to treat in rosacea. Topical Oxymetazoline cream 1% has been used to treat persistent facial erythema in rosacea patients for some years.

Objective

To quantitatively synthesize the benefits and harms of Oxymetazoline cream 1% in real-world clinical management of treatment response and adverse events.

Methods

The clinical researches before June 1, 2022 published on online databases including PubMed, Web of Science, Embase and Cochrane Library were meta-analyzed.

Results

A total of 2298 participants were included, and the improvement rate of two-grade Clinician Erythema Assessment score (CEA) and Subject Self-Assessment for rosacea facial redness score (SSA) in Oxymetazoline group was 38% (95%CI 28–48) and 25% (95%CI 22–27), respectively, at the 4th week of the dosing. The comprehensive rate of treatment-related TEAEs in Oxymetazoline group was 7% (95%CI 5–8). The rate of stinging/burning was 15% (95%CI 10–19), pruritus was 15% (95%CI 9–22), dryness was 23% (95%CI 18–28), and scaling was 17% (95%CI 12–22) in analysis of dermal tolerability. And topical Oxymetazoline cream 1.0% presented a very low rebound rate of erythema (1%, 95%CI 0–2).

Conclusions

These real-world data on Oxymetazoline cream 1% in rosacea-associated erythema may help making clinic decision and informing treatment expectations, and more clinic trials on longer-term dosing or the combination treatment with oral medication and energy-based therapy are worth exploring.     

Photometric and clinical assessment of localized UVB phototherapy systems for the high‐dosage treatment of stable plaque psoriasis

BACKGROUND: Ultraviolet‐B (UVB) light sources are widely used for the safe and effective treatment of inflammatory skin conditions. The recent commercial introduction of fiber‐coupled UVB phototherapy systems facilitates the selective exposure and treatment of localized psoriasis plaques while permitting the safe use of high‐dosage treatments.

OBJECTIVE: In this study, the performance characteristics and clinical outcome of psoriasis treatments were assessed when using two technologically distinct sources of high‐intensity, fiber‐optically delivered therapeutic UVB.

METHODS: A pulsed, monochromatic 308?nm excimer laser and a continuous‐wave, incoherent UVB light source were compared using photosensitive recording papers, images captured with a CCD camera, and on the healthy and lesional skin of ten psoriasis patients.

RESULTS: Beam profile analyses and minimal erythema dose (MED) test spots revealed distinct energy distribution patterns from the two devices. The Guassian‐type laser beam energy distribution complicated MED determinations, whereas skin exposed to light from the incoherent UVB system developed a more uniform erythema. Both systems cleared the treated psoriasis plaques equivalently, requiring no more than two to five weeks of high‐dose treatments.

CONCLUSION: When used at equally erythemogenic high doses, both systems produced rapid plaque clearance with minimal side effects. Unlike conventional phototherapy, localized UVB minimizes exposure to the healthy skin, making it suitable for patients with mild to moderate psoriasis, individuals with recalcitrant plaques and for the successful treatment of lesions occurring on most body sites.