Evaluation of safety and efficacy of topical prostaglandin E2 in treatment of vitiligo

Background  Prostaglandin E₂ (PGE₂) has stimulant and immunomodulatory effects on melanocytes and regulates their proliferation.
Objectives  To study the efficacy and safety of topical PGE₂ in treating stable vitiligo patches involving < 5% body surface area.
Methods  Fifty-six consecutive patients with clinically diagnosed stable vitiligo of types vulgaris, focal, segmental, lip and genital applied a translucent PGE₂ (0·25 mg g⁻¹) gel twice daily for 6 months. Evaluation was fortnightly for 3 months and monthly thereafter up to 6 months. Assessment was based on degree of repigmentation in treated patches ranging from 0% (no change) to 100% (complete repigmentation). Overall response was graded as: poor, 1–25% repigmentation; moderate, 26–50%; good, 51–75%; excellent, > 75%.
Results  Vitiligo vulgaris was the most common type ( n  =   22; 39%), followed by focal and lip vitiligo, with lesions being mostly on the face (25%) and lips. Repigmentation was seen in 40 of 56 patients (71%), with mean onset at 2 months. Patients with disease duration of 6 months or less repigmented best, with face and scalp responding earliest (1–1·5 months). Complete clearance occurred in eight of 40 patients, six of the eight having face lesions. Excellent response was seen in 22 of 40 patients. All neck, scalp and trunk lesions, 33% genital, 29% lip vitiligo, 100% segmental and 63% focal patches showed moderate to excellent response. Incidence of side-effects was 18%, mainly a transient burning sensation especially on the lips.
Conclusions  The efficacy and safety of topical PGE₂ make it a promising therapy for localized stable vitiligo.     

TNF-α, RANTES, and MCP-1 are major chemoattractants of murine Langerhans cells to the regional lymph nodes

We have previously reported that lymph node cells generated chemotactic factors for Langerhans cells (LCs) in the induction phase of contact dermatitis. In order to clarify the chemotactic factors involved in migration to the regional lymph nodes, we investigated the migratory activity of murine LCs toward several cytokines and chemokines in vitro . One-day cultured LC-enriched epidermal cells were added to the upper compartment of a modified Boyden chamber and cytokines were added to the lower compartment. We counted dendritic cells migrated to the lower chamber as LCs under phase contrast microscopy. About 99% of migrated dendritic cells were positively reacted with anti-Ia^d and NLDC145 antibodies and considered to be LCs. We could detect LC migration more accurately by this direct examination than by counting the migrated cells in the filter membrane of a Boyden chamber. In our system, migration of murine epidermal LCs was stimulated by TNF-β, RANTES and MCP-1, but not by GM-CSF, IL-1β, IL-4, and IL-6. TNF-α induced LC migration at concentrations from 4X10³ U/ml to 5X10⁴ U/ml. RANTES at concentrations from 10 to 100 ng/ml and MCP-1 a concentration of 100 ng/ml induced LC migration in a dose-dependent manner. These data confirmed that TNF-α, RANTES, and MCP-1 induced LC migration from epidermis during contact sensitization.     

Immunohistochemical and ultrastructural features of Langerhans cells in condyloma acuminatum

Background:  There are few studies on the abnormal morphology of Langerhans cells (LCs) in condyloma acuminatum (CA) lesions and the essence of the abnormal morphology of LCs in CA lesions is still not well elucidated. The aim of this study was to further investigate the morphological features of LCs in CA lesions.
Methods:  CD1a⁺ LCs in 13 CA lesions and in 13 normal controls were labeled using immunohistochemistry and examined by light microscopy. Ultrastructural investigation on LCs in six CA lesions and in six normal controls was performed by electron microscopy.
Results:  Compared with those in normal controls, most CD1a⁺ LCs in CA lesions exhibited dysplastic dendrities and abnormal distribution. The number of CD1a⁺ LCs in CA lesions (26.31 ± 18.84) was statistically lower (p < 0.001) than that in normal controls (72.00 ± 27.40). Electron microscopy showed that the number of Birbeck granules within lesional LCs (4.00 ± 2.94) was significantly decreased (p < 0.001) than that within normal LCs (10.80 ± 4.78). The ultrastructures of most lesional LCs displayed degenerative changes.
Conclusions:  The morphology of most LCs in CA lesions shows degenerative changes, which suggest that these LCs have been functionally impaired.     

Frequency of sensitization to methyl aminolaevulinate after photodynamic therapy

Background:  Allergic contact dermatitis to methyl aminolaevulinate (Metvix™) after topical application in photodynamic therapy (PDT) has previously been described in case reports.
Objective:  To compare the frequency of sensitization to Metvix^® cream in a group of patients previously treated at least five times with Metvix-PDT with the frequency observed in an unexposed control group.
Methods:  Twenty patients treated five times or more with Metvix-PDT and 60 controls with no prior exposure to Metvix^® were patch tested with Metvix^® cream and Metvix^® placebo cream. Subsequently, the patients were interviewed to determine the relevance of a positive patch test reaction to Metvix^®.
Results:  Of 20 patients treated with Metvix-PDT, 7 were sensitized to Metvix^® cream, giving a sensation risk of 35%. In the control group, 1 of 60 became sensitized after a single exposure to Metvix^® cream (1.7%). There was no reaction to the placebo cream. The positive patch tests to Metvix^® were considered relevant in four of seven patients (57%).
Conclusions:  This study demonstrates a considerable risk of sensitization after Metvix-PDT. We suggest that the patients are interviewed to detect late or persistent local reactions after PDT. These reactions are often considered to be local infections but may represent allergic contact dermatitis, and therefore, patients should be offered patch testing with Metvix^® cream.     

Quantitative and 3-dimensional analysis of Langerhans cells in basal cell carcinoma. A comparative study using light microscopy and confocal laser scanning microscopy

Summary We have analysed Langerhans cells (LCs) in basal cell carcinoma (BCC) and in healthy skin in 15 patients, using three different techniques: light microscopic examination of horizontal sheets, and of 6-μm-thick vertical skin sections, and confocal laser scanning microscopy (CLSM) of 25-μm-thick vertical sections. The use of CLSM enables both a quantitative and a three-dimensional (3-D) analysis of the cells in the same tissue volume. A statistically significant reduction in the relative volume of epidermal CDla reactivity confined to tumour areas was found with CLSM. This difference was confirmed when the number of LCs in horizontal sheets were counted. In contrast, no significant reduction in epidermal CDla⁺ cells was found in thin vertical sections. This is probably due to the smaller tissue sample examined, and to variations in the number of CDla⁺ cells, with less cells directly overlying the tumour nests. The ratio of CDla-expressing cells in the epidermis/dermis was significantly reduced in BCCs, compared with healthy looking skin. Few LCs were observed in tumour nests, but they were numerous in the surrounding stroma of the dermis. Three-dimensional reconstructions of CDla⁺ cells in BCC revealed striking morphological changes; they had a reduced number of dendrites, and these were often short and had few branches. The results demonstrate that CLSM is a suitable technique for quantitative and morphological analysis of CDla-expressing cells in the skin. We suggest that the alterations in LC numbers, distribution and morphology in BCC most probably are secondary to changes in the local environment.     

Stimulation of Langerhans cells with ketoprofen plus UVA in murine photocontact dermatitis to ketoprofen

BACKGROUND: Ketoprofen (KP) clinically evokes the allergic type of photocontact dermatitis when applied to the skin and irradiated with ultraviolet A (UVA). We have established a murine model of photocontact dermatitis to KP, which is a T cell-mediated delayed type hypersensitivity. OBJECTIVE: To further explore the mechanism underlying this sensitivity, we investigated whether KP plus UVA activates the antigen-presenting ability of Langerhans cells (LCs). METHODS: We analyzed the expression of surface molecules on LCs in the murine epidermis treated with KP plus UVA by immunohistochemistry and flow cytometry. Changes in the cytokine expression of epidermal cells from KP-phototreated skin were also examined by real-time PCR. RESULTS: LCs became larger after treatment with KP plus UVA. The number of LCs was significantly decreased 2-3 days after KP phototreatment and recovered on day 5. A flow cytometric analysis revealed that KP plus UVA increased the percentage of LCs that highly expressed MHC class II, CD86, CD80, CD54 and CD40, whereas neither KP nor UVA alone enhanced the expression. KP phototreatment augmented the expression of I-A and CD86 on LCs in KP and UVA dose-dependent manners. A real-time PCR analysis of KP-phototreated skin showed that the expression of mRNA for IL-1alpha and GM-CSF was immediately increased after treatment. CONCLUSION: A photosensitizing regimen of KP plus UVA activates LCs at least partly by stimulating keratinocytes to produce cytokines. Two strains of mice (BALB/c and AKR) differ in responsiveness to KP and the difference is not related to the activation of keratinocytes.     

CD28 T-cell costimulatory molecule expression in pemphigus vulgaris

Background  CD28 superfamily of immune costimulatory molecules could play an important role in autotolerance control. CD28 costimulation seems to be necessary for regulatory T cell (Treg) activation and successive suppressive activities involved in autoimmunity protection. This study investigates CD28 expression, especially inducible costimulator fraction, on T lymphocytes in pemphigus vulgaris (PV) patients.
Methods  CD28 expression on T lymphocytes was assessed in 16 PV patients during acute attack. All patients and 10 healthy control subjects were tested for lymphocyte populations, T-cell subpopulations (T-CD4⁺, T-CD8⁺), Treg and CD28 expression on T-cell subpopulations.
Results  T, B and natural killer cells average values in PV patients were close to the control group values. Compared with control group, PV values showed lower Treg (2.2% compared with 4.7%), slightly decreased CD4⁺ CD28⁺ T cells (91% compared with 95%), higher CD4⁺ CD28⁻ T cells (9% compared with 5%), decreased CD8⁺ CD28⁺ T cells (57% and 73%, respectively) and significantly enhanced CD8⁺ CD28⁻ T cells (43% compared with 27%).
Conclusions  These data suggest that Treg-mediated suppressor T-cell effects could be diminished in PV, together with an abnormal or ineffective subsequent helper T-cell suppression. CD28 high expression on helper T cells and low expression on suppressor T cells are arguments for a potential CD28 role in PV autoimmune response mechanism.

Conflicts of interest

None declared     

Epidermal Langerhans cells, HIV-1 infection and psoriasis

Summary Langerhans cells (LCs) subserve an important antigen-presenting function in the skin immune system. They bear CD4 receptors, which make them potential targets for infection with the human immunodeficiency virus (HIV-1).
The observation of reduced numbers of LCs in the skin of patients with the acquired immunodeficiency syndrome (AIDS), and the association of severe psoriasis with HIV-1 infection, raise interesting questions regarding the role of LCs in the skin of HIV-1-positive psoriatic patients.
In this study, LCs were quantified in the lesional and non-lesional skin of seven HIV-1-positive psoriatic patients, and the results were compared with age-, sex- and site-matched HIV-1-negative psoriatic patients. The number of LCs was determined by staining skin sections with S-100 polyclonal antibody, using the three-step avidin—biotin immunoperoxidase method. The S-100-positive cells above the basal layer were quantified in two ways: cells/mm² of epidermal area, and cells/mm of length of basement membrane.
HIV-1-positive psoriatic patients showed a reduction in the number of epidermal LCs compared with HIV-1-negative psoriatic patients using both methods of quantification, in both lesional and non- lesional skin (P <0·05, Mann-Whitney test). In addition, a reduction in the number of LCs in lesional compared with non-lesional skin was observed in both HIV-1-positive and -negative patients when LCs were quantified per mm² of epidermal area (P<0·05, Wilcoxon test). This reduction was also observed when LCs were quantified per mm length of basement membrane, but the reduction was not statistically significant in the control group of HIV-1-negative psoriatic patients. Our findings of a reduced number of LCs in the epidermis of HIV-1 -positive psoriatic patients may be associated with the clinical deterioration of psoriasis in these patients.     

Relationship of protoporphyrin IX synthesis to photodynamic effects by 5-aminolaevulinic acid and its esters on various cell lines derived from the skin

Background  5-Aminolaevulinic acid (ALA) and its esters act as precursors to the fluorescent photosensitizer protoporphyrin IX (PpIX) in photodynamic therapy (PDT). There is little information about how ALA and its esters induce PpIX synthesis and photodynamic effects in cell lines derived from the skin.
Objectives  We compared the amount of PpIX synthesis induced by ALA and its esters in skin cell lines, and evaluated the relationship of PpIX synthesis to photodynamic effects by ALA and its esters in vitro .
Methods  Four cell lines, including human epidermal keratinocytes (HEK), human dermal fibroblast (hF), A431, and TXM13 were used. Cell survival was evaluated by the MTT assay. Fluorescence spectroscopy was used to measure the amount of PpIX synthesis induced by ALA and its esters. Flow cytometry measured cell death induced by ALA- and its esters-mediated PDT.
Results  ALA and its esters were not toxic at concentrations lower than 2 mmol L⁻¹ in all cell lines. PpIX synthesis was dose-dependent at low doses (0·01–0·1 mmol L⁻¹), and ALA esters were more effective than ALA. Cell death occurred from necrosis rather than apoptosis just after light irradiation illumination on both ALA and its esters-treated cells. Cell death related more to PpIX synthesis than the irradiation light dose.
Conclusions  PpIX production by ALA and its esters was induced on both normal and malignant cell lines derived from the skin, and cell death of PDT responses is closely related to the amount of PpIX synthesis rather than to the irradiation dose.     

Skin and systemic pharmacokinetics of tacrolimus following topical application of tacrolimus ointment in adults with moderate to severe atopic dermatitis

Background  Systemic exposure to tacrolimus following topical application of tacrolimus ointment is minimal. There are, however, no data on the distribution of tacrolimus in the skin.
Objectives  To assess the distribution of tacrolimus in the skin and the systemic pharmacokinetics of tacrolimus in adults with moderate to severe atopic dermatitis after first and repeated application of tacrolimus ointment.
Methods  We investigated skin distribution of topically applied tacrolimus and systemic pharmacokinetics of percutaneously absorbed tacrolimus in adults with atopic dermatitis after topical application of tacrolimus 0·1% ointment twice daily for 2 weeks. Tacrolimus concentrations were assessed in full-thickness skin biopsies and blood samples.
Results  Of 14 patients, 11 completed treatment and were analysed. Mean ± SD tacrolimus concentrations in the skin at 24 h after first and last ointment applications were 94 ± 20 and 595 ± 98 ng cm⁻³, respectively. At 168 h after stopping treatment, values were 97% lower than at 24 h after last application. Tacrolimus concentration decreased with increasing skin depth. Systemic tacrolimus exposure after ointment application was low and highly variable, with 31% of samples below the limit of quantification (0·025 ng mL⁻¹) and 94% below 1 ng mL⁻¹. Blood concentrations at 24 h after the first and last ointment applications were 750 and 1800 times lower, respectively, than those in skin. Physicians' assessments showed that tacrolimus ointment was effective and well tolerated.
Conclusions  Tacrolimus was primarily partitioned in the skin, with minimal systemic absorption after topical application, in patients with atopic dermatitis.     

Systematic administration of chloroquine in discoid lupus erythematosus reduces skin lesions via inhibition of angiogenesis

Background.  Discoid lupus erythematosus (DLE) is a chronic cutaneous form of lupus erythematosus, characterized by inflammation and scarring skin lesions, with lymphocyte infiltration and vasodilation. Antimalarial drugs have beneficial therapeutic effects in DLE, partially resulting from their immunomodulating and photoprotective properties. The possible influence of these drugs on angiogenesis has not been previously evaluated.
Aims.  To investigate the impact of chloroquine (CQ) treatment on the expression of vascular endothelial growth factor (VEGF, a major regulator of angiogenesis) and CD34 (a transmembrane glycoprotein expressed on endothelial cells and involved in tethering lymphocytes) in patients with DLE.
Methods.  A 3-mm skin biopsy was taken from typical skin lesions in 10 people with DLE. Another biopsy was taken from the same area after 3 months of treatment with CQ (250 mg/day). Skin sections were stained with monoclonal antibodies directed against VEGF and CD34. The intensity of epidermal VEGF expression, and the number and area of CD34-positive dermal blood vessels were assessed.
Results.  CQ treatment induced a reduction in epidermal VEGF expression. It also resulted in a significant decrease in the median number of CD34+ dermal blood vessels (from 219 to 125 vessels per mm²). Furthermore the median vessel area was significantly lowered from 9.76 × 10⁶ to 6.92 × 10⁶ mm² per mm² of the dermis.
Conclusions.  These results indicate that one beneficial effect of CQ treatment in DLE may be due to its antiangiogenic properties.     

Ibuprofen and hydrogel-released ibuprofen in the reduction of inflammation-induced migration in melanoma cells

Background  There is growing evidence that inflammation may exacerbate cancer metastasis and several clinical studies show that taking nonsteroidal anti-inflammatory drugs appears to reduce metastases.
Objectives  The aims of this study were: (i) to examine the effects of ibuprofen on the major proinflammatory cytokine tumour necrosis factor (TNF)-α induction of migration of C8161 and HBL human melanoma cells; (ii) to develop ibuprofen-releasing hydrogels (Pluronics F127) for future topical use in reducing metastatic spread of primary melanoma; and (iii) to examine whether the actions of ibuprofen might be explained by induction of apoptosis.
Methods  Melanoma cells were exposed to 300 U mL⁻¹ TNF-α for a 24-h period prior to making a scratch wound to which ibuprofen or ibuprofen-loaded hydrogels were then added. The effects of relevant concentrations of ibuprofen on cell viability and apoptosis were examined.
Results  Ibuprofen at 10⁻³ mol L⁻¹ significantly reduced TNF-α-stimulated migration of both cell types to that of nonstimulated cells ( P  < 0·001). TNF-α-unstimulated cell migration was not significantly affected. Cells responded similarly to SS and SR forms of ibuprofen. Cells treated with ibuprofen sodium salt-loaded hydrogels showed a significant reduction in migration when compared with unloaded hydrogels. Ibuprofen induced apoptosis in HBL cells but had no effect on C8161 melanoma cells apoptosis at concentrations that reduced migration.
Conclusions  These results demonstrate that TNF-α upregulated malignant melanoma migration in vitro and that this could be reduced by ibuprofen both in solution and delivered from a hydrogel. These effects of ibuprofen cannot be attributed simply to induction of apoptosis.     

Pimecrolimus does not affect Langerhans cells in murine epidermis

BACKGROUND: Langerhans cells (LCs) function as specialized antigen-presenting cells in the epidermis, and therefore play a critical role in cutaneous immunological reactions. Topical treatment with corticosteroids is associated with a decrease in epidermal LC number and antigen-presenting capacity in laboratory animals and humans. OBJECTIVES: To examine whether pimecrolimus, a nonsteroidal inflammatory cytokine inhibitor recently introduced for the topical treatment of atopic dermatitis, differs from corticosteroids in effects on LCs. METHODS: Groups of BALB/c mice were treated twice daily on one to five consecutive days on the inner surface of the right ear with 10 micro L of ethanolic solutions of the test compounds at their clinically used concentrations (1% pimecrolimus, 0.1% betamethasone-17-valerate, 1% hydrocortisone and 0.05% clobetasol propionate) or with the vehicle (controls) alone. At selected time points after the treatment epidermal sheets were prepared and examined histomorphometrically for LCs immunolabelled with antibodies to major histocompatibility complex (MHC) class II and DEC 205, and adenosine diphosphatase staining. RESULTS: No changes in number or morphology of LCs were observed in epidermal sheets of mice treated for 5 days with pimecrolimus. In contrast, an almost complete depletion of LCs was observed in skin samples treated with hydrocortisone, betamethasone or clobetasol. Even a single-day treatment schedule with hydrocortisone, betamethasone or clobetasol caused a significant reduction in MHC class II+ LCs, by 31%, 62% and 87%, respectively. CONCLUSIONS: It is therefore unlikely that topically applied pimecrolimus affects epidermal LCs, in contrast to corticosteroids.     

Ultraviolet B radiation suppresses Langerhans cell migration in the dermis by down-regulation of alpha4 integrin

Background/Purpose: Ultraviolet B (UVB) radiation affects the migration and function of epidermal Langerhans cells (LC) and causes immunosuppression of contact hypersensitivity. It is known that LC leaves the epidermis after exposure to UVB. To know the behavior of LC in the dermis after UVB radiation, we studied the effect of UVB radiation on the expression of integrin families on freshly isolated or cultured murine LC. We also examined whether UVB radiation affects the migration of LC to secondary lymphoid tissue chemokine (SLC/6Ckine).
Methods: Integrin expressions of murine LC cultured in epidermal cell suspension were analyzed using flowcytometry. We used murine LC sorted flowcytometrically for binding assay to extracellular matrix and for migration assay to chemokine. Skin explant assay and immnohistochemical staining for 'cords formation' were performed as previously described.
Results: Twenty and 40 mJ/cm² of UVB radiation down-regulated the expression of α4 integrin on 24 h-cultured LC, but not that of α6, β1, or β4 integrin. The number of cultured LC adhered to fibronectin, a ligand for α4 integrin, was decreased after UVB irradiation, while that to laminin, a ligand for α6 integrin, was not influenced. UVB radiation reduced the number of migrating LC to SLC. Furthermore, skin sheet explant experiments showed that UVB radiation inhibited the 'cords' formation in dermal vessels of the 48 h-cultured skin.
Conclusions: These data suggest that UVB radiation may suppress the migration of LC from the dermis to lymphatic vessels. UVB radiation may downregulate the adherence of LC to dermal fibronectin and migration to SLC, and consequently suppress the migration of LC from the UVB-irradiated dermis to lymphatics.     

Skin application of ketoprofen systemically suppresses contact hypersensitivity by inducing CD4+ CD25+ regulatory T cells

BackgroundKetoprofen (KP) is a widely used nonsteroidal anti-inflammatory drug that inhibits prostaglandin biosynthesis. We have previously shown that topical KP treatment at the sensitizing site inhibits the development of contact hypersensitivity (CHS) to picryl chloride (PCl).ObjectiveWe investigated the mechanism underlying the KP-induced immunosuppression of CHS by application of KP.MethodsWe analyzed the CHS responses to the non-sensitizing site and subsequent sensitization with PCl, and by transfer of the draining lymph node cells (LNCs) from KP-tolerated mice to recipient mice. Changes in the Foxp3 expression of LNCs from KP-phototreated skin were also examined by real-time PCR.ResultsTopical application of KP to not only the sensitizing but also non-sensitizing site suppressed CHS response. The immunosuppression was transferred with LNCs from mice treated with PCl plus KP, but not from mice treated oxazolone plus KP. In this transfer study, the CD4⁺ CD25⁺ subset of LNCs exerted the suppressive effect, while CD25⁺ cell-depleted LNCs lost the inhibitory ability. CTLA-4 blocking with a specific antibody, but not IL-10 blocking, abrogated the activity of CD4⁺ CD25⁺ cells. Moreover, Foxp3 mRNA expression was remarkably increased in LNCs from PCl and KP-treated mice.ConclusionThe immunosuppression of CHS by topical application of KP is systemic and haptein-specific. Treg cells play an important role in the suppressive effect by KP.     

Protective effects of green tea extracts on photoaging and photommunosuppression

Objectives: This study aimed to investigate whether the sunscreen-containing 2–5% green tea extracts (GTEs) protect ultraviolet irradiation (UVR)-induced photoaging and photoimmunosuppression.
Materials and methods: Twenty volunteers were exposed to repetitive solar-simulated UVR (ssUVR) on the upper back at a dosage of 1.5 minimal erythema doses (MED) per day for four consecutive days. Thirty minutes before each UVR and 6, 24, and 48 h after the last UV exposure, the products containing vehicle, and 2–5% GTEs were applied onto five sites on the dorsal skin, respectively. The skin biopsies were obtained 72 h after the last UVR. The thickness of the stratum corneum and epidermis was measured under the microscope and the expression of cytokeratins (CK)-5/6, CK16, metalloproteinases (MMP)-2, MMP-9, and the CD1a⁺ Langerhans cells (LCs) were determined using immunohistochemistry.
Results: Our results showed that UVR substantially induced cutaneous erythema, thickening of the epidermis, overexpression of CK5/6, CK16, MMP-2, MMP-9, and depletion of CD1a⁺ LCs. The sunscreens containing different concentrations of GTEs conferred significant protection against the photoaging and photoimmunology-related biological events. Interestingly, the protective effects were not parallel to the concentrations of GTEs, with 2% and 3% GTEs showing the most efficacious photoprotection.
Conclusions: GTEs-containing sunscreens have potential photoprotective effects on UVR-induced photoaging and photoimmunosuppression.     

Mid-infrared spectroscopy on skin using a silver halide fibre probe in vivo

Background/aim: Mid-infrared spectroscopy is a versatile method for in vivo investigation of skin after topical treatment with skin care products.
Methods: FTIR-spectrometer (Bruker Optics) with a flexible silver halide fibre probe (Infrared Fiber Sensors).
Results: Absorbance spectra from 700 to 3000 cm⁻¹ have been recorded to gain information about proteins (amide-I and amide-II vibrations at 1650 and 1550 cm⁻¹), esters (1740 cm⁻¹), carboxylic acid (1710 cm⁻¹), polyalcohols (1050 cm⁻¹) and hydrocarbons (CH _n vibrations at 2800–3000 cm⁻¹).
Conclusions: Using the particular light guide, we were able to measure for the first time the effects of lip care products on lips directly. Furthermore, water binding and glycerol content of the skin could be determined simultaneously, as well as the replenishment of lipids by lipid-enriched bath oil.