Lim Photodermatology, An Issue of Dermatologic Clinics

1. Auflage 2014
ISBN: 978-0-323-31180-9
Verlag: Elsevier HealthScience EN
Format: EPUB
Kopierschutz: Adobe DRM (»Systemvoraussetzungen)

E-Book, Englisch, Band Volume 32-3, 217 Seiten

Reihe: The Clinics: Dermatology

Dr Henry Lim, renown for expertise and research in photodermatology leads this issue of Dermatologic Clinics. Photodermatology in this issue addresses dermatoses brought on or accelerated by light as well as light forms for dermatology therapies. Photodermatology is used to diagnosis and treat many common conditions that bring patients to the dermatologist. Topics include: Introduction to photobiology; Evaluation of patients with photodermatologic conditions; Photoimmunology; Photoaging; Photocarcinogenesis; Polymorphous Light Eruption (PMLE); Actinic Prurigo; Hydroa vacciniforme and solar urticaria; Chronic actinic dermatitis; drug-induced photosensitivity; Cutaneous porphyrias; Photoaggravated dermatoses; Ultraviolet (UV) based therapy; Photodynamic therapy; Photoprotection. Dr Lim works with one his residents, So Yeon Paek, as his co-Editor on this issue.

Autoren/Hrsg.

Lim, Henry

Inhaltsverzeichnis

1;Front Cover;1
2;Photodermatology;2
3;copyright
;3
4;Contributors;4
5;Contents;8
6;Dermatologic Clinics
;12
7;Preface
;14
8;Introduction to Photobiology;16
8.1;Key points;16
8.2;Introduction;16
8.3;UVR;16
8.3.1;Solar Radiation;16
8.3.2;UVR;17
8.3.3;Light-Skin Interactions;17
8.3.3.1;Reflection, scattering, and absorption;17
8.3.3.2;Photochemical reactions;18
8.4;Basic principles of phototherapy;18
8.4.1;MED;19
8.4.2;Acute and Chronic Effects of UVR;20
8.4.3;UV Damage on a Molecular Level;20
8.4.3.1;DNA damage and repair;20
8.4.3.2;UVR-induced apoptosis;21
8.4.3.3;Role of lipids;21
8.4.3.4;Role of proteins;21
8.4.4;UV Damage on a Clinical Level;21
8.4.4.1;Sun exposure: acute and chronic effects;21
8.4.4.1.1;Sunburn and tanning;21
8.4.4.1.2;Vitamin D production;22
8.4.4.1.3;Photoaging;22
8.4.4.1.4;Carcinogenesis;24
8.4.4.2;Phototherapy;24
8.4.5;Phototesting with Artificial Light Sources;24
8.4.5.1;Arc lamps;25
8.4.5.2;Excimer;25
8.4.5.3;Fluorescent lamps;25
8.4.5.4;Light-emitting diodes;25
8.4.5.5;Lasers;25
8.5;Summary;26
8.6;References;26
9;Evaluation of Patients with Photodermatoses;28
9.1;Key points;28
9.2;Overview;28
9.3;History;29
9.3.1;Age of Onset;29
9.3.2;Seasonal Variation, Interval Before Onset, Duration of the Eruption;30
9.3.3;Family History;30
9.3.4;Systemic Abnormalities;30
9.3.5;Window Glass;30
9.3.6;Exposure to Photosensitizers;31
9.4;Epidemiology and prevalence;31
9.5;Pathophysiology;32
9.6;Clinical findings;32
9.6.1;Histology;33
9.6.2;Laboratory and Photobiology Tests;33
9.6.2.1;Blood tests;33
9.6.2.2;Phototesting;34
9.6.2.3;Photopatch testing;34
9.7;Treatment;35
9.8;Summary;35
9.9;References;35
10;Photoimmunology;38
10.1;Key points;38
10.2;Evidence of photoimmunologic effects of UV radiation in humans;38
10.3;Experimental evidence for the photoimmunologic effects of UV radiation;39
10.4;Mechanisms of UV-induced immune suppression;39
10.4.1;Regulatory T Cells;39
10.4.2;APCs;40
10.4.3;Initial Molecular Events;41
10.4.4;Cytokines and Other Soluble Mediators;42
10.4.5;TLRs and Innate Immunity;43
10.5;Photoimmunologic diseases;44
10.5.1;PMLE;44
10.5.2;Chronic Actinic Dermatitis;44
10.5.3;Cutaneous Lupus Erythematosus;44
10.6;Photoimmunologic effects of phototherapy;46
10.7;Summary;47
10.8;References;47
11;Photoaging;52
11.1;Key points;52
11.2;Introduction;52
11.3;History;52
11.4;Epidemiology;52
11.5;Pathogenesis;53
11.6;Clinical manifestations;54
11.7;Histology;54
11.8;Photobiologic evaluation;54
11.9;Treatment;55
11.9.1;Topical Retinoids;56
11.9.2;Cosmeceuticals;56
11.9.3;Chemical Peels;57
11.9.4;Neuromodulators;57
11.9.5;Soft Tissue Fillers;58
11.9.6;Light Sources;58
11.10;Summary;59
11.11;References;59
12;Photocarcinogenesis;62
12.1;Key points;62
12.2;Introduction;62
12.3;Biologic effects of UV;62
12.3.1;DNA Damage;63
12.3.2;Cell-Cycle Arrest;63
12.3.3;DNA Repair;64
12.3.4;Apoptosis;64
12.3.5;UV Effects on the Immune System;64
12.4;Nonmelanoma skin cancer;65
12.4.1;Epidemiology;65
12.4.2;Genetic Predisposition for NMSC;65
12.4.3;Sporadic Formation of NMSC;65
12.4.4;Occupational Exposure and NMSC;66
12.4.5;Indoor Tanning and NMSC;67
12.5;Melanoma;67
12.5.1;Genetic Predisposition to Melanoma;68
12.5.2;Sporadic Melanoma;69
12.5.3;Occupational Exposure and Melanoma;69
12.5.4;Indoor Tanning and Melanoma;69
12.6;UVR, vitamin D, and skin cancer;70
12.7;Summary;71
12.8;References;71
13;Polymorphous Light Eruption;76
13.1;Key points;76
13.2;Introduction;76
13.3;History;77
13.4;Epidemiology;77
13.4.1;General Epidemiology;77
13.5;Clinical manifestations;77
13.5.1;Quality of Life;78
13.5.2;Relation to Lupus Erythematosus;78
13.6;Histology and immunohistochemistry;79
13.7;Photobiologic evaluation;79
13.7.1;Waveband Aspects;79
13.8;Pathogenesis;80
13.8.1;Genetics;80
13.8.2;Potential Antigens in PMLE;80
13.8.3;General Immunologic Aspects;81
13.8.4;Cell Migration Patterns and Cytokines;82
13.8.5;Antimicrobial Peptides;84
13.8.6;Hormonal Factors;84
13.8.7;Vitamin D;85
13.8.8;Relation to Skin Carcinogenesis;85
13.9;Management;86
13.9.1;Prevention;86
13.9.2;Photohardening;86
13.9.3;Established Treatments;87
13.9.4;Experimental Approaches;87
13.10;Summary and perspectives;88
13.11;Acknowledgments;88
13.12;References;88
14;Actinic Prurigo;96
14.1;Key points;96
14.2;Introduction;96
14.3;History;96
14.4;Epidemiology;97
14.5;Pathogenesis;97
14.6;Association with HLA;98
14.7;Clinical manifestations;98
14.8;Histology;99
14.9;Laboratory findings;99
14.10;Photobiological evaluation;100
14.11;Treatment;100
14.12;Summary;102
14.13;References;102
15;Hydroa Vacciniforme and Solar Urticaria;106
15.1;Key points;106
15.2;Hydroa vacciniforme;106
15.2.1;History;106
15.2.2;Epidemiology;106
15.2.3;Pathogenesis;107
15.2.4;Clinical Manifestations;107
15.2.4.1;Mucocutaneous manifestations;107
15.2.4.2;Systemic manifestations;107
15.2.5;Histology;108
15.2.6;Differential Diagnosis;108
15.2.7;Laboratory Findings;108
15.2.8;Photobiological Evaluation;108
15.2.9;Management;108
15.3;Solar urticaria;108
15.3.1;History;108
15.3.2;Epidemiology;109
15.3.3;Clinical Manifestations;109
15.3.4;Associated Conditions;109
15.3.5;Differential Diagnosis;109
15.3.6;Pathogenesis and Classification;109
15.3.7;Action Spectrum;109
15.3.8;Inhibition Spectrum;110
15.3.9;Augmentation Spectrum;110
15.3.10;Photobiological Evaluation;110
15.3.11;Management;110
15.3.11.1;Medical therapy;110
15.3.11.1.1;Antihistamines;110
15.3.11.1.2;Cyclosporine;111
15.3.11.1.3;Methotrexate;111
15.3.11.1.4;Intravenous immunoglobulin;111
15.3.11.1.5;Omalizumab;111
15.3.11.1.6;a–Melanocyte stimulating hormone analogue;111
15.3.11.2;Procedural therapy;111
15.3.11.2.1;Phototherapy and photochemotherapy;111
15.3.11.2.2;Plasmapheresis;112
15.3.12;Prognosis;112
15.4;References;112
16;Chronic Actinic Dermatitis;116
16.1;Key points;116
16.2;History;116
16.3;Epidemiology;116
16.4;Pathogenesis;117
16.5;Diagnosis;117
16.5.1;Clinical Manifestations;117
16.5.2;Differential Diagnoses;117
16.5.3;Histology;117
16.5.4;Photobiological Evaluation;117
16.5.5;Laboratory Evaluation;118
16.6;Management;118
16.7;Prognosis;119
16.8;Summary;119
16.9;References;120
17;Drug-Induced Photosensitivity;124
17.1;Key points;124
17.2;Introduction;124
17.3;Epidemiology;125
17.4;Pathogenesis;125
17.5;Clinical manifestations;126
17.6;Laboratory findings;126
17.7;Photobiological evaluation;126
17.8;Management;127
17.9;References;128
18;The Cutaneous Porphyrias;130
18.1;Key points;130
18.2;Introduction;130
18.3;History;130
18.4;Pathogenesis of skin lesions;131
18.5;Diagnostic approach in cutaneous porphyria;132
18.6;General photoprotection;133
18.7;Porphyrias presenting with acute photosensitivity;133
18.7.1;Erythropoietic and X-Linked Dominant Protoporphyria;133
18.7.1.1;Epidemiology;133
18.7.1.2;Clinical features;134
18.7.1.3;Differential diagnosis;134
18.7.1.4;Laboratory findings;135
18.7.1.5;Management;135
18.8;Porphyrias presenting with fragile skin;135
18.8.1;Porphyria Cutanea Tarda;135
18.8.1.1;Epidemiology and pathogenesis;135
18.8.1.2;Clinical features;136
18.8.1.3;Differential diagnosis;136
18.8.1.4;Laboratory findings;136
18.8.1.5;Management;137
18.8.1.6;Complications;137
18.8.2;The Autosomal Dominant Acute Porphyrias;137
18.8.2.1;Epidemiology;137
18.8.2.2;Pathogenesis of acute attacks;137
18.8.2.3;Clinical manifestations;138
18.8.2.4;Laboratory findings;138
18.8.2.5;Management;138
18.8.3;Congenital Erythropoietic Porphyria;139
18.8.3.1;Epidemiology;139
18.8.3.2;Clinical manifestations;139
18.8.3.3;Laboratory findings;140
18.8.3.4;Differential diagnosis;140
18.8.3.5;Management;140
18.8.3.6;Complications;141
18.9;Rare porphyria variants;141
18.10;References;141
19;Photoaggravated Disorders;146
19.1;Key points;146
19.2;Introduction;146
19.3;Diseases usually exacerbated by UVR;147
19.3.1;Cutaneous Lupus Erythematosus;147
19.3.1.1;Introduction;147
19.3.1.2;History;147
19.3.1.3;Epidemiology;147
19.3.1.4;Pathogenesis;148
19.3.1.5;Clinical manifestations;148
19.3.1.6;Histology;149
19.3.1.7;Laboratory findings;149
19.3.1.8;Management;149
19.3.2;Darier Disease;150
19.3.2.1;Introduction;150
19.3.2.2;History;150
19.3.2.3;Epidemiology;150
19.3.2.4;Pathogenesis;150
19.3.2.5;Clinical manifestations;150
19.3.2.6;Histology;150
19.3.2.7;Management;150
19.3.3;Dermatomyositis;151
19.3.3.1;Introduction;151
19.3.3.2;History;151
19.3.3.3;Epidemiology;151
19.3.3.4;Pathogenesis;151
19.3.3.5;Clinical manifestations;151
19.3.3.6;Histology;151
19.3.3.7;Laboratory findings;152
19.3.3.8;Photobiologic evaluation;152
19.3.3.9;Management;152
19.3.4;Lichen Planus Actinicus;152
19.3.4.1;Introduction;152
19.3.4.2;Epidemiology;152
19.3.4.3;Pathogenesis;152
19.3.4.4;Clinical manifestations;152
19.3.4.5;Histology;152
19.3.4.6;Management;152
19.3.5;Pellagra;152
19.3.5.1;Introduction;152
19.3.5.2;Epidemiology;152
19.3.5.3;Pathogenesis;152
19.3.5.4;Clinical manifestations;153
19.3.5.5;Laboratory findings;153
19.3.5.6;Management;153
19.3.6;Rosacea;153
19.3.6.1;Introduction;153
19.3.6.2;History;153
19.3.6.3;Epidemiology;153
19.3.6.4;Pathogenesis;153
19.3.6.5;Clinical manifestations;153
19.3.6.6;Histology;153
19.3.6.7;Management;153
19.3.7;Smith-Lemli-Opitz Syndrome;154
19.4;Diseases sometimes exacerbated by UVR;154
19.4.1;Atopic Dermatitis;154
19.4.2;Pemphigus;154
19.4.3;Psoriasis;154
19.5;References;155
20;UV-Based Therapy;160
20.1;Key points;160
20.2;Introduction;160
20.3;History;160
20.4;UV-B;161
20.4.1;Mechanism of Action;161
20.4.2;Modes of Delivery;161
20.4.2.1;BB–UV-B phototherapy;161
20.4.2.2;NB–UV-B phototherapy;161
20.4.3;Targeted Phototherapy: Excimer Lasers and Lamps;162
20.4.4;Indications;162
20.4.5;Contraindications;162
20.4.6;Treatment Protocol;163
20.4.7;Expected Outcome;165
20.4.8;Side Effects;165
20.5;PUVA and UV-A1;165
20.5.1;Mechanism of Action;165
20.5.2;Modes of Delivery;166
20.5.2.1;PUVA;166
20.5.2.2;UV-A1;166
20.5.3;Indications;166
20.5.4;Contraindications;166
20.5.5;Expected Outcome;166
20.5.6;Treatment Protocol;167
20.5.7;Side Effects;167
20.6;Summary;169
20.7;References;169
21;Photodynamic Therapy;176
21.1;Key points;176
21.2;Introduction;176
21.3;Historical perspective;176
21.4;Mechanism of action;177
21.5;Sensitizer;177
21.6;Light source;177
21.7;Therapeutic applications and expected outcomes;178
21.7.1;Photorejuvenation;178
21.7.2;Acne Vulgaris;179
21.7.3;Verrucae;180
21.7.4;Actinic Keratosis;180
21.8;NMSC;181
21.8.1;Bowen Disease;181
21.9;BCC;182
21.10;Management of adverse events;182
21.10.1;Pain;182
21.10.1.1;Cold air;183
21.10.1.2;Injectable anesthetics;183
21.10.1.3;Interruption of treatment;183
21.10.1.4;Topical anesthetics;184
21.10.2;Phototoxicity;184
21.10.3;Infection;184
21.10.4;Immunosuppression;184
21.10.5;Scarring;184
21.10.6;Pigmentation;184
21.10.7;Risk of Carcinogenesis;185
21.11;Summary;185
21.12;References;185
22;Sunscreens;188
22.1;Key points;188
22.2;Introduction;188
22.3;Mechanism of action;189
22.4;Health benefits of using sunscreen;189
22.4.1;Prevention of AK and SCC;190
22.4.2;Reduction of Basal Cell Carcinoma;191
22.4.3;Prevention of Melanoma;192
22.4.4;Prevention of Skin Aging;192
22.4.5;Management of Photodermatoses;192
22.5;FDA regulation on sunscreen labeling and effectiveness testing;192
22.6;Controversies associated with sunscreens;195
22.6.1;Safety of Oxybenzone;195
22.6.2;Safety of Nanoparticles;195
22.6.3;Sunscreen-Induced Vitamin D Deficiency;196
22.7;Limitations of sunscreen use;196
22.8;Summary;196
22.9;References;196
23;Photoprotection;200
23.1;Key points;200
23.2;Introduction;200
23.3;Photoprotection by glass;200
23.3.1;Main Types of Glass;200
23.3.2;UV Transmission Through Residential Glass;201
23.3.3;UV Exposure in Automobiles;201
23.3.4;Automobile Glass;201
23.3.4.1;UV transmission through automobile glass;202
23.3.4.2;Window films;202
23.4;Photoprotection with sunglasses;203
23.4.1;UV Exposure and the Eye;203
23.4.2;Sunglasses Guidelines;203
23.5;Photoprotection by clothing;204
23.5.1;Methods for Assessing the UPF of Textiles;204
23.5.1.1;In vitro method;204
23.5.1.2;In vivo method;205
23.5.2;Influence of Fabric Parameters on UPF;206
23.5.3;Porosity, Weight, and Thickness;206
23.5.4;Type of Fabric;206
23.5.5;Color of Fabrics;206
23.5.6;Laundry;206
23.5.7;Moisture Content;206
23.5.8;Stretch;207
23.5.9;Fabric to Skin Distance;207
23.5.10;Fabric Processing;207
23.5.11;UV Absorbers;207
23.6;Summary;207
23.7;References;208
24;Index;210

Leseproben

Introduction to Photobiology
Elma D. Baron, MDa*[e-mail] and Amanda K. Suggs, MDb,     aDepartment of Dermatology, University Hospitals Case Medical Center, Louis Stokes Cleveland Veterans Affairs Medical Center, Case Western Reserve University, 11100 Euclid Avenue, Lakeside 3500, Mailstop 5028, Cleveland, OH 44106-5028, USA; bDepartment of Dermatology, University Hospitals Case Medical Center, Case Western Reserve University, 11100 Euclid Avenue, Cleveland, OH 44106, USA *Corresponding author. Photobiology is the study of the local and systemic effects of incident radiation on living organisms. Solar radiation is made up of ultraviolet, visible and infrared radiation. Ultraviolet radiation is made up of UV-C, UV-B, and UV-A. Sun exposure can lead to sunburn, tanning, vitamin D production, photoaging, and carcinogenesis. Phototherapy is the use of nonionizing radiation to treat cutaneous disease. Various types of artificial light sources are used for photo testing and phototherapy. Keywords Ultraviolet radiation Ultraviolet light Phototherapy Photobiology Sunburn Melanogenesis Vitamin D production Photoaging Key points
• Solar radiation is made up of ultraviolet, visible, and infrared radiation. • Ultraviolet radiation is made up of UV-C, UV-B, and UV-A. • Most ultraviolet radiation that reaches the earth is UV-A. • Sun exposure has a wide range of biological effects, including sunburn, tanning, vitamin D production, photoaging, and carcinogenesis. • Phototherapy uses properties of ultraviolet light that are useful in the treatment of certain dermatologic conditions. Introduction
Photobiology deals with the local and systemic effects of incident radiation on living organisms. This introductory article on cutaneous photobiology focuses on the effects of ultraviolet (UV) radiation (UVR), both from its natural source (ie, the sun) and artificial sources (ie, those used in phototherapy), on skin function and diseases. Although visible light and infrared radiation also have effects on skin cells, there is more information on UVR. Phototherapy is the use of nonionizing radiation to treat cutaneous disease. For more than a century, phototherapy has played a pivotal role in the treatment of dermatologic diseases. In 1903, Niels Finsen received the Nobel Prize in Medicine for using light to treat a cutaneous mycobacterial disease. In the middle of the 20th century, advancements in UV-B light therapy expanded treatment options for patients with psoriasis. In the 1970s, photochemotherapy (ie, using psoralen as a photosensitizer in combination with UV-A radiation [PUVA]) made its debut. PUVA became an established player in the treatment of skin diseases in the last quarter of the 20th century. More recent advances in the last few decades (ie, narrowband UV-B therapy, laser therapy, targeted phototherapy, photodynamic therapy [PDT], UV-A1) have also revolutionized photodermatology.1,2 UVR
Solar Radiation
The rays of the sun hit the earth in the form of UVR, visible, and infrared radiation. These 3 entities are components of the electromagnetic spectrum, which also includes radiowaves, microwaves, radiographs, and ? radiation (Fig. 1). Solar radiation is made up of approximately 50% visible light, 40% infrared, and 9% UVR.3 Visible radiation is that which is perceived by the human eye.4 Each color of visible light represents a different wavelength range (see Fig. 1). UVR is the area of the electromagnetic spectrum that is considered most biologically active and therefore of greatest impact on health and disease.
Fig. 1 Electromagnetic spectrum. UVR
UVR spans the wavelengths 100 to 400 nm and is subdivided into UV-C, UV-B, and UV-A. There are subtle differences in the subdivisions described in the literature. In this article, the subdivision most commonly chosen in photobiology is used (ie, UV-C, 200–290 nm; UV-B, 290–320 nm; and UV-A, 320–400 nm).4 Other ranges referenced in the literature include: UV-C at 200 to 280 nm, UV-B at 280 to 320 nm, UV-A at 320 to 400 nm, UV-C at 200 to 280 nm, UV-B at 280 to 315 nm, and UV-A at 315 to 400 nm.5 The stratospheric ozone prevents wavelengths shorter than approximately 290 nm from hitting the earth. Most UV radiation that reaches the earth is UV-A. Only a small percentage (approximately 5%) of UV-B is present in terrestrial sunlight. UV-C is typically filtered by the ozone layer.6 The amount of solar energy at a specific wavelength that can affect the earth varies with season, region, altitude, pollution, and the path that the solar radiation traverses through the ozone.7 The amount of UV in sunlight also varies throughout the day. Being of a longer wavelength, UV-A is present consistently from sunrise to sunset, whereas UV-B peaks around noon. Approximately 50% of UV-A exposure occurs in the shade as a result of surface reflection and its penetration to cloud cover. Windows and automotive glass do not shield against UV-A but do shield against UV-B.8 For the purposes of phototherapy, UV-B has been further subdivided into broadband UV-B (290–320 nm) and narrrowband UV-B (311 nm–313 nm). UV-A radiation has been subdivided into UV-A1 (340–400 nm) and UV-A2 (320–340 nm), primarily because the biological effect of UV-A2 is closer to that of UV-B. The specific applications of these modalities are discussed in more detail in the article by Rkein and Ozog elsewhere in this issue. Light-Skin Interactions
Light has both the properties of waves and particles known as photons. In cutaneous photobiology, it is important to understand what happens to photons when they encounter the skin surface. They can undergo reflection, scattering, or absorption. According to the Grothus-Draper law, light can have a biological effect only if it is absorbed. Once radiation is absorbed by molecules in the skin (termed chromophores), energy is transferred to produce heat or drive photochemical reactions. This process results in detectable responses at the cellular and molecular levels that could lead to a clinical outcome (Fig. 2).9,10
Fig. 2 Light-skin interaction pathway. Reflection, scattering, and absorption Reflection happens at the skin surface. Light reflected from the skin can be used for diagnostic purposes but does not have much of a therapeutic role. Scattering alters the direction of the light transmission through the skin. How deep a photon can go is influenced by how much it is scattered by structures in the skin. Most scattering takes place in the dermis as a result of the presence of collagen. Scattering of radiation is also wavelength dependent; shorter wavelengths scatter more, whereas longer wavelengths penetrate deeper.9,10 The depth of light penetration is critical for phototherapy. UV-B is generally absorbed in the epidermis and upper dermis, whereas UV-A (because of its longer wavelengths) penetrates well into the dermis (Fig. 3). Shorter wavelength visible light such as blue light can be used in PDT for epidermal growths (such as actinic keratoses). Red light, which is of a longer visible wavelength, can target deeper structures such as sebaceous glands and thicker lesions.11 Nonetheless, penetration depth is only 1 part of the equation. The light must also be of the appropriate wavelength to be absorbed by the target molecule or chromophore. Only on absorption can a photon exert a clinical effect.
Fig. 3 UV wavelength and depth of skin penetration. Different wavelength(s) target different chromophores, which results in a variety of cutaneous effects.11 Chromophores can be cellular/molecular components, such as amino acids, nucleotides, lipids, and 7-dehydrocholesterol (a vitamin D precursor). They can also be porphyrins (exogenous or endogenous), tattoo pigments, or photosensitizing drugs (eg, psoralens).10 DNA directly absorbs UV-B and is therefore a chromophore targeted by UV-B phototherapy. In cosmetic laser treatments, endogenous chromophores targeted are mainly hemoglobin, melanin, and water.12 Exogenous substances (ie, aminolevulinic acid solution, which converts to protoporphyrin IX) may also be used to act as chromophores, depending on the phototherapeutic modality. Absorption is wavelength dependent and is influenced by the physicochemical structure of the chromophore.4,10 Each chromophore has an absorption spectrum, which is the range of wavelengths that are absorbed by that molecule. For example, the absorption spectrum for melanin is 250 to 1200 nm.13 The...