Shimizu's Dermatology E-Book

Hiroshi Shimizu

• Herausgeber: John Wiley & Sons
• Kategorie: Fachliteratur
• Sprache: Englisch

Seitenzahl: 1059

Veröffentlichungsjahr: 2016

Beschreibung

Shimizu's Dermatology, Second Edition provides practical, didactic, and rapid-reference advice on diagnosis and management of the most common dermatologic conditions.

Written by one of the world's leading experts, and a best-seller in Japan where it was first published, the second edition is cohesive, richly illustrated, attractively presented, and fully revised to reflect the latest in clinical developments. This complete dermatology resource offers:

• Over 2,000 clinical images to aid rapid and easy diagnosis
• 100% clinically focused chapters describing the clinical features, classifications, pathogeneses, pathologies, treatments and lab findings of diseases
• Key points and tips and tricks in every chapter for practical guidance
• Attractive color presentation throughout, with high-quality clinical images
• Improve your knowledge of skin conditions and their management with this concise, user-friendly, alternative to larger reference books.

Shimizu's Dermatology is ideal for specialists in clinical practice, trainees managing patients at clinics or hospitals or preparing for board exams, and medical students.

Leseprobe

Table of Contents

Cover

Title Page

CHAPTER 1: Structure and function of the skin

Overview of the skin

Epidermis

Dermis

Subcutaneous fat tissue

Appendages

Immunology of the skin

CHAPTER 2: Histopathology of the skin

Skin biopsy

Dermatopathology

Immunohistochemistry

Electron microscopy and immunoelectron microscopy

CHAPTER 3: Dermoscopy

Dermoscope

Diagnostic algorithm

Dermoscopic findings in melanocytic lesions

Dermoscopic findings in seborrheic keratosis

Dermoscopic findings in basal cell carcinoma

Dermoscopic findings in vascular lesions, including hemorrhages

Dermoscopic findings in other cutaneous diseases

CHAPTER 4: Description of skin lesions

Primary skin lesions

Secondary skin lesions

Enanthema

Lesions with elevation of the skin

Lesions associated with hair follicles

Lesions with color changes

Lesions accompanied by multiple blisters and pustules

Lesions associated with changes in the stratum corneum

Lesions accompanied by other changes

Dermatological phenomena

CHAPTER 5: Diagnosis of skin diseases

General diagnostic methods (Fig. 5.1)

Allergy test

Photosensitivity test

Ultrasonography

Skin function test

Fungal examination

Diascopy

Wood’s lamp test

Cytological diagnosis (Tzanck test)

Enzyme‐linked immunosorbent assay

Western blot

DNA analysis

Other general medical tests

CHAPTER 6: Treatment of skin diseases

Topical therapies

Systemic treatments

Laser therapies

Physical therapies

Skin surgery

CHAPTER 7: Eczema and dermatitis

Eczema (synoym: dermatitis)

Clinical features

Pathogenesis

Pathology

Classification

Eczema with unidentified cause

Contact dermatitis

Specific types of eczema

CHAPTER 8: Urticaria, prurigo, and pruritus

Urticaria and angioedema

Prurigo

Pruritus cutaneous

CHAPTER 9: Erythema and erythroderma

Erythema

Erythroderma (synonyms: exfoliative dermatitis)

CHAPTER 10: Drug‐induced skin reactions and graft‐versus‐host disease

Drug‐induced skin reactions (DISRs)

Graft‐versus‐host disease (GVHD)

CHAPTER 11: Vasculitis, purpura, and other vascular diseases

Vasculitis

Vasculitis in small vessels

Vasculitis in small and medium‐sized arteries

Other diseases related to vasculitis in small and medium‐sized blood vessels

Purpura

Thrombocytopenic purpura

Cryoglobulinemia

Pigmented purpuric dermatosis (synonyms: idiopathic pigmentary purpura, purpura pigmentosa chronica)

Senile purpura

Purpura simplex

Steroid purpura

Other vascular diseases

Arteriosclerosis obliterans (ASO)

Diabetic gangrene

Raynaud’s phenomenon, Raynaud’s disease

Chronic venous insufficiency (synonyms: venous insufficiency, venous stasis syndrome)

Livedo

Livedo vasculopathy (synonyms: livedo vasculitis, livedo reticularis with summer/winter ulcerations, livedoid vasculopathy)

Erythromelalgia (synonyms: erythralgia, acromelalgia)

Lymphangitis

Lymphedema

Ataxia telangiectasia (synonym: Louis–Bar syndrome)

CHAPTER 12: Collagen diseases

Lupus erythematosus

Scleroderma

Other collagen diseases

Rheumatic diseases whose main symptom is arthritis

CHAPTER 13: Physicochemical injury and photosensitive diseases

Physicochemical injury

Photodermatosis

CHAPTER 14: Blistering and pustular diseases

Blistering diseases

Genetic blistering diseases

Autoimmune blistering diseases

Pustular diseases

Palmoplantar pustulosis (synonym: pustulosis palmaris et plantaris (PPP))

Subcorneal pustular dermatosis (synonym: Sneddon–Wilkinson disease)

Eosinophilic pustular folliculitis (Ofuji) (EPF) (synonym: eosinophilic pustular dermatosis)

Acute generalized pustular bacterid (AGPB)

Infantile acropustulosis

CHAPTER 15: Disorders of keratinization

Hereditary keratoses

Ichthyoses

Palmoplantar keratoderma (PPK)

Other hereditary keratoses

Acquired keratoses

Inflammatory keratosis

Non‐inflammatory keratosis

CHAPTER 16: Disorders of skin color

Diseases of depigmentation

Hyperpigmentation

Diseases caused by extrinsic deposition

CHAPTER 17: Metabolic disorders

Amyloidoses

Mucinoses

Xanthomas

Electrolyte abnormalities

Vitamin deficiencies

Porphyria

Skin manifestations associated with diabetes

Other metabolic disorders

CHAPTER 18: Disorders of the dermis and subcutaneous fat

Disorders of the dermis

Cutaneous atrophy

Dysplasia

Perforating dermatosis

Granulomatous disorders

Hereditary connective tissue disease

Disorders of the subcutaneous fat

Panniculitis

Lipodystrophy

CHAPTER 19: Disorders of the skin appendages

Disorders of the sweat glands

Disorders of sebaceous glands

Disorders of the hair

Disorders of the nails

Color changes of the nail plates

Abnormal formation of the nails

CHAPTER 20: Nevi and neurocutaneous syndromes

Nevus

Melanocytic nevi

Epidermal nevi

Mesenchymal cell nevi

Other nevi accompanied by skin pigmentation

Neurocutaneous syndromes

CHAPTER 21: Benign skin tumors

Tumors originating from epidermal components

Follicular tumors

Sebaceous tumors

Sweat gland tumors

Cysts

Neural tumors

Vascular tumors

Hemangiomas

Vascular malformations

Fibrous tumors

Histiocytic tumors

Fat cell tumors

Muscular tissue tumors

Osteosis tumors

Hematopoietic tumors

CHAPTER 22: Malignant skin tumors, lymphomas,and melanomas

Malignant skin tumors

Epidermal and follicular tumors

Sebaceous gland tumors

Follicular tumors

Sweat gland tumors

Nervous system tumors

Mesenchymal tumors

Metastatic carcinoma of the skin

Malignant lymphomas and other hematopoietic tumors

Cutaneous T cell lymphoma

Cutaneous B cell lymphoma

Other hematopoietic tumors

(Malignant) melanoma

CHAPTER 23: Viral infections

Viral infections whose main symptom is blistering

Viral infections whose main symptom is verruca

Viral infections with generalized skin lesions

Specific viral infectious diseases

CHAPTER 24: Bacterial infections

Acute pyoderma

Chronic pyodermas

Systemic infections

Other bacterial infections

CHAPTER 25: Fungal diseases

Superficial mycoses

Tinea (dermatophytosis)

Candidiasis

Malassezia infections

Subcutaneous mycoses

CHAPTER 26: Mycobacterial infections

Mycobacterium tuberculosis infections

(True) Cutaneous tuberculosis

Tuberculid

Non‐tuberculous mycobacterial infections

Mycobacterium leprae infection (synonyms: leprosy, Hansen’s disease)

CHAPTER 27: Sexually transmitted infections

Syphilis

Chancroid

Lymphogranuloma venereum (synonyms: lymphogranulomatosis inguinale, chlamydia)

CHAPTER 28: Skin diseases caused by arthropods (insects, spiders, crustaceans) and other noxious animals

Diseases caused by insects and other noxious animals

Skin diseases transmitted by insects and other animals

Diseases caused by parasitic worms

Appendix Main genodermatoses and their causative genes and proteins

Index

End User License Agreement

List of Tables

Chapter 01

Table 1.1 Expression regions of main keratin pairs, and congenital disorders from mutations of keratins.

Table 1.2 Types of collagen fibers.

Table 1.3 Association between HLA complex and skin diseases.

Table 1.4 Basic characteristics of immunoglobulins.

Table 1.5 Main cytokins secreted by keratinocytes.

Table 1.6 Classification of allergy.

Chapter 02

Table 2.1 Specific stains used in dermatology.

Table 2.2 Diseases with inflammatory infiltration into the skin.

Table 2.3 Antibodies frequently used in dermatology.

Chapter 05

Table 5.1 Readings and interpretation of patch test reactions.

Table 5.2 Readings of scratch test reactions.

Table 5.3 Readings of intradermal test reactions (in 15 minutes).

Table 5.4 Typical type IV allergy tests.

Table 5.5 Fluorescence under Wood's lamp.

Table 5.6 Major autoantibodies detected in Western blot and their molecular weights.

Chapter 06

Table 6.1‐1 Principles of adsorption and infiltration of topical medicine.

Table 6.1‐2 Relative absorption rate of topical steroids by skin region (forearm=1).

Table 6.2 Characteristics of vehicles.

Table 6.3 Topical steroids.

Table 6.4 Side effects of topical steroids.

Table 6.5 Common antihistamines.

Table 6.6 Common antibiotics and their mechanisms.

Table 6.7 Side effects of corticosteroids.

Table 6.8 Various corticosteroids: comparison of the duration and dose for the same effects.

Table 6.9 Biologic (molecular‐targeted) agents.

Table 6.10 Main side effects of anticancer agents.

Table 6.11 Other dermatological drugs.

Table 6.12 Common lasers.

Chapter 07

Table 7.1 Eczema classified by pathogenesis.

Table 7.2 Main allergens in allergic contact dermatitis.

Table 7.3 Contact dermatitis: Locations and main causes.

Chapter 08

Table 8.1 Types and characteristics of physical urticaria.

Table 8.2 Causes of cutaneous pruritus.

Chapter 09

Table 9.1 Conditions associated with erythema multiforme.

Table 9.2 Erythema multiforme: differential diagnosis.

Table 9.3 Diagnostic criteria for Stevens–Johnson syndrome.

Table 9.4 Disorders associated with Sweet syndrome.

Table 9.5 Classification of annular erythema.

Table 9.6 Causative conditions of erythroderma.

Table 9.7 Examinations useful for diagnosis and treatment of erythroderma.

Chapter 10

Table 10.1 Drug‐induced skin reactions and their typical causative drugs.

Table 10.2 Drug‐induced skin reactions classified by mechanism.

Table 10.3 Diagnostic criteria for drug‐induced hypersensitivity syndrome (DIHS).

Table 10.4 Classification of graft‐versus‐host disease (GVHD).

Table 10.5 Clinical staging of organ dysfunction.

Table 10.6 Grading of acute graft‐versus‐host disease (GVHD).

Chapter 11

Table 11.1 Main clinical symptoms and findings of Churg–Strauss syndrome (based on classification criteria proposed by the American College of Rheumatology).

Table 11.2 Diagnostic criteria of Behçet’s disease.

Table 11.3 Differentiation between Buerger’s disease and arteriosclerosis obliterans.

Table 11.4 Major causes of secondary thrombocytopenic purpura.

Table 11.5 Major types of pigmented purpuric dermatosis.

Table 11.6 Causes of Raynaud’s phenomenon.

Table 11.7 Conditions with livedo (reticularis).

Chapter 12

Table 12.1 Lesions of cutaneous lupus erythematosus.

Table 12.2 1982 Revised criteria for classification of systemic lupus erythematosus.

Table 12.3 Factors associated with onset of SLE.

Table 12.4 Major autoantibodies found in SLE patients.

Table 12.5 Classification of systemic sclerosis (SSc).

Table 12.6 Clinical symptoms of systemic sclerosis (SSc).

Table 12.7 Preliminary criteria for classification of systemic sclerosis (SSc).

Table 12.8 Major specific autoantibodies in collagen diseases and in related diseases.

Table 12.9 Classification criteria for dermatomyositis and polymyositis.

Table 12.10 Revised version of the European classification criteria for Sjögren syndrome (2002).

Table 12.11 Major complications of Sjögren syndrome.

Table 12.12 1987 revised criteria for the classification of rheumatoid arthritis.

Table 12.13 Diagnostic criteria for adult Still's disease.

Chapter 13

Table 13.1 Diagnosis of burn by depth and clinical features.

Table 13.2 Parkland (Baxter) formula.

Table 13.3 Classification of acute radiodermatitis.

Table 13.4 Main drugs that induce photosensitive dermatosis. (Blue font indicates frequently used drugs.)

Table 13.5 Classification of photosensitive dermatosis and pages in which described.

Table 13.6 Phototoxic reaction and photoallergic reaction.

Table 13.7 Comparison between types of xeroderma pigmentosum.

Chapter 14

Table 14.1 Classification of epidermolysis bullosa (EB).

Table 14.2 Types of pemphigus groups.

Table 14.3 Autoantibody against desmoglein detected by ELISA, and confirmed diagnosis.

Table 14.4 Autoimmune blistering diseases that cause subepidermal blisters.

Chapter 15

Table 15.1 New international classification of ichthyosis (the terms in brackets are those used before revision).

Table 15.2 Comparison between types of ichthyosis.

Table 15.3 Major ichthyosis syndromes.

Table 15.4 Major types of palmoplantar keratoderma.

Table 15.5 Types and findings of psoriasis.

Table 15.6 Differential diagnosis of psoriasis.

Table 15.7 Simplified table for calculating for PASI score (assessment of psoriasis severity).

Table 15.8 Classification of pustular psoriasis.

Table 15.9 Classification and features of parapsoriasis.

Table 15.10 Diseases that are differentiated from pityriasis rosea.

Chapter 16

Table 16.1 Major types of oculocutaneous albinism (OCA).

Chapter 17

Table 17.1 Classification of cutaneous amyloidoses.

Table 17.2 Classification of cutaneous amyloidoses.

Table 17.3 Major types of porphyria.

Chapter 18

Table 18.1 Major congenital premature aging syndromes.

Table 18.2 Types of Ehlers–Danlos syndrome (EDS).

Table 18.3 Infection, underlying disease, etc. that cause erythema nodosum.

Chapter 19

Table 19.1 Diseases thought to cause anhidrosis.

Chapter 20

Table 20.1 Underlying diseases of connective tissue nevus.

Table 20.2 Comparison of café au lait spot and Becker’s nevus.

Table 20.3 Diagnostic criteria of neurofibromatosis type 1.

Table 20.4 Major cutaneous symptoms accompanying gastrointestinal polyposis.

Chapter 21

Table 21.1 Classification of hemangiomas and vascular malformation.

Table 21.2 Classification of cutaneous mastocytosis.

Chapter 22

Table 22.1 Preexisting lesions of squamous cell carcinoma.

Table 22.2 TNM classification and stage grouping of SCC (UICC,2002).

Table 22.3 Histopathological findings of actinic keratosis.

Table 22.4 Clinical differences between keratoacanthoma and squamous cell carcinoma (SCC).

Table 22.5 Classification of malignant fibrous histiocytoma (MFH).

Table 22.6 Types of primary cutaneous lymphoma.

Table 22.7 Stage grouping of mycosis fungoides and Sézary syndrome (ISCL/EORTC, 2007).

Table 22.8 Therapeutic examples of CHOP used in the tumor stage of mycosis fungoides.

Table 22.9 Clinical characteristics and types of adult T cell leukemia/lymphoma.

Table 22.10 Differentiation of B cells and cellular surface traits.

Table 22.11 Clinical and pathological findings of the four major types of melanoma.

Table 22.12 Clinical characteristics of melanoma (ABCDE).

Table 22.13 TNM classification of melanoma.

Table 22.14 Classification of anatomical stage of melanoma (AJCC/UICC, 2010).

Chapter 23

Table 23.1 HPV types and clinical symptoms.

Table 23.2 Diagnostic criteria for infectious mononucleosis in infants.

Chapter 25

Table 25.1 Classification of dermatophytes (Blue letters indicate the more important ones).

Table 25.2 The

Candida

species most frequently cultured from humans.

Chapter 26

Table 26.1 Classification of tuberculosis.

Table 26.2 Classification of leprosy.

Chapter 27

Table 27.1 Interpretation of STS and TPHA results, and courses of action.

Chapter 28

Table 28.1 Stages and symptoms of Lyme disease.

Table 28.2 Comparisons between tsutsugamushi disease and diseases that resemble it.

List of Illustrations

Chapter 01

Fig. 1.1

Structure of the skin.

Fig. 1.2

Appearance of the skin surface.

a: Cristae cutis (triangle), sulci cutis and openings of the sweat glands. b: Sweat pores fed by sweat glands open to the cristae cutis (arrows).

Fig. 1.3

Cleavage lines (Langer cleavage lines).

Fig. 1.4

Blaschko's lines.

Fig. 1.5

The four layers of the epidermis.

Fig. 1.6

Ultrastructural anatomy of the epidermis.

Fig. 1.7 Intercellular positions of desmosomes, gap junctions, and hemidesmosomes.

Fig. 1.8

The stratum lucida, which is found in the palms and soles (arrows).

Fig. 1.9

Stratum corneum.

Fig. 1.10

Electron microscopy of the border between the granular cell layer and the stratum corneum.

Fig. 1.11

Electron microscopy of the epidermal basement membrane.

AF, anchoring fibril; HD, hemidesmosome; LD, lamina densa; LL, lamina lucida; Tf, tonofilament.

Fig. 1.12

Microstructure of the basement membrane zone.

Fig. 1.13

Electron microscopy of the basement membrane zone.

Fig. 1.14

Ultrastructural image and illustration of the desmosome.

Fig. 1.15

Molecular components of the gap junction.

Fig. 1.16

Expression of keratin types in the epidermis.

Fig. 1.17

Profilaggrin and filaggrin.

Profilaggrin, which is in phosphorylated form, is stored in the keratohyalin granules of the granular cell layer. Profilaggrin is degraded into filaggrin through the process of dephosphorylation at the time of keratinization. Filaggrin aggregates and binds with keratin fibers in the stratum corneum to form the keratin pattern. Filaggrin ultimately degrades to low molecular weight substances such as urocanic acid and becomes a natural moisturizing factor that is involved in moisture retention and ultraviolet absorption.

Fig. 1.18

The border between the epidermis and stratum corneum.

Fig. 1.19

Melanocytes.

Melanocytes are seen as clear cells (arrows) under hematoxylin and eosin staining, because the cytoplasm of melanocytes shrinks during fixation.

Fig. 1.20

Biosynthesis of melanin.

Fig. 1.21

Maturation of melanosomes.

Fig. 1.22

Langerhans cell (immunostaining against CD1a).

Fig. 1.23

Birbeck granules of Langerhans cell (arrows).

Fig. 1.24

Structure of the dermis.

Fig. 1.25

Electron microscopy of the dermal matrix.

a: Collagen fibers (stars) and elastic fibers (arrows). b: High‐power magnification of collagen fibers. Stripes approximately 60–70 nm in width are seen.

Fig. 1.26

Stripes of collagen fibers.

Fine fibrils (tropocollagens) have cross‐links, giving the fibers the appearance of stripes with intervals of 60–70 nm.

Fig. 1.27

Fibroblasts (arrows).

Fig. 1.28

Histiocytes (arrows).

Fig. 1.29

Mast cells.

a: Hematoxylin and eosin staining. b: Metachromasia is seen by toluidine blue staining.

Fig. 1.30

Mast cell sensitization.

Fig. 1.31

Plasma cells (arrows).

Fig. 1.32

Distribution of blood vessels in the dermis.

Fig. 1.33

Cross‐section of a blood vessel (hematoxylin and eosin).

Fig. 1.34

Cross‐section of lymphatic vessels (hematoxylin and eosin).

Fig. 1.35

Cross‐section of nerve fibers.

a: Myelinated nerve fibers. b: Unmyelinated nerve fibers. c: Electron microscopy.

Fig. 1.36

Meissner corpuscles (arrows).

Fig. 1.37

Pacinian corpuscle (hematoxylin and eosin staining).

Fig. 1.38

Tunica dartos.

Fig. 1.39

Longitudinal section of the hair follicle.

Fig. 1.40‐1

Longitudinal cross‐section of the structure of the hair follicle (hematoxylin and eosin staining).

Fig. 1.40‐2

Cross‐section of the structure of the hair follicle (hematoxylin and eosin staining).

a: Hair follicular isthmus. b: Lower part of a hair follicle. c: Hair bulb. (See Fig. 1.39 for the longitudinal positions.)

Fig. 1.41

Hair cycle.

Fig. 1.42

Sebaceous and sweat glands.

Fig. 1.43

Types of secretion.

Fig. 1.44

Eccrine sweat gland.

a: Cross‐section. b: Longitudinal section of the duct in the epidermis. c: Longitudinal section of the duct in the dermis.

Fig. 1.45

Apocrine sweat gland.

Fig. 1.46

Apocrine (beheading) secretion of the sweat gland.

Fig. 1.47

Anatomy of the nail.

Fig. 1.48

Myelogenous cells composing the immune system.

Fig. 1.49

HLA (human leukocyte antigen) genes on the short arm of chromosome 6. Genetic recombination causes the HLA pattern to differ for each individual.

Fig. 1.50

Immune reactions classified by MHC class.

Each class of MHC presents antigen information to a different type of T cell.

Fig. 1.51

Basic structure of human immunoglobulin (IgG).

Fab, fragment antigen binding. Fc, crystallizable fragment. VL, variable light chain. CL, constant light chain. VH, variable heavy chain. CH, constant heavy chain.

Fig. 1.52

Eosinophils.

The cytoplasm is eosinophilic (red in hematoxylin‐eosin staining). Note the multiple nuclei.

Fig. 1.53

Neutrophils.

In skin, the cytoplasm of neutrophils is less eosinophilic than that of eosinophils. A neutrophil has a multi‐segmented nucleus.

Fig. 1.54

Langerhans cell electron micrograph.

A high‐power magnification of the part in the red square is shown in Fig. 1.55.

Fig. 1.55

Birbeck granules (arrows).

A high‐power magnification of the part in the red square in Fig. 1.54. In cross‐section, Birbeck granules look like tennis rackets.

Fig. 1.56

Mechanism of allergic contact dermatitis.

Chapter 02

Fig. 2.1

Procedure of skin biopsy.

a–c: Punch biopsy. d: Incisional biopsy with a scalpel.

Fig. 2.2‐1

Normal skin (hematoxylin and eosin staining).

a: Normal skin of the forearm. The horny cell layer has a basket‐weave appearance. The gaps between the stained horny cell layers are lipids that dissolved during fixation. These gaps indicate that the skin is well protected by moisturizing lipids.

Fig. 2.2‐2

Normal skin (hematoxylin and eosin staining).

a: Normal skin of the sole. A thick stratum corneum is seen. b: Scalp. Many follicles can be seen. c: Face. Sebaceous glands are abundant.

Fig. 2.3

Patterns of acanthosis.

Fig. 2.4

Acanthosis

(Chronic eczema)

Fig. 2.5

Epidermal atrophy

(Dermatomyositis)

Fig. 2.6

Hyperkeratosis

(Chronic eczema)

Fig. 2.7

Parakeratosis

(Psoriasis vulgaris)

Fig. 2.8

Dyskeratosis

(Bowen’s disease)

Fig. 2.9

Hypergranulosis

(Parapsoriasis)

Fig. 2.10

Granular degeneration

(Epidermolytic ichthyosis)

Fig. 2.11

Spongiosis

(Acute eczema)

Fig. 2.12

Intracellular edema

(Herpes simplex)

Fig. 2.13

Acantholysis

(Hailey–Hailey disease)

Fig. 2.14

Bulla

(Bullous pemphigoid)

Fig. 2.15

Munro’s microabscess

(Psoriasis vulgaris)

Fig. 2.16

Kogoj’s spongiform pustule

(Pustular psoriasis)

Fig. 2.17

Pautrier’s microabscess

(Mycosis fungoides)

Fig. 2.18

Vacuolar degeneration.

a: Graft‐versus‐host disease. Dyskeratosis is also seen from the apoptosis of the epidermal keratinocytes. b: Lichen planus. Civatte bodies are seen immediately below the epidermis (arrow).

Fig. 2.19

Foreign‐body granuloma.

a: Folliculitis. Giant cells are clearly seen. b: Cholesterol crystal embolization (CCE) (blue toe syndrome). Cholesterin crystals (arrows).

Fig. 2.20

Giant cells originating from histiocytes.

Fig. 2.21

Differences between septal panniculitis and lobular panniculitis.

Fig. 2.22

Septal panniculitis

(Erythema nodosum)

Fig. 2.23

Lobular panniculitis

(Erythema induratum)

Fig. 2.24

Mechanisms of immunofluorescence (bullous pemphigoid)

Fig. 2.25

Immunofluorescence (bullous pemphigoid).

a: Direct immunofluorescence. Linear IgG deposition is seen along the basement membrane of the patient’s skin. b: Indirect immunofluorescence (IIF). A 1/320 dilution of the patient’s serum is used on the skin sample from a healthy person. Anti‐basement membrane antibodies are seen in the blood.

Fig. 2.26

Immunoelectron microscopy of the bullous antigen in normal human skin labeled with gold colloid.

a: BP230 is immediately inside the basal cell membrane, a component of the hemidesmosome. b: BP180 (type XVII collagen), a transmembrane protein in the basement membrane zone. NC16a, the most important domain for BP pathogenesis, is in the basal cell membrane.

Chapter 03

Fig. 3.1

Dermoscopes.

a: Delta10 (Heine). b: Lumio (3Gen). c: Derma9500 (Derma Medical). d: DermLite II Pro (J. Hewitt). e: DermLiteDL100 (J. Hewitt).

Fig. 3.2

Dermoscopic images (clarification by using gel)

Fig. 3.3

Diagnostic algorithm (two‐phase diagnosis)

Fig. 3.4

Parallel pattern

Fig. 3.5

Parallel furrow pattern

(nevus cell nevus)

Fig. 3.6

Parallel ridge pattern

(malignant melanoma)

Fig. 3.7

Fibrillar pattern

(nevus cell nevus)

Fig. 3.8

Pigment network

(nevus cell nevus)

Fig. 3.9

Pigment network

Fig. 3.10

Pseudo‐network

(malignant melanoma)

Fig. 3.11

Globules

Fig. 3.12

Cobblestone pattern

(nevus cell nevus)

Fig. 3.13

Streaks: starburst pattern

(Spitz nevus)

Fig. 3.14

Homogeneous pattern: homogeneous blue pigmentation

(blue nevus)

Fig. 3.15

Multicomponent pattern: malignant melanoma

Fig. 3.16

Comedo‐like opening.

Fig. 3.17

Multiple milia‐like cysts.

Fig. 3.18

Fingerprint‐like structures: light‐brown

Fig. 3.19

Cerebriform pattern/brain‐like appearance

(with fissure and ridges).

Fig. 3.20

Arborizing vessels

Fig. 3.21

Spoke wheel areas

Fig. 3.22

Leaf‐like structures

Fig. 3.23

Multiple blue‐gray globules/large blue‐gray ovoid nests.

Fig. 3.24

Red‐blue lacunae

(angiokeratomas)

Fig. 3.25

Red‐bluish to reddish‐black homogeneous areas

(venous lake)

Fig. 3.26

Dotted vessels in the paronychium

(dermatomyositis)

Fig. 3.27

Linear vessels

(spider telangiectasia)

Fig. 3.28

Dermatofibroma

Fig. 3.29

White fibrous papulosis of the neck

Chapter 04

Fig. 4.1

Erythema

(Annular erythema in a patient with Sjögren syndrome)

Fig. 4.2

Skin lesions.

Macule colors and their respective changes.

Fig. 4.3

Purpura

(Henoch–Schönlein purpura)

Fig. 4.4

Pigmented macule

(Senile freckle)

Fig. 4.5 Association between the site of melanin deposition and the color of the lesion.

Fig. 4.6

Leukoderma

(Vitiligo vulgaris)

Fig. 4.7 Various papules.

Fig. 4.8

Papule

(Lichen nitidus)

Fig. 4.9

Nodule

(Dermatofibrosarcoma protuberans)

Fig. 4.10

Blisters.

Fig. 4.11

Blisters.

a: Bullous pemphigoid. b: Insect bite.

Fig. 4.12

Pustule, cyst, and wheal.

Fig. 4.13

Pustule

(Palmoplantar pustulosis: localized pustular psoriasis)

Fig. 4.14

Cyst

(Epidermal cyst)

Fig. 4.15

Wheal

(Acute urticaria)

Fig. 4.16

Atrophy

(Widespread striae atrophicae)

Fig. 4.17

Atrophy and hypertrophic scar.

Fig. 4.18

Scaling

(Psoriasis vulgaris)

Fig. 4.19

Crusts.

a: Epidermolysis bullosa simplex. b: Psoriasis vulgaris.

Fig. 4.20

Keloid

Fig. 4.21

Erosion

(Bullous pemphigoid)

Fig. 4.22

Ulcer

(Chronic radiochematic)

Fig. 4.23

Ulcer. Chronic radiation dermatitis.

[was Fig. 4.22]

Fig. 4.24

Fissure

(Angular cheilitis)

Fig. 4.25

Aphtha

(Patient with Behçet’s disease)

Fig. 4.26

Leukoplakia.

Fig. 4.27

Lichen

(Lichen amyloidosis)

Fig. 4.28

Lichenification

(Atopic dermatitis)

Fig. 4.29

Plaque.

a: Extramammary Paget’s disease. b: Mycosis fungoides.

Fig. 4.30

Condyloma

(Left: Condyloma acuminatum. Right: Condyloma latum)

Fig. 4.31

Acne

(Acne vulgaris)

Fig. 4.32

Comedo.

a: Solitary giant comedo. b: Favre–Racouchot syndrome.

Fig. 4.33

Sycosis

(Sycosis vulgaris)

Fig. 4.34

Erythroderma

(Patient with Hodgkin’s disease)

Fig. 4.35

Livedo reticularis.

Fig. 4.36

Herpes

(Herpes zoster)

Fig. 4.37

Impetigo

(Impetigo contagiosa)

Fig. 4.38

Pityriasis

(Pityriasis rosea)

Fig. 4.39

Ichthyosis

(Lamellar ichthyosis)

Fig. 4.40

Poikiloderma

(Dermatomyositis)

Fig. 4.41

Sclerosis

(Morphea)

Fig. 4.42

Alopecia

(Alopecia areata)

Fig. 4.43

Köbner phenomenon

(Verruca plana)

Fig. 4.44

Darier’s sign

(Mastocytosis.) Edema is marked.

Fig. 4.45

Dermographism

(Factitious urticaria)

Fig. 4.46

White dermographism

(Atopic dermatitis)

Chapter 05

Fig. 5.1

Lesion shapes.

Fig. 5.2

Lesion profiles.

Fig. 5.3

Shapes of elevation.

Fig. 5.4

Patch test.

a: The antigens are spread on adhesive plasters that are included in the patch test unit. These are then stuck to the back of the patient. b: If the patient is allergic to the antigen, various allergic reactions (edematous erythema and papules (arrows)) are seen 48 hours later.

Fig. 5.5

Prick lancet.

Fig. 5.6

Ultra‐violet photo test for minimal erythema dose (MED).

Erythema appears at the site of 30 mJ/cm

2

irradiation. The MED for this patient is 30 mJ/cm

2

.

Fig. 5.7

Ultrasound test.

a: Equipment. b: Pilomatricoma in the upper arm (the area encircled by the broken line; see Chapter 21). An area with acoustic shadow that reflects calcification is observed (arrows).

Fig. 5.8

Thermography.

The hands of a patient with systemic sclerosis (see Chapter 12). The second and third fingers of the right hand show markedly low skin temperature.

Fig. 5.9

Sweat function test.

The forearm of a patient with cholinergic urticaria. Sweat is detected by using starch‐iodine.

Fig. 5.10

Electric hygrometer: measuring transepidermal water loss (TEWL).

Fig. 5.11

Diagnosing tinea pedis.

Scales or swabbed blister contents are sampled from the interdigital area. Microscopic examination is made with potassium hydrate.

Fig. 5.12

Diascopy.

a: Transparent glass plate for diascopy. b,c: Erythema disappears with pressure from the glass plate. d,e: Purpura does not disappear with such pressure.

Fig. 5.13

a: Wood’s lamp. b: Photodynamic diagnosis of extramammary Paget’s disease.

Wood’s lamp reveals the area of the lesion, after δ‐aminolevulinic acid ointment is applied in an occlusive dressing.

Fig. 5.14

Western blotting.

Serum from a bullous pemphigoid patient reacts against skin antigens (molecular weights of 180 kDa (type XVII collagen) and 230 kDa (BP230)).

Fig. 5.15

DNA analysis of type VII collagen in a patient with dystrophic epidermolysis bullosa.

A point mutation (6781 in exon 86) causes a nonsense mutation. Instead of arginine (CGA), a stop codon (TGA) occurs at 2261 amino acid.

Chapter 06

Fig. 6.1

Size of molecule versus estimated permeability in skin under various conditions.

AD, atopic dermatitis skin; M, mucosa; NS, normal skin; US, ultrasound‐treated human skin without stratum corneum.

Fig. 6.2

Illustration of water‐in‐oil (w/o) emulsified ointment and oil‐in‐water (o/w) cream.

a: w/o emulsified ointment. Water granules are dispersed in oil by emulsion. b: o/w emulsive cream. Oil granules are dispersed in water.

Fig. 6.3

Topical agents with various vehicles.

a: Oleaginous ointment. b: Cream. c: Lotion.

Fig. 6.4

30% Salicylic acid plaster.

Wound dressing.

Fig. 6.5

Zinc oxide sheet.

Fingertip unit.

Fitzpatrick; classification. Japan; Japanese classification.

Fig. 6.6

Laser therapy.

a: Dye laser. b: Alexandrite laser. Skin whitening is seen immediately after laser irradiation.

Fig. 6.7

Lasers.

a: Carbon dioxide laser. b: Dye laser. c: Alexandrite laser. d: Ruby laser.

Fig. 6.8

Optical absorption spectrum in human skin.

Fig. 6.9

UV irradiation instrument (narrow‐band UVB/UVA).

Fig. 6.10

Cryotherapy (using stype).

Fig. 6.11

Cryotherapy (using spray).

Fig. 6.12

Excision and suture.

Fig. 6.13

Excision of keratoacanthoma:

Skin defect was closed by V‐T flap.

Fig. 6.14

Surgery of malignant melanoma on the heel (skin flap).

a: Melanoma on the right heel. b: Presurgical design. The inner plantar artery is located by Doppler blood flow sensor (shown by the x's). c: The prepared skin flap. d: The flap is moved to the site where the melanoma was removed. e: Mesh grafting is done on the sole. f–j: Follow‐up photos.

Fig. 6.15

Skin thicknesses and various graft procedures.

Fig. 6.16

Various pedicled flaps.

Fig. 6.17

Split‐thickness skin graft was obtained using silver knife.

Fig. 6.18

Skin grafting and tie‐over.

Fig. 6.19

Electrocoagulation.

Chapter 07

Fig. 7.1

Eczema.

a: Eczema with reddening. b: Eczema with crusts and partial infiltration.

Fig. 7.2

Course and symptoms of eczema.

Fig. 7.3

Various factors causing eczema:

Extrinsic and intrinsic factors interact, resulting in eczema formation.

Fig. 7.4

Histopathology of eczema.

a: Acute eczema. Spongiosis (arrows) has formed from intercellular edema. Lymphocytic infiltration is also seen. b: Chronic eczema. Hyperkeratosis, regular acanthosis and elongation of epidermal rete ridge are noted. Spongiosus is not severe.

Fig. 7.5

Acute eczema.

a: Multiple edematous erythema on the face. b: Pruritic erythema with scattered papules. Some vesicles are seen.

Fig. 7.6

Chronic eczema.

Hyperkeratosis is severe, as in tylosis. Erythema and fissures are seen.

Fig. 7.7‐1

Contact dermatitis.

a: From an unknown cause, probably a surfactant such as soap or detergent. b: From a clothing. c: Systemic contact dermatitis called “Shiitake dermatitis”, which occurs after raw shiitake mushrooms are eaten. The erythema is strongly itchy and infiltrative. d: Contact dermatitis from tattooing. Erythema with itchiness and infiltration occur as an allergic reaction to red pigments.

Fig. 7.7‐2

Contact dermatitis.

From an NSAID plaster.

Fig. 7.8

Contact dermatitis from gold earrings.

Diaper dermatitis and lip licker's dermatitis.

Fig. 7.9‐1

Atopic dermatitis.

a: Adult male. Erythema is seen on the face and neck. Erosion and infiltration from scratching are seen. Thinning of the outer edges of the eyebrows (Hertoghe's sign) is observed. b: A line in the skin below the lower eyelid (Dennie–Morgan fold) is observed. c: “Dirty neck”. Poikilodermatous pigmentation is seen on the neck and upper chest. d: Poikilodermatous pigmentation is widespread on the upper body. e: Adult male. Scattered eruptions from scratching are seen. f: Scars from scratching and hair loss are seen in the occipital region of the head, a complication of trichotillomania (Chapter 19, p. 350) from mental stress. g: Complicated with ichthyosis vulgaris (Chapter 15, p. 251). h: Rapidly aggravated infiltrative erythema, consistent with non‐bullous impetigo (Chapter 24, p. 489).

Fig. 7.9‐2

Atopic dermatitis.

a: Child. b: Multiple pruritus from scratching. c: Erythrodermic atopic dermatitis.

Fig. 7.9‐3

Atopic dermatitis.

a: Atopic dermatitis of the hands with contact dermatitis. b, c: Erythema, scales and exfoliation on the flexor of the lower leg.

Fig. 7.10

White dermographism in a patient with atopic dermatitis.

Fig. 7.11

Seborrheic dermatitis.

a: Scalp. Erythema with scales. b: Face.

Fig. 7.12

Nummular eczema.

Multiple round eczema of 1 to 5 cm in diameter.

Fig. 7.13

Lichen simplex chronicus (lichen Vidal).

Long‐time friction from clothes is the cause. It is a chronic eczema.

Fig. 7.14‐1

Autosensitization dermatitis.

Disseminated eczematous eruptions are seen.

Fig. 7.14‐2

Autosensitization dermatitis.

Infantile eczema.

Fig. 7.15

Stasis dermatitis.

Edematous, dark‐red erythema with scales.

Fig. 7.16

Asteatotic eczema.

Wiskott–Aldrich syndrome.

Fig. 7.17

Pompholyx.

Multiple vesicles on the palm.

Fig. 7.18

Dyshidrotic eczema.

Chapter 08

Fig. 8.1

Eruption of urticaria

. It is characteristically itchy, with slightly elevated erythema and wheals.

Fig. 8.2

Chronic urticaria.

Fig. 8.3

Mechanism of urticaria

. Chemical mediators such as histamines from mast cells induce vascular hyperpermeability, which causes intradermal edema.

Fig. 8.4

Dermographism

. Mechanical stimuli such as rubbing cause wheals (urticaria).

Fig. 8.5

Cholinergic urticaria.

a: Small, multiple wheals are seen. b: Sweating test reveals that wheals appear at locations of sweat glands.

Fig. 8.6

Angioedema.

a: Severe swelling on the right palpebra. b: Severe edema on the lower lip. c: Angioedema on the right side of the tongue.

Fig. 8.7

Prurigo nodularis.

Small, severely itchy nodules of 5–20 mm diameter are noted. Excoriation is also seen.

Fig. 8.8

Histopathological findings of prurigo nodularis.

Acanthosis and inflammatory cell infiltration in the upper dermis are noted. Excoriation induces even more severe acanthosis.

Fig. 8.9

Prurigo chronica multiformis.

Fig. 8.10

Prurigo pigmentosa.

a: Prurigo pigmentosa in a female patient in her 20s. Fresh red erythema is mixed with old lesions, which are seen as reticular hyperpigmented macules. b: Erythematous macules (arrows) are seen at the center of reticular hyperpigmentation. This is a recurrence of prurigo pigmentosa.

Chapter 09

Fig. 9.1‐1

Erythema multiforme

. Well‐demarcated edematous exudative erythema disseminates on the dorsal hand (a) and elbow (b). The size is up to 2 cm. Note the central concavities.

Fig. 9.1‐2

Erythema multiforme

. The central concavities give a characteristic iris‐like appearance.

Fig. 9.2‐1

Stevens–Johnson syndrome

. Erythema multiforme rapidly spreads over the entire body. Some lesions overlap to form large plaques on the back. A bull’s‐eye pattern, characteristic of erythema multiforme, is seen at the border of a plaque.

Fig. 9.2‐2

Stevens–Johnson syndrome

. Erosions and blistering are seen in some parts (arrows).

Fig. 9.3

Sweet syndrome

.

Fig. 9.4

Histopathology of Sweet’s disease.

Dense neutrophilic infiltration on the entire dermis without apparent vasculitis.

Paper money skin.

Fig. 9.5‐1

Erythema annulare centrifugum

.

Fig. 9.5‐2

Erythema annulare centrifugum

.

Fig. 9.6

Erythema gyratum repens

.

Fig. 9.7‐1

Erythroderma

. A case of atopic dermatitis that became erythroderma.

Fig. 9.7‐2

Erythroderma associated with Hodgkin’s disease

. Flushing and marked scaling are seen on the entire body. The severity of the skin lesions mirrors that of Hodgkin’s disease.

Fig. 9.7‐3

Erythroderma

. a: A case that accompanied Hodgkin’s disease. Normal skin appears on the abdomen and shoulders, where the conditions of Hodgkin’s disease are improving (arrows). b: A case that accompanied mycosis fungoides.

Fig. 9.8

Deck‐chair sign.

A case of Ofuji papuloerythroderma.

Chapter 10

Fig. 10.1‐1

Drug‐induced skin reaction.

Diffuse edematous erythema on the back. Each eruption was an erythema multiforme‐like erythema of 1–2 cm in diameter that gradually enlarged and tended to coalesce.

Fig. 10.1‐2

Drug‐induced skin reaction

. a: Drug‐induced erythema enlarge and coalesce to form erythroderma. b: Hand‐foot syndrome caused by the chemotherapy drug tegafur.

Fig. 10.2‐1

Various types of drug‐induced skin reaction.

a,b: Erythema multiforme‐like. Although uniformly colored erythematous plaques are mainly seen, newly formed erythema is seen at the periphery, some parts of which show the target‐like appearance that characterizes erythema multiforme. c: Purpuric. Dark red macules up to 1 cm in diameter are observed. These do not disappear by diascopy pressure, which indicates that the eruption is purpura.

Fig. 10.2‐2

Various types of drug‐induced skin reactions

. Urticarial drug eruptions. Edematous erythema resembling urticaria is seen on the trunk and palms.

Fig. 10.3

Fixed drug eruption (FDE).

a: Early FDE on the right eyelid. Early lesions are edematous erythema without pigmentation. b: FDE on the abdomen. Repeated intake of causative drug results in a severely pigmented FDE lesion. c,d: FDE on the thigh. The center of the lesion shows characteristic pigmentation caused by chronic inflammation. The periphery is erythematous, which suggests recent intake of the causative drug. e: FDE on the interdigital area. Erythema and bullous lesions are seen.

Fig. 10.4‐1

Toxic epidermal necrolysis (TEN)

.

Fig. 10.4‐2

Toxic epidermal necrolysis

.

Fig. 10.5

The pathogenic association of fixed drug eruption (FDE), toxic epidermal necrolysis (TEN), Stevens–Johnson syndrome (SJS), and erythema multiforme (EM).

Fig. 10.6

Toxic epidermal necrolsis (Lyell’s syndrome); Occurred in a black man.

Fig. 10.7

Drug‐induced hypersensitivity syndrome (DIHS).

Fig. 10.8

Acute generalized exanthematous pustulosis.

Fig. 10.9

Hand‐foot syndrome.

Fig. 10.10‐1

Acute graft‐versus‐host disease

. a: Diffuse erythema on the back after bone marrow transplantation. Clinically, differential diagnosis from drug eruption is almost impossible. b,c: Severe acute GVHD. Severe exfoliation similar to toxic epidermal necrolysis is seen.

Fig. 10.10‐2

Acute graft‐versus‐host disease

. a: Small, diffuse, multiple erythema appear, and partly coalescing eruptions are seen. The eruptions coalesce and form plaques on the lower leg. b: Erosions on the lips and mucosa.

Fig. 10.11

Chronic graft‐versus‐host disease.

Multiple purplish red plaques are seen on the forearm. The lesions are clinically similar to those of lichen planus.

Chapter 11

Fig. 11.1

Cutaneous small vessel vasculitis

. The skin lesion presents a mix of purpura, papules, nodules, pustules, blisters, erosions, and ulcers. It is accompanied by sharp pain.

Fig. 11.2

Cutaneous vasculitis and the depth of the affected vessels.

Fig. 11.3‐1

Cutaneous small‐vessel vasculitis (CSVV)

. The disease presents various cutaneous clinical features including purpura, erythema, bloody blisters, and ecchymosis.

Fig. 11.3‐2

Cutaneous small‐vessel vasculitis (CSVV).

Fig. 11.4

Histopathology: Fibrinoid degeneration of the vessel walls in the upper dermis.

Fig. 11.5‐1

Henoch–Schönlein purpura.

Palpable purpura may be accompanied by bloody blisters in some cases.

Fig. 11.5‐2

Henoch–Schönlein purpura.

Fig. 11.6

Direct immunofluorescence of Henoch‐Schönlein purpura.

IgA deposition on the vascular wall in the upper dermis is observed.

Fig. 11.7

Erythema elevatum diutinum.

a: Elevated reddish‐purple plaques and fibrotic tissues are seen. b: Blisters may form.

Fig. 11.8

Polyarteritis nodosa.

a: Nodules with palpable, severe infiltration. b: Coalesced purpura. c: Advanced polyarteristis nodosa accompanied by ulceration.

Fig. 11.9

Histopathology of PN

. Thickened vessel walls of medium‐sized arteries, fibrinoid degeneration, and leukocytoclastic vasculitis are accompanied by neutrophilic infiltration.

Fig. 11.10

Churg–Strauss syndrome.

Infiltrative subcutaneous nodules, purpura, and erythema are seen.

Fig. 11.11

Wegener’s granulomatosis

a: Gangrenous papules. b: Ulceration in the oral cavity. c: Multiple subcutaneous nodules on the back.

Fig. 11.12‐1

Behçet’s disease

. a,b: Recurrent aphtha in the oral cavity accompanied by sharp pain. c: Deep ulceration in the genitalia.

Fig. 11.12‐2

Behçet’s disease

. a: Deep ulceration in the genitalia. b,c: Nodular erythema‐like eruptions. d,e: Folliculitis‐like eruptions.

Fig. 11.13

Kawasaki's disease

. Firm edema and scaling in characteristic pattern.

Fig. 11.14

Pyoderma gangrenosum

. Various clinical features are seen.

Fig. 11.15

Buerger's disease

. a: Bluish discoloration (cyanosis) of the first toe. b: Progressive ulceration of the first toe. c: Necrosis of the first toe caused by impaired blood circulation.

Fig. 11.16

Mondor disease

. Subcutaneous, cordlike indurations (arrow) are observed.

Fig. 11.17

Histopathology of Mondor's disease.

Fig. 11.18

Pigmented purpuric dermatosis.

Fig. 11.19

Histopathology of pigmented purpuric dermatosis

. Perivascular lymphocytic infiltration in the upper dermis, hemorrhage, and deposition of hemosiderin.

Fig. 11.20

Steroid purpura.

Fig. 11.21

Raynaud's phenomenon.

Erythema ab igne.

Fig. 11.22 Varicose veins. Superficial veins of lower legs enlarge in serpentine, nodular or cystiform patterns.

Fig. 11.23 Chronic venous insufficiency (livedo).

Fig. 11.24 Livedo.

Fig. 11.25 Livedo vasculopathy. a: Livedo on the dorsa of foot. b: Ulcerations with livedo are seen on the lower legs. c: Ulceration on the lower leg, accompanied by atrophie blanche (arrows).

Fig. 11.26 Lymphedema. a: Marked swelling occurs secondarily in the lower leg. b: A skin lesion with extremely hypertrophic changes resembles elephant skin.

Chapter 12

Fig. 12.1‐1

Systemic lupus erythematosus (SLE)

. a: Butterfly rash and edematous erythema on the cheeks of a young woman. The skin lesion does not usually spread to the nasolabial groove and lips. Butterfly‐shaped erythema. b: Butterfly rash from recurrence of SLE in a woman in her 30s. Such rashes may recur with aggravation of the SLE.

Fig.12.1‐2

Systemic lupus erythematosus.

Fig. 12.1‐3

Systemic lupus erythematosus (SLE)

. a: Diffuse alopecia caused by SLE. In this case, discoid lupus erythematosus (DLE) is present at the sites with alopecia. b: Edematous erythema and papules on the trunk during the acute stage. c: A large ulcer in the pharyngeal region. Large oral mucosal ulcers may be seen in SLE. d: Diffuse erythema on the sole and toes. e: Skin lesion on fingers caused by DLE. Tenderness may be present.

Fig. 12.2

Main eruptions caused by systemic lupus erythematosus and their frequency (% of cases).

Fig. 12.3

Lupus band test.

Normal skin in the unexposed area of a patient with SLE, observed by direct immunofluorescence. There is linear deposition of IgG (fluorescent green) in the epidermal basement membrane. The nuclei stain orange.

Fig. 12.4‐1

Discoid lupus erythematosus (DLE).

a: Affected nasal skin of a man in his 20s. The skin lesion consists of a sharply demarcated macule with a reddish‐pink center. The periphery of the lesion has a brown discoloration and is accompanied by scaling. b: A sharply demarcated skin lesion accompanied by dilated hair follicles on the cheek of a woman in her 20s. The lesion is partly erosive. c: A lesion of DLE at a comparatively early stage on the cheek. d: A skin lesion present on the right cheek of a woman in her 30s. Multiple DLE lesions develop and gradually enlarge or coalesce into large plaques.

Fig.12.4‐2

Discoid lupus erythematosus (DLE).

a: DLE on the auricle, particularly noticeable on the lobule. The center of the lesion is scarred. b: DLE on the lips. Erythema and purple eruptions are present. It should be differentiated from lichen planus. DLE of the lips may induce squamous cell carcinoma. c: DLE on the dorsum of the hand and fingers.

Fig. 12.5

Widespread discoid lupus erythematosus (DLE).

Large areas on the trunk and arms are involved.

Fig. 12.6

Histopathology of discoid lupus erythematosus (DLE).

There is a vascular degeneration in the basal cell layer, lymphocytic infiltration in the blood vessels and peripheral skin appendages, and severe edema and mucin deposition in the dermis. Neutrophils and eosinophils are rarely seen.

Fig. 12.7

Lupus erythematosus profundus.

Large panniculitis in the skin of a patient with SLE. DLE eruptions are present on the skin surface.

Fig. 12.8

Subacute cutaneous lupus erythematosus (SCLE)

. a: Annular polycyclic SCLE on the back. The center of the lesion heals centrifugally. This condition resembles the annular erythema of Sjögren syndrome. b: Papules with scaling.

Fig. 12.9

Annular erythema in neonatal lupus erythematosus.

a: Annular erythema on the cheek of an infant with neonatal lupus erythematosus. It begins as erythema of 5–10 mm diameter and gradually enlarges. The center of the lesion tends to regress; however, marked edema and elevation occur in the periphery. b: Two annular erythema on the face.

Fig. 12.10

Bullous lupus erythematosus.

Bullous LE in a patient with SLE. Vesicles form not only on the LE erythema but also on the normal‐looking skin.

Fig. 12.11‐1

Systemic sclerosis.

a: There is intense sclerosis and impaired movement in the fingers. b: The sclerosis leads to reduced finger extension, a condition known as “prayer sign.” c: The fingertips, particularly those of the index finger, are lost or shortened due to necrosis from impaired circulation.

Fig. 12.11‐2

Systemic sclerosis.

a: Mask‐like face. b: Microglossia. c: Ulceration and gangrene in the first and second digits.

Fig. 12.12

Localized scleroderma (morphea).

a: A sclerotic plaque of 10 cm diameter on the extensor surface of the forearm. The center of the lesion appears ivory‐colored, with a glossy texture. A lilac ring with a faint erythema is present around the lesion. b,c: Morphea on the precordial region. d: Linear scleroderma (lip of a child).

Fig. 12.13

Scleroderma en coup de sabre.

Linear scleroderma with facial hemiatrophy. Alopecia and sclerosis on the head. It resembles the slash of a sword. Atrophy occurs in the hypodermic scalp.

Fig. 12.14

Eosinophilic fasciitis.

The skin on the lower legs is hardened and glossy. Skin hardening is not seen on the dorsa of the foot or toes.

Fig. 12.15‐1

Dermatomyositis (DM)

. Diffuse, edematous erythema accompanied by itching on the trunk. Flagellate erythema (arrows) caused by scratching is seen on the left precordial region.

Fig. 12.15‐2

Dermatomyositis (DM)

, Edematous erythema (a, b), Poikiloderma (c, d).

Fig. 12.15‐3

Dermatomyositis (DM).

a: Multiple, scattered, sharply demarcated keratotic papules of several millimeters in diameter on the extensor joints of DIP and PIP of fingers (Gottron’s sign). b: Gottron’s sign. c: Papules may occur on the flexor joints (reverse Gottron’s sign). d: Intense edema and purplish eruptions on the eyelids (heliotrope rash). e: Telangiectasia of the nail folds.

Fig. 12.16

Dermatomyositis (DM) in children.

a: Diffuse erythema accompanied by scaling on the face and trunk. b,c: The cheeks are most commonly involved. The skin lesion clinically resembles the butterfly rash of SLE.

Fig. 12.17

Cutaneous symptom of dermatomyositis (mechanic’s hand).

Fig. 12.18

Mixed connective tissue disease (MCTD).

Fig. 12.19

Antiphospholipid antibody syndrome (APS)

. Intractable skin ulcer and purpura on the lower leg of a middle‐aged postmenopausal woman. The ulceration results from circulatory disorder caused by angioma that is induced by antiphospholipid antibodies.

Fig. 12.20

Sjögren syndrome

. It begins with elevated, edematous erythema 1 cm in diameter. The erythema gradually enlarges and becomes ring‐shaped. It occurs multiply in most cases. The center of the erythema tends to heal, and there is severe infiltration at the periphery. Sjögren syndrome resembles the skin lesions seen in neonatal lupus erythematosus.

Fig. 12.21

Relapsing polychondritis.

Fig. 12.22

Rheumatoid arthritis

. a: Rheumatoid nodules. b: Ulceration from rheumatic vasculitis in the lower extremity.

Fig. 12.23

Adult‐onset Still’s disease.

Chapter 13

Fig. 13.1

Second‐degree burn

. Mix of superficial dermal burn (SDB) and deep dermal burn (DDB), caused by hot water.

Fig. 13.2

First‐ and second‐degree burns caused by explosion of a cigarette lighter.

Fig. 13.3

Burns

. a,b: Second‐degree burns caused by hot water. Marked blistering is present. c: The epidermis has exfoliated with the stripping of clothes that were wetted by the scalding water. Third‐degree burn is also present.

Fig. 13.4

Third‐degree low‐temperature burn

. a: This burn was caused by a heated pad that was adhered to the skin for a long time during sleep. Although the burn seems small and superficial, it is deep and third degree. b: Third‐degree burn caused by a hot water bottle during sleep. The patient has diabetes and diminished sensation in the peripheral nerves.

Fig. 13.5

Chilblains (pernio).

Fig. 13.6‐1

Chemical burn.

Fig. 13.6‐2

Chemical burn.

Fig. 13.7

Electric burn.

Fig. 13.8

Acute radiodermatitis

. Blistering after electron beam irradiation.

Fig. 13.9

Chronic radiodermatitis

. a: Chronic radiodermatitis on buttocks exposed to therapeutic irradiation for uterine cancer. Poikiloderma and ulcerations are seen in some areas. The skin lesions are potential sites for the development of squamous cell carcinoma. b: Chronic radiodermatitis in a 62‐year‐old male. Chronic radiation‐induced actinic keratosis is present on the flexor of a DIP joint. This patient was diagnosed with tinea manus about 30 years earlier and had been treated with therapeutic soft X‐ray irradiation.

Fig. 13.10 Pressure ulcer, decubitus.

Fig. 13.11

Areas most likely to be affected by pressure ulcers.

The most frequently involved areas are the sacral region, the ischial tuberosity and the bony areas of the skin, including the ankles, which tend to be subjected to pressure from the body weight during bed rest.

Fig. 13.12

Akatsuki disease in a woman in her 20s

. There is marked deposition of keratin. This patient hardly ever washed her nipples for fear that she would contract a skin disease.

Fig. 13.13

Navel stone

. This is so‐called bellybutton lint. The patient consulted a doctor on what seemed to be a black tumor in the navel. When it was pulled out, there was a grimy mass of keratin. The patient had believed the superstition that the navel must not be washed.

Fig. 13.14‐1

Solar dermatitis, sunburn.

a: Solar dermatitis caused by sleeping for 3 h on the beach. Blistering is marked. The cutaneous symptoms are equivalent to those of first‐degree and second‐degree burns.

Fig. 13.14‐2

Solar dermatitis, sunburn.

Note the marked difference between skin that was covered by swimwear and skin that was exposed to direct sunlight.

Fig. 13.15

Mechanism of photoallergic reaction

. Secondary and further intake of the causative substance (elicitation).

Fig. 13.16

Photo‐patch testing.

Fig. 13.17‐1

Chronic actinic dermatitis.

a: Intractable eczema presents as lichenified plaques that progress slowly. b: The skin lesions improved significantly after topical application of tacrolimus for several months. c: The skin lesions recurred after sun exposure.

Fig. 13.17‐2

Chronic actinic dermatitis (CAD).

a: Chronic eczematous skin lesions accompanied by intense itching on the occipital region. b: A clearly demarked red plaque on the occipital region. Involvement of sunlight is suggested. c: Flatly elevated plaques on the cheek. d: Lichenoid plaque and prurigo nodularis on the dorsa of the hands.

Fig. 13.18

Hydroa vacciniforme.

Fig. 13.19

Xeroderma pigmentosum (group D).

a: Pigmentation is seen on the face of a woman in her 40s. b: Pigmentation mainly on the sun‐exposed areas of a male in his teens. c: A woman in her 40s. She had experienced frequent basal cell carcinomas since her 30s. d: A man in his 20s. The disorder was accompanied by mental retardation and apraxia of gait. e,f: Pigmentation on the sun‐exposed areas of the precordial region and upper back of the patient in (b). g: Basal cell carcinoma on the nasal dorsum of the patient in (d).

Chapter 14

Fig. 14.1

What is epidermolysis bullosa?

Epidermolysis bullosa is a group of hereditary diseases in which even slight mechanical stimuli produces blisters, erosions, and ulcers. This photo shows dystrophic epidermolysis bullosa (RDEB, severe generalized).

Fig. 14.2

The mechanism of epidermolysis bullosa and the location of minute cleavage formation.

Epidermolysis bullosa simplex with mottled pigmentation.

Fig. 14.3

Epidermolysis bullosa simplex (localized type).

Blistering is localized on the hands and feet. Blistering is induced by friction, such as from long walks.

Fig. 14.4

Epidermolysis bullosa simplex (Dowling–Meara type).

Blisters form ring shapes and heal without scarring.

Fig. 14.5

Epidermolysis bullosa simplex (other, generalized type).

Blistering occurs on the whole body surface. The clinical severity is between those of the Dowling–Meara and the localized types.

Fig. 14.6

Electron microscopic image of epidermolysis bullosa simplex.

The arrows indicate the lamina densa. The cytoplasm of the basal cells (indicated by stars) on the basement membrane is disrupted, leading to blistering.

Fig. 14.7

Aggregated keratin fibers seen in the Dowling–Meara type.

Fig. 14.8

Junctional epidermolysis bullosa, Herlitz type.

Intractable, erosive ulcers cover the whole body surface. The ulcerations gradually enlarge.

Fig. 14.9

Junctional epidermolysis bullosa, non‐Herlitz type.

Blistering and pigmentation occur on the whole body surface. Non‐scarring alopecia also occurs on the scalp. Mutation in collagen type XVII is identified.

Fig. 14.10

Junctional epidermolysis bullosa associated with pyloric atresia.

Aplasia cutis congenita‐like ulceration of the skin and congenital pyloric atresia occur as complications. Mutation in the integrin β4 gene is identified.

Fig. 14.11

Electron microscopic image of junctional epidermolysis bullosa.

A blister (star) forms in the lamina lucida, between the plasma membrane of the basal keratinocytes (purple arrows) and the lamina densa (black arrows).

Fig. 14.12

Dystrophic epidermolysis bullosa (dominant type).

a: Blistering and scarring occur on areas subjected to friction, such as the knees. b: Deformity in the toenails.

Fig. 14.13

Dystrophic epidermolysis bullosa (recessive, severe generalized type).

a: Blistering and ulceration are relatively mild at birth. b,c: Intractable blisters form as the patient grows. d: Marked blistering is present on the whole body. e: Hypoplasia of the teeth is present. f,g,h: Adhesion is seen in the fingers and toes.

Fig. 14.14‐1

Dystrophic epidermolysis bullosa (recessive, other generalized type).

Scarring blisters, crusts, and adhesion occur in the fingers; however, these are milder than in the recessive, severe generalized type. Expression of collagen type VII is present but reduced.

Fig. 14.14‐2

Dystrophic epidermolysis bullosa (recessive, other generalized type).

Cases with squamous cell carcinoma (arrows).

Fig. 14.15

Light microscopic image of dystrophic epidermolysis bullosa.

Typical subcutaneous blistering and slight inflammatory cellular infiltration are present.

Fig. 14.16

Electron microscopic image of dystrophic epidermolysis bullosa.

Anchoring fibrils are absent, and blistering is observed immediately beneath the lamina densa (arrows).

Fig. 14.17

Hailey–Hailey disease.

a,b: Vesicles, erosions, impetigo, and pustules form in the groin. c,d: Axillary fossae. The blisters shown in photo (c) may appear, although only rarely.

Fig. 14.18

Histopathology of Hailey–Hailey disease.

Intraepidermal acantholysis.

Fig. 14.19

Distribution of desmoglein 1 and desmoglein 3 in the epidermis, and the pathomechanism of pemphigus.

Diseases with intraepidermal blistering are classified according to the desmoglein molecules that are impaired (see also Fig. 14.23).

Fig. 14.20

Direct immunofluorescence of pemphigus foliaceus.

Intercellular deposition of IgG is observed in the epidermis.

Fig. 14.21

Pemphigus vulgaris.

a: Edematous itching erythema and blisters on the trunk. b: The blisters easily rupture and become erosive. c: Erosion on the membrane of the genitalia (glans penis). d: A mix of blisters, erosions, and crusts is present on the trunk. e,f: Intractable erosion on the lips and in the oral cavity. g: The skin appears healthy except for the blister.

Fig. 14.22

Histopathology of pemphigus vulgaris.

Acantholysis is observed immediately above the basal cells.

Fig. 14.23

Expression patterns of desmogleins in the skin and mucosa.

The pemphigus type depends on whether the autoantibodies target desmoglein 1 or desmoglein 3 (see also Fig. 14.19).

Fig. 14.24

Pemphigus vegetans.

Fig. 14.25‐1

Pemphigus foliaceus.

a: Erosion on the back. b: Erythema and pigmentation on the chest.

Fig. 14.25‐2

Pemphigus foliaceus.

a: Erosions, erythema, and pigmentation on the chest. b: Exfoliation and erythema on the face. The blisters are thin and easily ruptured; tense blisters are rarely seen.

Fig. 14.26

Pemphigus erythematosus.

Erythema and erosions on the cheek. The lesions resemble those of pemphigus foliaceus.

Fig. 14.27

Pemphigus induced by D‐penicillamine.

Erythema and vesicles are present. When induced by D‐penicillamine, the skin lesions tend to persist even after the medication is discontinued.

Fig. 14.28

Difference between an intradermal blister and a subepidermal blister.

Fig. 14.29

Bullous pemphigoid.

a: Precordial region. b: Back. The lesion resembles erythema multiforme. c: Large blisters are seen. d: Itching, edematous erythema, and tense bullae on the extremities. This is a typical skin manifestation of bullous pemphigoid. e: Upper arm. f: Comparatively large erythema and blisters. g: Chest. h: Palms.

Fig. 14.30

Histopathology of bullous pemphigoid.

A distinct subepidermal blister. Inflammatory cells including eosinophils are seen.

Fig. 14.31

Direct immunofluorescence of the skin of a patient with bullous pemphigoid.

Linear deposition of IgG is observed in the epidermal basement membrane.

Differential diagnosis between bullous pemphigoid and epidermolysis bullosa acquisita using salt split‐skin analysis.

Fig. 14.32

Mucous membrane pemphigoid.

a,b: Erosion in the eye and scarring occur. c,d: Erosion in the oral cavity.

Fig. 14.33‐1

Epidermolysis bullosa acquisita.

Blistering, erosion, and ulceration occur, which may be partially accompanied by scarring.

Fig. 14.33‐2

Epidermolysis bullosa acquisita.

Fig. 14.34

Dermatitis herpetiformis.

Eczema and blisters accompanied by intense itching are present.

Fig. 14.35

Histopathology of dermatitis herpetiformis.

Fig. 14.36

Linear IgA bullous dermatosis.

Fig. 14.37‐1

Palmoplantar pustulosis (PPP).

Fig. 14.37‐2

Palmoplantar pustulosis (PPP).

Multiple pustules aggregate on the hands and feet.

Fig. 14.38

Subcorneal pustular dermatosis.

Fig. 14.39

Eosinophilic pustular folliculitis.

Follicular papules and pustules aggregate, accompanied by itching.

Chapter 15

Fig. 15.1‐1

Ichthyosis vulgaris.

The skin dries and pityriasis‐like lamellar exfoliation occurs.

Fig. 15.1‐2

Ichthyosis vulgaris.

Fig. 15.2

X‐linked ichthyosis.

Relatively large scales are present. The symptoms are more severe than those of ichthyosis vulgaris.

Fig. 15.3

Harlequin ichthyosis.

There is marked hyperkeratosis on the whole body surface. Ectropion of the eyelids results in reddening above the eyes. Normal eyeballs are present underneath.

Fig. 15.4

Lamellar ichthyosis

. Large, dark brown scales are characteristic of lamellar ichthyosis.

Fig. 15.5

Congenital ichthyosiform erythroderma.

Erosive flushing and fine scales are seen on the whole body. Blistering does not occur.

Fig. 15.6‐1

Epidermolytic ichthyosis.

Skin lesions accompanied by flushing and thick keratinization occur on the whole body surface.

Fig. 15.6‐2

Epidermolytic ichthyosis.

Flushing appears on the whole body. Severe, dark keratinization with a dirty appearance occurs on the hands and feet (often in cases of mutation in the keratin 10 gene).

Fig. 15.7 Histopathology of epidermolytic ichthyosis. Granular degeneration occurs in the epidermis.

Fig. 15.8

Superficial epidermolytic ichthyosis.

The clinical symptoms of flushing and hyperkeratosis are those of a mild case.

Fig. 15.9

Netherton syndrome.

a: It is accompanied by atopic dermatitis‐like eruptions and congenital ichthyosiform erythroderma‐like eruptions. b: The scalp hair becomes knotted and easily breaks at the knots, resulting in short hair (bamboo hair).

Fig. 15.10

Sjögren–Larsson syndrome.

Congenital ichthyosiform erythroderma‐like eruptions occur.

Fig. 15.11

KID syndrome.

Hair loss and hyperkeratotic papules are seen.

Fig. 15.12

Dorfman–Chanarin syndrome

. Clinically, skin lesions similar to those of congenital ichthyosiform erythroderma are present.

Fig. 15.13

Acquired ichthyosis.

a: A case that accompanied Hodgkin's disease. b: A case that accompanied mycosis fungoides.

Fig. 15.14‐1

Palmoplantar keratoderma.

Fig. 15.14‐2

Palmoplantar keratoderma.

Keratinization of varying severity is present on the hands and feet. It is often difficult to determine the subtype by the clinical findings alone.

Fig. 15.15

Keratosis palmoplantaris mutilans (Vohwinkel).

Fig. 15.16‐1

Darier’s disease.

Dark brown, keratotic papules on the whole body.

Fig. 15.16‐2

Darier’s disease.

a,b: Keratotic papules. c: Verrucous keratinization on the palm. d: Changes of nail plates.

Fig. 15.17

Histopathology of Darier’s disease.

Acantholysis, fissures, and villi are seen.

Fig. 15.18

Erythrokeratodermia variabilis.

Sharply demarcated keratotic erythema.

Laboratory findings on psoriasis: wax‐fragment phenomenon, Auspitz phenomenon, Köbner phenomenon.

Fig. 15.19

Cases of psoriasis vulgaris.

Erythema is accompanied by marked silvery‐white scales.

Fig. 15.20

Histopathology of psoriasis.

There is hyperkeratosis and club‐shaped extension of the epidermis (regular acanthosis).

Fig. 15.21

Histopathology of pustular psoriasis (Kogoj’s spongiform pustule (arrows)).

Spongiosis with infiltration of neutrophils is seen in the suprabasal cell layer.

Fig. 15.22‐1

Psoriasis vulgaris.

Fig. 15.22‐2

Psoriasis vulgaris.

Fig. 15.22‐3

Psoriasis vulgaris.

Sharply demarcated, thick, silver‐gray scales adhere to the surface of the erythematous plaques. Characteristic nail deformities.

Fig. 15.23

Pustular psoriasis.

The main skin lesions are sterile pustules.

Fig. 15.24

Psoriatic erythroderma.

Fig. 15.25

Psoriatic arthritis.

Fig. 15.26‐1

Pityriasis rubra pilaris.

There are follicular papules, orange psoriatic plaques and diffuse keratinization on the palms.

Fig. 15.26‐2

Pityriasis rubra pilaris.

Fig. 15.27

Parapsoriasis en plaque.

Mild, relatively sharply demarcated erythema is present.

Fig. 15.28

Pityriasis lichenoides chronica (PLC).

Old eruptions are rarely seen simultaneously with new ones on the lesion. Ulceration does not occur.

Fig. 15.29‐1

Pityriasis lichenoides et varioliformis acuta (PLEVA).

There are intense acute inflammatory symptoms, and old and new eruptions are present. These are accompanied by diffuse ulcers.

Fig. 15.29‐2

Pityriasis lichenoides et varioliformis acuta (PLEVA).

Fig. 15.30

Histopathology of pityriasis lichenoides et varioliformis acuta.

Vacuolar degeneration of basal cells and intense lymphocytic infiltration are observed.

Fig. 15.31‐1

Lichen planus.

A typical case.

Fig. 15.31‐2

Lichen planus.

Various clinical features are seen. a,b: Lichen planus annularis. It is important to differentiate this from porokeratosis. Erythema at the periphery of the lesion is characteristic of lichen planus. c: Lichen planus pigmentosus. d: A typical case of lichen planus on the lower leg. e: It is necessary to differentiate this from lichen sclerosus. f: Multiple lichen planus on the foreskin and glans penis. g,h: Affected lips. i: Linear, white lichen planus near the molar teeth in the buccal mucous membrane. j: Typical lichen planus on the wrist.

Fig. 15.32

Nail deformities in lichen planus.

Atrophic changes to the nails.

Fig. 15.33

Histopathology of lichen planus.

Hyperkeratosis and hypergranulosis without parakeratosis characterize the disorder. Saw‐toothed acanthosis, band‐like lymphatic infiltration in the upper dermal layer and vacuolar degeneration in the basal layer are also seen.

Fig. 15.34

Lichen striatus.

Fig. 15.35

Lichen nitidus.

Small, scattered, multiple papules of a few millimeters in diameter and normal skin color or yellowish‐white occur.

Fig. 15.36

Pityriasis rosea.

a: The eruptions are distributed in a Christmas tree pattern. b: Pityriasis caused by pityriasis rosea. c: The first rash, called a herald patch.

Fig. 15.37

Clavus, corn.

Fig. 15.38

Diagram of clavus and callus.

Fig. 15.39

Callus, tylosis.

Fig. 15.40‐1

Keratosis pilaris.

Fig. 15.40‐2

Keratosis pilaris.

Fig. 15.41

Erythromelanosis follicularis faciei.

Erythematous plaques caused by follicular keratotic papules are observed on the preauricular area and cheek.

Fig. 15.42‐1

Acanthosis nigricans.

Fig. 15.42‐2

Acanthosis nigricans.

Fig. 15.43

Confluent and reticulated papillomatosis.

Fig. 15.44

Paraneoplastic acrokeratosis.

Fig. 15.45

Keratosis follicularis squamosa.

Fig. 15.46

Histopathology of keratosis follicularis squamosa.

Chapter 16

Fig. 16.1

Electron microscopic image of a melanocyte (Mel) from a healthy person (a) and from a patient with oculocutaneous albinism (OCA1A) (b).

a: In a melanocyte from a healthy person, the cytoplasm contains large amounts of mature, blackish, stage IV melanosomes (arrows). The melanocytes transport melanosomes to neighboring keratinocytes. b: In oculocutaneous albinism, most melanosomes are immature, not progressing beyond stage II. Mature melanosomes are not seen in the cytoplasm.

Fig. 16.2

Oculocutaneous albinism (OCA1A) in a girl.

The hair will be white throughout her lifetime from lack of melanin production. A mutation in the tyrosinase gene was identified. Tyrosinase mutation (+).

Fig. 16.3

Oculocutaneous albinism (OCA4).

This patient had white hair at birth; however, pigmentation gradually appeared in the hair with age. Her hair is now blonde. MATP mutation (+).

Fig. 16.4

Hermansky‐Pudlak syndrome (HPS).

This patient had blonde hair and a fair complexion; however, more pigment gradually appeared as she grew. There was a hemorrhagic tendency in this case. Symptoms such as pulmonary fibrosis and intestinal catarrhs often appear after the patient reaches a certain age.

Fig. 16.5‐1

Vitiligo vulgaris on various sites.

a: Chest. b: Back. c: Lips. d: Sharply demarcated depigmented macules occur on the dorsum of the hands.

Fig. 16.5‐2

Vitiligo vulgaris on various sites.

On the forehead.

Fig. 16.6

Suction blister treatment of vitiligo vulgaris.

a: Vacuum aspiration is applied on normal skin to artificially produce a suction blister. b: Vacuum aspiration is applied on skin with vitiligo vulgaris to produce a suction blister. The covering of the vitiligo vulgaris blister is removed and replaced with the covering of the normal skin blister.

Fig. 16.7

Sutton nevus

. Sharply demarcated leukoderma appears around the nevus cells.

Fig. 16.8‐1

Vogt‐Koyanagi–Harada disease.

Irregularly shaped leukoderma is sporadically seen.

Fig. 16.8‐2

Vogt–Koyanagi–Harada disease.

Fig. 16.9

Nevus depigmentosus.

Fig. 16.10

Ephelides.

Fig. 16.11

Melasma, chloasma.

Brown spots on the cheeks.

Fig. 16.12

Friction melanosis.

Diffuse, reticular, brown pigmentation occurs on the trunk, particularly on the back. The eruptions are blackish papules of several millimeters in diameter. On histopathology, amyloid deposition is observed.

Fig. 16.13

Dyschromatosis symmetrica hereditaria.

Multiple brownish macules of 3–8 mm diameter occur on the dorsum of the hands. They coalesce to present a reticular pattern. Depigmentation is also seen.

Fig. 16.14

Senile lentigo.

Sharply demarcated brown patches appear. They may partially elevate and progress to seborrheic keratosis in some cases.

Fig. 16.15

Addison’s disease.

Fig. 16.16

Pigmentatio petaloides actinica.

This skin lesion occurred after PUVA therapy for vitiligo vulgaris (center of photo).

Fig. 16.17

Erythema dyschromicum perstans, ashy dermatosis.

Grayish‐blue patches and erythematous eruptions are seen around the patches.

Fig. 16.18

Carotenemia.

a: Color changes are seen in the hands. b: Multiple brown pigmented macules of 2–10 mm diameter occur on the dorsum of hand. The macules coalesce to form reticular patterns. Hypopigmented macules are also seen.

Fig. 16.19

Tattoo. Pigments of various colors have been injected.

Fig. 16.20

Traumatic tattoo.

Chapter 17

Fig. 17.1

Histopathology of amyloidosis.

Amyloids stain reddish brown in direct fast scarlet staining.

Fig. 17.2

Lichen amyloidosis.

Multiple light brown papules appear and aggregate, accompanied by intense itching.

Fig. 17.3

Macular amyloidosis.

Fig. 17.4

Nodular cutaneous amyloidosis.

Fig. 17.5

AL amyloidosis.

a: Amyloid deposition in the fingers results in hardening of the skin that resembles systemic scleroderma. b: Nail deformity is caused by amyloid deposition in the nail matrix and nail beds. c: Macroglossia. The tongue is markedly firm and swollen from amyloid deposition.

Fig. 17.6

Dialysis‐related amyloidosis.

Fig. 17.7

Scleredema

. Marked hardening of the skin on the neck and upper back.

Fig. 17.8

Histopathology of scleredema

. Deposition of mucin.

Fig. 17.9

Reticular erythematous mucinosis.

Fig. 17.10

Follicular mucinosis

. The skin lesion is accompanied by relatively sharply demarcated, reddish infiltration of 3–4 cm in diameter, and alopecia.

Fig. 17.11

Tuberous xanthoma.

a: A lesion on the left pollex. b: Lesions on the metacarpophalangeal joints and proximal interphalangeal joints. Redness is seen in some of the affected sites.

Fig. 17.12

Plane xanthoma that occurred secondarily after lymphedema on the upper arm.

There are vaguely demarcated yellow plaques.

Fig. 17.13

Xanthelasma palpebrarum.

Flatly elevated yellow plaques occur on the inner canthus of the upper and lower eyelids, accompanied by mild infiltration.

Fig. 17.14

Eruptive xanthoma.

Fig. 17.15

Histopathology of xanthoma.

Foamy histiocytes that have phagocytosed fat droplets are observed in the dermis.

Fig. 17.16‐1

Zinc deficiency syndrome.

A large area of impetigo‐like erythema around the external genitalia. Blisters and pustules form in some parts.

Fig. 17.16‐2

Zinc deficiency syndrome.

Fig. 17.17

Hemochromatosis.

Fig. 17.18

Histopathology of hemochromatosis.

a: Melanin deposition is observed in the epidermal basal keratinocytes. b: There is iron deposition in the dermis (the portions stained blue).

Fig. 17.19

Calcinosis cutis on the extensor surface of an infant’s forearm.

Multiple papules of several millimeters in diameter are caused by calcium deposition. Some rupture and coalesce, discharging their contents.

Fig. 17.20

Calcinosis cutis on the scrotum.

Fig. 17.21

Calciphylaxis.