Hidradenitis Suppurativa E-Book

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

Seitenzahl: 134

Veröffentlichungsjahr: 2017

Beschreibung

Hidradenitis Suppurativa: A Diagnostic Atlas provides a unique visual aid to the diagnosis of Hidradenitis Suppurativa (HS), also known as "acne inversa." The book covers the epidemiology and pathogenesis of the disease, its typical presentation, differences in manifestations of cutaneous versus systemic instances, and considerations for clinical and histopathological differential diagnosis. Guidance is also provided for the classification of disease severity and for managing the impact of HS on the patient's quality of life. The book is packed with high-quality, full-color clinical images for each of the most common HS diagnostic imaging techniques, such as videodermatoscopy, ultrasound, computed tomography, and magnetic resonance imaging. As a clinical atlas, it helps dermatologists with differential diagnoses and correct assessments of disease severity, as well as possible complications of the condition. The book: * Is highly focused on acne inversa, which can have a debilitating impact on quality of life * Includes over 200 outstanding diagnostic clinical images * Covers all imaging modalities used in the diagnosis and management of Hidradenitis Suppurativa This book is a key resource for dermatologists, dermatopathologists, and dermatology nurses working with patients with HS.

Leseprobe

HidradenitisSuppurativa

A Diagnostic Atlas

First Edition

EDITED BYGiuseppe Micali, MD

Chair, Professor of Dermatology Department of Dermatology University of Catania, Italy

This edition first published 2017© 2017 Wiley

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Library of Congress Cataloging-in-Publication DataNames: Micali, Giuseppe, editor. Title: Hidradenitis suppurativa : a diagnostic atlas / [edited by] Giuseppe Micali. Other titles: Hidradenitis suppurativa (Micali) Description: First edition. | Hoboken, NJ : Wiley, 2017. | Includes bibliographical references and index. Identifiers: LCCN 2017011126 | ISBN 9781119272953 (pbk.) Subjects: | MESH: Hidradenitis Suppurativa–diagnosis | Atlases Classification: LCC RL201 | NLM WR 17 | DDC 616.5/2–dc23 LC record available at https://lccn.loc.gov/2017011126

Cover images courtesy of the authorCover design by Wiley

CONTENTS

List of contributors

Foreword

Chapter 1 Introduction

References

Chapter 2 Epidemiology and pathogenesis

2.1 Epidemiology

2.2 Pathogenesis

References

Chapter 3 Clinical features and diagnostic clues

3.1 Cutaneous findings

3.2 Alternative clinical phenotypes

3.3 Diagnostic clues

References

Chapter 4 Histopathology

4.1 Histopathological features

4.2 Immunohistochemistry

4.3 Histological differential diagnoses

References

Chapter 5 Classification and severity scales

References

Chapter 6 Correlation between severity and its impact on quality of life

6.1 Quality of life questionnaires

References

Chapter 7 Comorbidities and complex syndromes

7.1 Comorbidities

7.2 Complex syndromes

References

Chapter 8 Complications

References

Chapter 9 Ultrasound imaging

9.1 Staging

9.2 Evaluation of the inflammatory activity

9.3 Monitoring

References

Chapter 10 Radiological imaging

10.1 Magnetic resonance imaging

10.2 Computed tomography

10.3 Positron emission tomography

References

Chapter 11 Skin imaging: dermatoscopy

References

Chapter 12 Differential diagnosis

References

Chapter 13 Conclusions

References

Index

EULA

List of Tables

Chapter 2

Table 2.1

Table 2.2

Table 2.3

Chapter 3

Table 3.1

Table 3.2

Table 3.3

Chapter 5

Table 5.1

Table 5.2

Table 5.3

Table 5.4

Chapter 6

Table 6.1

Table 6.2

Chapter 7

Table 7.1

Table 7.2

Table 7.3

Chapter 8

Table 8.1

Chapter 9

Table 9.1

Table 9.2

Table 9.3

Table 9.4

Chapter 12

Table 12.1

Table 12.2

List of Illustrations

Chapter 2

Figure 2.1

. Pathogenesis of HS

Chapter 3

Figure 3.1

. HS cutaneous lesions in different stages of evolution: highly inflamed, coalescent nodules along with cord-like scars (arrows) from previous flares on the left axilla

Figure 3.2

. HS cutaneous lesions in different stages of evolution: highly inflamed, multiple draining nodules and abscesses on the left axilla. Multiple scars can be appreciated (arrow)

Figure 3.3

. Same patient of Figure 3.2 in a resolution stage showing less inflammatory lesions

Figure 3.4

. HS cutaneous lesions in different stages of evolution: multiple papules/pustules and draining nodules (yellow arrows) along with multiple small atrophic scars (red arrows)

Figure 3.5

. HS presenting with multiple inflammatory nodules in the right axilla in a patient with bilateral involvement. HS severity grade: moderate

Figure 3.6

. HS showing a single recurrent nodule on the left axilla in a patient with bilateral involvement. HS severity grade: mild

Figure 3.7

. HS with multiple discharging nodules on inguinal folds along with postinflammatory hyperpigmentation and scarring from previous inflammatory episodes. HS severity grade: severe

Figure 3.8

. HS presenting with inflammatory nodules and scarring on the right axilla in a patient with bilateral involvement. HS severity grade: severe

Figure 3.9

. HS affecting the gluteal area with inflammatory discharging nodules and fibrotic tissue resulting from previous recurrent episodes. HS severity grade: severe

Figure 3.10

. HS complications: vulvar lymphedema

Figure 3.11

. HS complications: penile and scrotal lymphedema

Figure 3.12

“Milk line”: distribution of apocrine-related mammary tissue in mammals

Figure 3.13

. HS predilection areas in males and females

Figure 3.14

. Typical primary lesion: solitary axillary inflammatory nodule

Figure 3.15

. Typical primary lesion: solitary axillary abscess

Figure 3.16

. Typical primary lesions: multiple axillary nodules, some of them eroded

Figure 3.17

. Typical secondary lesions: single infiltrated plaque of the buttock with multiple draining sinuses, some of them showing purulent discharge

Figure 3.18

. Typical secondary lesions: multiple plaques of the inguinal fold showing dry draining sinuses (red arrow) along with discharge draining ones (yellow arrows)

Figure 3.19

. Typical secondary lesions: sero-purulent discharge from a draining sinus on the buttock

Figure 3.20

. Outcome of chronic inflammation: pyogenic granulomas developing on scarring area

Figure 3.21

. Outcome of chronic inflammation: ulcerative nodules showing granulation tissue

Figure 3.22

. Outcome of chronic inflammation: fibrotic plaques localized in the inguinal folds

Figure 3.23

. Outcome of chronic inflammation: fibrosis of the scrotum

Figure 3.24

. Outcome of chronic inflammation: severe fibrosis of the gluteal fold altering the anatomic outline

Figure 3.25

. Typical tertiary lesions: double-ended pseudocomedones

Figure 3.26

. Typical tertiary lesions: bridging scars on the right axilla

Figure 3.27

. Typical tertiary lesions: cord-like scars on the left axilla

Figure 3.28

. Typical tertiary lesions: multiple bridging scars (yellow arrows) on the right inguinal fold

Figure 3.29

. Typical tertiary lesions: linear scars

Figure 3.30

. Typical tertiary lesions: multiple, circinate atrophic scars on the pubic area

Figure 3.31

. Typical tertiary lesions: hyperpigmented atrophic scars

Figure 3.32

. Typical tertiary lesions: hypertrophic scar

Figure 3.33

. Typical tertiary lesions: multiple hypertrophic scars with some of them showing bridging (yellow arrow)

Figure 3.34

. Typical tertiary lesions: keloids

Figure 3.35

. Typical tertiary lesions: keloids

Figure 3.36

. Other cutaneous lesions: follicular papules and pustules

Figure 3.37

. Other cutaneous lesions: follicular papules and pustules

Figure 3.38

. Other cutaneous lesions: multiple epidermal cysts

Figure 3.39

. Other cutaneous lesions: multiple epidermal cysts

Chapter 4

Figure 4.1

. Hyperkeratosis, occlusion, and dilatation of hair infundibulum with hyperplasia of follicular epithelium

Figure 4.2

. Follicular hyperkeratosis with superficial folliculitis made by neutrophils and lymphocytes

Figure 4.3

. (A) Acute suppurative folliculitis with occlusion and dilatation of hair infundibulum, perifolliculitis, and stasis in apocrine glands; (B) superficial folliculitis with follicular hyperkeratosis; (C) acute suppurative deep folliculitis

Figure 4.4

. Occlusive folliculitis with initial rupture of the follicle, inflammatory infiltrate with giant cell granulomatous reaction, and apocrinitis

Figure 4.5

. Extension of inflammatory reaction to apocrine glands

Figure 4.6

. (A) Fully developed apocrinitis with dilation of the lumen and mainly intraluminal inflammatory neutrophilic infiltrate; (B) apocrinitis with mainly extraluminal infiltrate with granulomatous features

Figure 4.7

. (A) Marked inflammatory infiltrate in the dermis with apocrinitis and extension on the inflammation to the close eccrine glands; (B) contemporary inflammation of apocrine and eccrine glands

Figure 4.8

. (A) Involment of the apocrine and eccrine glands by the inflammatory reaction; (B) folliculitis with adjacent involvement of eccrine glands

Figure 4.9

. (A) Draining sinus tracts lined by stratified squamous epithelium in the form of dissecting burrows throughout the inflamed and necrotic dermis; (B) draining sinus tracts lined by stratified squamous whose epithelial wall is broken down

Figure 4.10

. Granulomatous reaction containing foreign-body giant cells related to fragments of keratin from ruptured follicles

Figure 4.11

. Extensive fibrosis with hyperplastic epidermis and residual perivascular superficial and deep inflammatory infiltrate as a late stage of HS

Figure 4.12

. Well-differentiated squamous cell carcinomas arising in long-standing HS lesion

Chapter 5

Figure 5.1

HS Hurley stage I

Figure 5.2

HS Hurley stage II

Figure 5.3

HS Hurley stage III

Figure 5.4

HS Canoui-Poitrine classification: LC1 (axillary) subtype

Figure 5.5

HS Canoui-Poitrine classification: LC1 (mammary) subtype

Figure 5.6

HS Canoui-Poitrine classification: LC2 (follicular) subtype

Figure 5.7

HS Canoui-Poitrine classification: LC2 (follicular) subtype

Figure 5.8

HS Canoui-Poitrine classification: LC3 (gluteal) subtype

Chapter 6

Figure 6.1

DLQI questionnaire

Figure 6.2

HS in a patient with a high DLQI score consistent with severe disease (Hurley stage III)

Figure 6.3

HS in a patient with a relatively mild disease (Hurley stage I) but a very high DLQI score resulting from a significant psychological impact

Figure 6.4

Deep erythematous nodules and evident depressed cribriform scarring causing social embarrassment and limiting sexual contacts and recreational activities such as sunbathing and swimming

Figure 6.5

Inflamed nodules and pilonidal cyst causing intense pain

Figure 6.6

Deep and superficial nodules, papules and pustules localized on the buttocks causing pain during sitting

Figure 6.7

Multiple inflammatory nodules on the abdomen that prevent wearing tight clothing

Figure 6.8

Pain VAS

Chapter 7

Figure 7.1

HS in a 44-year-old woman with severe obesity

Figure7.2

A 37-year-old overweight man with HS on the abdominal crease

Figure7.3

A 52-year-old man with severe obesity, HS, and a giant abdominal hernia

Figure 7.4

mTOR gene expression HS. (A) mTOR was increased in lesional (LS) and non-lesional (NLS) skin compared to normal skin (NS) of controls; (B) mTOR fold increase, obtained from LS versus NS of controls and normalized to 18S, correlated with Sartorius score. (

c

) Insulin resistance in HS. Serum levels of insulin after 75 g of glucose load (oral glucose tolerance test, OGTT) significantly differed in HS patients with respect to controls; (

d

) BM of insulin-resistant HS patients correlated well with Sartorius score. (

e

) mTOR and insulin resistance in HS patients. mTOR fold increase, obtained from LS versus NS of controls and normalized to 18S, correlated with serum levels of insulin after 75 g of glucose load (OGTT) at 30 min; (

f

) mTOR fold increase, obtained from LS versus NS of controls and normalized to 18S, correlated with serum levels of insulin after 75 g of glucose load (OGTT) at 60 min

Figure7.5

Acanthosis nigricans, psoriasis, and HS occurring in an obese patient

Figure7.6

A 58-year-old woman affected by PG and HS in perianal region

Figure7.7

Coexistence of histologically confirmed PG and HS: superficial diffuse dermatitis with deep inflammatory process showing prevalence of neutrophils

Figure7.8

Coexistence of histologically confirmed PG and HS: edema in the papillary dermis with perivascular, lymphohistiocytic inflammatory infiltrate, and neutrophilic polymorphonuclear leukocytes, extending into the hypodermis

Figure7.9

Mild acne (A) in a woman with HS localized at the inframammary fold (B)

Figure7.10

Coexistence of acne conglobata (A) and axillary HS (B) in a male patient

Figure7.11

Open pilonidal cyst in an HS patient

Figure7.12

Pilonidal cyst (yellow circle) in an HS patient

Figure7.13

Psoriasis in a woman affected by mild HS

Chapter 8

Figure 8.1

Inflammatory nodules, abscesses and scarring with surrounding erythema on the right axilla in a 28-year-old girl, suffering from HS since the age of 16

Figure 8.2

Multiple cysts and superficial erosions on the right axilla in a 40-year-old woman, with a 15-year history of HS

Figure 8.3

Vulvar lymphedema with nodules, scarring and multiple ulcerations in a 60-year-old woman with long-standing HS

Figure 8.4

Scrotal elephantiasis with scarring and ulcerations in a 57-year-old man with long-standing HS

Figure 8.5

Gluteal lichen simplex chronicus in a 50-year-old man, with long-standing HS

Figure 8.6

(A) Gluteal HS with

draining abscess

(red arrow) and SCC (black arrow) (by courtesy of Prof. G. Fabbrocini). (B) Moderately to well-differentiated SCC (HE × 250) (by courtesy of Prof. G. Fabbrocini)

Chapter 9

Figure 9.1

Follicular HS Hurley stage I

Figure 9.2

US examination of the lesions of Figure 9.1 showing widening of the hair follicles (red arrow) and thickening of the dermis (blue arrow) (US, 18 MHz probe, B-Mode)

Figure 9.3

Nodule of the left thigh

Figure 9.4

US examination of the lesion of Figure 9.3. Dermal pseudocystic nodule. (A) Longitudinal axis (US, 18 MHz probe, B-mode); (B) transversal axis (US, 18 MHz probe, B-mode); (C) color Doppler flow mode negative (non-inflammatory nodule), longitudinal axis (US, 18 MHz probe, CFM-mode); (D) color Doppler flow mode negative (non-inflammatory nodule), transversal axis (US, 18 MHz probe, CFM-mode)

Figure 9.5

Abscess of the left axilla

Figure 9.6

US examination of the lesion of Figure 9.5. Fluid collection. (A) Longitudinal axis (US, 18 MHz probe, B-mode); (B) transversal axis (US, 18 MHz probe, B-mode); (C) color Doppler flow mode positive (inflamed abscess), longitudinal axis (US, 18 MHz probe, CFM-mode); color Doppler flow mode positive (inflamed abscess), transversal axis (US, 18 MHz probe, CFM-mode)

Figure 9.7

Linear structure located on the right axilla, compatible with a simple fistula

Figure 9.8

US examination of the lesion of Figure 9.7. Simple fistula. (A) Longitudinal axis (US, 18 MHz probe, B-mode); (B) transversal axis (US, 18 MHz probe, B-mode); (C) color Doppler flow mode positive (inflamed fistula), longitudinal axis (US, 18 MHz probe, CFM-mode); (D) color Doppler flow mode positive (inflamed fistula), transversal axis (US, 18 MHz probe, CFM-mode)

Figure 9.9

Swollen, indurated, ill-defined plaque on the left axilla

Figure 9.10

US examination of the lesion of Figure 9.9. Complex fistula. (A) Longitudinal axis (US, 18 MHz probe, B-mode); (B) transversal axis (US, 18 MHz probe, B-mode); (C) color Doppler flow mode positive (inflamed fistula), longitudinal axis (US, 18 MHz probe, CFM-mode); (D) color Doppler flow mode positive (inflamed fistula), transversal axis (US, 18 MHz probe, CFM-mode)

Figure 9.11

Simple fistula on the left groin befeore (A) and after (B) 12 weeks after treatment with adalimumab (week 0: 160 mg; week 2: 80 mg; from week 4: 40 mg/week)

Figure 9.12

Sequential US examination of the lesion of Figure 9.11. (A) Pretreatment: simple fistula Doppler flow mode positive (US, 18 MHz probe, CFM-mode); (B) week 4: simple fistula Doppler flow mode negative (US, 18 MHz probe, CFM-mode); (C) week 8: partial tissue repair with hyper- and isoechogenic structures; (D) week 12: complete resolution with a remnant area occupied by hyperechogenic structures

Chapter 10

Figure 10.1

Axial T2-weighted image, without (A) and with (B) fat suppression. Ill-defined hyperintense areas are shown in A (white arrows), located along inguinal and gluteal folds. These lesions involve the cutaneous and subcutaneous planes, as well demonstrated after fat suppression (B). The high signal depicted after fat suppression reflects the presence of edema and inflammation (white arrows)

Figure 10.2

Fat suppressed T2-weighted image (A) and DWI (B). Inflammatory lesions appear hyperintense in both sequences and are well recognized in gluteal regions (white arrows)

Figure 10.3

Chronic longstanding HS. Axial T2-weighted image (A) shows an ill-defined area in the intergluteal cleft, with a horseshoe appearance (white arrow); this finding represents a gluteal abscess close to the anal canal. The same alteration is well depicted in DWI (B, white arrow)

Figure 10.4

Plaques and nodules on the right breast (A); CT revealing hyperdense thickening of the affected skin (B, green arrow)

Figure 10.5

Male patient with positive history of recurrent HS inflammatory lesions with no apparent active disease (A); axial CT image showing enlarged lymph nodes in both inguinal regions (B, green arrows)

Figure 10.6

Scrotal fibrosis from long-standing HS (A). Coronal multiplanar reformatted CT image showing hypervascularization of the scrotum (green arrows), with increased calibre of scrotal arteries; enlarged inguinal nodes are also recognizable (B, green asterisks)

Figure 10.7