References

1. Velpeau A. Dictionnaire de Medicine, un Repertoire General des Sciences Medicales Sous La Rapport Theorique et Pratique. Aiselle, Bechet, 1839

2. Verneuil A. Etudes sur les tumours de la peau et quelques maladies des glandes sudoripares. Arch Gen Med 1854; 4:447-468

3. Schiefferdecker B. Die Hautdrusen des Menschen, und der Saugetierre, ihre Histologische und rassenanatomische Bedeutung Sowie die Muscularis Sexu-alis. Schweizerbart, Stuttgart, 1922

4. Brunsting HA. Hidradenitis suppurativa; abscess of apocrine sweat glands - a study of clinical and pathological features with a report of 22 cases and a review of the literature. Arch Dermatol Syphilol 1939; 39:108-120

5. Shelly WB, Cahn MM. The pathogenesis of hidradenitis suppurativa in man. Arch Dermatol 1955; 72: 562-565

6. Yu CCW, Cook MG. Hidradenitis suppurativa: a disease of follicular epithelium, rather than apocrine glands. Br J Dermatol 1990; 122:763-769

7. Attanoos RL, Appleton MAC, Douglas-Jones AG. The pathogenesis of hidradenitis suppurativa: a closer look at apocrine and apoeccrine glands. Br J Dermatol 1995; 133:254-258

8. Boer J, Weltevreden EF. Hidradenitis suppurativa or acne inversa: a clinicopathological study of early lesions. Br J Dermatol 1996; 135:721-725

9. Brunsting HA. Hidradenitis and other variants of acne. Arch Dermatol Syphilol 1952; 65:303-315

10. Mortimer PS. Hidradenitis suppuritiva - diagnostic criteria. In: Marks R, Plewig G (eds) Acne and Related Disorders. Martin Dunitz, London, 1989, pp 359-360

11. Jemec GBE, Hansen U. Histology of hidradenitis suppurativa. J Am Acad Dermatol 1996; 34:994999

12. Mortimer PS, Lunniss PJ. Hidradenitis suppurativa. J R Soc Med 2000; 93:420-422

13. Weedon D. Skin Pathology. Churchill Livingstone, Edinburgh, 1999, p 390

14. Fitzpatrick JE. Inflammatory reactions of the sweat unit. In: Farmer ER, Hood EF (eds) Pathology of the Skin. Appleton and Lange, Norwalk, 1990, pp 461-462

15. Heller DS, Haefner HK, Hameed M. J Reprod Med 2002; 47(9):695-689

16. Norris JFB, Cunliffe WJ. A histological and im-munohistochemical study of early acne lesions. Br J Dermatol 1988; 118:651-659

17. Layton AM, Morris C, Cunliffe WJ, Ingham E. Im-mmunohistochemical investigation inflammation in lesions of acne. Clin Exp Dermatol 1998; 7:191197

18. Kurokawa I, Nishijima S, Kusumoto K. Immuno-histochemical study of cytokeratins in hidradeni-tis suppurativa (acne inversa). J Int Med Res 2002; 30:131-136

19. Pillsbury DM, Shelley WB, Kligman AM. Dermatology. Saunders, Philadelphia, 1956, p 481

20. Plewig G, Steger M. Acne inversa (alias acne triad, acne tetrad or hidradenitis suppurativa). In: Marks R, Plewig G (eds) Acne and Related Disorders. Martin Dunitz, London, 1988, pp 345-357

21. Kurokawa I, Nishijima S, Suzuki K. Cytokeratin expression in pilonidal sinus. Br J Dermatol 2002; 146:409-413

22. Attanoos RI, Appleton MA, Hughes LE. Granulo-matous HS and cutaneous Crohn's disease. Histo-pathology 1993; 23:111-115

23. Church JM, Fazio VW, Lavery IC. The differential diagnosis and comorbidity of HS and perianal Crohn's disease-a further support to this association. Int J Colorectal Dis 1993; 8:117-119

Chapter 5

Imaging

5

Ximena Wortsman, Gregor B.E. Jemec

Hidradenitis lesions extend into the deeper tissue

Imaging may facilitate the assessment of disease severity and treatment

Imaging may aid differential diagnosis

Key points axillae, the ano-genital region or under the breasts, they may penetrate far from the skin, and may reach distant sites. If this is not properly identified before treatment the presence of such lesions may adversely affect the outcome of, for example, surgery. Similarly, appropriate visualization of the extent of all lesions may help in the planning of surgery; finally, non-invasive visualization of lesions may be used to monitor the effect of, for example, medical therapy. Im aging of this debilitating skin disease may therefore have broad positive consequences for the patients. Two methods have been used for the study of HS: high-frequency ultrasound and

Introduction 34 MR scanning.

Ultrasound 34

Magnetic Resonance Imaging (MRI) 36 H 5.2 Ultrasound

X-Ray Examination 35

. _. Ultrasound imaging is determined by the tis-

sues physical properties. These physical pro-

References 37 perties delay the propagation of sound waves.

The sound propagation velocity is usually set at

1540 m/s, although it varies slightly in different tissues; for example in the skin it has been shown to be 1580 m/s. The sound is emitted from a

Hidradenitis suppurativa (HS) is a chronic, re- transducer, which also serves as a piezoelectric current and often devastating disease with long- receiver of the reflected echoes, transforming term evolution and severe psychological impact the discrete pressure of an echo into an electric on patients. For practical management of pa- current. The current is then transformed into a tients as well as for pathogenetic research, skin surrogate black/white image which can be used imaging at a lesser magnification than used for for tissue analysis by a trained ultrasonogra-

histopathology may also be of interest. In vivo pher.

imaging in the millimetre range allows visual- Ultrasound equipment is widely available ization of the hair follicle structure as well as the in many hospitals, and therefore offers an excel-identification of associated inflammation and lent opportunity for monitoring the subcuta-the spread of the disease into deeper tissues. neous spread of HS. More pathogenetic in-This may be of considerable benefit to patients. vestigations are however also possible. Using When abscess and sinus tracts develop in the high-frequency ultrasound machines, with fre-

Contents

5.1 Introduction

Fig. 5.2. Dermal fluid collection in a patient with extensive hidradenitis lesions

Fig. 5.1. Dermal focal hypoechoic nodular lesion. Hi-dradenitis patient with subclinical lesion in the axillary zone not suspected by the clinician quencies of 15-20 MHz, detailed visualization of hair follicle structure is possible. It has been shown that hair follicles of predisposed regions in HS patients differ from those of healthy controls [1, 2]. The patients appear to have hair follicles with a larger hypoechoic or echolucent diameter at the deeper end, which may reflect either an actual distortion of the follicle lumen or ongoing, subclinical inflammation. In addition to such observations, studies of HS complications or spread of disease are also possible.

To illustrate this point we have studied 5 patients (4 women and 1 man) with HS and 13 healthy control subjects using Philips 5000 and Philips IU 22 Real Time and High Resolution Ultrasound Machines with 15- and 17-MHz frequency linear probes. Images were acquired by a radiologist skilled in the ultrasound examina

Fig. 5.2. Dermal fluid collection in a patient with extensive hidradenitis lesions tion of skin, and presented as easily detected, characteristic patterns.1-1

Ultrasound morphological changes of HS can be classified as follows:

Dermal fluid collections (indicating inflammation)

Dermal increase of thickness (secondary to inflammation)

Dermal decrease of echogenicity (oedema) Dermal increase of echogenicity (fibrosis or long-term inflammatory changes) showing hair follicle enlargement Dermal hypoechoic focal nodular lesions (subclinical)

In particular the existence of dermal hypoechoic nodular lesions (see Figs. 5.1, 5.2) is important in the management of the disease.

1) Data on file

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