Ultrasound In‐Depth Characterization and Staging of Hidradenitis Suppurativa

BACKGROUND The clinical diagnosis of fistulous tracts and recurrent fluid collections in hidradenitis suppurativa (HS) may be complex. Information on subclinical involvement and grading of severity may improve management. OBJECTIVE To study HS lesions and evaluate the relevance of adding ultrasound (US) to the clinical examination. METHODS AND MATERIALS We reviewed the sonograms of consecutive patients with HS from January 1, 2010 to May 31, 2012. The abnormalities observed in the US examinations were organized, classified, and integrated into a clinical‐sonographic scoring system (SOS‐HS), to stage the disease. RESULTS Thirty‐four patients with HS with a total of 142 lesional areas were evaluated. US findings included subclinical fluid collections in 76.4% of the patients, fistulous tracts in 29.4%, dermal pseudocysts in 70.6%, and widening of the hair follicles in 100%. Concordance with the clinical HS scoring performed by dermatologists showed a significant fair agreement (k = 0.30; p < .001); concordance of SOS‐HS with clinical scores was acceptable but significantly lower (k = 0.27; p = .02) because clinical scores consistently underestimated disease stage and severity. CONCLUSION US examination of HS lesions provides anatomic information that is clinically unavailable. HS is possible to stage sonographically.

[1]  J. Hamilton,et al.  Finasteride for the treatment of hidradenitis suppurativa in children and adolescents. , 2013, JAMA dermatology.

[2]  R. Paus,et al.  Immunohistological pointers to a possible role for excessive cathelicidin (LL‐37) expression by apocrine sweat glands in the pathogenesis of hidradenitis suppurativa/acne inversa , 2012, The British journal of dermatology.

[3]  G. Jemec Clinical practice. Hidradenitis suppurativa. , 2012, The New England journal of medicine.

[4]  Ximena Wortsman,et al.  Common Applications of Dermatologic Sonography , 2012, Journal of ultrasound in medicine : official journal of the American Institute of Ultrasound in Medicine.

[5]  J. Laman,et al.  Alterations in leucocyte subsets and histomorphology in normal‐appearing perilesional skin and early and chronic hidradenitis suppurativa lesions , 2012, The British journal of dermatology.

[6]  Egil Lien,et al.  NLRP3 inflammasomes are required for atherogenesis and activated by cholesterol crystals , 2010, Nature.

[7]  E. Efstathopoulos,et al.  Ultrasound aids in diagnosis and severity assessment of hidradenitis suppurativa , 2010, The British journal of dermatology.

[8]  J. Lapins,et al.  Interobserver variability of clinical scores in hidradenitis suppurativa is low , 2010, The British journal of dermatology.

[9]  Jacobo Wortsman,et al.  Clinical usefulness of variable-frequency ultrasound in localized lesions of the skin. , 2010, Journal of the American Academy of Dermatology.

[10]  G. Jemec,et al.  Lymph Nodes in Hidradenitis Suppurativa , 2009, Dermatology.

[11]  K. Moore,et al.  Loss of SR-A and CD36 Activity Reduces Atherosclerotic Lesion Complexity Without Abrogating Foam Cell Formation in Hyperlipidemic Mice , 2009, Arteriosclerosis, thrombosis, and vascular biology.

[12]  H. Kurzen,et al.  What causes hidradenitis suppurativa? , 2008, Experimental dermatology.

[13]  G. Jemec,et al.  Real‐Time Compound Imaging Ultrasound of Hidradenitis Suppurativa , 2007, Dermatologic surgery : official publication for American Society for Dermatologic Surgery [et al.].

[14]  B. Ganapathi,et al.  Hidradenitis suppurativa treated with finasteride , 2005, The Journal of dermatological treatment.

[15]  T. Jansen,et al.  Acne inversa (alias hidradenitis suppurativa) , 2001, Journal of the European Academy of Dermatology and Venereology : JEADV.

[16]  A. Ohkawara [Structure and function of the skin]. , 1983, Iyo denshi to seitai kogaku. Japanese journal of medical electronics and biological engineering.

[17]  Gerrity Rg The role of the monocyte in atherogenesis: I. Transition of blood-borne monocytes into foam cells in fatty lesions. , 1981 .

[18]  R. Gerrity,et al.  The role of the monocyte in atherogenesis: II. Migration of foam cells from atherosclerotic lesions. , 1981, The American journal of pathology.

[19]  R. Gerrity The role of the monocyte in atherogenesis: I. Transition of blood-borne monocytes into foam cells in fatty lesions. , 1981, The American journal of pathology.