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25 Rheumatoid andSystemic Collagenosis Vasculitis
183
25.4.4 Approach fortheWound
Infection
25.4.5 Several Adjuvant Devices
intheManagement ofHardto- Heal Wounds
25.4.2 Topical Wound Treatment
25.4.3 Occlusive Dressings
184
ab c
Fig. 25.6 (a) The photograph shows the unsatisfactory
25.5 Surgical Wound Closure
forPatients withRA
M. Fujioka
25 Rheumatoid andSystemic Collagenosis Vasculitis
185
Fig. 25.7 (a) The
a b
ab c
Fig. 25.8 (a) The photograph shows the venous stasis
186
25.6 Prevention ofRecurrence
Acknowledgments None.
References
M. Fujioka
Open Access
Giant Cell Arteritis
PaulineLecerf andSophieGolstein
26
26.1 Introduction/ Physiopathology
Giant cell arteritis (GCA) or Horton’s disease is a
systemic granulomatous vasculitis. According to
the Chapel Hill classication, it affects large vessels, namely, the aorta and its main branches.
This is an antigen-driven disease with local T-cell
and macrophage activation in the vessel wall and
with an important role of proinammatory cytokines. GCA is also called “temporal arteritis”
because it involves often the supercial temporal
arteries. The condition affects especially the
extracranial branches of the carotid artery, but
GCA has been recognized to also affect limb
arteries and the aorta [1, 2].
GCA typically affects adults older than
50 years of age with a peak incidence at the
eighth decade of life [1]. Most patients will have
laboratory evidence of acute inammation (elevation of erythrocyte sedimentation rate and
C-reactive protein).
26.2 Diagnosis
26.2.1 Medical Context
• GCA is the most common vasculitis in the
elderly.
• Incidence increases with aging of the
population.
• GCA affects mainly white individuals over
50years of age, with a peak incidence in the
70–79-year-old age group (Figs. 26.1, 26.2
and 26.3).
• Women are mostly affected (sex ratio 3:1) [3, 4].
P. Lecerf (*) · S. Golstein
Department of Dermatology, University Hospital
Brugmann and Saint-Pierre, Université Libre de
Bruxelles, Brussels, Belgium
© The Author(s) 2024
L. Téot et al. (eds.), Skin Necrosis, https://doi.org/10.1007/978-3-031-60954-1_26
187
188
Fig. 26.1 Vast ulceration and necrosis of the buttock due
to giant cell arteritis in a 76-year-old female, with associated signs: jaw claudication, temporal artery pulseless,
weight loss, visual manifestations, and amputations of the
left forefoot weeks before. Improvement of the ulcerations of the seat after initiation of glucocorticoid
therapy
P. Lecerf and S. Golstein
Fig. 26.3 Same patient with giant cell arteritis, left side
of the scalp
Fig. 26.2 Patient with giant cell arteritis, right side of the
scalp
26.2.2 Semiology
Symptoms are correlated with the localization of
the vasculitic involvement of the arteries.
Classical form of GCA, with involvement of the
extracranial branches of the carotid artery
Early Headache, jaw claudication, purpuric
lesions and tender nodules in temporal
region, temporal artery pain, temporal
artery pulseless, weight loss, fever,
visual manifestations, polymyalgia
rheumatica (in 30–50% of the cases) [5]
Late Ulceration and/or gangrene of
frontotemporal scalp or tongue
Involvement of limb arteries [6–8]
Early Swelling, pain, claudication
Late Ulceration, necrosis (Fig.26.1),
gangrene of the distal parts of the limbs
Major complications
Ischemic optic neuritis/blindness, stroke (mainly
vertebrobasilar territory), aortic complications
(aneurysms, dissection) [6]
26 Giant Cell Arteritis
189
26.2.3 Criteria (Table26.1)
Table 26.1 ACR classication criteria for giant cell
arteritis
Age≥50years at disease onset
New onset of localized headache
Temporal artery tenderness or decreased temporal
artery pulse
ESR ≥50mm/h
Biopsy: Necrotizing arteritis; mononuclear cell
inltrates, or a granulomatous process with
multinucleated giant cells
Presence of≥3/5: Sensitivity of 93% and specicity of
91% for distinguishing GCA from other primary
vasculitis syndromes
American College of Rheumatology (ACR), 1990
26.2.4 Routine Evaluation
(a) Biology
– Elevated C-reactive protein (CRP), eryth-
rocyte sedimentation rate (ESR).
– Thrombocytosis.
– Anemia.
– Abnormal liver function tests, particularly
raised alkaline phosphatase.
– Raised α1 and α2 globulins on serum
electrophoresis.
– No autoimmune disorders [2].
(b) Histology
• Temporal artery biopsy (TAB)
– Recommended in all suspected cases.
– Should be performed soon after the
onset of treatment.
– The sensitivity and specicity of TAB
have been reported to be around 75%
and 90%, respectively.
– Histological features: inammation of
the vessel wall by inltration of T cells
and macrophages, presence of giant
cells, granulomatous lesions, intimal
hyperplasia and destruction of elastic
bers, and arterial lumen partially or
completely occluded.
– Histologic signs of inammation may be
missed in TABs performed in arteritisfree segments because GCA affects
vessels focally and segmentally.
• Skin biopsies
– Histological features from limb ulcer
edge, nodule, and purpuric patch show
nonspecic ulceration if the biopsy is
supercial and do not include deep
medium or large vessels. The extracranial large vessel had similar histopathologic features to those seen in the
temporal arteries and showed a lymphocytic panarteritis with a variable
number of giant cells. Direct immunouorescence is negative [9].
(c) Imaging
The prevalence of limb arteries’ involvement in GCA is clinically underestimated.
Imaging studies are useful in identifying the
involvement of the latter [2]:
• Ultrasonography.
• Positron-emission tomography (PET).
• Computed tomography angiography (CTA).
• Magnetic resonance angiography (MRA).
It is also recommended to perform a
screening for aortic aneurysms and for extraaortic large-vessel involvement.
26.3 Treatment
High-dose glucocorticosteroid therapy is the
rst-line therapy as soon as the diagnosis has
been established or if there is a strong clinical
suspicion of GCA to prevent visual loss [10, 11].
1. Recommended starting dosages of glucocorticosteroids are:
190
P. Lecerf and S. Golstein
Uncomplicated GCA
(no jaw claudication
or visual disturbance)
Evolving visual loss or
amaurosis fugax
(complicated GCA)
Established visual loss 60mg prednisolone daily
40–60mg prednisolone
daily
500mg to 1g of i.v.
methylprednisolone for
3days before oral
glucocorticosteroids
to protect the contralateral
eye
Do not forget bone protection and proton pump
inhibitors for gastrointestinal protection.
2. Symptoms of GCA should respond rapidly to
high-dose glucocorticosteroid treatment, followed by resolution of the inammatory
response. Failure to do so should raise the
question of an alternative diagnosis.
3. Glucocorticosteroid reduction:
(a) Should be considered only in the absence
of clinical symptoms, signs, and laboratory abnormalities suggestive of active
disease.
(b) Introduction of MTX or alternative
immunosuppressants should be considered as adjuvant therapy for recurrent
relapse.
26.4 Tocilizumab
Tocilizumab is an anti-interleukin-6 receptor
monoclonal antibody. Recent American recommendations propose to use a combination of
prednisone and tocilizumab as rst-line therapy
in new-onset GCA.
It can be used in newly diagnosed GCA
patients already presenting corticosteroid-related
adverse events (AE) or at high risk for such AE
[10–13].
26.5 Methotrexate
Methotrexate is initially associated with systemic corticosteroids in patients presenting or at
high risk of corticosteroid-related AE (as an
alternative to tocilizumab) and allows the gradual tapering of the systemic corticosteroid treatment. Although stronger clinical evidence
supports the use of tocilizumab compared to
methotrexate, the latter can be considered if the
patient is at risk of recurrent infections or for
cost reasons [14].
References
1. Kesten F, Aschwanden M, Gubser P, Glatz K, Daikeler
T, Hess C. Giant cell arteritis—a changing entity.
Swiss Med Wkly. 2011;28:141.
2. Borchers AT, Gershwin ME. Giant cell arteritis:
a review of classication, pathophysiology, geoepidemiology and treatment. Autoimmun Rev.
2012;11(6–7):A544.
3. Gonzalez-Gay MA, Vazquez-Rodriguez TR, LopezDiaz MJ, Miranda-Filloy JA, Gonzalez-Juanatey
C, Martin J, et al. Epidemiology of giant cell arteritis and polymyalgia rheumatica. Arthritis Rheum.
2009;61(10):1454–61.
4. Salvarani C, Cantini F, Boiardi L, Hunder
GG. Polymyalgia rheumatica and giant-cell arteritis
[review]. N Engl J Med. 2002;347:261–71.
5. Weyand CM, Goronzy JJ. Giant-cell arteritis
and polymyalgia rheumatica. Ann Intern Med.
2003;139:505–15.
6. Assie C, Janvresse A, Plissonier D, Levesque H, Marie
I.Long-term follow-up of upper and lower extremity
vasculitis related to giant cell arteritis: a series of 36
patients. Medicine (Baltimore). 2011;90:40–51.
7. Kermani TA, Matteson EL, Hunter GC, Warrington
KJ. Symptomatic lower extremity vasculitis in
giant cell arteritis: a case series. J Rheumatol.
2009;36:2277–83.
8. Kermani TA, Warrington KJ.Lower extremity vasculitis in polymyalgia rheumatica and giant cell arteritis.
Curr Opin Rheumatol. 2011;23(1):38–42. https://doi.
org/10.1097/BOR.0b013e3283410072.
9. Klein RG, Campbell RJ, Hunder GG, Carney
JA.Skip lesions in temporal arteritis. Mayo Clin Proc.
1976;51:504–10.
10. Maz M, Chung SA, Abril A, et al. 2021 American
College of Rheumatology/Vasculitis Foundation
guideline for the management of giant cell arteritis and Takayasu arteritis. Arthritis Rheumatol.
2021;73:1349–65.
11. Gonzalez-Gay M. The diagnosis and management
of patients with giant cell arteritis. J Rheumatol.
2005;32:1186–8.
12. Greigert H, Ramon E, Tarris G, Martin L, Bonnotte
B. Temporal artery vascular diseases. J Clin Med.
2022;11:275.
13. Unizony SH, Dasgupta B, Fisheleva E, Rowell L,
Schett G, Spiera R, Zwerina J, Harari O, Stone
JH. Design of the tocilizumab in giant cell arteritis
trial. Int J Rheumatol. 2013;2013:912562. https://doi.
org/10.1155/2013/912562.
14. Golstein S, Delguste T, Lesage V, Vandergheynst F,
Debusscher C.Rapid-onset bilateral scalp ulceration
with visual loss. JAAD Case Rep. 2022;28:97–9.
26 Giant Cell Arteritis
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191
Hidradenitis Suppurativa
KianZarchi, VéroniqueDel Marmol,
andGregorB.E.Jemec
27
27.1 Introduction
Hidradenitis suppurativa is a chronic inammatory skin disease affecting approximately 1% of
the adult population [1, 2]. It presents clinically
as painful inammatory nodules, draining
sinuses, and abscesses, causing considerable
pain, suppuration, and malodor. It has a substantial negative impact on the quality of life, more so
than many other skin diseases, such as eczema
and psoriasis [3]. The disease is associated with
physical and psychological morbidity, such as
depression, metabolic syndrome, and an
increased risk of skin cancer.
The typical age of onset is the early 20s, but
the disease may present in younger ages, and
occasionally affection of prepubertal children is
seen. Symptoms persist for years to decades,
characterized by periods of ares and remission.
The disease activity often diminishes with age, as
the prevalence decreases among adults aged
50years and older. The sex ratio is 3:1, female to
GB Jemec and V Del Marmol are part of ERN skin
network.
K. Zarchi (*) · G. B. E. Jemec
Department of Dermatology, Roskilde Hospital,
Faculty of Health and Medical Sciences, University
of Copenhagen, Roskilde, Denmark
V. Del Marmol
Department of dermatology, Hopital Erasme HUB,
Univesité Libre de Bruxelles, Bruxelles, Belgium
e-mail: Veronique.delmarmol@hubruxelles.be
male. Family history is reported by one in three
patients, and an autosomal dominant pattern of
inheritance has been described [1, 2]. Other risk
factors include obesity and smoking, both being
associated with severe disease.
27.2 Diagnosis
Patients with hidradenitis suppurativa are usually
diagnosed several years after the onset of symptoms, mostly due to failure on the part of healthcare professionals to recognize the disease. The
diagnosis is primarily clinical, based on the presence of recurring noninammatory and inammatory nodules, abscesses, and sinus tracts. The
inammatory nodules and abscesses are erythematous, tender, and not uncommonly painful.
They may persist for weeks to months without
any considerable change, or they may rupture,
yielding purulent discharge. In moderate and
severe disease, drainage also occurs through
sinus tracts, causing malodorous suppuration.
The lesions are distributed characteristically with
predilection sites being the axillary, inguinofemoral, and anogenital regions. Extensions beyond
these areas are occasionally seen.
The most commonly used classication system
for hidradenitis suppurativa is that of Hurley (stages
I–III), stage I representing solitary or multiple nodules and abscesses, stage II recurrent abscesses with
sinus tract formation and scarring (Fig.27.1), and
stage III diffuse involvement of the area with mul-
© The Author(s) 2024
L. Téot et al. (eds.), Skin Necrosis, https://doi.org/10.1007/978-3-031-60954-1_27
193