The Use of Elastocompressive Therapy in a Patient With Acroangiodermatitis of the Lower Limb

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Author(s): 
Antonio Giovanni Richetta, PhD;Valentina Carboni, MD; Valentina Carlomagno, MD; Elisa Maiani, MD; Manuela Cimillo, MD; Carlo Mattozzi, MD; Stefano Calvieri, MD

Disclosure: This work was supported by the ARRD (Associazione Romana Ricerca Dermatologica).

Acroangiodermatitis is a vasoproliferative disease of the lower limbs associated with congenital or acquired vascular alterations. It is clinically characterized by circumscribed, slowly-evolving, red violaceous or dusky macules, papules, or plaques.1,2

This condition closely mimics Kaposi’s sarcoma in regard to clinical and histopathological features. For this reason it is also called pseudo-Kaposi sarcoma.1 Immunolabeling makes the two diseases different: endothelial marker CD34, von Willebrand’s factor, and Ulex European agglutinin I lectin are not present in acroangiodermatitis.3

There are two main clinical variants of acroangiodermatitis—the Mali type, associated with venous hypertension, and the Stewart-Bluefarb type, associated with arteriovenous malformation or acquired (iatrogenic) arteriovenous fistula (in patients with chronic renal failure).Vascular alterations may be associated with A) paralysis of the affected limb;B) damage of vessels after amputation and poorly fitting prosthesis or intravenous (IV) drug abuse; C) carriage of the thrombophilic 20210A mutation in the prothrombin gene; D) Klippel-Trénaunay syndrome.4–6

Therapeutical options consist of corrective arteriovenous shunts through embolization or surgery, surgical ligation of vessels, or elastic compression therapy in chronic venous insufficiency. Anticoagulant therapy is useful in patients with thrombophilic alterations.1

Case Study

A 63-year-old white man, with an erythematous redviolaceous macule on the anterior tibial region of the right leg in part covered by yellow-brownish crusts presented to the authors’ facility (Figure 1).

 

Prior to presentation at the author’s facility, the patient had undergone surgical interventions for bladder polyposis and was given a permanent bladder catheter. The patient also had a duodenal ulcer that was controlled with oral esomeprazole.

A cutaneous biopsy of the lesion was performed and the histopathology image showed hyperkeratosis of the epidermis, presence of new vessels in lobular arrangement, and hemosiderin deposits in the papillar and the upper part of the reticular dermis (Figure 2). Diagnosis of acroangiodermatitis was made.

After several months, the erythematous area extended to the external and internal malleolar regions of the right leg and became completely covered by crusts. Upon removal,an intensely erythematous,exuding,malodorous, exulcerated skin was seen (Figures 3–5).

 

Laboratory assays showed mild reduction of hemoglobin (11.8), hematocrit (36.7), MCV (70.7%), ferreamia (35.8), ferritin (9), and elevation of transferrin (408). Although hepatitis C virus (HCV) antibodies resulted positive (1.26 s/co), quantitative and qualitative dosage for HCV-RNA by polymerase chain reaction (PCR) was negative. Autoantibodies (ANA, p-ANCA, c-ANCA), anticardiolipin, and cryoglobulins were not present. Inflammation signs (ie, VES, PCR, rheumatoid factor) were normal. A thrombophilic screening showed only a mild reduction of APTT (24 sec or 0.85 ratio), while PT, fibrinogen, ATIII, protein C,protein S,and APCR were normal.Mutations for Leiden’s factor V (G16961A1),methylene tetrahydrofolate reductase (MTHFR, C677T), and prothrombin (G20210A) by PCR were not found.

Several bacterial cultures from the lesion were taken and showed growth of several microorganisms:

• Escherichia coli, Proteus species, Enterococcus faecalis— treated with systemic antibiotic therapy ampicillin and imipenem

• E coli, Proteus mirabilis, Staphylococcus aureus— responsive to topical gentamicin and systemic cefepime

References: 

References

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