P1516Varicella zoster virus brachioplexitis associated with granulomatousvasculopathy

John Fleming, MBBS, King’s College Hospital, London, United Kingdom; AbigailFogo, MBBS, King’s College Hospital, London, United Kingdom; Roderick Hay,MBBS, King’s College Hospital, London, United Kingdom; Salman Haider, MBBS,King’s College Hospital, London, United Kingdom; Saqib Bashir, MD, MBBS,King’s College Hospital, London, United Kingdom

Varicella zoster virus (VZV) iswell-known to lead to the clinical disease of varicella inprimary infection and zoster upon reactivation. However, the manifestations of VZVinfection can be altered in the immunocompromised, and our case highlights thepotential for motor nerve involvement. We report the case of a 63-year-old man witha prolonged, multidermatomal, nonvesicular rash with VZV PCR positivity onaffected skin, limb paresis secondary to brachioplexitis, and histology consistentwith granulomatous vasculopathy. Because of the significant motor weakness, nerveconduction studies and electromyography were performed, which revealed absentsensory potentials and biceps denervation, suggesting C5 pathology. In addition, aT2-weighted MRI scan showed root enhancement of the left brachial plexus,supporting the diagnosis of a left brachial radiculoplexitis. No other systemicfeatures of vasculitis developed, a vasculitic screen was negative, and a lumbarpuncture excluded the presence of VZV DNA. After 3 months of oral valaciclovir 1 gtds and regular physiotherapy, his motor neuropathy improved with 5/5 power inelbow flexion and extension, but a reduced range of movement and weakness inshoulder abduction persists. His papular red-brown eruption has settled slowly 8months after the initial presentation. The clinical course of cutaneous zoster inimmunocompromised individuals is often recurrent, protracted, and multiderma-tomal. In such individuals, it can penetrate into deeper tissue and result in a diversespectrum of disorders, including myelitis, meningoencephalitis, and cerebral orsmall-vessel vasculopathic or vasculitic changes. This case discusses the unusualfinding of disuse muscle wasting secondary to limb paresis from brachioplexitis andthe potential role of MRI to investigate cases where a prolonged albeit atypicaleruption coincides with motor weakness and pain. The challenges posed bypotential central nervous system complications after immunosuppressive treatmentare also highlighted. Prolonged oral treatment with valaciclovir improves aciclovirbioavailability and may obviate the need for increasing immunosuppression whenthese concerns exist.

FEBRUARY

cial support: None identified.

Commer

P1517Annular elastolytic giant cell granuloma

Jose Aneiros-Fernandez, MD, San Cecilio Clinical Hospital, Department ofPathology, Granada, Spain; Husein Husein-ElAhmed, MD, San Cecilio ClinicalHospital, Department of Dermatology, Granada, Spain; Ines Aroca-Siendones,MD, San Cecilio Clinical Hospital, Tumor Bank, Granada, Spain; Jose Aneiros-Cachaza, MD, San Cecilio Clinical Hospital, Department of Pathology, Granada,Spain; Salvador Arias-Santiago, MD, San Cecilio Clinical Hospital, Department ofDermatology, Granada, Spain

Background: Annular elastolytic giant cell granuloma is a rare dermatosis ofunknown origin that is characterized by a loss of elastic fibers and elastophagocy-tosis by multinucleated giant cells. It affects photoexposed areas.

Case report: A 45-year-old woman reported that more than 1 year ago, a lesionappeared on her neck after a burn. A physical examination revealed an incompleteannular lesion that was bright, consisted of erythematous papules, and wassometimes itchy. The rest of the skin was normal. The histologic study shows thepresence of multiple giant cells, which are not lattice or caseous necrosis,accompanied by few cells located in superficial dermis. Some giant cells had elasticconnective tissue debris (elastophagocytosis).

Discussion: The etiology is unknown, although cases have been reported on burnscars, after intense sun exposure, and from phototoxicity associated with doxycy-cline. The clinical course is chronic, and treatment has been effective with topicalcorticosteroids, intralesional or systemic, chloroquine, acitretin, and cyclosporin.The differential diagnosis must be made with granuloma annulare, erythemaannulare centrifugum, necrobiosis lipoidica, sarcoidosis, and granulomatousinfections.

cial support: None identified.

Commer

2011

P1518Importance of histopathologic diagnosis of acroangiodermatitis

Ana Maria Mosca de Cerqueira, PhD, Hospital Menino Jesus, Rio de Janeiro,Brazil; Clarissa Caramez, Policlinica Geral do Rio de Janeiro, Rio de JAneiro,Brazil; Joana Orli, Policlinica Geral do Rio de Janeiro, Rio de Janeiro, Brazil; MariaAuxiliadora Jeunon, Hospital Universit�ario Pedro Ernestro, Rio de Janeiro, Brazil

Background: Acroangiodermatitis is a very rare disease. It is characterized byerythematous violaceous cutaneous lesions, localized mainly in the legs and feet,resembling Kaposi sarcoma. Acroangiodermatitis is a disease that is usually associ-ated with different disorders, such as chronic venous insufficiency, arteriovenousmalformation, and arteriovenous shunt. This case adds your learning difficultyprenatal.

Summary: A 62-year-old white woman who was a resident of Rio de Janeiropresented with lesions that were erythematous, violaceous, painless, and pruritic,with an evolution of approximately 1 year. The physical examination revealed thepresence of varicose veins of varying sizes in her legs. Routine laboratory exami-nations did not reveal alterations. Histopathology revealed hyperplastic epidermisand, in the papillary dermis and the middle reticular dermis, a proliferation of bloodvessels amid a moderate interstitial lymphohistiocytic infiltrate and depositinghemosiderin. Immunohistochemistry lookup antigen CD34 was negative, excludingthe diagnosis of Kaposi sarcoma, whose cells are 100% positive CD34.

Conclusion: Acroangiodermatitis is a disorder that is clinically and histologicallysimilar to Kaposi sarcoma and that is characterized by violaceous papules andnodules grouped into anatomic ends. It seems to be caused by changes in the localcirculation, causing a reactive proliferation. This is frequently associated with othervascular disorders. The histopathologic differential diagnosis of Kaposi sarcoma isnot always easy; however, in acroangiodermatitis, the vessels are quite regularwithout the fissures that are very common in Kaposi sarcoma. In the latter, theleakage of red blood cells is not so intense and there is a lesser amount ofhemosiderin. There are cases, however, in which the differential diagnosis becomesdifficult. In such cases, clinicians should use the CD34 antigenwhich is expressed in100% of the cases of Kaposi sarcoma and absent in acroangiodermatitis, according tothe work of Kanitakis et al.

cial support: None identified.

Commer

DERMATOPHARMACOLOGY/COSMECEUTICALS

P1600Simple vasoconstriction may be a primary antiinflammatory mechanismof topical corticosteroids

Christopher Kroodsma, MD, University of Illinois College of Medicine Peoria,Peoria, IL, United States

The vasoconstrictor assay is used as a method to measure corticosteroid potency,because their ability to constrict blood vessels has been found to correlate well withantiinflammatory efficacy. Yet this vasoconstriction is generally not considered to bean antiinflammatory mechanism. An experimental model was designed with thepurpose of showing the effect that simple diameter differences may have on bloodvessel walls. Distensible latex material containing microscopic holes (representingintercellular spaces) was used to create a cylindrical lumen with diameters of 0.5’’proximally and 1’’ distally. Water was allowed to flow through the lumen andpressure was increased by blocking the distal end. As fluid pressure increased, onlythe larger diameter segment became visibly distended, although pressure was equalthroughout the lumen. No fluid escaped through the luminal wall holes initially, butas the larger diameter segment distended, fluid began to flow rapidly through theholes in this region but not through those in the narrower segment. Thesephenomena are explained by the LaPlace Law, which holds that T ¼ DP�R (whereT ¼ wall tension, DP ¼ transmural pressure, and R ¼ radius) for a distensiblecylindrical lumen. The term tension (T) represents a force directed along thecircumference of the luminal wall that promotes distension and stretch. A narrowervessel, simply as a function of its smaller diameter, is relatively protected from walltension. Vessels in many inflammatory processes are either temporarily or chron-ically dilated are therefore exposed to increased wall tension/stretch force. Physicalstretch of blood vessel walls and endothelium has been shown experimentally toresult in release of numerous proinflammatory cytokines, including VEGF, TNFa,MCP-1, IL-6, and IL-8. Also, as shown in the above experiment, increased walltension may result in the opening of typically closed gaps in vessel walls, facilitatingmovement of fluid and/or inflammatory cells into the surrounding tissues. It followsthat with corticosteroid-induced decreases in vessel diameter and subsequentlydecreased wall tension, as defined and predicted by the LaPlace Law, inflammationmay be accordingly decreased.

cial support: None identified.

Commer

J AM ACAD DERMATOL AB69