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Granuloma Annulare in a Zoster Scar of a Patient with Multiple Myeloma

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Granuloma Annulare in a Zoster Scar of a Patient with Multiple Myeloma Granuloma Annulare in a Zoster Scar of a Patient With Multiple Myeloma Navid Ezra, BS; Jennifer Ahdout, MD; Jennifer C. Haley, MD; Melvin W. Chiu, MD, MPH Granuloma annulare (GA) is a common benign of localized GA at the site of scars from prior HZ inflammatory skin disorder with an unknown infection in a patient with multiple myeloma who pathogenesis. Granuloma annulare occurring in had received an autologous peripheral stem cell prior sites of herpes zoster (HZ) infection is rarely transplant (PSCT). reported; however, it is the most common granu- lomatous reaction described at these sites. We Case Report report a case of localized GA on scars of prior A 54-year-old woman presented to our clinic with HZ infection in a patient with multiple myeloma persistent shingles on the left side of her back and who had received an autologous peripheral stem abdomen. She had a 2-year history of multiple cell transplant (PSCT). This patient’s GA was myeloma and received thalidomide, dexamethasone, successfully treated with intralesional corticoste- palliative radiation to the thoracic spine, and high- roid injections. dose melphalan chemotherapy followed by autolo- Cutis. 2011;87:240-244. gous PSCT. The lesions were pruritic and painful. Two months prior to presentation and 2 weeks prior CUTISto her PSCT, the patient developed a painful and ranuloma annulare (GA) is a common benign pruritic eruption on the left side of her back and inflammatory skin disorder with an unknown abdomen. She initially attributed the discomfort to G pathogenesis. Associations with several dis- a previously diagnosed pathologic rib fracture but eases such as diabetes mellitus and lymphoprolif- was subsequently diagnosed with HZ and started on erative malignancies have been well-established, yet a 7-day course of valacyclovir. The lesions crusted the exact mechanism has not been determined.1-3 over and healed in approximately 2 weeks; she then It hasDo been suggested that a cell-mediatedNot immune underwent Copy autologous PSCT while on prophylactic response triggered by a local or systemic stimulus doses of valacyclovir approximately 1 month prior may be involved in the disorder.4-7 to presentation. Localized GA has been reported to occur in sites At presentation the patient had grouped pink affected by trauma, vaccinations,8,9 or insect bites; to violaceous papules in a dermatomal distribution resolving lesions of varicella and verruca vulgaris; along the left side of her back, flank, and abdomen sun-damaged skin4; and skin following tuberculin (Figures 1A and 1B). There were no hemorrhagic tests.1,3,10,11 Some cases have been reported of occur- crusts or vesicles, but the papules were slightly rence on dermatomal areas previously affected by tender to palpation. At that time, her diagnosis herpes zoster (HZ) infection.1,3,12-15 We report a case was postherpetic neuralgia with hypertrophic scars from HZ. A skin punch biopsy was performed and the patient was started empirically on gabapentin Mr. Ezra and Dr. Chiu are from, Dr. Ahdout was from, and Dr. Haley with progressively increasing dosages up to 300 mg was from the Division of Dermatology, Department of Medicine, 3 times daily. David Geffen School of Medicine at University of California, Los Angeles. Dr. Ahdout currently is from the Department of Skin biopsy demonstrated palisading granulomas Dermatology, University of California, Irvine. Dr. Haley currently is in the upper dermis with a lymphocytic infiltrate from Kaiser Permanente, Panorama City, California. (Figure 2). Several multinucleated giant cells were The authors report no conflict of interest. apparent. Acellular areas were present within the Correspondence: Melvin W. Chiu, MD, MPH, Division of center of the granulomas and showed positive stain- Dermatology, Department of Medicine, David Geffen School of Medicine at UCLA, 52-121 Center for the Health Sciences, ing for mucin with colloidal iron and Alcian yellow- 10833 Le Conte Ave, Los Angeles, CA 90095 toluidine blue (Leung) stains. Acid-fast and periodic ([email protected]). acid–Schiff stains were negative for organisms. 240 CUTIS® WWW.CUTIS.COM Copyright Cutis 2011. No part of this publication may be reproduced, stored, or transmitted without the prior written permission of the Publisher. Granuloma Annulare in a Zoster Scar A C CUTIS B D Figure 1. Grouped erythematous papules in a zosteriform distribution on the left side of the back (A) and an ery- thematous plaque on the left side of the abdomen (B). One month following intralesional triamcinolone acetonide injections, the patient demonstrated flattening of papules and decreased erythema on the back (C) and abdomenDo (D). Not Copy The patient was diagnosed with GA occurring Prior reports of GA after HZ infection show an in HZ scars. The gabapentin had not relieved her equal sex distribution and an onset during the fourth pain; as a result, she was given an intralesional tri- or fifth decades of life.19 Granuloma annulare may amcinolone acetonide injection at a concentration develop at sites of resolved HZ with variable latency of 10 mg/mL. At 1-month follow-up she reported periods between the infection and the granuloma- resolution of pain and pruritus at the locations of her tous reaction.2 Based on reported cases, the interval prior eruptions. On physical examination her lesions between the eruption of HZ and the onset of GA demonstrated considerable flattening and decreased is short, ranging from 1 week to 14 months.19 The erythema (Figures 1C and 1D). lesions typically are papules that precisely trace the HZ scar. Histologic examination typically reveals Comment foci of necrobiotic collagen surrounded by a pali- Etiology—Although GA occurring in prior sites sade of histiocytes in the deep dermis and subcutis. of HZ infection is rarely reported, it is the most Mucin deposits may be seen within the center of the common granulomatous reaction described at palisaded granuloma with possible scattered multi- these sites. Granulomatous reactions following nucleated giant cells.19 HZ are rare and include GA, sarcoidosis, tuber- Pathogenesis—Although the pathogenesis remains culoid granulomas, granulomatous vasculitis, unclear, 3 different mechanisms have been proposed granulomatous panniculitis, and nonspecific granu- to explain the association of GA and HZ infec- lomatous reactions.1-3,10,11,14-18 tion: an isotopic phenomenon, an immune complex WWW.CUTIS.COM VOLUME 87, MAY 2011 241 Copyright Cutis 2011. No part of this publication may be reproduced, stored, or transmitted without the prior written permission of the Publisher. Granuloma Annulare in a Zoster Scar within early (,1 month) but not older postzoster GA lesions by using polymerase chain reaction anal- ysis.2,30 The presence of varicella-zoster virus DNA in early lesions that histologically do not display viral cytopathic changes suggests the virus induces an atypical delayed hypersensitivity reaction not affected by antiviral therapy.2 Another study using immunohistochemistry and in situ hybridization techniques to look at early granulomatous lesions concluded that major viral envelope glycoproteins (GpI and GpII) rather than complete viral particles could be responsible for delayed hypersensitivity reactions and could trigger granuloma formation fol- lowing HZ infection.31 Localized GA also has been reported on HZ scars Figure 2. Superficial dermis with scattered granulomas from prior infection 3 months after autologous PSCT and multinucleated giant cells (H&E, original magnifica- in a man with Hodgkin disease.32 Many cases of GA tion 3100). occur after the diagnosis of a malignancy, suggesting that either the malignancy itself or immunosuppres- sion caused by the cancer treatment is responsible reaction, and an atypical delayed hypersensitiv- for GA development.33,34 Generalized GA lesions ity reaction to HZ viral antigen.1,12,13,20 The term in a patient with Hodgkin disease have been seen isotopic response was used to describe the occurrence 3 weeks following autologous bone marrow trans- of a new skin disorder at the site of another unre- plant.35 Because of the altered lymphocyte-mediated lated and already healed skin disease. It was thought immune response during the immune system’s that introducing the new term and classifying all the early recovery period following transplantation,36 cases under a single keyword CUTISwould make it possible a delayed hypersensitivity reaction to HZ antigens to group occurrences of these phenomena together may lead to the development of GA in HZ scars. and simplify the search for an underlying mecha- It has been suggested that granulomatous reactions nism.21 The pathogenesis stems from the fact that on HZ scars are mainly due to atypical lymphocytic herpesviruses are known to specifically damage sen- immune reactions to local antigenic stimuli.32 sory nerve fibers,22,23 which leads to a dysregulation Treatment—Localized GA, including GA associ- of the neuropeptides secreted from these fibers in the ated with HZ infection, is generally self-limited and dermis.Do These changes locally Notaffect several immune resolves Copy within 1 to 2 years, whereas disseminated and angiogenic responses,20,24 which may result in a disease lasts longer.37 No treatment other than reas- type of postherpetic neuroimmune dysregulation.25 surance may be necessary for localized GA, yet there This imbalance may be responsible for the predilec- are no well-designed randomized controlled trials tion and initiation of a localized isotopic response.25 of treatment
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