Clinical image: chronic skin ulcers in a patient with rheumatoid arthritis on immunosuppressant therapy
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CLINICAL IMAGE
Clinical image: chronic skin ulcers in a patient with rheumatoid arthritis on immunosuppressant therapy Takaaki Kobayashi 1
&
Brian L. Swick 2 & Christine Cho 1,3
Received: 29 May 2020 / Revised: 12 June 2020 / Accepted: 18 June 2020 # International League of Associations for Rheumatology (ILAR) 2020
Presentation A 50-year-old woman with a history of rheumatoid arthritis (RA) and interstitial lung disease (ILD) on prednisone, methotrexate, and hydroxychloroquine presented with a 3-month history of chronic left leg ulcers. Lesions were initially red patches that later blistered and ulcerated. She did not have any associated systemic symptoms. She had never received any biologic agents such as tumor necrosis factor inhibitors for RA and ILD. Empiric treatment with topical gentamicin and clobetasol did not resolve skin lesions. Physical examination demonstrated multiple ulcerated lesions with surrounding erythema in various stages of healing along the left leg (Fig. 1a). Basic metabolic panel, complete blood count, and inflammatory markers were within normal limits. Human immunodeficiency virus screen was negative. An interferon-gamma release assay was negative. Chest radiograph showed known increased interstitial lung markings due to ILD, which were stable without new infiltration. Punch biopsy of proximal lesion demonstrated numerous suppurative granulomas with long beaded acidfast bacilli (AFB, × 1000 magnification) (Fig. 1b). AFB culture was negative, but 16s ribosomal RNA gene sequencing detected Mycobacterium haemophilum. She was treated with ciprofloxacin, clarithromycin, rifampin,
* Takaaki Kobayashi [email protected] 1
Department of Internal Medicine, University of Iowa Hospitals & Clinics, 200 Hawkins Drive, SW34 GH, Iowa, IA, USA
2
Department of Pathology, University of Iowa Hospitals & Clinics, Iowa, IA, USA
3
Iowa Inflammation Program, Roy J. and Lucille A. Carver College of Medicine, University of Iowa, and Veterans Administration Medical Center, Iowa, IA, USA
and intravenous amikacin for 2 months followed by ciprofloxacin, clarithromycin, and rifampin for 4 months. Due to drug-drug interaction, hydroxychloroquine was held, but the rest of immunosuppressive therapy was continued. At the end of therapy, her lesions significantly improved (Fig. 1c).
Discussion M. haemophilum is a slow-growing, aerobic, fastidious mycobacterium that requires heme-supplemented medium and lower incubation temperature (30–32 °C) [1]. M. haemophilum is presumed to be ubiquitous, but its exact habitat has not been defined [2]. Therefore, we could not identify the source of infection in our patient. M. haemophilum can cause a wide range of infections (cutaneous, pyomyositis, lymphadenitis, pulmonary, or disseminated infection), especially in immunocompromised patients [3]. Cutaneous disease is the most common clinical manifestation, as seen in our patient. Most strains of M. haemophilum demonstrate in vitro susceptibility to ciprofloxacin, clarithromycin, rifamycins, and clofazimine; variable
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