Multifocal Osteoarticular Tuberculosis in a Lupus With Sjogren Syndrome Patient

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To the Editor:
A 41-year-old woman from Senegal was admitted to our facility for physical therapy. She had a history of systemic lupus erythematosus (SLE), Sjogren syndrome, and untreated latent tuberculosis infection (LTBI). Before admission, she was diagnosed with an SLE flare and avascular necrosis of the hips and right proximal tibia in the other facility receiving autoimmune therapy.
Although inpatient urine tract infection was diagnosed and treated, despite the completion of treatment, she continued experiencing intermittent high-grade fevers. Physical examination showed bilateral hip tenderness and a mild swollen right knee. Laboratory revealed white blood cell count 3280/mm3, antinuclear antibody titer 1:128, erythrocyte sedimentation rate 57 mm/hour, and C-reactive protein 82 mg/L. Hip x-ray showed bilateral degenerative destruction of the femoral heads with loss of joint spaces.
Subsequently, she underwent right total hip arthroplasty and arthrocentesis of the right knee. Intraoperative findings revealed a thick yellow viscous fluid material in the right hip and tissue with liquefaction extending to the ipsilateral gluteus maximus. Biopsy of the hip showed caseating granuloma with chronic inflammation. Fluid cultures of the right hip and knee revealed Mycobacterium tuberculosis sensitive to first-line drugs. The patient started quadruple antituberculosis therapy; however, she developed complications such as hepatotoxicity, hospital-acquired pneumonia, candidemia, sepsis, and multiorgan failure.
Tuberculosis (TB) is one of the most deadly communicable diseases in the world. In the United States, a total of 9412 new cases were reported in 2014.1,2 Although the lungs are the most commonly affected organ, extrapulmonary involvement is commonly seen in immunocompromised hosts.3,4 Bone and skeletal involvement account for 10%–15% of the extrapulmonary forms.5
A greater percentage of extrapulmonary TB was described in patients with SLE than those in general population, and the main risk factor was higher daily or cumulative doses of steroids during the year before diagnosis.6 An increased risk for TB infection in patients with Sjogren syndrome has been described as well.7
Tuberculous arthritis is usually monoarticular; nonetheless, multiple-joint involvement is rare, about 5%–15% in endemic countries.5,8 Rich vascular supply of the vertebra, growth plates of long bones, and its hematogenous spread may explain preference toward large joints.9,10
The clinical manifestation of TB is diverse especially in extrapulmonary presentation. The diagnosis of multifocal tuberculosis is even more complex and is often delayed because of its rarity.5 Common misdiagnoses include inflammatory arthritis, septic arthritis, malignancy, osteoporotic fractures, and connective tissue flare. Patients with delayed diagnosis may be prone to dreadful consequences such as spreading of the infection from infected bone to adjacent soft tissue and other joints or permanent disability. Therefore, a high degree of suspicion should be maintained especially when images demonstrate multiple destructive lesions.5,9
Identification and treatment of LTBI reduce the likelihood of reactivation; our patient had a positive tuberculin skin test performed in the other facility years ago, but unfortunately did not receive any prophylaxis. In patients who need long and rigorous immunosuppression due to any autoimmunity, physicians must not only seek for LTBI but also treat it. If LTBI had been treated in parallel to immunosuppression, the patient might not have developed the active disease.

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