The patient was a 70-year-old man with no notable medical history. Chest abnormal shadows were detected by chest X-ray during a health examination. Chest computed tomography (CT) performed at another hospital for a close examination detected nodular and granular shadows suggestive of lung tuberculosis in the right upper lobe (Fig. 1A). The patient was asymptomatic. Sputum culture was positive for Mycobacterium tuberculosis, and the diagnosis of lung tuberculosis was made.
Antituberculosis treatment was initiated with isoniazid, rifampicin, ethambutol, and pyrazinamide in June 2021. He developed a persistent fever three months after the initiation of treatment, and the drugs were discontinued, as drug fever was suspected. However, the fever persisted, and the cause remained unknown. Therefore, he was referred to our hospital in November 2021 for a further examination.
During the first examination, he was febrile and exhausted due to the persistent fever. A laboratory examination showed an elevated MPO-ANCA titer of 36.1 IU/mL and a normal level of creatinine. The drug-induced lymphocyte stimulation (DLST) test was positive for isoniazid. No abnormal findings were detected on a urinalysis (Table). Purpura, arthralgia, neuropathy, and fecal occult blood were not confirmed. Chest CT showed nodular and granular shadows in the right upper lobe, along with no findings suggestive of interstitial pneumonia (Fig. 1B). Chest shadows slightly improved compared with those confirmed at the diagnosis. Enhanced abdominal CT and magnetic resonance imaging (MRI) of the spine showed no findings that could cause a fever, such as intra-abdominal abscess or tuberculous spondylitis. Transthoracic echocardiography revealed no vegetations, and no significant microorganisms were detected in blood, sputum, or urine cultures, including M. tuberculosis.
Since the patient complained of mild grasp pain in his thighs, MRI of the lower extremities was performed, and fat-suppression T2 imaging showed a linear and reticular high signal, suggestive of vasculitis in the thigh muscles of both sides (Fig. 2). Based on these findings and an elevated MPO-ANCA titer, MPA was suspected. Therefore, a muscle biopsy was performed on the right biceps femoris. A histopathological examination revealed monocyte infiltration around the small vessels and fibrinoid necrosis of the vessel walls (Fig. 3). According to the classification criteria for MPA proposed by the American College of Rheumatology/European Alliance of Associations for Rheumatology, the present case had a classification score of six and was thus classified as having MPA.
Radiological worsening of lung tuberculosis lesions and signs of extrapulmonary tuberculosis were not detected, and sputum culture was negative for M. tuberculosis. The patient had used drugs that could induce MPA. Therefore, we excluded active tuberculosis mimicking MPA and made a diagnosis of drug-induced MPA.
The fever and grasp pain were alleviated immediately after the administration of prednisolone 30 mg/day, accompanied by a decrease in the MPO-ANCA titer. Antituberculosis drugs rifabutin, levofloxacin, and ethionamide were administered. Tapering of prednisolone and treatment for tuberculosis will continue accordingly.