Use of (18)F-fluorodeoxyglucose Positron Emission Tomography to Monitor Disease Activity in Patients With Giant Cell Arteritis on Tocilizumab

使用 (18)F-氟代脱氧葡萄糖正电子发射断层扫描监测接受托珠单抗治疗的巨细胞动脉炎患者的疾病活动度

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Abstract

OBJECTIVE: The objective of this study was to assess the value of (18)F-fluorodeoxyglucose (FDG)- positron emission tomography (PET) scans to monitor disease activity in patients with giant cell arteritis (GCA) on tocilizumab. METHODS: Patients with GCA were recruited into a prospective cohort in which they underwent clinical, laboratory, and imaging assessments, including FDG-PET. FDG-PET scans were interpreted as active or inactive based on global impression by two independent readers. The PET Vascular Activity Score (PETVAS) was calculated to quantify arterial FDG uptake (scale 0-27). Vascular FDG-PET findings were described in patients with GCA on tocilizumab for at least six months. For patients in established clinical remission, FDG-PET findings were compared between those treated with tocilizumab versus glucocorticoid monotherapy. RESULTS: A total of 36 patients with GCA underwent FDG-PET imaging on tocilizumab. Five patients had active clinical symptoms, and FDG-PET scans were active in all cases (PETVAS range: 20-27). For the 31 patients in clinical remission on tocilizumab, FDG-PET was active in 16 of these patients (52%) across a wide range of PETVAS (range 11-27). There were no associations between FDG-PET activity during remission and historical clinical features or longitudinal outcomes, including relapse risk or angiographic progression of disease. PETVAS was significantly lower during clinical remission in patients treated with tocilizumab compared to an additional 12 patients treated with glucocorticoid monotherapy (PETVAS 18 vs 24; P = 0.02). CONCLUSION: FDG-PET has limited value to guide management decisions or inform prognosis when obtained during remission in patients with GCA on tocilizumab. Compared to glucocorticoid monotherapy, tocilizumab significantly reduces, but often does not eliminate, vascular inflammation in GCA.

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