TY - JOUR
T1 - Effect of the TNF-α inhibitor adalimumab in patients with recalcitrant sarcoidosis: a prospective observational study using FDG-PET
AU - Milman, Nils
AU - Graudal, Niels
AU - Loft, Annika
AU - Mortensen, Jann
AU - Larsen, Janni
AU - Baslund, Bo
N1 - © 2011 Blackwell Publishing Ltd.
PY - 2012/10
Y1 - 2012/10
N2 - Background: Tumour necrosis factor-alpha (TNF-α) plays a crucial role in sarcoidosis. In severe disease, treatment with TNF-α inhibitors may be effective. Objectives: Changes in sarcoid disease activity were assessed by fluorine-18-fluorodeoxyglucose positron emission tomography (FDG-PET) in patients with recalcitrant sarcoidosis treated with adalimumab. Methods: Prospective 24-week observational study. Patients continued medication with steroids and antimetabolites and received adalimumab 40mg subcutaneously every other week. Ten patients with biopsy-proven sarcoidosis (two men) were included with a median age of 47 years (range 35-73). An FDG-PET showing uptake indicating sarcoid activity was required at inclusion and repeated at the end of the study. FDG-PET uptake was assessed by calculated standardised uptake value (SUV). Blood samples and lung function tests were performed regularly. Quality of life was assessed by the short-form health survey (SF-36) questionnaire. Results: Following treatment with adalimumab, FDG-PET uptake decreased in nine patients (P=0.011) and increased in one patient. Maximum SUV fell from median 14.1 to 7.0 (P<0.03), and mean SUV fell from median 6.5 to 2.9 (P<0.02). Six patients had uptake in the lungs, which decreased after treatment (P=0.035). Six patients had uptake in the lymph nodes, which decreased after treatment in five patients (P=0.035). Four patients had non-lymphatic extrathoracic uptake, which decreased after treatment (P=0.05). There was no effect of adalimumab on pulmonary function tests, serum angiotensin I converting enzyme and blood lymphocyte (CD3+, CD4+, CD8+) concentrations. Physical component summary score (SF-36) increased during treatment, mental component summary score was unchanged. Conclusion: In sarcoidosis, treatment with adalimumab can reduce disease activity, as assessed by FDG-PET.
AB - Background: Tumour necrosis factor-alpha (TNF-α) plays a crucial role in sarcoidosis. In severe disease, treatment with TNF-α inhibitors may be effective. Objectives: Changes in sarcoid disease activity were assessed by fluorine-18-fluorodeoxyglucose positron emission tomography (FDG-PET) in patients with recalcitrant sarcoidosis treated with adalimumab. Methods: Prospective 24-week observational study. Patients continued medication with steroids and antimetabolites and received adalimumab 40mg subcutaneously every other week. Ten patients with biopsy-proven sarcoidosis (two men) were included with a median age of 47 years (range 35-73). An FDG-PET showing uptake indicating sarcoid activity was required at inclusion and repeated at the end of the study. FDG-PET uptake was assessed by calculated standardised uptake value (SUV). Blood samples and lung function tests were performed regularly. Quality of life was assessed by the short-form health survey (SF-36) questionnaire. Results: Following treatment with adalimumab, FDG-PET uptake decreased in nine patients (P=0.011) and increased in one patient. Maximum SUV fell from median 14.1 to 7.0 (P<0.03), and mean SUV fell from median 6.5 to 2.9 (P<0.02). Six patients had uptake in the lungs, which decreased after treatment (P=0.035). Six patients had uptake in the lymph nodes, which decreased after treatment in five patients (P=0.035). Four patients had non-lymphatic extrathoracic uptake, which decreased after treatment (P=0.05). There was no effect of adalimumab on pulmonary function tests, serum angiotensin I converting enzyme and blood lymphocyte (CD3+, CD4+, CD8+) concentrations. Physical component summary score (SF-36) increased during treatment, mental component summary score was unchanged. Conclusion: In sarcoidosis, treatment with adalimumab can reduce disease activity, as assessed by FDG-PET.
U2 - 10.1111/j.1752-699x.2011.00276.x
DO - 10.1111/j.1752-699x.2011.00276.x
M3 - Journal article
SN - 1752-6981
VL - 6
SP - 238
EP - 247
JO - Clinical Respiratory Journal
JF - Clinical Respiratory Journal
IS - 4
ER -