Adalimumab/etanercept

Abstract

Dementia: case report An approximately 51-year-old man developed progressive dementia following anti-tumour necrosis factor α (anti-TNFα) treatments with adalimumab and etanercept [durations of treatments to reactions onsets not stated; not all routes stated]. In September 2014, a man aged 50 years, was diagnosed with active ankylosing spondylitis (AS). Treatment with unspecified nonsteroidal anti-inflammatories [non-steroidal anti-inflammatory drugs; NSAID] was insufficient to control the disease. In January 2015, he started receiving SC adalimumab 40mg once every two weeks. The treatment lead to rapid improvement of the AS symptoms; however, progressively, he developed short-term memory loss, word-finding difficulty, decreased concentration and psychic slowdown. Intially differential diagnosis of depression was considered in May 2015 and he was treated with escitalopram, but improvement was not seen. In July 2015, neurologic explorations for the cognitive disorder were negative, with an exception of mild attention difficulties. Brain MRI showed no cerebral atrophy or stroke/ encephalitis. No infectious disease was observed in serological investigations. Testing for autoimmunity, endocrine, TSH, homocysteine and vitamins B1, B6, B9 and B12 levels etiologies yielded normal results. The thoracic-abdominopelvic CT scan and cerebrospinal fluid (CSF) testing results were normal. The CSF markers of Alzheimer’s disease (AD) were in the normal range. The conginitive impairment continued progressively. Thus, a relationship between cognitive impairment and adalimumab use was suspected. Thus, the man’s adalimumab treatment was discontinued in October 2015. He started receiving treatment with another antiTNFα drug etanercept 50mg once per week; however cognitive impairment continued progressively and etanercept was withdrawn in January 2016. After withdrawal of second anti-TNFα drug etanercept, his cognitive functions started to improve slowly. In September 2016, however, he still presented with major neurocognitive disorders. A complete neuropsychological assessment confirmed dementia, with a Mattis dementia scale score of 90/144. The evaluation showed attention and executive disorders, but also encoding disorders in episodic memory. Behavioral disorders have also been observed (e.g. impulsivity). In March 2017, about fourteen months after anti-TNF α treatment cessation, a second neuropsychological assessment showed a significant improvement in cognitive and behaviour functions with a Mattis dementia scale score of 141/144 with only few persistent memory and concentration difficulties. In February 2018, cognitive performances and the Mattis dementia scale score remained stable. In July 2016, a cerebral FluoroDeoxy-Glucose Positron Emission Tomog-raphy (FDG-PET) SCAN showed abnormalities with a moderate bilateral fronto-temporal hypo-metabolism. No evidence of vasculitis was seen. In July 2017 a second brain PET scan detected the same abnormalities. The etiology for persistent alterations of cerebral PET-scan results remained unclear. The authors concluded that, the complete recovery of the cognitive function suggested towards imputability of anti-TNF drugs in the dementia.