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Hypnotic medication may be ineffective in the long-term in primary care and potentially exacerbates the problem, this exacerbation may be due to a specific problem of tolerance and addiction related to both persistence and medication use [ 29].
Furthermore, P. gingivalis infection exacerbated collagen-induced arthritis (CIA), and this exacerbation was dependent on the expression of P. gingivalis PAD [46].
Importantly, this exacerbation is dependent on MOG recognition by the human-derived antibodies.
This exacerbation of endothelial inflammatory phenotype occurs through nuclear factor κB overactivation.
Due to this exacerbation, treatment with new high-dose oral corticosteroid dose, bilateral intravitreal injection of ranibizumab and dexamethasone and adalimumab (Humira®) every 15 days was performed.
This exacerbation was associated with either reduced (moderate dose) or unaltered (low dose) hepatic levels of the pro-inflammatory cytokines tumor necrosis factor alpha (TNF-α) and interferon gamma (IFN-γ).
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This phenotypical exacerbation in the absence of two translational repressors was mirrored in aggravated epileptogenesis in vivo.
This caused exacerbation of headaches and in 2 patients (with aneurysms of the cavernous carotid artery) worsening opthalmoplegia.
This symptom exacerbation is temporary and will subside with a rest period [ 12].
Distinguishing this from exacerbation is challenging but important as access to prompt treatment at exacerbation is associated with earlier recovery [ 2], while treating symptom variation as exacerbation might result in unnecessary exposure to therapy.
In this cohort, exacerbation frequency was not significantly different between the patients with a low FFMI and patients with a normal FFMI (3.7 exacerbations per year versus 2.9 excaerbations per year respectively, p = 0.47).
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