Korte, S. Mechiel and Straub, Rainer H. (2019) Fatigue in inflammatory rheumatic disorders: pathophysiological mechanisms. RHEUMATOLOGY, 58 (Suppl5). pp. 35-50. ISSN 1462-0324, 1462-0332
Full text not available from this repository. (Request a copy)Abstract
Today, inflammatory rheumatic disorders are effectively treated, but many patients still suffer from residual fatigue. This work presents pathophysiological mechanisms of fatigue. First, cytokines can interfere with neurotransmitter release at the preterminal ending. Second, a long-term increase in serum concentrations of proinflammatory cytokines increase the uptake and breakdown of monoamines (serotonin, noradrenaline and dopamine). Third, chronic inflammation can also decrease monoaminergic neurotransmission via oxidative stress (oxidation of tetrahydrobiopterin [BH4]). Fourth, proinflammatory cytokines increase the level of enzyme indoleamine-2, 3-dioxygenase activity and shunt tryptophan away from the serotonin pathway. Fifth, oxidative stress stimulates astrocytes to inhibit excitatory amino acid transporters. Sixth, astrocytes produce kynurenic acid that acts as an antagonist on the alpha 7-nicotinic acetylcholine receptor to inhibit dopamine release. Jointly, these actions result in increased glutamatergic and decreased monoaminergic neurotransmission. The above-described pathophysiological mechanisms negatively affect brain functioning in areas that are involved in fatigue.
| Item Type: | Article |
|---|---|
| Uncontrolled Keywords: | TUMOR-NECROSIS-FACTOR; TO-BRAIN COMMUNICATION; INDUCED SICKNESS BEHAVIOR; QUALITY-OF-LIFE; INTERFERON-ALPHA; ANKYLOSING-SPONDYLITIS; PREFRONTAL CORTEX; IMMUNE-SYSTEM; PROINFLAMMATORY CYTOKINES; NOREPINEPHRINE RELEASE; fatigue; rheumatic disorders; inflammation; pathophysiology; mechanisms |
| Subjects: | 600 Technology > 610 Medical sciences Medicine |
| Divisions: | Medicine > Lehrstuhl für Innere Medizin I |
| Depositing User: | Dr. Gernot Deinzer |
| Date Deposited: | 24 Mar 2020 06:38 |
| Last Modified: | 24 Mar 2020 06:38 |
| URI: | https://pred.uni-regensburg.de/id/eprint/25912 |
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