Experimental Evaluation of an Altered Tryptophan Metabolism in Fibromyalgia

Psychiatric Hospital, University of Munich, Nussbaumstr. 7, D - 80336 Munich, Germany.
Advances in Experimental Medicine and Biology (Impact Factor: 1.96). 02/2003; 527:265-75. DOI: 10.1007/978-1-4615-0135-0_30
Source: PubMed


Fibromyalgia (FM) is a prevalent syndrome with chronic pain and a hypothesised underlying disturbance of the tryptophan (TRP) metabolism. We performed a tryptophan depletion (TD) test in 17 FM patients and 17 controls. TRP, 5-hydroxyindoleacetic acid (5-HIAA), kynurenine (KYN), and Interleukin-6 (IL-6) were measured. Additionally pain perception was monitored in the FM patients. FM patients and controls exhibited a decrease of TRP and KYN during TD. 5-HIAA levels also decreased in all controls and in 11 FM patients, but showed a marked increase in 6 FM patients. IL-6 significantly increased during TD in the patients, but not in the controls. Pain perception was not affected in the FM patients. These data demonstrate an altered TRP metabolism in a subgroup of FM patients, where the TD seems to activate 5-HT metabolism and IL-6 production. Our findings may have diagnostic as well as therapeutic implications in the field of fibromyalgia.

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    • " et al . , 1976 ; Jokinen et al . , 2009 ; Chatzittofis et al . , 2013 ) . Tryptophan depletion ( a method of lowering brain serotonin , used as a model of depressive disorders ) not only worsens depres - sive symptoms ( Fields et al . , 1991 ; Booij et al . , 2005 ; van Steen - bergen et al . , 2012 ) and also can increase the sensation of pain ( Schwarz et al . , 2003 ; Supornsilpchai et al . , 2006 ; Wei et al . , 2010 ) . The system of antinociception operates primarily through sero - tonin 5 - HT1A and 5 - HT2 receptors ; the stimulation of 5 - HT3"
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    ABSTRACT: Neither pain, nor depression exist as independent phenomena per se, they are highly subjective inner states, formed by our brain and built on the bases of our experiences, cognition and emotions. Chronic pain is associated with changes in brain physiology and anatomy. It has been suggested that the neuronal activity underlying subjective perception of chronic pain may be divergent from the activity associated with acute pain. We will discuss the possible common pathophysiological mechanism of chronic pain and depression with respect to the default mode network of the brain, neuroplasticity and the effect of antidepressants on these two pathological conditions. The default mode network of the brain has an important role in the representation of introspective mental activities and therefore can be considered as a nodal point, common for both chronic pain and depression. Neuroplasticity which involves molecular, cellular and synaptic processes modifying connectivity between neurons and neuronal circuits can also be affected by pathological states such as chronic pain or depression. We suppose that pathogenesis of depression and chronic pain shares common negative neuroplastic changes in the central nervous system (CNS). The positive impact of antidepressants would result in a reduction of these pathological cellular/molecular processes and in the amelioration of symptoms, but it may also increase survival times and quality of life of patients with chronic cancer pain.
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    • "An increased density of 5-HT receptors on platelets in patients with FMS (Russell et al 1992b) and abnormal transport of serum tryptophan (Yunus et al 1990), which have also been reported, indicate a general disturbance of serotonergic neurotransmission. Interestingly, however, tryptophan depletion in FMS patients had no effect on their pain severity (Schwarz et al 2003). "
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    ABSTRACT: Fibromyalgia syndrome is a chronic disease of widespread and debilitating pain whose cause is unknown and whose risk factors are poorly understood. It is often comorbid with rheumatoid and other pain disorders as well as psychiatric disorders such as anxiety and depression. Although they are not officially approved for this indication, antiepileptics and antidepressants are often used to treat fibromyalgia. The tricyclic antidepressants (TCAs), particularly amitriptyline, are among the most common treatment strategies. Because of the poor tolerability of the tricyclics, the newer antidepressants have been widely tested in fibromyalgia. The selective serotonin reuptake inhibitors (SSRIs) and the reversible monoamine oxidase inhibitors do not seem to be particularly helpful. The serotonin and norepinephrine reuptake inhibitors (SNRIs), duloxetine and milnacipran, on the other hand, have been shown in placebo-controlled trials to offer significant relief to patients suffering from fibromyalgia. Although no direct comparative studies have been performed, these compounds appear to be as effective as the TCAs but much better tolerated. The effectiveness of the SNRIs as well as other dual acting antidepressants, such as mirtazapine, but not the SSRIs, implies that a dysfunction of both serotonin and norepinephrine neurotransmission probably exists in fibromyalgia. The effectiveness of antidepressants appears to be independent of their effect on comorbid depression.
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