This forum is for questions about medical issues and research aspects of
Hepatitis C such as, questions about being newly diagnosed, questions about current treatments, information and participation in discussions about research studies and clinical trials related to Hepatitis. If you would like to communicate with other people who have been touched by Hepatitis, please visit our new
Hepatitis Social/Living with Hepatitis forum
It's crazy, because I was always asymptomatic. (without symptoms but you probably knew the meaning) however once I found out, I was really scared about being sick.
There are studies that correlate HCV with depression, but I'm skeptical as most studies correlate hep c with all kinds of things that we might have anyway. I was on a/d's before I found out. Some could say the hep c caused it, but what a coincidence, I have 3 siblings and a father that suffer from anxiety/depression and they don' have hep c.
Take care, it'll be ok, it just takes awhile to get used to the idea.
Bug
FB
I took Peg-Intron and had to wait for 3 months to get it. I have a friend on Pegasys, he is doing ok with it, I hope you get clear! Just live a clean life, eat well and stay away from alchohol is all you can do.
SEE: http://www.tiny.cc/PWuG2
"HCV-Related Morphologic and Functional Alterations in the CNS
Significant progress toward understanding the impact of HCV infection on the CNS has been accomplished through evaluation of morphological and functional alterations found in HCV-infected patients.
Cerebral Magnetic Resonance Spectroscopy
Using proton magnetic resonance spectroscopy, Forton and colleagues[50] evaluated patients with histologically defined mild HCV and found significant elevations in cerebral choline-to-creatine ratios compared with healthy controls and hepatitis B virus–infected individuals. Choline-to-creatine ratios were specifically elevated in the basal ganglia and white matter of the HCV-infected individuals. Furthermore, metabolite elevations were unrelated to hepatic encephalopathy or a history of intravenous drug abuse. Taken together, these findings suggest that a biological mechanism underlies the CNS-related symptoms observed in patients chronically infected with HCV. Consistent with these findings, other researchers have demonstrated metabolite abnormalities, including increased choline and reduced N-acetylaspartate relative to creatine levels, in the brains of HCV-infected patients.[39,51] However, the association between observed cerebral metabolite abnormalities and cognitive impairment was not strong in these patients.[52]
Electroencephalogram Activity in HCV Patients
In a separate study, Weissenborn and colleagues[53] demonstrated that patients with HCV infection (n = 30) had impaired cognitive function, more anxiety and depression, and impaired QOL compared with healthy controls (n = 15). They also showed a decrease in the cerebral cortex N-acetylaspartate-to-creatine ratio and a significant slowing of electroencephalogram activity in approximately 25% of the HCV patients, possibly reflecting changes in cerebral neurotransmission. The reported deficits in neural activity seemed to primarily affect patients that had reported moderate fatigue symptoms. This study further supports the hypothesis that HCV infection directly impairs CNS function.
Alterations in CNS Neurotransmitter Action
Additional reports suggest that HCV infection affects monoaminergic neurotransmission, particularly in the subgroup of patients with symptoms of fatigue and cognitive impairment, although these alterations could also explain HCV-associated depressive symptoms.[53] Although not previously demonstrated, it is plausible that HCV infection could affect serotonergic neurotransmission and lead to clinical symptoms of depression.
In a small sample of HCV-infected patients (n = 20) suffering from disabling fatigue and cognitive decline of unknown aetiology other than HCV positivity, 60% showed impaired dopamine transporter binding whereas 50% demonstrated impaired serotonin transporter binding (Table 2).[53] Of interest, patients with decreased function in both the monoamine transporters showed significantly impaired performance in applied neuropsychological tests. Furthermore, no significant correlation was found between the dopamine and serotonin transporters binding function and fatigue or QOL scores, indicating the specificity of the relationship....."
"Recent studies have demonstrated that—as with interferon-linked depression—treatment with a selective serotonin reuptake inhibitor (eg, escitalopram) is highly effective and safe in HCV-associated depression.[54,55] Nevertheless, as a precaution, it is recommended that a specialist be included in such instances where HCV-infected patients display clinically relevant symptoms of mental disorders (especially depression) or inappropriate coping styles, partly to determine whether the depressive symptoms are caused by the HCV infection or alternative mechanisms. Additional forms of antidepressant or stabilising therapy might be considered as well: Concomitant psychotherapeutic intervention and support groups might be sufficient for those patients with milder forms of depression."
Mike
It is:
Risk and Mechanisms of Depression in HCV
Source: Depression Associated With HCV Infection and Its Therapy: Impact on Patient Management
By: Michael R. Kraus, MD, PhD