Aa
My 3 week post Tx Lab Results
Hello to All:
I have just received my lab results after 6 mth of Tx PEG/Riba. Last shot #26/24 was on Apr 8th 2004 & Riba was taken for an additional week. Lab results look GREAT:
ALK.PHOSPHAT. 78.00 IU/L ( 35.00- 141.00
(....*....) (ALT(GPT) 26.00 IU/L ( 5.00- 40.00
(...*.....) (AST(GOT) 27.00 IU/L ( 5.00- 40.00
(.......*.) (BILIRUB.TOTAL 0.30 MG/DL ( 0.10- 1.10
(....*....) (BUN 16.00 MG/DL ( 8.00- 23.00
(......*..) (CALCIUM-SERUM 9.30 MG/DL ( 8.40- 11.00
(...*.....) (CREATININE-S 1.00 MG/DL ( 0.50- 1.30
(......*..) (SODIUM-SERUM 139.00 MMOL/L ( 133.00- 153.00
(......*..) (POTASSIUM-SERU 4.10 MMOL/L ( 3.50- 5.30
*(.........) (GGT(GAMMA GT) 91.00 IU/L ( 5.00- 50.00
(....*....) (PHOSPHORUS 3.90 MG/DL ( 2.50- 4.80
(.......*.) (URIC ACID 3.30 MG/DL ( 2.40- 7.70
(......*..) (WBC 6.60 K/UL ( 4.00- 12.00
(......*..) (NEUTROPHILS 3.50 K/UL ( 2.00- 6.90
(......*..) (NEUTROPHILS % 52.80 % ( 37.00- 80.00
(....*....) (LYMPHOCYTES 2.10 K/UL ( 0.60- 3.40
Good Luck to us all :)
I have just received my lab results after 6 mth of Tx PEG/Riba. Last shot #26/24 was on Apr 8th 2004 & Riba was taken for an additional week. Lab results look GREAT:
ALK.PHOSPHAT. 78.00 IU/L ( 35.00- 141.00
(....*....) (ALT(GPT) 26.00 IU/L ( 5.00- 40.00
(...*.....) (AST(GOT) 27.00 IU/L ( 5.00- 40.00
(.......*.) (BILIRUB.TOTAL 0.30 MG/DL ( 0.10- 1.10
(....*....) (BUN 16.00 MG/DL ( 8.00- 23.00
(......*..) (CALCIUM-SERUM 9.30 MG/DL ( 8.40- 11.00
(...*.....) (CREATININE-S 1.00 MG/DL ( 0.50- 1.30
(......*..) (SODIUM-SERUM 139.00 MMOL/L ( 133.00- 153.00
(......*..) (POTASSIUM-SERU 4.10 MMOL/L ( 3.50- 5.30
*(.........) (GGT(GAMMA GT) 91.00 IU/L ( 5.00- 50.00
(....*....) (PHOSPHORUS 3.90 MG/DL ( 2.50- 4.80
(.......*.) (URIC ACID 3.30 MG/DL ( 2.40- 7.70
(......*..) (WBC 6.60 K/UL ( 4.00- 12.00
(......*..) (NEUTROPHILS 3.50 K/UL ( 2.00- 6.90
(......*..) (NEUTROPHILS % 52.80 % ( 37.00- 80.00
(....*....) (LYMPHOCYTES 2.10 K/UL ( 0.60- 3.40
Good Luck to us all :)
Sue..... The lowest limit of that test is 615IU's. The < means "less than"......So, all this test says is that you are "less than" 615IU/ml. If your prior test was only 39, then y0u should have had a more sensitive test. I am surprised that they would use this test for you. But it's still good. Since Hcv is most often measured in the Millions of copies, then this is still a good sign. The currently best tests I've seen measure all the way down to 5.
you need a better test.
you need a better test.
thanks for you input. I will mention this to my doctor the next time I go for bloodwork.
I have learned so very much from all of you and this group. I really appreciate it. Had I not, I would have gone into this so blindly, who knows what would have happened???
Thank you all again!
Love you all.
Sue
I have learned so very much from all of you and this group. I really appreciate it. Had I not, I would have gone into this so blindly, who knows what would have happened???
Thank you all again!
Love you all.
Sue
From the earlier fibrosis/damage discussion: Cute, I totally agree that even a grade1 stage 0 must be addressed and not ignored as if no damage will ever occur. I guess that is where people diverge as to what constitutes "addressing the situation".
Chev: Alas! As I was about to embark upon my quest for a "pretty doc", I suddenly realized that the lovely Marchessa would likely not approve. And I have learned over the years it is best to not provoke the Marchessa or "damage" will likely occur. Oh well, "to sleep, perchance to dream ..."
Chev: Alas! As I was about to embark upon my quest for a "pretty doc", I suddenly realized that the lovely Marchessa would likely not approve. And I have learned over the years it is best to not provoke the Marchessa or "damage" will likely occur. Oh well, "to sleep, perchance to dream ..."
GEE, all I see in those results is undetectable vl by their measurements.
CONGRATS!
different labs use differents assay methods and maybe the one 3 yrs ago used the copies/ml measurement, that is why they provide the formula for conversion. Right now I don't see anything for you to convert. 0 by this one. the heptimax test goes to much lower than the 615IU range this test uses. If your insurance covers it perhaps you can suggest that one next time. I use Quest.
Am I seeing this correctly guys? is it clear?
CONGRATS!
different labs use differents assay methods and maybe the one 3 yrs ago used the copies/ml measurement, that is why they provide the formula for conversion. Right now I don't see anything for you to convert. 0 by this one. the heptimax test goes to much lower than the 615IU range this test uses. If your insurance covers it perhaps you can suggest that one next time. I use Quest.
Am I seeing this correctly guys? is it clear?
When I last wrote, I told you all that my Doc said at my 12week check the virus level dropped considerably..but I didn't have the actual numbers at that time. I finally got my written report and I'm not sure how to read it. Hopefully one of you will be able to help. All I know is 3 years ago my viral load was 39..For some reason before I started treatment, I did not have this repeated. I'm just going to type exactly what I have in front of me........
HCV QN by bDNA, S: <615 IU/mL
Assay dynamic range is 615 IU/mL to 7,692,310 IU/mL.
to convert IU/mL to copies/mL, muliply the IU/mL result by 5.2
This is what is says......Tell me HOW this is LESS then 39???
Thanks you all.
Sue
HCV QN by bDNA, S: <615 IU/mL
Assay dynamic range is 615 IU/mL to 7,692,310 IU/mL.
to convert IU/mL to copies/mL, muliply the IU/mL result by 5.2
This is what is says......Tell me HOW this is LESS then 39???
Thanks you all.
Sue
You Guys are probably right about using a link. Pls forgive me for my hormones were playing havoc with me. I intend to RESERVE a SEAT on the SVR-Bound USS DRAGON-SLAYER for Indiana as well.
However, ALL are welcome!
However, ALL are welcome!
HAHAHAHAHAHAHAHA WOW I think I just wore out my mouse button!
Congratulations of getting through tx. Your counts look awfully good. Looks like you're comming back nicely. Welcome back to the "Land of the Living".
I agree with Galen.....links would work better.
I've got a seat all ready for ya on the SVR bus.
Congratulations of getting through tx. Your counts look awfully good. Looks like you're comming back nicely. Welcome back to the "Land of the Living".
I agree with Galen.....links would work better.
I've got a seat all ready for ya on the SVR bus.
I am glad to hear that you are doing so well.
You might want to consider posting links to these sites instead of copying them in total. For one thing, copyrights are infringed upon and our "Terms and Conditons" prohibit them. Another reason is the sheer length of the posts. Thank you for the info, tho.
You might want to consider posting links to these sites instead of copying them in total. For one thing, copyrights are infringed upon and our "Terms and Conditons" prohibit them. Another reason is the sheer length of the posts. Thank you for the info, tho.
Additional Data from May 2004 HCV Advocate:
May 2004 HCV Advocate
Download printable version
--------
Update from EASL
Alan Franciscus, Editor-in-Chief
The European Association for the Study of Liver Disease recently held its annual conference in Berlin, Germany. The majority of noteworthy clinical data on current treatment options have been previously reported in the press or at other conferences. This report will mainly focus on experimental therapies for treating chronic hepatitis C and one report on the treatment of acute hepatitis C.
Fibromyalgia and Hepatitis C
Liz Highleyman
Many people with hepatitis C experience symptoms such as fatigue, muscle and joint aches, "brain fog," and depression, either due to HCV itself or as side effects of treatment with interferon. But some hepatitis C patients also have fibromyalgia (FM), a condition marked by widespread bodily pain.
HealthWise: Herbs and Hepatitis C: Part 1
Lucinda K. Porter, RN, CCRC
The use of herbs for medicinal purposes has a long and interesting history. The use of herbs, however, is controversial in contemporary western medicine due to the lack of evidence-based research to support safety and efficacy.
Stay informed on the latest news ..click here to register for email alerts
Update from EASL
Alan Franciscus, Editor-in-Chief
The European Association for the Study of Liver Disease recently held its annual conference in Berlin, Germany. The majority of noteworthy clinical data on current treatment options have been previously reported in the press or at other conferences. This report will mainly focus on experimental therapies for treating chronic hepatitis C and one report on the treatment of acute hepatitis C.
This year's EASL conference highlighted many new compounds under study for treatment of hepatitis C. It is important to remember that most drugs in clinical trials will never be approved by the FDA for marketing. Generally, new therapies in clinical trials are divided into three phases. Phase IV trials are usually considered post-marketing studies after the initial FDA approval of the new drug. The further along a drug is in testing or clinical phase the more likely the drug will be FDA approved for marketing.
Study Phases
In Phase I clinical trials, researchers test a new drug or treatment in a small group of people (20-80) for the first time to evaluate its safety, determine a safe dosage range, and identify side effects.
In Phase II clinical trials, the study drug or treatment is given to a larger group of people (100-300) to see if it is effective and to further evaluate its safety.
In Phase III studies, the study drug or treatment is given to large groups of people (1,000-3,000) to confirm its effectiveness, monitor side effects, compare it to commonly used treatments, and collect information that will allow the drug or treatment to be used safely.
In Phase IV studies, the drug is already on the market for a particular indication, but is now being tested for a different indication, use, or disease.
Experimental Therapies
Albuferon
Albuferon (XTL Biopharmaceuticals Ltd) is a form of interferon that is fused with human serum albumin allowing the interferon to remain in the body for a longer period of time. A clinical trial by V. Balan and colleagues studied the safety, pharmacokinetics and pharmacodynamics of Albuferon in single and double dose-escalation in hepatitis C positive individuals who did not respond to a previous course of interferon containing medications. Ninety-seven percent of the trial participants were genotype 1 (the hardest to treat). Adverse events or side effects were mild to moderate and were not dose dependent. The preliminary analyses suggest a median terminal half-life (how long it stays in the body) of 143 hours in the two highest single injection groups. Reduction in HCV viral load (>0.5 log reduction) was observed in 62.5% (25/40) of the participants in the single injection group (120-160 mcg). The authors of this study concluded that "Albuferon was safe and well-tolerated. Dosing every 2-4 weeks is supported by pharmacokinetics. Anti-viral response was observed in the higher single dose groups."
Merimepodib
Merimepodib (MPB) (VX-497) is a selective inhibitor of IMPDH. In a study by P. Marcellin and colleagues, 31 patients with genotype 1 who were nonresponders to prior interferon and ribavirin therapy were enrolled. The participants were randomized to receive VX-497, 25 or 50 mg every twelve hours, or a placebo drug in combination with pegylated interferon plus ribavirin for 24 weeks. Trial participants with no detectable viral load at 24 weeks received treatment for an additional 24 weeks. All participants were then followed post-treatment to determine sustained virological response.
The report for the 24 weeks (preliminary results) found that the highest dose of VX-950 when com-bined with pegylated interferon plus ribavirin produced the highest number of patients with unde-tectable viral load
May 2004 HCV Advocate
Download printable version
--------
Update from EASL
Alan Franciscus, Editor-in-Chief
The European Association for the Study of Liver Disease recently held its annual conference in Berlin, Germany. The majority of noteworthy clinical data on current treatment options have been previously reported in the press or at other conferences. This report will mainly focus on experimental therapies for treating chronic hepatitis C and one report on the treatment of acute hepatitis C.
Fibromyalgia and Hepatitis C
Liz Highleyman
Many people with hepatitis C experience symptoms such as fatigue, muscle and joint aches, "brain fog," and depression, either due to HCV itself or as side effects of treatment with interferon. But some hepatitis C patients also have fibromyalgia (FM), a condition marked by widespread bodily pain.
HealthWise: Herbs and Hepatitis C: Part 1
Lucinda K. Porter, RN, CCRC
The use of herbs for medicinal purposes has a long and interesting history. The use of herbs, however, is controversial in contemporary western medicine due to the lack of evidence-based research to support safety and efficacy.
Stay informed on the latest news ..click here to register for email alerts
Update from EASL
Alan Franciscus, Editor-in-Chief
The European Association for the Study of Liver Disease recently held its annual conference in Berlin, Germany. The majority of noteworthy clinical data on current treatment options have been previously reported in the press or at other conferences. This report will mainly focus on experimental therapies for treating chronic hepatitis C and one report on the treatment of acute hepatitis C.
This year's EASL conference highlighted many new compounds under study for treatment of hepatitis C. It is important to remember that most drugs in clinical trials will never be approved by the FDA for marketing. Generally, new therapies in clinical trials are divided into three phases. Phase IV trials are usually considered post-marketing studies after the initial FDA approval of the new drug. The further along a drug is in testing or clinical phase the more likely the drug will be FDA approved for marketing.
Study Phases
In Phase I clinical trials, researchers test a new drug or treatment in a small group of people (20-80) for the first time to evaluate its safety, determine a safe dosage range, and identify side effects.
In Phase II clinical trials, the study drug or treatment is given to a larger group of people (100-300) to see if it is effective and to further evaluate its safety.
In Phase III studies, the study drug or treatment is given to large groups of people (1,000-3,000) to confirm its effectiveness, monitor side effects, compare it to commonly used treatments, and collect information that will allow the drug or treatment to be used safely.
In Phase IV studies, the drug is already on the market for a particular indication, but is now being tested for a different indication, use, or disease.
Experimental Therapies
Albuferon
Albuferon (XTL Biopharmaceuticals Ltd) is a form of interferon that is fused with human serum albumin allowing the interferon to remain in the body for a longer period of time. A clinical trial by V. Balan and colleagues studied the safety, pharmacokinetics and pharmacodynamics of Albuferon in single and double dose-escalation in hepatitis C positive individuals who did not respond to a previous course of interferon containing medications. Ninety-seven percent of the trial participants were genotype 1 (the hardest to treat). Adverse events or side effects were mild to moderate and were not dose dependent. The preliminary analyses suggest a median terminal half-life (how long it stays in the body) of 143 hours in the two highest single injection groups. Reduction in HCV viral load (>0.5 log reduction) was observed in 62.5% (25/40) of the participants in the single injection group (120-160 mcg). The authors of this study concluded that "Albuferon was safe and well-tolerated. Dosing every 2-4 weeks is supported by pharmacokinetics. Anti-viral response was observed in the higher single dose groups."
Merimepodib
Merimepodib (MPB) (VX-497) is a selective inhibitor of IMPDH. In a study by P. Marcellin and colleagues, 31 patients with genotype 1 who were nonresponders to prior interferon and ribavirin therapy were enrolled. The participants were randomized to receive VX-497, 25 or 50 mg every twelve hours, or a placebo drug in combination with pegylated interferon plus ribavirin for 24 weeks. Trial participants with no detectable viral load at 24 weeks received treatment for an additional 24 weeks. All participants were then followed post-treatment to determine sustained virological response.
The report for the 24 weeks (preliminary results) found that the highest dose of VX-950 when com-bined with pegylated interferon plus ribavirin produced the highest number of patients with unde-tectable viral load
Sx were considerable in my case however, the results were worth every micron of adversity.
Here's a recent (Apr. 04) HCV neuropsychiatric study:
Minimizing the Impact of Neuropsychiatric Effects During Chronic HCV Disease and Treatment
Robert G. Gish , M.D.
(To see the figures and illustrations in this article, please download the pdf version.)
New data are emerging that implicate direct effects of the hepatitis C virus (HCV) on the central nervous system, along with side effects of both peginterferon and ribavirin as causes of multiple symptoms during treatment of HCV. Neuropsychiatric symptoms are of great concern in patients with hepatitis C because they are common, may reduce quality of life, and can limit treatment adherence and effect the outcome of treatment. To improve patient well-being and the likelihood of successful anti-HCV therapy, it is critical that physicians screen patients for neuro-psychiatric symptoms and manage these problems and symptoms proactively.
Pre-existing neuro-psychiatric symptoms are common in hepatitis C patients. In fact, 35% to 57% of patients with chronic HCV infection may have depression upon diagnosis or before starting any therapy. Furthermore, new neuropsychiatric symptoms emerge in an additional 30% to 40% of patients receiving peginterferon / ribavirin treatment. Cognitive deficits, particularly those affecting concentration, memory, and psychomotor speed, have been identified in patients with even mild HCV infection as well.
The pathophysiology of these toxic effects of HCV remain poorly defined. One theory is that HCV may infect the brain via macrophage or microglial cells. Another is that toxins may accumulate in the blood secondary to impaired clearance by a cirrhotic liver, causing impaired cognition. Cirrhosis may be predictive of poorer cognitive function due to clinical or subclinical encephalopathy, and progressive hepatic injury in the HCV-infected patient without cirrhosis also may play a role in the development of neurocognitive problems although this is rarely seen in patients without significant fibrosis and portal hypertension. Antiserotonergic effects of interferon have been proposed as a mechanism in the development of interferon-related depression and may explain why patients symptoms from interferon therapy can be profoundly improved with SSRI type antidepressants.
A recent prospective cohort study found that although only 11% of patients treated with peginterferon/ribavirin met criteria for major depression, yet more than one third developed symptoms of moderate to severe depression during treatment. Whereas interferons are generally known to be associated with psychiatric side effects, this study was one of the first to identify a dose-related association between PEG interferon/ribavirin treatment and depression.
Due to the chronic nature and nonspecific symptoms of HCV infection, distinguishing the somatic complaints of disease chronicity from a depressive syndrome is a major clinical challenge. Patients with major depression often feel ill, experiencing somatic and/or cognitive symptoms and a perceived state of "brain fog" and other symptoms that impair the patients functional level. These symptoms can easily be confounded by the presence of a chronic HCV infection. Nonsomatic symptoms of depression may include low self-esteem, feelings of guilt, worthlessness, hopelessness, and in the most severe cases, suicidal ideation. Some depression screening tools-such as the Hospital Anxiety and Depression Scale (HADS)-are geared toward assessment of nonsomatic symptoms of depression, and may be useful in HCV-infected patients who exhibit symptoms of major depression. The Center for Epidemiologic Studies of Depression (CES-D) self-administered scoring sheet also may be useful in an office practice.
The impact of depression on the patient can be significant, causing irritability, fatigue, apathy, lack of concentration, and in extreme situations, suicidal ideation or suicide. It is therefore not surprising that depression can have a negative impact on adherence to anti-HCV therapy. Moreover, another prospective cohort study found a correlation between depression symptoms and clearance of HCV RNA at week 24, even after adjusting for ribavirin dose assignment, genotype, age, antidepressant usage, dose reduction of peginterferon or ribavirin, and knowledge of viral status during treatment. Periodic assessment for depression during treatment is imperative, with expert psychiatric referral provided as needed if signs and symptoms of depression progress during treatment.
Profound improvement can be achieved with antidepressant pharmacotherapy and formal psychotherapy for treatment of depression. There are no placebo-controlled studies evaluating the treatment of interferon-induced depression. An open-label trial of citalopram conducted in 15 patients with HCV infection demonstrated a significantly positive response in interferon-treated patients. Prophylactic therapy in patients with a recent or remote history of depression may be controversial; but recent studies have shown a benefit and proactive antidepressant therapy is strongly advised in clinical practice, both from this author's clinical experience and from surveys of practitioners who manage HCV treatment. Patients with major depression may also benefit from support groups, but this should not be a replacement for pharmacologic therapy and psychotherapy.
Pharmacologic guidelines for general treatment of neuropsychiatric disorders may offer the best approach to managing depression in the peginterferon-treated patient. These guidelines emphasize individualized selection of an agent, often exploiting the side-effect profile of the various medications available. For example, agents that promote sleep may be most appropriate for patients who have a primary sleep disturbance, whereas patients experiencing fatigue may benefit most from activating agents.
Patients with a history of major depression or significant depressive symptoms including history of suicide attempts, or bipolar disorder or psychosis, should be referred for expert psychiatric diagnosis and management prior to treatment initiation. Patients with a pre-existing history of bipolar disorder should be monitored closely while receiving interferon therapy, and, whenever possible, treated prophylactically with a mood stabilizer such as olanzapine or quetiapine (lithium or valproic acid can also be considered, with close follow-up). Any patient for whom the medical practitioner is not comfortable starting antidepressant therapy should be referred for clearance before starting anti-HCV treatment, and psychiatric follow-up should continue periodically during therapy.
In summary, neuropsychiatric symptoms are common in HCV-infected patients both at baseline and as side effects of peginterferon therapy. Without appropriate intervention, these symptoms can have serious consequences for the patient and can also limit adherence to, and therefore success of, antiviral therapy. Fortunately, depression and other neuropsychiatric side effects can generally be managed effectively with available pharmacologic therapies, thereby allowing patients to stay on anti-HCV therapy with the best chance of treatment success.
Important References
Bonaccorso S, Marino V, Puzella A, et al. Increased depressive ratings in patients with hepatitis C receiving interferon-alpha-based immunotherapy are related to interferon-alpha-induced changes in the serotonergic system. J Clin Psychopharmacol. 2002;22:86-90.
Fontana RJ. Neuropsychiatric toxicity of antiviral treatment in chronic hepatitis C. Dig Dis. 2000;18:107-116.
Gleason OC, Yates WR. Five cases of interferon-alpha-induced depression treated with antidepressant therapy. Psychosomatics. 1999;40:510-512.
Gleason OC, Yates WR, Isbell MD, Philipsen MA. An open-label trial of citalopram for major depression in patients with hepatitis C. J Clin Psychiatry. 2002;63:194-198.
Hilsabeck RC, Perry W, Hassanein TI. Neuropsychological impairment in patients with chronic hepatitis C. Hepatology. 2002;35:440-446.
Ho SB, Nguyen H, Tetrick LL, Opitz GA, Basara ML, Dieperink E. Influence of psychiatric diagnoses on interferon-alpha treatment for chronic hepatitis C in a veteran population. Am J Gastroenterol. 2001;96:157-164.
Hosoda S, Takimura H, Shibayama M, Kanamura H, Ikeda K, Kumada H. Psychiatric symptoms related to interferon therapy for chronic hepatitis C: clinical features and prognosis. Psychiatry Clin Neurosci. 2000;54:565-572.
Levenson JL, Fallon HJ. Fluoxetine treatment of depression caused by interferon-alpha. Am J Gastroenterol. 1993;88:760-761.
Menkes DB, MacDonald JA. Interferons, serotonin and neurotoxicity. Psychol Med. 2000;30:259-268.
Meyers CA, Scheibel RS, Forman AD. Persistent neurotoxicity of systemically administered interferon-alpha. Neurology. 1991;41:672-676.
Musselman DL, Lawson DH, Gumnick JF, et al. Paroxetine for the prevention of depression induced by high-dose interferon alfa. N Engl J Med. 2001;344:961-966.
Raison CL, Borisov AS, Broadwell SD, et al. Depression during IFN-alfa plus ribavirin therapy: prevalence and prediction [abstract 345]. Hepatology. 2003;38(suppl 1):326A.
Raison CL, Broadwell SD, Borisov AS, et al. Depressive symptoms during IFN-alpha/ribavirin therapy are associated with reduced viral clearance in patients with hepatitis C [abstract 344]. Hepatology. 2003;38(suppl 1):325A.
Renault PF, Hoofnagle JH, Park Y, et al. Psychiatric complications of long-term interferon alfa therapy. Arch Intern Med. 1987;147:1577-1580.
Rifflet H, Vuillemin E, Oberti F, et al. Suicidal impulses in patients with chronic viral hepatitis C during or after therapy with interferon alpha. Gastroenterol Clin Biol. 1998;22:353-357.
Schramm TM, Lawford BR, Macdonald GA, Cooksley WG. Sertraline treatment of interferon-alfa-induced depressive disorder. Med J Aust. 2000;173:359-361.
Valentine AD, Meyers CA, Kling MA, Richelson E, Hauser P. Mood and cognitive side effects of interferon-alpha therapy. Semin Oncol. 1998;25(suppl 1):39-47.
Back to Medical Writers' Circle
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Here's a recent (Apr. 04) HCV neuropsychiatric study:
Minimizing the Impact of Neuropsychiatric Effects During Chronic HCV Disease and Treatment
Robert G. Gish , M.D.
(To see the figures and illustrations in this article, please download the pdf version.)
New data are emerging that implicate direct effects of the hepatitis C virus (HCV) on the central nervous system, along with side effects of both peginterferon and ribavirin as causes of multiple symptoms during treatment of HCV. Neuropsychiatric symptoms are of great concern in patients with hepatitis C because they are common, may reduce quality of life, and can limit treatment adherence and effect the outcome of treatment. To improve patient well-being and the likelihood of successful anti-HCV therapy, it is critical that physicians screen patients for neuro-psychiatric symptoms and manage these problems and symptoms proactively.
Pre-existing neuro-psychiatric symptoms are common in hepatitis C patients. In fact, 35% to 57% of patients with chronic HCV infection may have depression upon diagnosis or before starting any therapy. Furthermore, new neuropsychiatric symptoms emerge in an additional 30% to 40% of patients receiving peginterferon / ribavirin treatment. Cognitive deficits, particularly those affecting concentration, memory, and psychomotor speed, have been identified in patients with even mild HCV infection as well.
The pathophysiology of these toxic effects of HCV remain poorly defined. One theory is that HCV may infect the brain via macrophage or microglial cells. Another is that toxins may accumulate in the blood secondary to impaired clearance by a cirrhotic liver, causing impaired cognition. Cirrhosis may be predictive of poorer cognitive function due to clinical or subclinical encephalopathy, and progressive hepatic injury in the HCV-infected patient without cirrhosis also may play a role in the development of neurocognitive problems although this is rarely seen in patients without significant fibrosis and portal hypertension. Antiserotonergic effects of interferon have been proposed as a mechanism in the development of interferon-related depression and may explain why patients symptoms from interferon therapy can be profoundly improved with SSRI type antidepressants.
A recent prospective cohort study found that although only 11% of patients treated with peginterferon/ribavirin met criteria for major depression, yet more than one third developed symptoms of moderate to severe depression during treatment. Whereas interferons are generally known to be associated with psychiatric side effects, this study was one of the first to identify a dose-related association between PEG interferon/ribavirin treatment and depression.
Due to the chronic nature and nonspecific symptoms of HCV infection, distinguishing the somatic complaints of disease chronicity from a depressive syndrome is a major clinical challenge. Patients with major depression often feel ill, experiencing somatic and/or cognitive symptoms and a perceived state of "brain fog" and other symptoms that impair the patients functional level. These symptoms can easily be confounded by the presence of a chronic HCV infection. Nonsomatic symptoms of depression may include low self-esteem, feelings of guilt, worthlessness, hopelessness, and in the most severe cases, suicidal ideation. Some depression screening tools-such as the Hospital Anxiety and Depression Scale (HADS)-are geared toward assessment of nonsomatic symptoms of depression, and may be useful in HCV-infected patients who exhibit symptoms of major depression. The Center for Epidemiologic Studies of Depression (CES-D) self-administered scoring sheet also may be useful in an office practice.
The impact of depression on the patient can be significant, causing irritability, fatigue, apathy, lack of concentration, and in extreme situations, suicidal ideation or suicide. It is therefore not surprising that depression can have a negative impact on adherence to anti-HCV therapy. Moreover, another prospective cohort study found a correlation between depression symptoms and clearance of HCV RNA at week 24, even after adjusting for ribavirin dose assignment, genotype, age, antidepressant usage, dose reduction of peginterferon or ribavirin, and knowledge of viral status during treatment. Periodic assessment for depression during treatment is imperative, with expert psychiatric referral provided as needed if signs and symptoms of depression progress during treatment.
Profound improvement can be achieved with antidepressant pharmacotherapy and formal psychotherapy for treatment of depression. There are no placebo-controlled studies evaluating the treatment of interferon-induced depression. An open-label trial of citalopram conducted in 15 patients with HCV infection demonstrated a significantly positive response in interferon-treated patients. Prophylactic therapy in patients with a recent or remote history of depression may be controversial; but recent studies have shown a benefit and proactive antidepressant therapy is strongly advised in clinical practice, both from this author's clinical experience and from surveys of practitioners who manage HCV treatment. Patients with major depression may also benefit from support groups, but this should not be a replacement for pharmacologic therapy and psychotherapy.
Pharmacologic guidelines for general treatment of neuropsychiatric disorders may offer the best approach to managing depression in the peginterferon-treated patient. These guidelines emphasize individualized selection of an agent, often exploiting the side-effect profile of the various medications available. For example, agents that promote sleep may be most appropriate for patients who have a primary sleep disturbance, whereas patients experiencing fatigue may benefit most from activating agents.
Patients with a history of major depression or significant depressive symptoms including history of suicide attempts, or bipolar disorder or psychosis, should be referred for expert psychiatric diagnosis and management prior to treatment initiation. Patients with a pre-existing history of bipolar disorder should be monitored closely while receiving interferon therapy, and, whenever possible, treated prophylactically with a mood stabilizer such as olanzapine or quetiapine (lithium or valproic acid can also be considered, with close follow-up). Any patient for whom the medical practitioner is not comfortable starting antidepressant therapy should be referred for clearance before starting anti-HCV treatment, and psychiatric follow-up should continue periodically during therapy.
In summary, neuropsychiatric symptoms are common in HCV-infected patients both at baseline and as side effects of peginterferon therapy. Without appropriate intervention, these symptoms can have serious consequences for the patient and can also limit adherence to, and therefore success of, antiviral therapy. Fortunately, depression and other neuropsychiatric side effects can generally be managed effectively with available pharmacologic therapies, thereby allowing patients to stay on anti-HCV therapy with the best chance of treatment success.
Important References
Bonaccorso S, Marino V, Puzella A, et al. Increased depressive ratings in patients with hepatitis C receiving interferon-alpha-based immunotherapy are related to interferon-alpha-induced changes in the serotonergic system. J Clin Psychopharmacol. 2002;22:86-90.
Fontana RJ. Neuropsychiatric toxicity of antiviral treatment in chronic hepatitis C. Dig Dis. 2000;18:107-116.
Gleason OC, Yates WR. Five cases of interferon-alpha-induced depression treated with antidepressant therapy. Psychosomatics. 1999;40:510-512.
Gleason OC, Yates WR, Isbell MD, Philipsen MA. An open-label trial of citalopram for major depression in patients with hepatitis C. J Clin Psychiatry. 2002;63:194-198.
Hilsabeck RC, Perry W, Hassanein TI. Neuropsychological impairment in patients with chronic hepatitis C. Hepatology. 2002;35:440-446.
Ho SB, Nguyen H, Tetrick LL, Opitz GA, Basara ML, Dieperink E. Influence of psychiatric diagnoses on interferon-alpha treatment for chronic hepatitis C in a veteran population. Am J Gastroenterol. 2001;96:157-164.
Hosoda S, Takimura H, Shibayama M, Kanamura H, Ikeda K, Kumada H. Psychiatric symptoms related to interferon therapy for chronic hepatitis C: clinical features and prognosis. Psychiatry Clin Neurosci. 2000;54:565-572.
Levenson JL, Fallon HJ. Fluoxetine treatment of depression caused by interferon-alpha. Am J Gastroenterol. 1993;88:760-761.
Menkes DB, MacDonald JA. Interferons, serotonin and neurotoxicity. Psychol Med. 2000;30:259-268.
Meyers CA, Scheibel RS, Forman AD. Persistent neurotoxicity of systemically administered interferon-alpha. Neurology. 1991;41:672-676.
Musselman DL, Lawson DH, Gumnick JF, et al. Paroxetine for the prevention of depression induced by high-dose interferon alfa. N Engl J Med. 2001;344:961-966.
Raison CL, Borisov AS, Broadwell SD, et al. Depression during IFN-alfa plus ribavirin therapy: prevalence and prediction [abstract 345]. Hepatology. 2003;38(suppl 1):326A.
Raison CL, Broadwell SD, Borisov AS, et al. Depressive symptoms during IFN-alpha/ribavirin therapy are associated with reduced viral clearance in patients with hepatitis C [abstract 344]. Hepatology. 2003;38(suppl 1):325A.
Renault PF, Hoofnagle JH, Park Y, et al. Psychiatric complications of long-term interferon alfa therapy. Arch Intern Med. 1987;147:1577-1580.
Rifflet H, Vuillemin E, Oberti F, et al. Suicidal impulses in patients with chronic viral hepatitis C during or after therapy with interferon alpha. Gastroenterol Clin Biol. 1998;22:353-357.
Schramm TM, Lawford BR, Macdonald GA, Cooksley WG. Sertraline treatment of interferon-alfa-induced depressive disorder. Med J Aust. 2000;173:359-361.
Valentine AD, Meyers CA, Kling MA, Richelson E, Hauser P. Mood and cognitive side effects of interferon-alpha therapy. Semin Oncol. 1998;25(suppl 1):39-47.
Back to Medical Writers' Circle
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Sx were considerable in my case however, the results were worth every micron of adversity.
Here's a recent (Apr. 04) HCV neuropsychiatric study:
Minimizing the Impact of Neuropsychiatric Effects During Chronic HCV Disease and Treatment
Robert G. Gish , M.D.
(To see the figures and illustrations in this article, please download the pdf version.)
New data are emerging that implicate direct effects of the hepatitis C virus (HCV) on the central nervous system, along with side effects of both peginterferon and ribavirin as causes of multiple symptoms during treatment of HCV. Neuropsychiatric symptoms are of great concern in patients with hepatitis C because they are common, may reduce quality of life, and can limit treatment adherence and effect the outcome of treatment. To improve patient well-being and the likelihood of successful anti-HCV therapy, it is critical that physicians screen patients for neuro-psychiatric symptoms and manage these problems and symptoms proactively.
Pre-existing neuro-psychiatric symptoms are common in hepatitis C patients. In fact, 35% to 57% of patients with chronic HCV infection may have depression upon diagnosis or before starting any therapy. Furthermore, new neuropsychiatric symptoms emerge in an additional 30% to 40% of patients receiving peginterferon / ribavirin treatment. Cognitive deficits, particularly those affecting concentration, memory, and psychomotor speed, have been identified in patients with even mild HCV infection as well.
The pathophysiology of these toxic effects of HCV remain poorly defined. One theory is that HCV may infect the brain via macrophage or microglial cells. Another is that toxins may accumulate in the blood secondary to impaired clearance by a cirrhotic liver, causing impaired cognition. Cirrhosis may be predictive of poorer cognitive function due to clinical or subclinical encephalopathy, and progressive hepatic injury in the HCV-infected patient without cirrhosis also may play a role in the development of neurocognitive problems although this is rarely seen in patients without significant fibrosis and portal hypertension. Antiserotonergic effects of interferon have been proposed as a mechanism in the development of interferon-related depression and may explain why patients symptoms from interferon therapy can be profoundly improved with SSRI type antidepressants.
A recent prospective cohort study found that although only 11% of patients treated with peginterferon/ribavirin met criteria for major depression, yet more than one third developed symptoms of moderate to severe depression during treatment. Whereas interferons are generally known to be associated with psychiatric side effects, this study was one of the first to identify a dose-related association between PEG interferon/ribavirin treatment and depression.
Due to the chronic nature and nonspecific symptoms of HCV infection, distinguishing the somatic complaints of disease chronicity from a depressive syndrome is a major clinical challenge. Patients with major depression often feel ill, experiencing somatic and/or cognitive symptoms and a perceived state of "brain fog" and other symptoms that impair the patients functional level. These symptoms can easily be confounded by the presence of a chronic HCV infection. Nonsomatic symptoms of depression may include low self-esteem, feelings of guilt, worthlessness, hopelessness, and in the most severe cases, suicidal ideation. Some depression screening tools-such as the Hospital Anxiety and Depression Scale (HADS)-are geared toward assessment of nonsomatic symptoms of depression, and may be useful in HCV-infected patients who exhibit symptoms of major depression. The Center for Epidemiologic Studies of Depression (CES-D) self-administered scoring sheet also may be useful in an office practice.
The impact of depression on the patient can be significant, causing irritability, fatigue, apathy, lack of concentration, and in extreme situations, suicidal ideation or suicide. It is therefore not surprising that depression can have a negative impact on adherence to anti-HCV therapy. Moreover, another prospective cohort study found a correlation between depression symptoms and clearance of HCV RNA at week 24, even after adjusting for ribavirin dose assignment, genotype, age, antidepressant usage, dose reduction of peginterferon or ribavirin, and knowledge of viral status during treatment. Periodic assessment for depression during treatment is imperative, with expert psychiatric referral provided as needed if signs and symptoms of depression progress during treatment.
Profound improvement can be achieved with antidepressant pharmacotherapy and formal psychotherapy for treatment of depression. There are no placebo-controlled studies evaluating the treatment of interferon-induced depression. An open-label trial of citalopram conducted in 15 patients with HCV infection demonstrated a significantly positive response in interferon-treated patients. Prophylactic therapy in patients with a recent or remote history of depression may be controversial; but recent studies have shown a benefit and proactive antidepressant therapy is strongly advised in clinical practice, both from this author's clinical experience and from surveys of practitioners who manage HCV treatment. Patients with major depression may also benefit from support groups, but this should not be a replacement for pharmacologic therapy and psychotherapy.
Pharmacologic guidelines for general treatment of neuropsychiatric disorders may offer the best approach to managing depression in the peginterferon-treated patient. These guidelines emphasize individualized selection of an agent, often exploiting the side-effect profile of the various medications available. For example, agents that promote sleep may be most appropriate for patients who have a primary sleep disturbance, whereas patients experiencing fatigue may benefit most from activating agents.
Patients with a history of major depression or significant depressive symptoms including history of suicide attempts, or bipolar disorder or psychosis, should be referred for expert psychiatric diagnosis and management prior to treatment initiation. Patients with a pre-existing history of bipolar disorder should be monitored closely while receiving interferon therapy, and, whenever possible, treated prophylactically with a mood stabilizer such as olanzapine or quetiapine (lithium or valproic acid can also be considered, with close follow-up). Any patient for whom the medical practitioner is not comfortable starting antidepressant therapy should be referred for clearance before starting anti-HCV treatment, and psychiatric follow-up should continue periodically during therapy.
In summary, neuropsychiatric symptoms are common in HCV-infected patients both at baseline and as side effects of peginterferon therapy. Without appropriate intervention, these symptoms can have serious consequences for the patient and can also limit adherence to, and therefore success of, antiviral therapy. Fortunately, depression and other neuropsychiatric side effects can generally be managed effectively with available pharmacologic therapies, thereby allowing patients to stay on anti-HCV therapy with the best chance of treatment success.
Important References
Bonaccorso S, Marino V, Puzella A, et al. Increased depressive ratings in patients with hepatitis C receiving interferon-alpha-based immunotherapy are related to interferon-alpha-induced changes in the serotonergic system. J Clin Psychopharmacol. 2002;22:86-90.
Fontana RJ. Neuropsychiatric toxicity of antiviral treatment in chronic hepatitis C. Dig Dis. 2000;18:107-116.
Gleason OC, Yates WR. Five cases of interferon-alpha-induced depression treated with antidepressant therapy. Psychosomatics. 1999;40:510-512.
Gleason OC, Yates WR, Isbell MD, Philipsen MA. An open-label trial of citalopram for major depression in patients with hepatitis C. J Clin Psychiatry. 2002;63:194-198.
Hilsabeck RC, Perry W, Hassanein TI. Neuropsychological impairment in patients with chronic hepatitis C. Hepatology. 2002;35:440-446.
Ho SB, Nguyen H, Tetrick LL, Opitz GA, Basara ML, Dieperink E. Influence of psychiatric diagnoses on interferon-alpha treatment for chronic hepatitis C in a veteran population. Am J Gastroenterol. 2001;96:157-164.
Hosoda S, Takimura H, Shibayama M, Kanamura H, Ikeda K, Kumada H. Psychiatric symptoms related to interferon therapy for chronic hepatitis C: clinical features and prognosis. Psychiatry Clin Neurosci. 2000;54:565-572.
Levenson JL, Fallon HJ. Fluoxetine treatment of depression caused by interferon-alpha. Am J Gastroenterol. 1993;88:760-761.
Menkes DB, MacDonald JA. Interferons, serotonin and neurotoxicity. Psychol Med. 2000;30:259-268.
Meyers CA, Scheibel RS, Forman AD. Persistent neurotoxicity of systemically administered interferon-alpha. Neurology. 1991;41:672-676.
Musselman DL, Lawson DH, Gumnick JF, et al. Paroxetine for the prevention of depression induced by high-dose interferon alfa. N Engl J Med. 2001;344:961-966.
Raison CL, Borisov AS, Broadwell SD, et al. Depression during IFN-alfa plus ribavirin therapy: prevalence and prediction [abstract 345]. Hepatology. 2003;38(suppl 1):326A.
Raison CL, Broadwell SD, Borisov AS, et al. Depressive symptoms during IFN-alpha/ribavirin therapy are associated with reduced viral clearance in patients with hepatitis C [abstract 344]. Hepatology. 2003;38(suppl 1):325A.
Renault PF, Hoofnagle JH, Park Y, et al. Psychiatric complications of long-term interferon alfa therapy. Arch Intern Med. 1987;147:1577-1580.
Rifflet H, Vuillemin E, Oberti F, et al. Suicidal impulses in patients with chronic viral hepatitis C during or after therapy with interferon alpha. Gastroenterol Clin Biol. 1998;22:353-357.
Schramm TM, Lawford BR, Macdonald GA, Cooksley WG. Sertraline treatment of interferon-alfa-induced depressive disorder. Med J Aust. 2000;173:359-361.
Valentine AD, Meyers CA, Kling MA, Richelson E, Hauser P. Mood and cognitive side effects of interferon-alpha therapy. Semin Oncol. 1998;25(suppl 1):39-47.
Back to Medical Writers' Circle
About Hepatitis | News Updates | Community & Support | Resource Library | About HCSP | Contact Us | Site Map | Resources en Espa
Here's a recent (Apr. 04) HCV neuropsychiatric study:
Minimizing the Impact of Neuropsychiatric Effects During Chronic HCV Disease and Treatment
Robert G. Gish , M.D.
(To see the figures and illustrations in this article, please download the pdf version.)
New data are emerging that implicate direct effects of the hepatitis C virus (HCV) on the central nervous system, along with side effects of both peginterferon and ribavirin as causes of multiple symptoms during treatment of HCV. Neuropsychiatric symptoms are of great concern in patients with hepatitis C because they are common, may reduce quality of life, and can limit treatment adherence and effect the outcome of treatment. To improve patient well-being and the likelihood of successful anti-HCV therapy, it is critical that physicians screen patients for neuro-psychiatric symptoms and manage these problems and symptoms proactively.
Pre-existing neuro-psychiatric symptoms are common in hepatitis C patients. In fact, 35% to 57% of patients with chronic HCV infection may have depression upon diagnosis or before starting any therapy. Furthermore, new neuropsychiatric symptoms emerge in an additional 30% to 40% of patients receiving peginterferon / ribavirin treatment. Cognitive deficits, particularly those affecting concentration, memory, and psychomotor speed, have been identified in patients with even mild HCV infection as well.
The pathophysiology of these toxic effects of HCV remain poorly defined. One theory is that HCV may infect the brain via macrophage or microglial cells. Another is that toxins may accumulate in the blood secondary to impaired clearance by a cirrhotic liver, causing impaired cognition. Cirrhosis may be predictive of poorer cognitive function due to clinical or subclinical encephalopathy, and progressive hepatic injury in the HCV-infected patient without cirrhosis also may play a role in the development of neurocognitive problems although this is rarely seen in patients without significant fibrosis and portal hypertension. Antiserotonergic effects of interferon have been proposed as a mechanism in the development of interferon-related depression and may explain why patients symptoms from interferon therapy can be profoundly improved with SSRI type antidepressants.
A recent prospective cohort study found that although only 11% of patients treated with peginterferon/ribavirin met criteria for major depression, yet more than one third developed symptoms of moderate to severe depression during treatment. Whereas interferons are generally known to be associated with psychiatric side effects, this study was one of the first to identify a dose-related association between PEG interferon/ribavirin treatment and depression.
Due to the chronic nature and nonspecific symptoms of HCV infection, distinguishing the somatic complaints of disease chronicity from a depressive syndrome is a major clinical challenge. Patients with major depression often feel ill, experiencing somatic and/or cognitive symptoms and a perceived state of "brain fog" and other symptoms that impair the patients functional level. These symptoms can easily be confounded by the presence of a chronic HCV infection. Nonsomatic symptoms of depression may include low self-esteem, feelings of guilt, worthlessness, hopelessness, and in the most severe cases, suicidal ideation. Some depression screening tools-such as the Hospital Anxiety and Depression Scale (HADS)-are geared toward assessment of nonsomatic symptoms of depression, and may be useful in HCV-infected patients who exhibit symptoms of major depression. The Center for Epidemiologic Studies of Depression (CES-D) self-administered scoring sheet also may be useful in an office practice.
The impact of depression on the patient can be significant, causing irritability, fatigue, apathy, lack of concentration, and in extreme situations, suicidal ideation or suicide. It is therefore not surprising that depression can have a negative impact on adherence to anti-HCV therapy. Moreover, another prospective cohort study found a correlation between depression symptoms and clearance of HCV RNA at week 24, even after adjusting for ribavirin dose assignment, genotype, age, antidepressant usage, dose reduction of peginterferon or ribavirin, and knowledge of viral status during treatment. Periodic assessment for depression during treatment is imperative, with expert psychiatric referral provided as needed if signs and symptoms of depression progress during treatment.
Profound improvement can be achieved with antidepressant pharmacotherapy and formal psychotherapy for treatment of depression. There are no placebo-controlled studies evaluating the treatment of interferon-induced depression. An open-label trial of citalopram conducted in 15 patients with HCV infection demonstrated a significantly positive response in interferon-treated patients. Prophylactic therapy in patients with a recent or remote history of depression may be controversial; but recent studies have shown a benefit and proactive antidepressant therapy is strongly advised in clinical practice, both from this author's clinical experience and from surveys of practitioners who manage HCV treatment. Patients with major depression may also benefit from support groups, but this should not be a replacement for pharmacologic therapy and psychotherapy.
Pharmacologic guidelines for general treatment of neuropsychiatric disorders may offer the best approach to managing depression in the peginterferon-treated patient. These guidelines emphasize individualized selection of an agent, often exploiting the side-effect profile of the various medications available. For example, agents that promote sleep may be most appropriate for patients who have a primary sleep disturbance, whereas patients experiencing fatigue may benefit most from activating agents.
Patients with a history of major depression or significant depressive symptoms including history of suicide attempts, or bipolar disorder or psychosis, should be referred for expert psychiatric diagnosis and management prior to treatment initiation. Patients with a pre-existing history of bipolar disorder should be monitored closely while receiving interferon therapy, and, whenever possible, treated prophylactically with a mood stabilizer such as olanzapine or quetiapine (lithium or valproic acid can also be considered, with close follow-up). Any patient for whom the medical practitioner is not comfortable starting antidepressant therapy should be referred for clearance before starting anti-HCV treatment, and psychiatric follow-up should continue periodically during therapy.
In summary, neuropsychiatric symptoms are common in HCV-infected patients both at baseline and as side effects of peginterferon therapy. Without appropriate intervention, these symptoms can have serious consequences for the patient and can also limit adherence to, and therefore success of, antiviral therapy. Fortunately, depression and other neuropsychiatric side effects can generally be managed effectively with available pharmacologic therapies, thereby allowing patients to stay on anti-HCV therapy with the best chance of treatment success.
Important References
Bonaccorso S, Marino V, Puzella A, et al. Increased depressive ratings in patients with hepatitis C receiving interferon-alpha-based immunotherapy are related to interferon-alpha-induced changes in the serotonergic system. J Clin Psychopharmacol. 2002;22:86-90.
Fontana RJ. Neuropsychiatric toxicity of antiviral treatment in chronic hepatitis C. Dig Dis. 2000;18:107-116.
Gleason OC, Yates WR. Five cases of interferon-alpha-induced depression treated with antidepressant therapy. Psychosomatics. 1999;40:510-512.
Gleason OC, Yates WR, Isbell MD, Philipsen MA. An open-label trial of citalopram for major depression in patients with hepatitis C. J Clin Psychiatry. 2002;63:194-198.
Hilsabeck RC, Perry W, Hassanein TI. Neuropsychological impairment in patients with chronic hepatitis C. Hepatology. 2002;35:440-446.
Ho SB, Nguyen H, Tetrick LL, Opitz GA, Basara ML, Dieperink E. Influence of psychiatric diagnoses on interferon-alpha treatment for chronic hepatitis C in a veteran population. Am J Gastroenterol. 2001;96:157-164.
Hosoda S, Takimura H, Shibayama M, Kanamura H, Ikeda K, Kumada H. Psychiatric symptoms related to interferon therapy for chronic hepatitis C: clinical features and prognosis. Psychiatry Clin Neurosci. 2000;54:565-572.
Levenson JL, Fallon HJ. Fluoxetine treatment of depression caused by interferon-alpha. Am J Gastroenterol. 1993;88:760-761.
Menkes DB, MacDonald JA. Interferons, serotonin and neurotoxicity. Psychol Med. 2000;30:259-268.
Meyers CA, Scheibel RS, Forman AD. Persistent neurotoxicity of systemically administered interferon-alpha. Neurology. 1991;41:672-676.
Musselman DL, Lawson DH, Gumnick JF, et al. Paroxetine for the prevention of depression induced by high-dose interferon alfa. N Engl J Med. 2001;344:961-966.
Raison CL, Borisov AS, Broadwell SD, et al. Depression during IFN-alfa plus ribavirin therapy: prevalence and prediction [abstract 345]. Hepatology. 2003;38(suppl 1):326A.
Raison CL, Broadwell SD, Borisov AS, et al. Depressive symptoms during IFN-alpha/ribavirin therapy are associated with reduced viral clearance in patients with hepatitis C [abstract 344]. Hepatology. 2003;38(suppl 1):325A.
Renault PF, Hoofnagle JH, Park Y, et al. Psychiatric complications of long-term interferon alfa therapy. Arch Intern Med. 1987;147:1577-1580.
Rifflet H, Vuillemin E, Oberti F, et al. Suicidal impulses in patients with chronic viral hepatitis C during or after therapy with interferon alpha. Gastroenterol Clin Biol. 1998;22:353-357.
Schramm TM, Lawford BR, Macdonald GA, Cooksley WG. Sertraline treatment of interferon-alfa-induced depressive disorder. Med J Aust. 2000;173:359-361.
Valentine AD, Meyers CA, Kling MA, Richelson E, Hauser P. Mood and cognitive side effects of interferon-alpha therapy. Semin Oncol. 1998;25(suppl 1):39-47.
Back to Medical Writers' Circle
About Hepatitis | News Updates | Community & Support | Resource Library | About HCSP | Contact Us | Site Map | Resources en Espa
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