"Are there any initial non-responders that have had success with the triple therapy? "
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Yes. There is data from trials that confirm this.
Also, go to frijole's profile page, click on the white sheets, and review her spread sheets. They contain the data for many of us who are treating and who have treated. The data includes information such as previous treatment and treatment response, viral load, liver fibrosis stage, Genotype, treatment progress, length of treatment, and end result of treatment;
http://www.medhelp.org/personal_pages/user/223152
"Am I better of waiting for the non-interferon option the future promises? More importantly, Can I wait? "
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Hector's post covered this pretty well and I agree with Hector.
However, I will add some information about extrahepatic manifestations of Hepatitis C. Many people do not realize how many and how severe these extrahepatic manifestations can be. In addition, some try to frighten others into not treating their Hepatitis C, so it is extremely important and advantageous to be aware of just how dangerous untreated Hepatitis C can be and just how common these extrahepatic manifestations and Hep C related disease processes are.
"Abstract: Cirrhosis and hepatocellular carcinoma are the prototypic complications of chronic hepatitis C virus infection in the liver. However, hepatitis C virus also affects a variety of other organs that may lead to significant morbidity and mortality. Extrahepatic manifestations of hepatitis C infection include a multitude of disease processes affecting the small vessels, skin, kidneys, salivary gland, eyes, thyroid, and immunologic system. The majority of these conditions are thought to be immune mediated. The most documented of these entities is mixed cryoglobulinemia. Morphologically, immune complex depositions can be identified in small vessels and glomerular capillary walls, leading to leukoclastic vasculitis in the skin and membranoproliferative glomerulonephritis in the kidney. Other HCV-associated entities include porphyria cutanea tarda, lichen planus, necrolytic acral erythema, membranous glomerulonephritis, diabetic nephropathy, B-cell non-Hodgkin lymphomas, insulin resistance, sialadenitis, sicca syndrome, and autoimmune thyroiditis. This paper highlights the histomorphologic features of these processes, which are typically characterized by chronic inflammation, immune complex deposition, and immunoproliferative disease in the affected organ ...........
Conclusion: Chronic hepatitis C virus infection is associated with multiple extrahepatic manifestations (EHMs) affecting various organs in the body. While there is some evidence that the virus may play a direct role in HCV-related B-cell lymphomas via direct HCV antigen stimulation of B-cells, most EHMs are generally believed to be secondary to the host immune response to the virus.In some conditions, the histopathologic changes of EHM are related to circulating immune complexes such as type II cryoglobulinemia, and their subsequent deposition in the small vessels and glomerular capillary walls, leading to leukoclastic vasculitis in the skin and membranoproliferative glomerulonephritis in the kidney.Other HCV-associated entities like sialadenitis, sicca syndrome, lichen planus, and autoimmune thyroiditis, while not associated with cryoglobulinemia, appear to be secondary to autoimmune processes resulting in chronic inflammatory infiltrates.In porphyria cutanea tarda, the disease process is thought not to be related to host immune response to HCV, but rather to HCV-associated liver dysfunction.The role of the virus in insulin resistance in HCV-associated diabetes is unclear, but it is thought to be secondary to either viral induced inflammation or direct interference of the virus on muscle insulin signaling.In summary, chronic HCV infection may result in a multitude of disease processes affecting the small vessels, skin, kidneys, salivary glands, eyes, thyroid, and immunologic system. The sequelae of extrahepatic HCV infection are seen histomorphologically as chronic inflammation, immune complex deposition, and immunoproliferative disease in the affected organs."
http://www.hindawi.com/journals/cdi/2012/740138/
http://www.ccjm.org/content/72/11/1005.full.pdf
http://www.hcvadvocate.org/hepatitis/factsheets_pdf/Extrahepatic.pdf
Best of luck.
We just fundamentally disagree on that point. The question has not been adequately or squarely addressed by the medical establishment. If one reviews the studies presented to the FDA and journal articles as to complication rates and accepts what the CDC says as to mortality rates, I just don't think the math works.
In my own experience (ie - the number of folks I know who have done INF, the number I know who have cleared without significant side effects, the number I know who suffered a lot from INF, or declared that they would never do it again notwithstanding that they did not clear the virus) INF,
as well as the research I have read in numerous journal articles with a critical eye to what is not being said or addressed,
as well as the anecdotal evidence on this forum
just lead me to a different conclusion. In fact (and to use the terminology in the warnings written by Roche) "many, but not all" come to the same conclusion. :-)
It's probably a really close question, so if you have chosen to treat with INF, well, okay. Do it. But treatment with INF is not the only rational option. The doctors say that.
A diagnosis of chronic Hep C infection DOES NOT mean that you will die from liver disease. Don't take my word for it. Read the CDC advice to physicians - "1 to 5% will die" and note that I've been using 5% (1 in 20) out of fairness and conservatism.
http://www.cdc.gov/hepatitis/HCV/HCVfaq.htm
How does 1 to 5% from the CDC translate in this forum to "If you have Hep C you are going to get ESLD and die?" Very hard to understand. Unfounded fear. Mistake of fact.
Good luck to all!