Thanks to a HepC positive organ donor last year, he is no longer on dialysis and is now getting treatment. Things are looking up - if the hands get well too, life will really be good again. Time will tell. The same hands that go fishing should also be able to wash a few dishes!--MsJoe
fibrotest 0.73 (f3/f4)
acti test 0.93 A3
VL 14,660,000+ (Jan 2016)
Started Harvoni 5/16/16
5/31/16 VL 239
If i correctly understand, symptomatic cryoglobulinemia (for example, cryoglobulinemic vasculitis with serious damaging of kidneys) due to HCV infection, usually, is an indication for rapid initiation of HCV treatment. Asymptomatic cryoglobulinemia often does not require treatment. Successful HCV treatment may lead to disappearance of cryoglobulinemia in majority of patients. From the other hand, there are some data, that successful HCV treatment itself may cause cryoglobulinemia:
Before treatment, cryoglobulins were detected in 25 subjects (50%). Only 1 of the 25 patients with asymptomatic mixed cryoglobulinemia had persistence of cryoglobulins at the end of the follow-up period. Unexpectedly, in 7 of 25 subjects without mixed cryoglobulinemia before treatment, cryoglobulins became detectable after antiviral therapy.
Thank you, Serge, for posting that link. This is a perplexing, study. It seems to raise as many questions as it answers. I find it difficult to see how successful treatment of hep c could cure cryo in one group of patients while causing it in another
The substance of the report, which the abstract says contains a discussion of possible explanations, lies behind a paywall. Without being able to access the full report it is difficult to know quite what to make of the study results from the abstract alone.
The study dates from 2005, before the advent of DAAs, and so inevitably refers to patients who cleared the virus through the old interferon and ribavirin treatment regime. This may be significant. Although I'm not an expert, I believe the old interferon and ribavirin treatment worked in very different ways to the new DAAs.
Nevertheless, I agree with you that the topic is under-researched. At least part of the explanation may be that Big Pharma, having no pill to treat cryo, has no reason to spend money researching it.
Male Geno 1a F3-4 Tx Naive
Contracted early 1970s Diagnosed 2012
Started 12 wks TWINVIR (Sof/Led) on 15 Nov 2015
Pre-treatment VL 1.8 million
UND at 8 Dec 2015; UND at 12 Jan 2016
Ended 12 wks TWINVIR on 6 Feb 2016
9 Feb 2016 EOT VL test <15 PCR Negative
UND at 3 May 2016 SVR12
ETA: Thurl was posting as I was writing this post. It appears we share some of the same insights.
It occurs to me that not all HCV treatments are equal in this respect. Some (e.g. Viekira Pak + Ribavirin) are known to damage the liver in the process of attempting to clear the virus, while others are not. I am not a medical person, but suspect that therapies which damage the liver during treatment are probably more likely to leave behind a higher level of Cryoglobulinemia than treatments which demonstrate improved liver function during treatment.
Many years ago, I had the experience of going from slightly elevated ALT/AST levels, to astronomically high ALT/AST levels upon Interferon therapy (ALT/AST are now only moderately elevated, but have remained far above tested levels prior to Interferon therapy). The side effects from interferon were so severe, I had to stop six months in.
Like many others (~50%) who have lived with this virus for many years, while not being specifically diagnosed with Cryoglobulinemia, I have some of the textbook symptoms. The outward symptoms ( occasional rash, bruising, edema in the lower legs) so far have been mild enough that others don't seem to notice them. However, I have undergone three major surgeries for joint problems that no one else in my family has ever experienced.
There is nothing to prove, or disprove that the joint problems I've experienced are related to chronic Hep C infection, but personally.... I strongly suspect that they are.
One of the reasons I am opting for genric Sof/Led treatment rather than accepting a cheaper treatment known to cause liver damage, is that at a fibrosis score of F3, I think my liver has endured quite enough.
While my insurer, and the physicians held captive by them, seem willing in the interest of saving a little bit of money - and honestly it is not that much - to roll the dice on additional liver damage, major drug interactions, severe side effects, etc., I am not.
As I've said in a previous post, I've been there, and done that.
I'll know soon enough whether the external and internal symptoms I am experiencing will abate with treatment, and I'll be sharing those experiences with my fellow forum members in future posts.