Not sure if this tells us much - non-cirrhotic HCV patients aren't likely to die within 2 years.
The way I read this is that you are more likely to die with HCV rather than because of it unless G3, have Cirrhosis and drink more than an itty bitty guppy. It sort of misses the point that fibrosis can segue to cirrhosis and then such a person is on the outside looking in. As for part about "not heavy alcohol" users...unless I'm, wrong (someone please check me) the 40 grams of alcohol is about 3 tablespoons.
Plus another dubious distinction for G3'ers...in addition to subdued response for some PI's.
I think even people that are not HCV+ die.
Flguy; according to this,
"In the United Kingdom, a unit of alcohol is defined as 10 milliliters (or approximately 8 grams) of ethanol (ethyl alcohol)
A 750 ml bottle of 12% wine contains 9 units. Many wines may contain 14% abv. (alcohol by volume?-Willy) or more, which is just over 10 units of alcohol per bottle."
Based on this 40 grams would be about one half bottle of wine per day, just for a sense of scale. Tablespoons of pure alcohol doesn't translate as well for me.
I also have to agree that the study doesn't say much. It reminds me of the quote. Something like; There's lies, there's *damned lies*, and then there's statistics. ; )
I think the same methodology could prove that smoking 2 packs a day won't harm anyone (not within 3 years, anyway) or that drinking a half bottle of Rye per day may not either, within similar time constraints, unless one drives. ; )
I think the real and more elusive question is what happens to large groups of people with liver disease given certain behaviors; (whether alcohol consumption in light or moderate amounts; heavy use is shown to have negative effects), diet choices, effects of diet and lifestyle choices, etc. These are very difficult to isolate and therefore, to study.
Example, one well known study on pot use and fibrosis also was contaminated (my own word and viewpoint) since they also drank alcohol;
the participants of the survey, not the researchers. ; )
I think that it may miss the point by making assumptions based on the results of the healthiest of the HCV infected.
On the other hand, such studies also are good because they are a means of being thorough and complete. They proved that nothing cataclysmic happened to this group given these behaviors. That still proves something, likewise sometimes things we "know" meaning *assume* may be disproven in such simple innocuous studies. We don't truly know it until it is proven over and over in different ways.
Thanks for the interpretation. It makes more sense when using equivalency of pure alcohol.
"Example, one well known study on pot use and fibrosis also was contaminated (my own word and viewpoint) since they also drank alcohol;
the participants of the survey, not the researchers. ; ) "...
Do you have some study data about the researchers to back that up?
Here is the article. You can go find the study.
My beef is the way that it gets reported. Look at the headline. Look at the first sentence.
The fact that the pot smokers also consumed alcohol gets under-reported.
The problem is that it is difficult to isolate these factors which could influence the rate of fibrosis/staging increase. I've read this study a few times and really, the only safe thing to read is the study, not the articles about the results of the study.
Perhaps I am wrong but my recollection was that the banner headline was about pot but in further digging it appeared that the smokers were also drinking alcohol. To my way of thinking a better way of writing it up would be to say that the use of both increased fibrosis.
A better way would be to have a study in which there was no alcohol, no tobacco use, etc. In the real world that's hard to do.
Please correct me if I'm wrong.
I've been wrong before. ; ) I want to get it right.
I actually was already in agreement with your viewpoint on the study, Willy.
My quip was about the use/no use of alcohol by the researchers (alas, forgot the ;) and completely missed the mark...) ~eureka
LOL; don't you hate having to explain jokes?
Sorry that I missed it. I may check out the actual study again myself anyway.
According to Dr Seef,et al, tranfusion acquired HCV seems to have the slowest course of progression and---no difference in their mortality rates than those without HCV. I seem to recall that G2 and G3 was associated with transfusion acquired HCV
at a higher rate than G1. I'll have to look for that. - ML
N Engl J Med. 1992 Dec 31;327:1906-11 1454085 Cit:364 Long-term mortality after transfusion-associated non-A, non-B hepatitis. The National Heart, Lung, and Blood Institute Study Group.
[My paper] L B Seeff, Z Buskell-Bales, E C Wright, S J Durako, H J Alter, F L Iber, F B Hollinger, G Gitnick, R G Knodell, R P Perrillo
BACKGROUND. Acute non-A, non-B hepatitis after blood transfusion often progresses to chronic hepatitis and sometimes culminates in cirrhosis or even hepatocellular carcinoma. However, the frequency of these sequelae and their effects on mortality are not known. METHODS. We traced patients with transfusion-related non-A, non-B hepatitis who had been identified in five major prospective studies conducted in the United States between 1967 and 1980. We matched each patient with two control subjects (identified as the first and second controls) who received transfusions but who did not have hepatitis. The mortality rates in the three groups were determined with use of data from the National Death Index and Social Security Death Tapes. Cause-specific mortality was determined by reviewing death certificates. RESULTS. Vital status was established for over 94 percent of the 568 patients who had had non-A, non-B hepatitis and the two control groups (526 first controls and 458 second controls). After an average follow-up of 18 years, the estimate by life-table analysis of mortality from all causes was 51 percent for those with transfusion-associated non-A, non-B hepatitis, as compared with 52 percent for the first controls and 50 percent for the second controls. The survival curves for the three groups were virtually the same. Mortality related to liver disease was 3.3, 1.1, and 2.0 percent, respectively, among the three groups (P = 0.033 for the comparison of the group with non-A, non-B hepatitis with the combined control group). Seventy-one percent of the deaths related to liver disease occurred among patients with chronic alcoholism. CONCLUSIONS. In this long-term follow-up study, there was no increase in mortality from all causes after transfusion-associated non-A, non-B hepatitis, although there was a small but statistically significant increase in the number of deaths related to liver disease.