im also around a 12 - it does fluctuate - the hepatologist at the transplant center told me a 15 was needed to get on the transplant list - i registered with them because it was recommended to do so early on - he said that generally speaking after having compensated cirrhosis for 10 years or so in most cases decompensation is usually only a few years away - i would seek treatment elswhere asap instead of messin around with a trial - they have their place its just not at my place - or generally speaking at yours either - if i may be so bold - im not sure exactly sure how long ive been cirrhotic but im guessing at least 10 years ( i was diagnosed with hep c over 6 years ago and i was cirrhotic then ) judging by what i now know about it - you may be in similar shoes or you may not - best to err on cautions side - best wishes
You're welcome. Others can tell you where 12 falls on the spectrum. I have compensated cirrhosis and have always been around 7 - I hit 6 once and 8 once.
Thanks much. I did it and it came back as 12-which hopefully buys me some time. :-)
Thanks again
MELD is a score acheived through an algorythm that looks at three blood markers. MELD is used an a standadized formula for measuring liver health and managing transplant lists - the higher the score the worse off you are. Google MELD calculator. That will lead you to what you need to calculate meld score.
Good luck.
Thank you so much for your information. There is so much I do not know yet about the liver, specifically mine. I won't be able to get a biopsy for about a month, but I just had a slew of blood tests, liver panels. Unfortunately, the Dr. at the county clinic won't be able to see me until the end of September, so unless the Dr. at the research clinic can enlighten me on the results, I am on my own, trying to figure out what it all means.
Through this forum, I am truly getting an education and I deeply appreciate all the feedback.
Thank you and all the best,
Rivll (Ps I don't know what MELD is, but maybe it will be on the latest tests I just took.)
Assessment of Fibrosis and Cirrhosis in Liver Biopsies
An Update
Posted: 06/24/2011;
"...Fibrosis regresses because successful treatment results in apoptosis of the fibrogenic cells, causing a favorable shift in the balance between the fibrolytic metalloproteinases and their profibrotic inhibitors in the tissue microenvironment, and leading to resolution of the excess extracellular matrix.
What is true for fibrosis at large, also applies to the excess fibrous tissue of the liver in the setting of cirrhosis, i.e., both progression and regression of fibrosis may occur in cirrhotic livers over time.[22–25] Actually, the work of Wanless et al[25] has demonstrated that regressive changes may occur simultaneously with progressive ones. Furthermore, suppression of the necro-inflammatory activity can result in gradual fibrous septum resorption and loss of nodularity. It has been suggested that the following histologic features are indicative of regressing fibrosis:[3,25] perforated delicate fibrous septa, isolated thick collagen fibers, delicate periportal fibrous spikes, hepatic vein remnants with prolapsed hepatocytes, hepatocytes within portal tracts or split septa, minute regenerative nodules ("buds"), aberrant parenchymal veins, and portal tract remnants. Based on morphologic changes, it has been suggested that regression of fibrosis and nodularity in cirrhotic livers may result in ISC (Fig. 3),[25] a condition that is characterized by persistent vascular changes resulting in portal hypertension.
In our daily practice of diagnostic pathology, we review an increasing number of liver biopsy specimens with features suggestive of fibrosis in regression, such as attenuated, and often perforated fibrous septa, as well as delicate periportal fibrous spikes (Fig. 4). Sometimes regression of fibrosis can be clearly documented by comparing the findings of the patient's current biopsy with those of previous ones. However, even when previous biopsies are unavailable, delicate remnants of fibrous septa are very characteristic of regressing fibrosis when seen in the absence of necro-inflammatory activity."
See: http://www.medscape.com/viewarticle/743946_4
Mike