This is for a friend of mine. I confess I don't understand. He had a biopsy in 2005 which pegged him at Stage 1, Grade 2. That was his last biopsy. In 2008, he got a diagnosis of cirrhosis via a CT scan with this comment - "there is some blood vessel changes, suggesting early esophageal variceal formation. "
"His liver function tests remain normal and his INR is normal, as is his albumin. His main problem is that his platelet count is low, this time at 45, the lowest it has been recorded, but really, in the past year, he has varied between 55 and now 45.
Nothing new to find on physical examination. There is no jaundice, no lymphadenopathy and no ascites, as well as no abdominal pain. "
Can you please tell me what this reads like to you? Does this sound like someone with cirrhosis? Has anyone done treatment with a similar situation and is he able to do treatment? And are they really able to tell all this with a CT scan?
I'd welcome your input please on what his options are.
I don't find CT Scan's ability to detect cirrhosis the most convincing, but my understanding is that it is pretty good at detecting vascularture -- it maybe well be worthwhile for your friend to have an upper endoscopy to look for varices (and treat as necessary) if they are suspected. If their presence is detected, it's another indicator for diagnosis.
Cirrhosis does not seem to follow a linear nor a predictable path, and my experience has taught me that it can very easily go undetected by routine screening. I'm always unconvinced without a multi-core biopsy, but that's my personal feeling (I've always been one of the serious doubters on the accuracy of staging techniques).
In regards to blood results, using my husband as (admittedly a rather extreme) example, post-resection, even with his left lobe gone and the right one cirrhotic, his bloodwork was for the most part deceptively "normal" -- and his INR and albumin continue to be in normal range. Even when his cirrhosis spawned an hcc the size of one's fist, he had no abdominal pain, and nothing apparent on physical exam either (and only "trace" ascities on recent CT-Scans).
I hope your friend is not stage 4, but if he is it sounds like it could be well-compensated cirrhosis. My guess is that he'd have to find an experienced liverhead and would need to be followed closely, but if he's class A (no or very minimal signs of decompensation), there's a good chance he might be a candidate for treatment. My husband's treatment has been difficult, and he is watched closely and monitored for possible decompensation, but it is doable for some stage 4s. Hope that helps. ~eureka
I do not believe that a CT scan can show cirrhosis, Mine didn't, nor did an MRI (done to search for hepatoma) . The low platelets can be an indicator of cirrhosis, as is a prolonged clotting time on PT/PTT (not evident in his INR). The only abnormality on my bloodwork besides those and ALT/AST was elevated AFP. Was that done? I would not trust a CT for such a serious diagnosis. I think that sometimes the image readers may be swayed by an HCV diagnosis. There is a possibility that the low platelets are related to something else. I am nearly positive that he will not be allowed TX with platelets that low.
CT-Scan for hep c protocol is done in three phases: arterial phase, portal venous phase, and equilibrium phase in order to observe liver dynamics -- I am not familiar with all the variables, but the last sentence is a good thing: he's cleared of hcc. The first sentence does seem to point to "collateral circulation." One of the ''decompensating" behaviors of cirrhosis as the liver increases rigidity is to alleviate portal vein pressure by developing additional blood vessels. (Still thinking an endoscopy might be the next best step for your friend...)
The mention of "Aside from a mild portal venous collateral circulation” to me suggests portal hypertension that is typically present with cirrhosis. Collateral circulation can occur when the liver can no longer filter and ‘plugs up’ the normal flow from the portal tract. This to me sounds rather significant; maybe others will comment?
If a CT scan is not reliable at detecting cirrhosis, what is used to determine this? Eureka, you mention endoscopy. If he has an endoscopy, if I understand you correctly, the presence or absence of varices is a better indication of how cirrhotic he may or may not be?
I think I will try to get him into MY liverhead. He is not faring at all well with the ones in his area and he needs a second opinion, in my mind.
Newleaf..unfortunately, I think his low platelets are most likely due to the fact he is cirrhotic. That is my feeling. I wish otherwise but I'm thinking that's it.
Thanks Bill. That's what I need, straight information.
Eureka, I'll ask him about the endoscopy, however he doesn't really get anything much from the doctor he's seeing. He goes for his appointment, the doctor looks at the results and they send him on home again and that's the extent of it. Very little dialogue, very little hope.
He says he has a ravenous appetite, can't eat enough but gains no weight.
I want to see if my docs will take him on or at the least, give him a second opinion and a referral to doctors they would consult with that he will feel has his best interests at heart.
Trish, I just noticed his albumin is well within range; this is a good sign, I think. I was told by my doc that this is one of the things he looks for to determine whether a liver is compensated, or starting to lose its edge.
I've learned over the years not to jump to conclusions about any symptoms of cirrhosis and their correlation to severity or survival. I'm definitely of the mind that biopsy is the still the best diagnostic tool for assessing liver damage (and, a skilled GI can also measure portal vein pressure during biopsy if cirrhosis is suspected).
As far as the endoscopy, if varices are confirmed, one would presume it to be a result of cirrhosis; however, I have yet to be convinced about whether the severity of varices could lead one to accurately conclude the amount of liver damage. (If cirrhosis is not homogenous, increased hepatic pressure could be localized, causing selective areas of developing vasculature.) Maybe not the answer you were looking for, but I've had interesting/similar discussions here in the past:
"I'm definitely of the mind that biopsy is the still the best diagnostic tool for assessing liver damage (and, a skilled GI can also measure portal vein pressure during biopsy if cirrhosis is suspected). "
I asked him about getting another biopsy done and he was told it isn't possible, too dangerous to have a biopsy with his stats. I'm asking opinions here .. is there any reason with his stats as posted that he should not have a biopsy or that it's risky?
My husband was ruled out for standard biopsy because of plavix therapy, so he had a transjugular biopsy -- much lower risk of bleeding, but I understand it's a pretty specialized procedure, and only a small percentage of radiologists are familiar with it. Maybe your liverhead's center could offer him that option if his doctors can't...
My docs have a Fibroscan, however I understand that's more reliable at lower stages of liver damage than at the more advanced stages. Regardless, they do have that technology available to them and perhaps that will be beneficial also?
They didn't have a Fibroscan when they started my treatment in Feb 2008, however by the time I was done and at 6 months post EOT, they did have one.
a mild portal venous collateral circulation
early esophageal variceal formation
I think he has cirrhosis and needs to be re-evaluated. The report from 2008 said,
"His liver function tests remain normal" but his ALT is 106 and AST 55.
They may say they can't do an endoscopy because of the low platelet count...but they can give him a platelet transfusion before the procedure. That's what they did for my mother any time she had a procedure that could cause bleeding.
"He says he has a ravenous appetite, can't eat enough but gains no weight."
He might be DIABETIC. Have him get checked. That's a sign of diabetes.
I will ask him about Diabetes. His HGB is between 14 and 15 so it doesn't seem to indicate anemia.
Thank you CoWriter for the comment on blood transfusion. Thanks to everyone for all the valuable input so quickly. I see much here to go on and much to talk to him about. What is also clear is that he needs very capable care. I hope we can find that for him.
I have to say...I keep reading also about ALA. OH is using ALA. I wonder about that for him also .. somewhat thinking out loud here but wondering on experiences with that also.
Thank you. It's a very good start and we'll see what happens. Some obstacles but I've encountered obstacles before plenty of times. We'll see how it goes.
"Both HCV infection and HH are associated with increased risk of developing diabetes. Diabetes is now recognized as one of the extra-hepatic manifestations of HCV infection.4-6 People with chronic HCV infection have a two- to fourfold higher likelihood of developing diabetes than nondiabetic control subjects."
"Advanced liver disease appears to potentiate the diabetogenic action of infection because as many as half of all patients with HCV cirrhosis develop diabetes. The clinical phenotype of a patient with HCV infection and diabetes is characterized by onset of diabetes in the fifth or sixth decade of life, BMI < 30 kg/m2, lower cholesterol level, and advanced liver disease"
I'll definitely ask him about diabetes. Thank you.
I'm aware he may not know he has it, he hasn't mentioned it - I intend to ask him to get tested for it.
There is a section in that article that mentions insulin resistance as well - it's a very good and enlightening read.
"Multiple factors may contribute to the pathogenesis of diabetes in patients with HCV infection.5,6 Insulin resistance is a core defect in development of HCV-associated diabetes. Increasing evidence indicates that decreased insulin action in the liver is caused by hepatic steatosis/fibrosis and surge in proinflammatory cytokines tumor necrosis factor (TNF)=α and interleukin-6, as well as impaired insulin action in peripheral tissues, primarily muscle, largely underlined by TNF-α effects. Autoimmunity and α-cell cytopathic mechanism are unlikely to represent a primary mechanism in the pathogenesis of diabetes in HCV infection. Based on available clinical evidence, testing is recommended for HCV in individuals with diabetes and elevated liver enzymes (AST and ALT).9"
I don't get the impression that steatosis is his problem however fibrosis certainly seems to be.
I'm aware that different tests have different ranges, but my albumin report lists normal as 3.3 to 4.9. Did you mean to write 4.0?
My lab's bilirubin range is .2 to 1.2 and GGT range is 4 to 49. Going by my lab's ranges he's out of whack on all but alk phosphatase. I agree that portal hypertension is a sign of cirrhosis. I'd be interested in the diabetes angle also. My doctor just mentioned that me that hep C has been documented as an actual cause of one of the forms of diabetes.
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