Eleven years since my last biopsy. 9.5 years undetected/post-tx. Sonograms at one year post-tx and four years post-tx show steatosis (fatty infiltration) of the liver. Since clearing my geno 3 HCV did not resolve this, sonogram cannot accurately gauge progression/regression, and other symptoms (blood pressure, cholestrol, insulin resistance) point to 'metabolic syndrome', gastro doc has said biopsy is unnecessary and I should get a CT scan. Part of this is standard follow up to SVR, since my understanding is we should all have regular screening for HCC post-tx.
My problem with CT is the high level of radiation you're exposed to and I'm wondering if an MRI could give the same info and be less of a 'necessary evil'. The only thing I could think of that might preclude MRI, is the small metal clip that is a souvenir of my gall bladder removal and still resides in my liver.
Any input from those with some imaging experience would be welcome.
Being cirrhotic I have to get regular screening for HCC, Doctor Kwo stopped doing the CT scans a couple years ago due to the radiation and now only does the MRI... Since either one doesn't matter to me and he likes the MRI better I just do it... But if I pushed the CT scan I really don't think he would have much of a problem.
Magnetic resonance imaging (MRI) is extremely useful in the detection and characterization of regenerating and dysplastic nodules and HCC (Table 1). Several studies have demonstrated the superiority of MRI in both lesion detection and characterization for focal hepatic lesions when compared to CT.
Abdominal CT's are comparable to receiving approx 100 single x rays at one time...repeated CT's is exposing yourself to an abundance of radiation
I have always been told MRI is better resolution and with no side effects . I push for this if a CT is ever recommended.
.MRI" here in CAN are much harder to get as there are not near as many machines and much costlier than CT ..however I tell them I will wait..
I would venture to guess that I have had at less a dozen of more CT scans and MRIs of my abdomen over the years. And maybe 8 ultrasounds. Since I have HCC that is not unusual. So what I have to say is based on my own experience and readings on HCC and its detection. Especially reading the AASLD Practice Guideline for "Management of Hepatocellular Carcinoma" which was updated last year. Which I consider the one best source regarding HCC.
"my understanding is we should all have regular screening for HCC post-tx."
If you had stage 4/cirrhosis you are correct the screening for HCC is still warranted.
IMPORTANT: (Maybe it is my HE but...)
Correct me if I am wrong. The the purpose of your imaging test is to screen for HCC? Or are you trying to "see" changes in your degree of cirrhosis or fibrosis?
Everything that follows is based on detecting HCC while having steatosis. Sorry if I misunderstood.
"CT is the high level of radiation you're exposed to and I'm wondering if an MRI could give the same info and be less of a 'necessary evil'."
* It is possible to screen for HCC using ultrasound. Is the problem that the steatosis which tends to make the liver echogenic, makes detecting lesions difficult?
From the AASLD Practice Guideline for HCC............
"The radiological test most widely used for surveillance is ultrasonography. A small HCC on ultrasound may take on one of several different appearances. The smallest lesions may be echogenic, because of the presence of fat in the cells. Other lesions may be hypoechoic, or show a ‘‘target lesion’’ appearance. None of these appearances is speciﬁc. Ultrasound has been reported to have a sensitivity of between 65% and
80% and speciﬁcity greater than 90% when used as a screening test.
However, the performance characteristics have not been as well deﬁned in nodular cirrhotic livers undergoing surveillance. These performance characteristics, although not ideal, are superior to any of the serological tests.
The most difﬁcult ultrasounds are in obese individuals with fatty liver disease and cirrhosis. However, no alternative strategy for surveillance has been adequately tested. Some reports suggest the use of CT scanning as
a screening test for HCC.
The performance characteristics of CT scanning have been developed
in diagnostic/staging studies in which some other test has raised the suspicion of HCC. Thus, these results come from biased populations. The performance characteristics of CT scanning in HCC surveillance are
unknown. In addition, for CT scanning to have maximum sensitivity this will require 4-phase scans, with the attendant high levels of radiation and potential long term carcinogenesis risk.
No recommendation can be made about CT scanning for individuals in
whom visibility on ultrasound is inadequate. It may be that some patients, particularly the obese, are just not good candidates for HCC surveillance despite their risk. Ideally, ultrasonographers performing HCC surveillance should receive special training, much as is done for mammographic surveillance in some jurisdictions.
Strategies such as alternating different surveillance modalities at intervals have no basis. The guiding principle should be that the best available screening test should be chosen, and it should be applied regularly.
Combined use of AFP and ultrasonography increases detection rates, but also increases costs and false-positive rates. AFP-only surveillance had a 5.0% falsepositive rate, ultrasound alone had a 2.9% false positive rate, but in combination the false positive rate was 7.5%.
Ultrasound alone cost about $2000 per tumor found, whereas the combination cost about $3000 per tumor found."
"small metal clip that is a souvenir of my gall bladder removal and still resides in my liver"
Whoa, you have it find out if that precludes all MRIs for you. I don't even want to pic what would happen if that clip is magnetic!!!
The only time a contrast-enhanced study (dynamic CT-scan or MRI) is needed is when a lesion is seen and it is not known if it is HCC or not. Only contrast-enhanced dynamic CT-scan or a MRI can detect the "classic" sign of HCC; the presence of arterial uptake enhancement followed by washout. This is because HCC is feed by the livers arterial blood supply.
By the way MRIs are the most expensive imaging test. Mine costs $5,000 per and I have then every 3 months.
As far as radiation...Since I have had a dozen or so, maybe that is why my girlfriends say I glow in the dark? ;-)
Please clarify the info you would like to know and I will share what I know with you.
Thank you. Looks like I've got some studying to do, but will probably push for the MRI if my ins. will cover. I sorta think my gastro has a buddy deal with the enoscope clinic next door and they 'just happen' to have a CT machine there.
Thanks Hector. My original intention was to try to get a handle on how bad my NAFLD is. I had thought steatosis put me at a higher risk for HCC, but I've never been diagnosed cirrhotic and gastro doc (not alwqays the sharpest tool in the shed) says, "No. All my fatty liver is probably due to 'metabolic syndrome' and I'm not actually at higher risk for HCC than the general population.
Really appreciate the extra info. It's a lot of work trying to be an 'informed healthcare consumer'.
"NAFLD - Encompasses the entire spectrum of fatty liver disease in individuals without significant alcohol consumption, ranging from fatty liver to steatohepatitis and cirrhosis."
The American Association for the Study of Liver Diseases, in collaboration with the American College of Gastroenterology and American Gastroenterological Association, have developed new guidelines for the diagnosis and management of Nonalcoholic Fatty Liver Disease (NAFLD). The practice guideline was co-published in the June 2012 issues of the official journals of the sponsoring societies.
The guideline is intended for physicians and allied health professionals and provides recommendations that suggest preferred approaches to the diagnosis, therapeutic and preventive aspects of care. While obesity is a risk factor for NAFLD, there is a very high prevalence in individuals with type 2 diabetes mellitus and progression to advanced fibrosis and mortality increases in older patients. The recommendations address NAFLD in children and adults.
All quotes are from this new guideline...you can get the pdf there too.
“The Adult Treatment Panel III clinical definition of the metabolic syndrome requires the presence of three or more of the following features:
(1) waist circumference greater than 102 cm in men or greater than 88 cm in women;
(2) triglyceride level 150 mg/dL or greater;
(3) high-density lipoprotein (HDL) cholesterol level less than 40 mg/dL in men and less than 50 mg/dL in women;
(4) systolic blood pressure 130 mm Hg or greater or diastolic pressure 85 mm Hg or greater; and
(5) fasting plasma glucose level 110 mg/dL or greater.”
“Patients with NAFLD are at increased risk for HCC, but this risk is likely limited to those with advanced fibrosis and cirrhosis. Several studies investigated the natural history of NASH cirrhosis in comparison to patients with hepatitis C cirrhosis. One large prospective US-based study observed a lower rate of decompensation and mortality in patients with NASH cirrhosis as compared to patients with hepatitis C cirrhosis. However, a more recent international study of 247 NAFLD patients with advanced fibrosis and cirrhosis followed over a mean duration of 85.6 ± 54.5 months showed an overall 10-year survival of 81.5% that was not different from matched patients with hepatitis C cirrhosis. Importantly, both studies have shown that patients with NASH cirrhosis are at significantly lower risk for HCC than patients with hepatitis C cirrhosis”
“The diagnosis of NAFLD requires that (a) there is hepatic steatosis by imaging or histology, (b) there is no significant alcohol consumption, (c) there are no competing etiologies for hepatic steatosis, and (d) there are no co-existing causes for chronic liver disease.
Common alternative causes of hepatic steatosis are significant alcohol consumption, hepatitis C, medications, parenteral nutrition, Wilson's disease, and severe malnutrition. When evaluating a patient with newly suspected NAFLD, it is important to exclude co-existing etiologies for chronic liver disease including hemochromatosis, autoimmune liver disease, chronic viral hepatitis, and Wilson's disease. Mildly elevated serum ferritin is common in patients with NAFLD and it does not necessarily indicate increased iron stores. Elevated serum ferritin and transferrin saturation in patients with suspected NAFLD should lead to testing for genetic hemochromatosis. Mutations in the HFE gene occur with variable frequency in patients with NAFLD and their clinical significance is unclear. One should consider a liver biopsy to assess hepatic iron concentration and to exclude significant hepatic injury and fibrosis in a patient with suspected NAFLD with elevated serum ferritin and a homozygote or compound heterozygote C282Y mutation in the HFE gene. Elevated serum autoantibodies are common in patients with NAFLD and are generally considered to be an epiphenomenon.3 In a recently published large study from the NASH Clinical Research Network, positive serum autoantibodies, defined as ANA > 1:160 or ASMA >1:40 were present in 21% of patients with well-phenotyped NAFLD and were not associated with more advanced histologic features.
7. When evaluating a patient with suspected NAFLD, it is essential to exclude competing etiologies for steatosis and co-existing common chronic liver disease. (Strength – 1, Evidence - A)
8. Persistently high serum ferritin and increased iron saturation, especially in the context of homozygote or heterozygote C282Y HFE mutations may warrant a liver biopsy. (Strength – 1, Evidence - B)
9. High serum titers of autoantibodies in association with other features suggestive of autoimmune liver disease (very high aminotransferases, high globulin) should prompt a more complete work-up for autoimmune liver disease. (Strength – 1, Evidence - B)”
When to obtain a liver biopsy in patients with NAFLD?
Liver biopsy remains the gold standard for characterizing liver histology in patients with NAFLD. However, it is expensive and carries some morbidity and very rare mortality risk. Thus, it should be performed in those who would benefit the most from diagnostic, therapeutic guidance, and prognostic perspectives.
13. Liver biopsy should be considered in patients with NAFLD who are at increased risk to have steatohepatitis and advanced fibrosis. (Strength – 1, Evidence - B)
14. The presence of metabolic syndrome and the NAFLD Fibrosis Score may be used for identifying patients who are at risk for steatohepatitis and advanced fibrosis. (Strength – 1, Evidence - B)
15. Liver biopsy should be considered in patients with suspected NAFLD in whom competing etiologies for hepatic steatosis and co-existing chronic liver diseases cannot be excluded without a liver biopsy. (Strength – 1, Evidence - B)”
MANAGEMENT OF PATIENTS WITH NAFLD
The management of patients with NAFLD consists of treating liver disease as well as the associated metabolic co-morbidities such as obesity, hyperlipidemia, insulin resistance and T2DM. As patients with NAFLD without steatohepatitis have excellent prognosis from a liver standpoint, treatments aimed at improving liver disease should be limited to those with NASH.
Many studies indicate that lifestyle modification may reduce aminotransferases and improve hepatic steatosis when measured either by ultrasound7 or MR imaging and spectroscopy. In a meta-analysis of 15 early case series and clinical studies spanning between 1967 through 2000, most studies reported reductions in aminotransferases and hepatic steatosis by ultrasound across a broad spectrum of diets of different caloric restriction intensities and macronutrient composition (low vs. high carbohydrate, low vs. high fat, saturated vs. unsaturated fat diets). However, these early studies were inconclusive as a result of being small, largely uncontrolled and few using histology as the primary endpoint. More recent uncontrolled studies also showed an improvement in aminotransferases and hepatic steatosis on histology with lifestyle modification.
Orlistat (an enteric lipase inhibitor) in conjunction with lifestyle modification was investigated in two randomized controlled trials. In the study by Ziegler-Sagi et al., orlistat reportedly improved ALT and steatosis by US, but its effect on liver histology could not be evaluated because the majority of patients did not undergo a follow-up liver biopsy. However, in the study by Harrison et al., orlistat did not improve body weight or liver histology.
The best evidence for weight loss as a means to improve liver histology in NASH comes from a trial that randomized 31 obese persons with NASH to intensive lifestyle changes (diet, behaviour modification and 200 minutes a week of moderate physical activity for 48 weeks) versus structured basic education alone. The intensive arm had 9.3% weight loss (versus 0.2% in the dietary counseling alone arm) and led to an improvement in steatosis, necrosis and inflammation, but not fibrosis. Importantly, participants with ≥ 7% weight loss had significant improvement in steatosis, lobular inflammation, ballooning, and NAFLD Activity Score (NAS). There was a similar pattern in the study by Harrison et al., where participants who lost > 5% body weight improved steatosis, whereas individuals with ≥ 9% weight loss had significant improvement in steatosis, lobular inflammation, ballooning, and NAS.
A number of recent studies used MR spectroscopy to assess changes in hepatic fat in response to lifestyle modification. The results from these studies using a variety of interventions, either by diet alone or in combination with different exercise prescriptions, have consistently reported a significant reduction in liver fat by an average of ∼40% (ranging from 20% to 81%). The degree of hepatic fat reduction was proportional to the intensity of the lifestyle intervention and generally required a body weight loss between ∼5 to 10%.
The effect of exercise without dietary modification on hepatic steatosis was investigated in four studies using MR spectroscopy. Exercise programs consisted of 2-3 sessions a week of 30-60 minutes over a period of 6 to 12 weeks. In all but one study liver fat content diminished without a significant change in body weight.
16. Weight loss generally reduces hepatic steatosis, achieved either by hypocaloric diet alone or in conjunction with increased physical activity. (Strength – 1, Evidence - A)
17. Loss of at least 3-5% of body weight appears necessary to improve steatosis, but a greater weight loss (up to 10%) may be needed to improve necroinflammation. (Strength – 1, Evidence - B)
18. Exercise alone in adults with NAFLD may reduce hepatic steatosis but its ability to improve other aspects of liver histology remains unknown. (Strength – 1, Evidence - B)”
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