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Post Info TOPIC: Fatty Livers (Steatosis) and "FibroScan" Measurements


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RE: Fatty Livers (Steatosis) and "FibroScan" Measurements
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Post-SVR "following" with Fibroscans (with Cap) being promoted:

(Coverage from the currently ongoing  2017 "Liver Meeting" - Washington)

Fatty Liver Common After Direct-Acting Antivirals for Hep C - Damian McNamara - October 30, 2017

 

WASHINGTON, DC - Evidence of steatosis is found in almost half the patients with hepatitis C who achieved a sustained virologic response after treatment with direct-acting antivirals, results from a prospective study show.

"Fatty liver is very common now that hepatitis C is being treated effectively," said Mazen Noureddin, MD, from Cedars-Sinai Medical Center in Los Angeles.

American and European guidelines state that a patient can be discharged from care in the absence of cirrhosis and elevated liver enzymes, but "we wanted to see what happens after direct-acting antiviral treatment," he said.

Steatosis was "very prevalent" in the study population, "although liver enzymes were normal," Dr Noureddin reported here at The Liver Meeting 2017.

Monitoring people for steatosis after a sustained virologic response is not common practice, he told Medscape Medical News, but these findings suggest that long-term monitoring is warranted.

 

Long-term Monitoring Needed

In their study, Dr Noureddin and his colleagues compared transient elastography findings (FibroScan, Echosens) in 101 patients  - 49 men and 52 women -  before and after they were treated with direct-acting antivirals. After each participant achieved a sustained virologic response, the researchers used the controlled attenuation parameter (CAP) to assess liver fat.

Mean age of the participants was 60 years and mean body mass index (BMI) was 28 kg/m˛. In addition, 36% of the patients were white, 25% were Hispanic, and 90% had diabetes. The hepatitis C infection was genotype 1 in 86% of the patients, genotype 2 in 13%, and genotype 4 in 1%. People with genotype 3 infection were excluded from the analysis because the etiology of hepatic steatosis is different in this population.

 

Decreases were significant in alanine transaminase (ALT) and aspartate transaminase (AST) levels and fibrosis scores from baseline to the achievement of sustained virologic response (P < .05).

In the study cohort, 48% of the patients showed evidence of steatosis after treatment, 6% of whom had advanced fibrosis. None of the 52% of patients without steatosis showed evidence of advanced fibrosis, defined as a score of at least 11 kPa.

For patients with steatosis, weight did not change during the study period. However, there were significant differences between these patients and those without steatosis.

Table. Mean Values After Patients Achieved a Sustained Virologic Response

Parameter

Patients With Steatosis

Patients Without Steatosis

P Value

BMI

29 m/kg˛

26 m/kg˛

<.05

Glucose level

108 mg/dL

96 mg/dL

<.05

ALT level

20 mg/dL

15 mg/dL

<.05

CAP score

297 dB/m

214 dB/m

<.05

Fibrosis score

7.0 kPa

5.3 kPa

<.05

 

"We need more follow-up," said Dr Noureddin. "We looked at patients 8 weeks after treatment. Next, we want to follow patients longitudinally to see if more patients with a fatty liver also develop fibrosis."

The study showed that even after achieving a cure for hepatitis C, approximately 50% of those patients demonstrated evidence of NAFLD.

"This is one of the most important studies presented at this meeting," said Naim Alkhouri, MD, from the Texas Liver Institute in San Antonio.

"The treatment of chronic hepatitis C infection has been revolutionized by the introduction of highly effective direct-acting antivirals, with cure rates of 95% or higher," he told Medscape Medical News. "However, the study showed that even after achieving a cure for hepatitis C, approximately 50% of those patients demonstrated evidence of NAFLD, which may increase their risk for liver cirrhosis and liver cancer."

"The use of FibroScan with CAP to assess for the presence of NAFLD and fibrosis progression should be considered in patients who are cured from hepatitis C infection," Dr Alkhouri said.

 

Dr Noureddin is a speaker and advisor for EchoSense. Dr Alkhouri has disclosed no relevant financial relationships.

 

The Liver Meeting 2017: American Association for the Study of Liver Diseases (AASLD): Abstract 2155. Presented October 23, 2017.



__________________

HCV/HBV 1973. HBV resolved. HCV undiagnosed to 2015. 64 y.o. F. Canada.

GT3a, Fibroscan F3/12 kPa - F4/12.6 kPa, VL log 7.01 (10,182,417), steatosis, high iron load.

SOF/VEL with/without GS-9857 trial - NCT02639338.

SOT March 10 - EOT May 5, 2016 - SOF/VEL/VOX 8 week trial.

 

(SEE UPDATES IN BIO)



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I was told I have a bit of a fatty liver for someone as thin as a rake :) Some reading to do here I see

SF



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65 yo, GT1A, , Cirrhosis, F-Scan F4 33.5, TX Naive Harvoni 12 wks

SOT 2/9/16 / ALT 187 AST 114 VL 2.3M.    POSTS

EOT 5/2/16  ALT 35/ AST/25  platlets 126 C/B VL UND

EOT +12 7/26/16  ALT 25 /AST 22/ ALP 83  platlets 129 C/B VL UND

EOT + 24 10/18/16 ALT 27/ AST 20/ ALP 71 platlets 153 C UND

 * SVR *

Tig


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The article is excellent for us Hep C geeks! I always thought the results of TE might be influenced by fatty liver/steatosis. It just makes sense that it would be impacted. Good to see the attention paid to these differences and the solutions being developed. Thanks for the article!



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Tig

63 yo GT1A - 5 Mil - A2/F3 - (1996) Intron A - Non Responder, (2013) Peg/Riba/Vic SOT:05/23/13 EOT:12/04/13 SVR 6+ years!

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Being that I was a longstanding GT3a, with a prior abdominal ultrasound showing "steatosis" (fatty liver), and a "FibroScan" showing F4 (12.6 kPa) that provided no CAP measurement (which would be an indicator of the degree of liver fat content) I have a vested interest in the accuracy in assessing the extent of my cirrhosis, fibrosis/liver stiffness and degree of fatty infiltration of my liver.

Since asking Mallani about the "value" of CAP assessments, I stumbled across Dr. Petta's study regarding possibly inaccurate higher fibroscan kPa scores due to fatty livers. Mind you the subjects higher BMI's were a factor. I found it all very interesting.

Both this editorial, and the actual abstract, are found in the Journal of "Hepatology" (Vol. 62, Issue 4). There is also an excellent on-line podcast via "Hepaology" of the study doctor Dr. Petta being interviewed about his findings, and expressing future studies needing to be done. (I would volunteer to be in his next study, with my low BMI)! The podcast was VERY good, but is a little hard to catch every word of Dr. Petta due to his delightful Italian accent.

 

EDITORIAL

 "Is liver stiffness measurement to stage fibrosis in patients with nonalcoholic fatty liver disease ready for clinical use?"

Authors - Michelle Lai

First Published: 30 June 2015,  Vol: 62, Pages: 997 - 998, DOI: 10.1002/hep.27902

Abstract

Full Text (HTML)

PDF (295.7KB) 

References

 

Abbreviations

BMI

body mass index

CAP

controlled attenuation parameter

LSM

liver stiffness measurement

NAFLD

nonalcoholic fatty liver disease

VCTE

vibration-controlled transient elastography

 

For a highly prevalent disease such as nonalcoholic fatty liver disease (NAFLD) which presents with a wide range of severity, staging of hepatic fibrosis is key to the clinical evaluation to assess the patient's risk of liver-related and overall mortality. It is vital to the clinician's, and the patient's, decision-making process as to how closely to monitor the patient, whether to screen for hepatocellular carcinoma or varices. In addition, as therapeutic options loom on the horizon, the staging of disease will be important in the decision of who and when to treat with a pharmacologic agent. The limitations of the current gold standard, a liver biopsy, including sampling variability and risks of complications, are well recognized.[1-4] With a high disease burden in the general population, the widespread use of a liver biopsy would result in a significant number of complications. The ideal tool for the evaluation and staging of a highly prevalent disease with a wide spectrum of severity such as NAFLD in the clinic is a noninvasive, rapidly performed, point-of-care test that allows the clinician to risk-stratify the patient and make clinical decisions at the time of the clinic visit. Vibration-controlled transient elastography (VCTE) by FibroScan (Echosens, Paris, France) has the potential to be such a tool. It measures liver stiffness as a surrogate marker of liver fibrosis. It is a rapid test, most validated in viral hepatitis, done at the bedside in the clinic to give an immediate result to inform the clinician and patient for their discussion of management. While it has been shown to be a reproducible and accurate test of liver fibrosis in patients with viral hepatitis, VCTE comes with its own set of limitations.[5]

Limitations of VCTE include reported short-term variations and failed or unreliable readings in one-fifth of patients and in a higher percentage of patients with body mass index (BMI) >30 kg/m2.[6] The rate of failed and unreliable readings is of concern in nonalcoholic steatohepatitis where patients have higher BMI. This seems to be addressed with the XL probe, which has a lower fail rate in patients with higher BMI. Nascimbeni et al. reported >20% variations in liver stiffness measurement (LSM) in about half of the 531 patients they studied with chronic liver diseases on short-term repeat LSM.[7] Repeat VCTE had been performed on these patients more than 1 day and less than 1 year after their initial VCTE test. The short-term variations observed produced a one-stage difference in about one-third of the patients and a two-stage or more difference in another one-tenth of the patients. They found both operator- and patient-specific factors that were associated with variations. Operator factors associated with variations were having two different operators perform the VCTE and a nonsenior operator perform the VCTE. Patient factors included higher baseline BMI, higher baseline LSM, interquartile range to median ratio, and a two-fold difference in alanine transaminase between measurements. The time interval between the VCTE testing was not associated with variations.

In this issue of Hepatology, Petta et al. present their results from a prospective cohort study of patients from Palermo, Italy, evaluating the impact of severe hepatic steatosis on the LSM using VCTE in patients with NAFLD.[8] They found that the median LSM was higher in patients with severe hepatic steatosis compared to those without severe hepatic steatosis for the same stage of fibrosis seen on liver biopsy. All subjects were assessed with a liver biopsy, LSM using VCTE with the M probe, and an ultrasound evaluation of the liver. Of the 306 subjects evaluated, there was unreliable LSM in 53 (17.3%). About one-third of subjects with BMI >30 kg/m2 had unreliable LSM. Those with reliable LSM were younger, were male, had lower BMI, were less likely to have hypertension or diabetes mellitus, and had less severe steatosis, while those with unreliable LSM had higher BMI and worse metabolic syndrome. In essence, those at higher risk for nonalcoholic steatohepatitis and more significant fibrosis are also the ones who are likely to have unreliable LSM. This is a problem for a couple of reasons. First, it biases the results as the authors do not have reliable data on this subgroup with more severe steatosis to obtain a more accurate assessment of the effect of steatosis on LSM. Second, this tool is limited in the patient population at highest risk for having more severe disease. The authors found that the ideal LSM cutoffs increased by 1.1-2.2 kPa with severe steatosis. Without accounting for severe steatosis, using a cutoff of 6.9 kPa to determine significant fibrosis would result in 13% of the subjects having false negatives and 17% of the subjects having false positives. Essentially, this would result in misclassification in about one-third of the patients.

What does this mean for clinical application? In evaluating a patient with NAFLD using VCTE, there needs to be quantification of steatosis in order to interpret the LSM score. Using another imaging modality for the quantification of steatosis undermines one of the biggest advantages of VCTE, which is to get an immediate result at the bedside while seeing the patient in the clinic for clinical decision making. The authors of this article also showed that the use of ultrasound to detect severe steatosis performed poorly, with a sensitivity rate of 48.6%. Echosens has addressed the fat quantification issue by adding the controlled attenuation parameter (CAP) function to the FibroScan machines. The CAP function has been shown to accurately measure the amount of steatosis,[9-11] with an area under the receiver operating characteristic curve of 0.84 for detecting severe steatosis. However, patients with a high BMI also had a higher failure rate of CAP measurements, with a failure rate of 19.4% in patients with BMI >30 kg/m2 and 58.4% in those with BMI >40 kg/m2.

Given the prevalence of NAFLD, there is a strong need for an accurate noninvasive tool to risk-stratify and monitor patients, and VCTE has the potential to be such a tool. However, Petta et al.[8] have shown that steatosis can significantly affect the LSM score. We therefore need good data to define the ideal LSM cutoffs in NAFLD for fibrosis staging for the M and XL probes that adjust for the amount of steatosis measured by CAP.

Michelle Lai, M.D., M.P.H.

Beth Israel Deaconess Medical Center

Harvard University

 

ACTUAL  ABSTRACT

 

"The severity of steatosis influences liver stiffness measurement in patients with nonalcoholic fatty liver disease"

Authors -  Salvatore Petta, Marcello Maida, Fabio Salvatore Macaluso, Vito Di Marco, Calogero Cammā, Daniela Cabibi, Antonio Craxė

First Published: 20 May 2015, Vol: 62, Pages: 1101 - 1110, DOI: 10.1002/hep.27844

ˇ         Abstract  

ˇ         Full Text (HTML)

ˇ         PDF (580.9KB) 

ˇ         References

 





__________________

HCV/HBV 1973. HBV resolved. HCV undiagnosed to 2015. 64 y.o. F. Canada.

GT3a, Fibroscan F3/12 kPa - F4/12.6 kPa, VL log 7.01 (10,182,417), steatosis, high iron load.

SOF/VEL with/without GS-9857 trial - NCT02639338.

SOT March 10 - EOT May 5, 2016 - SOF/VEL/VOX 8 week trial.

 

(SEE UPDATES IN BIO)

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