To assess the degree of fibrosis, I used FIB-4, NAFLD fibrosis score and, according to this, a transient Elastography or ultrasonido CAP.

NAFLD is usually associated with insulin resistance.

I guess weight loss, exercise especially shaping up your abs helps a lot.

If not responding i had seen people responding to metformin and statins.

Anyway improved eating patterns with lifestyle helps.

Warms regards

Dr Sikandar

Usual management is a combination of several measures directed to loss weight such as a low fat diet, more physical exercise, and rational use of statins and other hypolipemic drugs

Usual Rx – weight loss in obese especially abdominal obesity [by exercise, drugs, bariatric surgery in morbid obese], control of diabetes and hyperlipidemias by drugs. Exclude secondary causes like metabolic liver disease [Wilson’s disease, autoimmune hepatitis, storage disorder in children] and hepatitis C. Holistic treatment should also include measurement of liver fat and fibrosis by MR elastography, fibroscan or liver biopsy for prognostication

I advise dietary modification, exercises, and Unani drug such as "Safoofe Mohazzil" which has substanciated its efficacy in metabolic syndrome in clinical studies. We have even treated even cirrhotic patient of NAFLD, and fibrosis decreased in fibroscan significantly after treatment. please follow the link: Article Unani Treatment Decreased Fibrosis and Improved Liver Functi...

I would like to thank all my colleagues for their participation and their recommendation of the discussion.

As it was expected the mainstay of the treatment which is recommended was the weight reduction, which can be achieved with change of diet and increasing of the exercise.

But the problem is that these changes from usual diet pattern and sedentary life is not so easy for most of the patients. The question is that how do you convince and encourage them to act properly?

Herbal and alternative medicine has been used in the treatment of fatty liver disease in a lot of studies. Honestly to say I had not heard anything on the issue that Shabnam has shared. I would like to ask her to further clarify their study and the results here in the discussion. I would also like to ask others to share their alike experiences in the field.

The best way is to provide examples e.g. One of my patients lost 10 kg weight in 6 months with substantial improvement in liver function tests without any medicine.

One of my female patients 45 years old, loosed 15 Kg. in one year with dieta and exercise without any other medical treatment

Following to results : Positive effect of SAMe on reducing liver enzyme levels, dyspeptic syndrome, asthenic syndrome, and a tendency toward a decrease in steatosis (Baranovsky AYU, Raykhelson KL, Marchenko NV. S-adenosylmethionine (Heptral®) in the treatment of patients with non-alcoholic steatohepatitis. Clinical Perspectives of Gastroenterology, Hepatology. 2010) and our own data, we using in routine clinical practice combination SAMe+BCAA and dipeptide glycil-glycin. We perform such medication on the background of weight loss and dosed physical exercise (control of sarcopenia).

physical exercise, weight loss, statins, Silybum marianum(Milk Thistle), May be low fat and sugar diet and 500 mg/resveratrol twice perday for 60kg weight

NAFLD, usually responds well to weight reduction through regular exercise, low carbohydrate balanced diet. Also vitamin E has been found to have benefit in clinical practice in reducing the transaminase elevation.

Weight loss, physical dailyexercise, statins, none of sugar and so on...

Use of Vitamin E has been issued By Sarin. I myself do not recommend Vitamin E anymore. As it was mentioned by Sarin, it can only decrease AST / ALT levels, but no proven effect in liver pathology has been shown.

My point of view is that prescribing any drug to these patients can make them think that they are doing something for their disease! so they can forget to focus on their diet and exercise. Any comment to this?

Weight loss through a nutrient-dense diet (adjusting for calories), physical activity, and probiotics. I am waiting for results of fecal microbiota transplantation (FMT) trials ( NCT02469272, NCT02721264 and NCT02496390 ) and probiotic trials (NCT03511365).

https://www.ncbi.nlm.nih.gov/m/pubmed/26059365/

https://www.google.co.in/amp/s/www.researchgate.net/publication/259181429_A_systematic_review_for_the_use_of_Vitamin_E_in_non-alcoholic_fatty_liver_disease_NAFLD_A_meta-analysis/amp

https://www.google.co.in/url?sa=t&source=web&rct=j&url=https://www.mdpi.com/2079-9721/6/4/86/pdf&ved=2ahUKEwjK8ujn_d_dAhWBXisKHVgKCssQFjAIegQIAhAB&usg=AOvVaw2HBdrEMS47Vy9gEWqWcxb2&cshid=1538216303642

I agree that even use of vitamin E is quiet limited. Various meta analysis has given conflicting reports. But given that life style modification and weight reduction is not effective in many , a drug even though of limited benefit may be considered in the ambit. That is my opinion.

Thank you Sarin for the references to the 2X different publications on Vitamin E. They have different conclusions.

Obviously, like so many areas of research, further corroborating studies are required to validate one or the other papers.

Thanks for Sarin and Patricia:

On the Vitamin E prescription, do you do a liver biopsy before prescribing it? As it is recommended in non-diabetics and in those who have NASH, which can only be diagnosed by liver biopsy. Of course having some degrees of fibrosis in Fibroscan etc can indirectly show an indirect to NASH in the liver, but the exact diagnosis of steatohepatitis needs liver Bx.

I would also ask Patricia to give some more information on the ongoing above mentioned studies.

I forgot to add that you should order IgA anti-tTg to rule out celiac disease. But even the gluten-free diet does not prevent NAFLD.

Tovoli F, Negrini G, Fari R, et al. Increased risk of nonalcoholic fatty liver disease in patients with coeliac disease on a gluten-free diet: beyond traditional metabolic factors. Alimentary pharmacology & therapeutics. 2018;48(5):538-546. PMID:10.1111/apt.14910.

I suggest following:

- Mile NAFLD: Exercise for mild Fatty liver/NAFLD with more emphasis on development of abdominal

-Moderate and those can't exercise: Very low fatty Acid Diets with marked reduction in saturated FAs PLUS some sort of exercise if possible

-Marked NAFLD: Very low fatty Acid Diets with marked reduction in saturated FAs + statins. Some do recommend metformin as well, but statin response is quicker but give you body aches sometimes.

Rest nutritionist MUST be consulted for long-term benefits in diet selection, as NAFLD is now considered as precursor to diabetes, NASH leading cirrhosis and sometime hepatocelullar carcinoma.

Regards

It seems great that we categorize NAFLD patients into mild, moderate and severe and manage them in concordance with it.

But how can we categorize them? On ultrasound findings? Lab data? Fibroscan? A combination of them? What is your suggestion? Do you practice for NAFLD patients based on such a categorization?

I fully agree with the suggestion from Dr. Maleki

I also agree with Dr Maleki and Prof Rodrigo.

Dear Iradj Maleki

Yes ultrasound mainly and currently with the help of radiologist we are doing it. Its mostly subjective but hen the radiologist did share some references for this.

Regards

In my obese adolescents with NAFLD, dietary modification with reduced calories and increased physical activity leading to weight loss and decreased abdominal adiposity, their livers have no more fatty infiltration and liver enzymes (ALT and AST) levels normalized.

I manage the NAFLD, obviously assuring an adequate control of Diabetes mellitus, Obesity, Dyslipidemia, Hypothyroidism and also diet more regular physical activity. In addition, use of Lactobacillus rhamnosus GG as an aid to improve dysbiosis.

For NASH I use Pioglitazone 45 mg / day, especially in diabetics.

To assess the degree of fibrosis, I used FIB-4, NAFLD fibrosis score and, according to this, a transient Elastography or ultrasonido CAP.

There is an existing system of ultrasonographic gradation of NAFLD into mild, moderate and severe. If finance is no problem then MRI can also be used to grade it better than USG. Fibroscan/NAFLD fibrosis score etc only picks up advanced disease when there is significant fibrosis as their name suggests.

In my practice I see adult patients and refer patients under 15 years to my pediatrician gastro colleagues. 

It is said that the course and prognosis of childhood NAFLD/ NASH is worse than adults and the response to treatment is less satisfying. 

I see that Sioksoan is managing patients in that field. I like to ask her if she is successful with these patients or not?

And on the ultrasound grading of the NAFLD score, I should tell that as you all know that US grading is based on steatosis alone. It has some inter-observer variations. But for NAFLD/NASH patients the level of inflammation and fibrosis is more important which cannot be diagnosed by US. Don't you think that grading on this isn't enough? How can one consider the those aspects (fibrosis / NASH) in the grading? Aside from the cost isn't it better to go for CAP/TE (Fibroscan, transient elastography)?

I saw success in resolution of steatosis among obese adolescents with weight reduction (more than 5-10% loss) and decrease waist circumference (attaining “healthy” waist).

Fibroscan only measures fibrosis [that too in advanced stages] but unfortunately there are no non invasive measures to determine exactly the level of inflammation [except liver biopsy of course].

Of course liver biopsy is the gold standard for diagnoses of NAFLD/NASH but we have many obstacles, as most patients refuse it, invasive and falsies in interpretations. So we need simple, non invasive, affordable tools for diagnoses and follow up of NAFLD especially in communities with high prevalence of NAFLD (Coming epidemic)

Liver biopsy is the official gold standard for the diagnosis of fatty liver disease and its' stages. But as Emad mentioned it has its' own problems (Cost, being invasive, small piece of sample for evaluation, inter and intra-observer variations in pathology report, complications of procedure ...). Of course for the diagnosing hepatitis (steatohepatitis) it is the only way.

Fibroscan, the Echosense transient elastography can measure the steatosis (CAP) as well as fibrosis, however its' accuracy should be further evaluated.

For the non-invasive evaluation of fibrosis some scores/ panels have been recommended and evaluated. Some of these scores are as FIB 4 and NFS score.

How much do YOU use these scores in your practice/ research? I like to add an algorithm from the latest EASL for the evaluation of NAFLD.

Matter remains much the same. EASL also finally recommends liver biopsy for high risk cases and the algorithm starts with advanced fibrosis [F3]. There are no non invasive markers for exacting the degree of INFLAMMATION. MR can measure liver fat and fibrosis but not inflammation.

I have found a reference where liver inflammation in hepatitis B was determined non invasively. e.g. Aspartate transaminase to platelet ratio index and gamma‐glutamyl transpeptidase‐to‐platelet ratio outweigh fibrosis index based on four factors and red cell distribution width‐platelet ratio in diagnosing liver fibrosis and inflammation in chronic hepatitis B

• December 2017 Journal of Clinical Laboratory Analysis 32(4).DOI:10.1002/jcla.22341
• Not sure whether same can apply for NAFLD; may be material for future study.

Basically, I use NAFLD score to initial screening in clinical suspected cases to guide liver biopsy in high risk patients. Management with focus on risk factors for cardiometabolic diseases; pioglitazone (in diabetics), liraglutide, and vitamin E due to evidences of reduction in liver fibrosis. There are also evidence of reduction in liver inflammation with dapagliflozin.

Dear all

I have been busy these days and the talks haven't been active for the last weeks.

We all know that the major cause of mortality in the NAFLD patients is not liver related. The major cause of mortality and probably morbidity is the cardiovascular system. Recent guidelines do recommend to check all NAFLD patient for their blood pressure and cardiovascular status. It has also been shown that ischemic heart disease and CV events are more common in NAFLD patients and NAFLD can be seen as a sole risk factor for CV events aside from diabetes and hyperlipidemia.

My question is that do you refer all NAFLD patients for a cardiology consult / evaluation? If not which patients are you choosing for that referral?

Yes, NAFLD has been shown to be a predictor of cardiovascular disease independent of metabolic risk factors (OR = 4.12; 95% CI: 1.58–10.75; p = 0.004).

Hamaguchi M, Kojima T, Takeda N, et al. Nonalcoholic fatty liver disease is a novel predictor of cardiovascular disease. World J Gastroenterol. 2007;13:1579–84.

Oni ET, Agatston AS, Blaha MJ, et al. A systematic review: burden and severity of subclinical cardiovascular disease among those with nonalcoholic fatty liver; should we care? Atherosclerosis. 2013;230(2):258-267.

Scientifically speaking, though recent research points towards association of NAFLD and CVD, this does not imply causation for sure. Points to note: [1] Both have many shared risk factors especially the metabolic syndrome, [2] Both occur with increasing frequency as age advances. So I would refer those patients to cardiology who have [1] symptomatic, [2]>40 years old with these risk factors including family history of CVD [3] >50 years old and has these risk factors [which occur in a significant proportion]. But referral will also depend on other aspects [insurance, legality, public health situation etc]

i feel some authorities label NAFLD as "pre-diabetes" , so i guess it increases the risk of cardiovascular disease

It's for sure that the relation between NAFLD and CV disease are not a causation type, good point from Guatam.

But some facts are available, The progression of fibrosis is doubled when hypertension is also present.

NAFLD associated strongly with an increased risk of CVD, subclinical atherosclerosis , coronary, cerebrovascular, and peripheral vascular disease, myocardial dysfunction, hypertrophy, and ventricular remodeling, valvular heart disease, arrhythmia & hypertension. (I have picked up these items from one of my colleagues talk, also to be considered the references provided by Patricia).

I myself think that as a gastroenterologist I have to be more aware of the CV system in the management of my NAFLD patients.

True. Vascular endothelial inflammation is the factor underlying both at microscopic level.

i guess sub clinical atherosclerosis could be the borader phenomena which was sometime back defined as insulin resistance syndrome or metabolic syndrome and NAFLD like PCOS and other are associated with this. in each of these categories impaired glucose, hypertension, nephropathy, NAFLD, PCOS evidence is there for sub clinical atherosclerosis.

So in the end its all linked with one entity.

With a low fat diet and physical exercise as main supporting measures

Bariatric surgery for weight loss gives best results with life style modificatios

vit E

GLP-1

Pioglitazones

No role for UDA or omega

Dear Fady

Thanks for your reply. I see that you are making some suggestions behind diet and exercise for weight reduction. My point is where and when are you going to suggest these drugs and the bariatic surgery?

I don't think that you suggest them to any NAFLD patient. Do you have some sub-categories or subgroups of NAFLD to whom these interventions apply?

Let's say for example does it differ between a fatty liver with or without diabetes, or fatty liver with or without morbid obesity?