Preamble: 4. The experience of the authors

Preamble:

This guidance describes a wide spectrum of approaches to
identify the adults, young people and children with non-alcoholic fatty liver
disease (NAFLD) who have advanced liver fibrosis and are most at risk of
further complications. It outlines the lifestyle changes and pharmacological
treatments that can manage NAFLD and advanced liver fibrosis. This guidance is
developed by a panel of expert hepatologist with data supported system.
Guidance document is little different from guideline as guidelines are developed
by a multidisciplinary panel of experts and rate the quality of the evidence
and the strength of each recommendation using the grading of recommendations,
assessment development, and evaluation system. Guidance
statements are not recommendations, but help clinicians to understand and
implement the most recent evidence.

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This is the first practice guidance on Nonalcoholic fatty liver
disease commissioned by Fatty liver study group of Hepatology society,
Bangladesh based on the following:

1.     
Review and analysis of the
recently published world literature on the topic

2.     
Research data on the topic
of south Asian region.

3.     
Guideline policies of
AASLD

4.     
The experience of the
authors and independent reviewers with regard to NAFLD.

 

This practice guidance is developed for use by physicians and
other health professionals. The data have been retrieved by an extensive PubMed
search up to December 2017. Specific guidance statements are evidence based
whenever possible, and, when such evidence is not available or is inconsistent,
guidance statements are made based on the consensus opinion of the authors.

 

 

Definitions:

Non-alcoholic
fatty liver disease has been defined as the accumulation of fat in the liver in
the absence of recent or ongoing intake of significant amount of alcohol. Two criteria must be fulfilled for defining NAFLD

(1) evidence of hepatic steatosis (HS), either by imaging or
histology, and

(2)
lack of secondary causes of hepatic fat accumulation such as significant
alcohol consumption,

NAFLD can be categorized histologically into nonalcoholic fatty
liver (NAFL) or nonalcoholic Steatohepatitis. NAFL is defined as the presence of ?5% HS
without evidence of hepatocellular injury in the form of hepatocyte ballooning.
NASH is defined as the presence of   ?5%
HS and inflammation with hepatocyte injury (e.g., ballooning), with
or without any fibrosis.Encompasses the entire
spectrum of FLD in individuals without significant alcohol consumption, ranging
from fatty liver to SH to cirrhosis.Presence of ?5% HS without
evidence of hepatocellular injury in the form of ballooning of the hepatocytes
or evidence of fibrosis. The risk of progression to cirrhosis and liver failure
is considered minimal.Presence of ?5% HS with
inflammation and hepatocyte injury (ballooning) with or without fibrosis. This
can progress to cirrhosis, liver failure, and rarely liver cancer.Presence of cirrhosis with
current or previous histological evidence of steatosis or SH.Till date, liver biopsy
remains the gold standard for diagnosing NASH. Though, liver biopsy is not
feasible in studies of the general population, there is no direct assessment of
the incidence or prevalence of NASH. But, there have been some attempts to
estimate the prevalence of NASH by indirect means.

There is a bidirectional association between NAFLD and
components of Mets. Features of metabolic syndrome (MetS) are highly prevalent
in patients with NAFLD, and also increase the risk of developing NAFLD. Table 3
showing some established and emerging conditions that are associated with
NAFLD.Worldwide,
obesity remains the most important and well-described risk factor for NAFLD.
The results of several cross-sectional studies and case-control studies have
shown that people with NAFLD have higher waist circumference (WC) or BMI than
those without NAFLD, and have reported significant associations between
abdominal obesity (OR = 1.10-1.13; 95% CI, 1.02-1.22 per 1-cm increase in WC)
and NAFLD.(108) In the Dionysos study, NAFLD was present in 94%, 67%, and 24.5%
of the obese, overweight, and normal weight populations, respectively.109  Although the mechanisms responsible for
the increased risk of NAFLD with abdominal obesity have not been fully
elucidated, current findings suggest that obesity leads to insulin resistance,
which, in turns, leads to NAFLD.110
At the other end of the distribution, data on the prevalence of NAFLD
among high-risk individuals with severe obesity have become widely published.
On average, these studies reported that 76% (range 33 to 99%) of the patients
undergoing bariatric surgery have steatosis, 37% (range 9.8 to 72.5%) have
NASH, 23% (range 7.3 to 49%) fibrosis, and 5.8% (range 1.6 to 10%) cirrhosis.Several
studies have described a higher prevalence of NAFLD among people with type 2
diabetes compared with nondiabetics, with prevalence estimates ranging from 40%
to 69.5%.61,86,87 Moreover, a recent
case-control study using proton-MRS demonstrated that people with type 2
diabetes have on average 80% more liver fat than age-, weight-, and sex-matched
controls. This difference was not explained by the type of medications used.
Furthermore, aspartate aminotransferase (AST) and alanine aminotransferase(ALT)
underestimated liver fat content among people with diabetes; for any given ALT
or AST level, adults with type 2 diabetes had 40 to 200% more liver fat than
nondiabetic adults.88
Patients with type 2 diabetes not only have a higher prevalence of NAFLD, but
also appear to have more severe forms of the disease, including NASH and
fibrosis.Dyslipidemia: Dyslipidemia that is characterized by high
triglyceride (TG) and low high-density lipoprotein cholesterol (HDL-C) levels predisposes
patients to arthrosclerosis.16
Approximately 20–80% of NAFLD patients also have dyslipidemia.17  The prevalence of
NAFLD in individuals with dyslipidemia attending lipid clinics has been
estimated to be 50%.(29,30) A very common change in the metabolic profile
among patients with T2DM, MS, and obesity is an alteration of serum lipid
levels (dyslipidemia), suggesting a close relationship between T2DM, MS, and
obesity and NAFLD. It has been shown that NASH significantly boosts the level
of oxidized low-density lipoprotein cholesterol (LDL-C). High LDL-C is a
well-established risk factor for arthrosclerosis.18 The
most common form of dyslipidemia in NAFLD patients is atherogenic dyslipidemia,
which is characterized by hypertriglyceridemia, low HDL-C levels, and high LDL-C
levels.Age, sex, and ethnicity: NAFLD is seen in all
age groups, prevalence peaks in the fourth decade in men and sixth decade in
women (Ruhl & Everhart 2003).The prevalence of NAFLD in India above 20
years age was 18.9% (Amarapurkar et al. 2007).The prevalence of NAFLD increased
with increasing age. More recent studies are showing that the prevalence of
NAFLD in men is equal to or greater than the prevalence in women (Amarapurkar
et al. 2007). But these findings are not consistent with our population.
Recently in a large cohort, it revealed that NAFLD is more prevalent in female
among Bangladeshi population and prevalence of NASH was 42.4% in NAFLD which is
much higher. (Alam et al. 2013). In fact, both the
prevalence of NAFLD and stage of liver disease appear to increase with age.

·     Despite using different diagnostic
tools, US population-based studies all found that Hispanics have the highest
and non-Hispanic blacks have the lowest prevalence of NAFLD. Echoing the
racial/ethnic differences in the NAFLD prevalence, Younossi et al17
recently reported that NASH was independently associated with being Hispanic
odds ratio (OR), 1.72; 95%CI: 1.28-2.33 and inversely associated with being
African-American (OR, 0.52; 95%CI: 0.34-0.78). Furthermore, in a study using
proton-MRS Peterson et al found that even after adjusting for BMI and age,
Asian Indian men have significantly higher HT compared with their Caucasian
counterparts (1.54 vs. 0.77%).103
It is intriguing that most of the recent data suggest that the
ethnic differences reported for NAFLD may be explained by the genetic variation
related to the patatin-like phospholipase domain-containing protein 3 (PNPLA-3)
gene.(40) In summary, the incidence of NAFLD varies across the world, ranging
from 28.01 per 1,000 person-years (95% CI, 19.34-40.57) to 52.34 per 1,000
person years (95% CI, 28.31-96.77).

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