2. NAFLD , Chronic HCV and DM
Multisystem systemic diseases with hepatic flavor
3.
4.
5. Non-alcoholic fatty liver disease, hepatitis C virus infection and type 2 diabetes: the “vicious circle”. The
liver plays a pathogenic role in the development of type 2 diabetes both in the context of
non-alcoholic fatty liver disease and hepatitis C virus infection through the development of systemic
and hepatic insulin resistance, partly mediated by the release of multiple pro-inflammatory cytokines,
diabetogenic hepatokines and reactive oxygen species. If left uncorrected, insulin resistance will
eventually lead to progressive pancreatic beta cell failure in predisposed individuals. Moreover, the
strong interconnection between type 2 diabetes and liver disease may result into a “vicious circle”
[25] eventually leading to liver disease progression with an excess risk of liver-related, i.e., cirrhosis
and hepatocellular carcinoma (HCC), and cardiovascular complications, i.e., atheroscler
6.
7. Review
Type 2 Diabetes in Non-Alcoholic Fatty Liver
Disease
and Hepatitis C Virus Infection—Liver: The
“Musketeer” in the Spotlight
Stefano Ballestri 1, Fabio Nascimbeni 2,3, Dante
Romagnoli 2, Enrica Baldelli 3,
Giovanni Targher 4 and Amedeo Lonardo 2,*
Received: 16 February 2016; Accepted: 2 March
2016; Published: 9 March 2016
13. Our understanding of the
pathogenesis, clinical spectrum and
epidemiology of GORD has
continuously evolved.
Historicaly
14. At first, reflux was synonymous with oesophagitis and
hiatus hernia.
Then, it was a motility disorder, defined by sphincter or
peristaltic dysfunction.
Next, it was an acid-peptic disorder.
Now, we see GORD emerging as a heterogeneous entity
encompassing elements of all these concepts
15. These developments
prompted the formation
of an international
consensus conference,
resulting in the
‘Montreal definition’ of GORD.
16.
17.
18.
19. Cowen, S. G. Therapeutic Categories Outlook (SG Cowen,2005)
20. While typical GERD symptoms are balanced between comparator groups, the distribution of
complications becomes progressively skewed in gender, geographic and racial distribution.
*GORD symptoms are similar between Western and Middle Eastern countries, but are lower in
Eastern countries.
Epidemiological trends in GORD-related disorders.
21. PATHOPHYSIOLOGY
The earlier belief that increased gastro
esophageal reflux mainly results from
one dominant mechanism has been
replaced by acceptance that GORD is
multifactorial
41. The intestinal microbiota lies strategically at the interface of the internal and external
environment of the gut.
It plays several important biological roles including: aiding in digestion and absorption of
nutrients from partially digested food, production of SCFA – a primary energy source for
intestinal epithelial cells (IECs), stimulating immune responses by releasing ligands, and
protection against enteropathogens by production of antimicrobial peptides (AMPs)
47. Is dysbiosis of the upper-GI tract to blame for
esophageal gastroesophageal reflux disease
(GERD) and it’s related conditions, Barrett’s
esophagus and adenocarcinoma?
48. Undoubtedly, we need to eradicate virulent H. pylori in
people with adverse clinical manifestations, but this
conclusion cannot be generalized to all H. pylori positive
subjects.
49. For the past four years we’ve known
that individuals with GERD have imbalances in
the microbial ecology of the distal esophagus.
One consequence of this microbial shift is increased
levels of Gram-negative bacteria, which harbor on
their cell surface an inflammatory membrane
component known as lipopolysaccharides (LPS)
or endotoxin
50. Clinical and Translational Gastroenterology (2015) 6, e91; doi:10.1038/ctg.2015.16; published online 18 June 2015
Type1-microbiota (Gram-positive predominant) with H. pylori provides a neutral esophageal
environment. Type-II microbiota (Gram-negative predominant) with loss of H. pylori invokes a
pro-inflammatory state in two ways. First, loss of H. pylori allow for increased acid secretion
resulting in gastroesophageal reflux disease and its sequelae. Second, predominance of Gram-
negative bacteria upregulate the pro-inflammatory cascade due to the
interaction between lipopolysaccharide and Toll-like receptor 4.
Gut microbiota & esophageal adenocarcinoma.
52. Probiotics, Prebiotics and Symbiotics
Probiotics are defined as live microorganisms which
confer health benefits to the host when taken in adequate
quantities.
Prebiotics are nondigestible food ingredients that beneficially
affect the host by selectively stimulating the growth
and/or activity of beneficial colonic bacteria.
Acombination of probiotics and prebiotics is termed symbiotics.
Various kinds of probiotics have been tested clinically as potential therapeutic
agents for both localized and systemic diseases.
57. It is a common belief that some foods may induce
or worsen GERD symptoms; in fact, in daily clinical
practice, this belief leads to advising patients to avoid
the suspect foods .
Further more, since GERD symptoms are most commonly
reported postprandially, the role of diet components in inducing
symptoms has been suggested.
However, different and conflicting results exist in the literature
for identifying the most “refluxogenic” foods
Festi etal.,World J Gastroenterol April 14, 2009
58. Dietary elements may ppt reflux episode via :
Increasing acid secretion e.g Coffee.
Decrease LOS pressure e.g peppermint & ess oils.
Slow gastric emptying e.g fatty food .
Impairing oesophageal motility e.g alcohol.
Triggering pain by irritating an already inflammed oesophageal
mucosa e.g Tomato, citrus, softdrinksandspicyfood.
59. Foods Not Recommended
It is recommended that a trial of limiting or eliminating the following foods may
reduce the symptoms of GERD:
• Peppermint and spearmint
• Chocolate
• Alcohol
• Caffeinated beverages (regular tea, coffee, colas, energy drinks, other caffeinated
soft drinks)
• Decaffeinated coffee and decaffeinated regular tea (herbal teas, except those with
peppermint or spearmint, are allowed)
• Pepper
• High-fat foods, including:
o 2% milk, whole milk, cream, high-fat cheeses, high-fat yogurt, chocolate milk,
cocoa
o Fried meats, bacon, sausage, pepperoni, salami, bologna, frankfurters/hot dogs
o Other fried foods (doughnuts, french toast, french fries, deep-fried vegetables)
o Nuts and nut butters
o Pastries and other high-fat desserts
o More than 8 teaspoons of oil, butter, shortening per day
• Any fruits or vegetables that cause symptoms. (These will vary from person to
person.)
American Dietetic Association.
60. Other Lifestyle Tips
• Exercise at least three or four times each week.
• Wear loose-fitting clothes.
• Do not smoke.
• Raise the head of your bed 6 to 9 inches. You can put a foam wedge
under the top part of the mattress, or prop up the legs on the head of the
bed with wooden blocks. (Stacking pillows is not effective.)
• Wait 3 hours after eating before lying down.
• Eat several small meals throughout the day.
• Eat in a calm, relaxed place. Sit down while you eat.
