Transcript Management

Introduction
• Diabetes causes a number of lethal complications affecting almost every
system of the body and hence the overall quality of life.
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The Gastrointestinal Tract (GIT) is no exception to diabetic complications;
it affects the digestive processes, motility as well as nervous control of the
entire system.
• Since the absorption and metabolism of glucose is mediated by GIT and
liver respectively, gastrointestinal (GI) complications commonly occur in
diabetes.
GASTROINTESTINAL COMPLICATIONS OF
DIABETES MELLITUS: AN OVERVIEW
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GI symptoms are more common in individuals with diabetes than nondiabetics.
It is seen that 76% of diabetics had at least one clinical manifestation of GI
complications.
Constipation was the most frequent amongst them (60% of cases). Also, upper GI
symptoms were more closely
associated with diabetes mellitus
Common GI symptoms among diabetics
PATHOPHYSIOLOGY
Gastrointestinal Complications of Diabetes
 Early identification and appropriate management of GI complications is important for
improving both diabetic care and quality of life of the patients.
 The common GI complications of diabetes have been discussed in the
subsequent sections.
GERD
LIVER
DISEASES
IBS
GASTROPARESIS
GIT
COMPLICATION
ALONG WITH
DIABETES
INCLUDE
FAECAL
INCONTINENCE
DIARRHOEA
CONSTIPATION
1. GASTRO-OESOPHAGEAL REFLUX DISEASE (GERD)
Epidemiology: Up to 50% of patients with diabetes have oesophageal abnormalities
that involve motility disturbance and/or acid reflux. A North Indian study revealed
that the prevalence of GERD was 16.2%, with diabetes as one of the co-morbidities.
Pathophysiology: Autonomic neuropathy and structural remodelling of the
oesophageal musculature in diabetes results in abnormal peristalsis, spontaneous
contractions and reduced lower oesophageal sphincter (LES) tone.
Clinical features of GERD in diabetes
 Heartburn and epigastric pain are known to be the most frequent GERD
associated symptoms, occurring in up to 90% of patients with proven type 2
diabetes mellitus (T2DM).
Diagnosis
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High resolution manometer and impedance manometer are newer modalities to
assess oesophageal motility
Upper GI endoscopy to detect hiatal hernia, oesophagitis
Barium oesophagogram
Oesophageal histology to detect oesophagitis, dysplasia, etc.
24-hour oesophageal pH monitoring
Endoscopy for the diagnosis of GERD
Prevention
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Glycemic control and weight management are the cornerstones for preventing
GERD in diabetes mellitus
Patient should be advised to:
– Raise the head end of the bed by 6–8 inches to avoid nighttime symptoms
– Refrain from lying down in recumbent position for 2–3 hours after the meals
– Abstain from smoking, drinking alcohol, soda and caffeine containing
beverages
– Avoid foods that reduce LES pressure like fatty foods, tea, coffee, etc.
Management
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H2 antagonists: Ranitidine, Famotidine, etc.
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Proton pump inhibitors: Pantoprazole, Rabeprazole, etc.
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Prokinetic drugs such as metoclopramide
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A 2-week course of erythromycin has been shown to reduce mean oesophageal
transit time and gastric emptying time in type 2 diabetics
2. DIABETIC GASTROPARESIS
• Gastroparesis is a motility disorder or an alteration of
neuromuscular function that may occur in association with diabetes
in the absence of any physical obstruction.
• Diabetic gastroparesis may occur in chronic diabetics, wherein there
is an evidence of end organ damage like nephropathy, retinopathy
and neuropathy.
Epidemiology:
• It affects up to 50% of patients with long standing diabetes mellitus.
• Delayed gastric emptying can be demonstrated in 27–65% of
patients with type 1 diabetes mellitus (T1DM) and about 30% of
patients with T2DM.
• The incidence of gastroparesis is higher
in women.
Pathogenesis
It is generally assumed that chronic hyperglycemia leads to neuropathic changes and
dysfunctional innervation of the stomach leading to delayed gastric emptying.
Clinical features
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Nausea
Vomiting
Early satiety
Postprandial fullness after few bites of food
Bloating
Upper abdominal pain
Palpitations and heartburn
About 53% of patients may experience weight loss, but 18–24% may experience
weight gain
Unexplained alternating hyper- and hypoglycemia due to a mismatch between
insulin action and carbohydrate absorption
Prolonged gastric distension increases propensity for transient relaxation of the
LES, thus exacerbating gastro-oesophageal reflux
Types of Gastroparesis
Diagnosis
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Detailed medical history
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Physical examination: Focus on abdominal and neurological examination
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Blood investigations
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Scintigraphy
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Plain X-ray abdomen
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Barium meal study
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GI endoscopy
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Tracer method of scintigraphy
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Ultrasonography
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Electrogastrography (EGG)
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Other modalities like magnetic resonance imaging (MRI)
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Computed tomography (CT)
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Impedance epigastrography
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Impedance tomography
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Real time ultrasonography
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Positron emission tomography (PET) can be used to document delayed gastric
emptying
Management
The therapeutic pyramid
Management
Dietary management:
• Patients should be advised to eat a diet low in fat content, and should be instructed to
consume frequent and small meals
• Preferentially consume a diet low in fiber
• Small particle size helps in accelerating gastric emptying. Hence, patients should be
instructed to chew their food adequately
• Food should be consumed in liquefied form. Taking fluids throughout the meal and
sitting upright or walking for 1–2 hours after meals may help the patient to accelerate
gastric emptying
• Low and high fermentable oligosaccharides, disaccharides, monosaccharides and
polyols (FODMAP) foods: A reduction of FODMAPs in a patient’s diet may improve
functional Gl symptoms
• Low FODMAP foods: To be eaten, High FODMAP foods: To be avoided
Pharmacotherapy
Pharmacotherapy Continued
Prevention:
• Keeping the blood glucose levels under control through compliance with diabetes
medications
• Lifestyle modifications like physical activities and dietary changes prevent damage
to the vagus nerve
• Maintenance of a normal body mass index (BMI)
3. CONSTIPATION
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Constipation is seen as a major GIT complaint in patients with diabetes than in
non-diabetics.
It affects up to 60% of patients with long-standing diabetes mellitus.
Hyperglycemia may directly inhibit intestinal transit in such patients.
Epidemiology:
• The prevalence of constipation is higher in women, and amongst those diabetic
patients who consume medications like calcium channel blockers, which cause
constipation.
Pathogenesis:
• Neuronal dysfunctions in large bowel along with impaired gastro colic reflex are
associated with constipation.
Clinical features
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Difficult, infrequent or seemingly incomplete defecation
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Straining at stools and hard stools
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Two or fewer bowel movements in a week
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Occasional massive amount of fecal material found in the large atonic and dilated
colon of diabetes patients
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It can infrequently lead to mega colon, pseudo-obstruction, perforation, etc.
Diagnosis
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Detailed history about bowel movements, straining at stools, duration, stool
consistency and associated bleeding, if any, should be obtained.
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Thorough physical examination with focus on abdominal examination and
auscultation for bowel sounds.
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Rule out other causes of constipation like hypothyroidism or medications .
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Constipation that does not respond to lifestyle changes or first-line medications
require further investigations.
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Anorectal inspection looks for skin excoriations, skin tags, anal fissures or
haemorrhoids.
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Digital rectal examination, aabdominal X-ray and barium enema, colonoscopy,
radio-opaque marker test
Prevention and Management
Management
• Laxatives: Sorbitol or lactulose can be used to treat constipation
• Osmotic laxatives and saline are reserved for severe cases
Prevention
• Patients should be enquired for medications like antidepressants
and calcium channel blockers, which can cause constipation and
advised to avoid the same
• Patients should be advised to:
– Consume large quantity of water i.e., around 2–3 liters per day. Warm
water early in morning can improve colonic motility
– Perform deep breath exercises and walking
– Have a diet high in fiber content like beans, cereals, vegetables and
fruits
– Set a particular time of defecation each day
4. DIARRHEA
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Intestinal and colonic motility disorders in both types of diabetes (1 and 2) can
lead to diarrhea.
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Diabetic diarrhea can be described as the presence of chronic diarrhea which is
usually brown, watery, profuse and might be associated with tenesmus.
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The diarrhea is long-lasting, typically episodic and consistent with hyperglycemia
and the presence of diabetic neuropathy.
Epidemiology
• Around 4–22% of people with diabetes suffer from diarrhea.
Diagnosis
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The diagnosis depends on a judicious clinical assessment accompanied by a
stepwise laboratory evaluation, which allows the differentiation of idiopathic
diabetic diarrhea from many other causes of diarrhea, that can occur in diabetes
and non-diabetes patients.
Pathophysiology
Clinical features
• Diarrhea associated with diabetes characteristically occurs at night following meals
and is watery
• Painless diarrhea is mainly associated with fecal incontinence
• Intermittent diarrhea can alternate with constipation
• Evidence of diabetic peripheral and autonomic neuropathy
Management
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The management chiefly relies on use of alpha-2 adrenergic agonist to stimulate
intestinal absorption of fluids and electrolytes
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Patients should be instructed to maintain strict glycaemic control and adequate
hydration
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Avoid medications like biguanides and alpha-glucosidase inhibitors
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Symptomatic measures like atropine, codeine sulphate and loperamide as
antimotility agents to relieve abdominal cramps
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Adrenergic agonists like clonidine that have antisecretory action Octreotide,
somatostatin based on their antisecretory and antimotility actions
Management (continued)
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Rifaximin, a GI selective antibiotic along with other antibiotics like amoxicillinclavulanic acid, doxycycline, ciprofloxacin, metronidazole, neomycin can be used to
eradicate the small intestinal bacterial overgrowth
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Clonidine 0.1–0.6 mg BD can reverse peripheral adrenergic resorptive
abnormalities, while octreotide 100–150 mcg is reserved for refractory cases
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If no specific cause of diarrhoea is identified, empiric therapy with simple
antidiarrhoeal agents (e.g., loperamide) is a reasonable starting point
Small intestinal bacterial overgrowth (SIBO)
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SIBO refers to bacterial overgrowth in the small intestine generally due to
intestinal stasis. It is seen in about 15% of patients with T2DM. Also, 44% of
patients with T1DM had autonomic neuropathy.
When to suspect SIBO?
• Predominant symptom is diarrhoea
• Marked milk intolerance
• Older age/ long duration diabetes
• Type 1 diabetics with autonomic neuropathy
• Marked abdominal bloating
• Marked flatulence
• Proton pump inhibitor therapy
• History of response to antibiotics/ probiotics
5. FAECAL INCONTINENCE
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Fecal incontinence is the inability to control bowel movements, causing stool to
leak unexpectedly from the rectum.
Epidemiology
• Reported in 20% of patients in a study on diabetic population
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Mainly affects the elderly patients
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The prevalence of fecal incontinence secondary to anorectal dysfunction has also
been reported to be increased in patients with diabetes
Pathogenesis
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Many factors like aberrant autonomic and enteric regulation of the internal anal
sphincter and rectal contraction are involved in the pathogenesis of faecal
incontinence
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Acute hyperglycemia also inhibits external anal sphincter function and decreases
rectal compliance
Clinical features
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It is characterised by normal or moderately increased stool volumes and anorectal
sensory and motor dysfunction
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It occurs more commonly at night
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Rectal prolapse can be demonstrated by asking the patient to attempt defaecation
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Anorectal examination reveals a reduced anal muscle tone and loss of anal wink
reflex (anus normally squeezes on stroking the skin around the anus)
Diagnosis
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Anorectal manometry
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Endoscopic examination of recto sigmoid region
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Rectal sensory testing
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Anal endosonography, MRI, defaecography Detailed neurological examination of
back and lower limbs
Management
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Strict glycaemic control
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Use of loperamide
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Laxatives for regular bowel movements
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Anal sphincter repair
6. IRRITABLE BOWEL SYNDROME (IBS)
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IBS is a functional bowel disorder characterized by abdominal pain or discomfort
and altered bowel habits in the absence of detectable structural abnormalities.
Epidemiology
• IBS is the most common reason for referral to gastroenterologists
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In South Asia and India, men are most commonly affected by IBS
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Data suggests that diabetics experience IBS symptoms significantly more
frequently than the general population
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Gut bacteria and metabolism are the common factors affected by IBS
Diagnosis
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History and physical examination
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Proctoscopy examination to rule out local anal fissures
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Routine stool examination is done for Amoebae and Giardia
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Sigmoidoscopy or colonoscopy is done in suspected cases
Clinical features
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Abdominal pain or discomfort localized in the periumbilical region or left
hypochondriac region
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Abdominal pain and other accompanying features like bloating are usually relieved
temporarily by defaecation
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In India, there is either constipation or diarrhea predominant pattern, which varies
regionally within the country
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Incomplete evacuation is a distressing symptom in constipation predominant form
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Stool consistency may vary from small-quantity semisolid or liquid with mucous in
those with diarrhea, to hard pellet-like with mucous in constipated subjects
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Abnormal psychological features have been reported in over 70% of patients
Management
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Reassurance and psychological support
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Restriction of milk and spicy food in those with diarrhea and restriction of milk,
legumes and cabbage in those with bloating
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Commercially available isabgol husk preparations can be taken with meals to
ensure an additional fiber intake of 15–20 g/day
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Tegaserod, a specific serotonin (5-HT4) agonist, can improve symptoms in patients
with IBS and constipation
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Patients with diarrhea benefit from loperamide and antispasmodics
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Selective chloride-channel activators lubiprostone; rifaximin, a GI selective
antibiotic and probiotics have proven to be beneficial in IBS
7. LIVER DISEASES
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The liver is a key organ involved in glucose metabolism and energy homeostasis. A
major amount of carbohydrates absorbed from the GIT undergo hepatic
processing and subsequent storage as glycogen or are metabolized into amino
acids or fatty acids.
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Hyperglycemia occurs owing to a combination of processes such as increased rate
of hepatic glucose output secondary to insulin resistance and diminished
peripheral uptake.
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There is a profound relationship between diabetes and liver disease.
Liver diseases occurring as a consequence of diabetes mellitus:
• Glycogen deposition, Steatosis and non-alcoholic steatohepatitis (NASH), Fibrosis
and cirrhosis, Biliary disease, cholelithiasis, cholecystitis, Complications of therapy
(cholestatic and necroinflammatory)
Diabetes mellitus and abnormalities of glucose homeostasis occurring as a
complication of liver disease:
• Hepatitis, Cirrhosis, Hepatocellular carcinoma
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Fulminant hepatic failure
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Post-orthotopic liver transplantation
Clinical features
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Glycogen deposition: Abdominal pain, nausea, vomiting and hepatomegaly, liver
enzyme abnormalities
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Fatty liver: Hepatomegaly, normal or only mildly abnormal transaminases and
normal bilirubin
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Cholelithiasis: Obesity and hyperlipidaemia are the confounding variables
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NAFLD: Most patients with non-cirrhotic NAFLD are initially asymptomatic, and are
diagnosed due to an incidental detection of raised liver enzymes or fatty liver on
ultrasonography.
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Presence of diabetes, elevated BMI and liver fibrosis were identified as risk factors
for progression to hepatocellular carcinoma (HCC) among NAFLD casesHCC:
Weight loss, jaundice, abdominal pain and deranged liver enzymes.
Management
• All pharmacological therapies should be supplemented with lifestyle modification
and weight reduction especially for NAFLD
• Insulin sensitising agents like metformin and pioglitazone; vitamin E; glucagon-like
peptide-1 (GLP1) analogues like liraglutide; omega-3 fatty acids; antiobesity drugs
like orlistat are the pharmacological options for management of NAFLD.
• Insulin management for diabetic control can benefit patients of glycogenic
hepatopathy within 4 weeks
• Glycaemic control, weight reduction and ursodeoxycholic acid are the therapeutic
options for fatty liver
Prevention
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Weight management is the single key aspect for preventing NAFLD
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Patients should be given a target for sustained weight loss of 7–10% of body weight
with a combination of a balanced, calorie-restricted diet.
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Lifestyle modification inclusive of exercise and alcohol cessation
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Improvement in glycaemic control
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Proper patient evaluation, counselling to prevent the development of hypertension