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  1. 1. ‫ ‬ ‫ ‬ ‫ ‬ ‫ ‬ ‫نيرفعد اللد الذنيند آمناواد من وُمد توالذنيند أتوتاواد ال ْلِل د َ (‬ ‫د َ َمْ د َ ْلِ َّ َّ ْلِ د َ د َ وُ ْلِ َمْك َمْ د َ َّ ْلِ د َ وُ وُ َمْع َمْمد ‬ ‫وُ‬ ‫درج اتد تواللد بم اد تع د َلاوند خبرير(‬ ‫د َ د َ د َ ٍ د َ َّ ْلِ د َ د َ َمْموُ د َ د َ ْلِ (ٌ‬ ‫وُ‬ ‫ ‬ ‫         )المجادلة: من الةية11(‬ ‫     صدق ال العظيم‬ ‫د ‬
  3. 3. The ‫د‬aim ‫د‬of ‫د‬this ‫د‬lecture ‫د‬is ‫د‬to ‫د‬study ‫د‬the ‫د‬ role ‫د‬of ‫د‬dietary ‫د‬habits ‫د د‬nutrient ‫د‬intake ‫د‬ in ‫د‬NASH ‫د د‬Chronic ‫د‬liver ‫د‬disease.
  4. 4. Definition • NASH ‫د‬is ‫د‬accumulation ‫د‬of ‫د‬lipid ‫د‬in ‫د‬the ‫د‬liver ‫د‬primarily ‫د‬in ‫د‬ the ‫د‬form ‫د‬of ‫د‬triglycerol ‫د‬in ‫د‬individual ‫د‬who ‫د‬don't ‫د‬consume ‫د‬ significant ‫د‬amount ‫د‬of ‫د‬alcohol ‫د 02د‬gm ‫د‬ethanol ‫د /د‬day ‫د‬ • ‫د‬NAFLD ‫د‬is ‫د‬recognized ‫د‬as ‫د‬the ‫د‬most ‫د‬common ‫د‬cause ‫د‬of ‫د‬ chronic ‫د‬liver ‫د‬disease ‫د‬world ‫د‬wide. ‫د د‬ • NAFLD ‫د‬refer ‫د‬to ‫د‬wide ‫د‬spectrum ‫د‬of ‫د‬clinicopathologic ‫د‬liver ‫د‬ disease ‫د‬ranging ‫د‬from ‫د‬relatively ‫د‬benign ‫د‬form ‫(د‬fatty ‫د‬liver) ‫د‬ to ‫د‬more ‫د‬severe ‫د‬form ‫د‬known ‫د‬as ‫د‬NASH. • ‫د‬NASH ‫د‬is ‫د‬a ‫د‬progressive ‫د‬form ‫د‬of ‫د‬liver ‫د‬injury ‫د‬that ‫د‬carry ‫د‬ risk ‫د‬for ‫د‬progressive ‫د‬fibrosis, ‫د‬cirrhosis, ‫د‬hepatocellular ‫د‬ carcinoma ‫د‬and ‫د‬liver ‫د‬failure. ‫د‬It ‫د‬may ‫د‬be ‫1د‬ry ‫د‬cause ‫د‬of ‫د‬up ‫د‬ to ‫د %51د‬of ‫د‬cryptogenic ‫د‬carcinoma. ‫د‬It ‫د‬represents ‫د‬the ‫د‬ hepatic ‫د‬manifestation ‫د‬of ‫د‬metabolic ‫د‬syndrome ‫د‬
  5. 5. History of NASH In ‫د ,0891د‬Ludwig ‫د‬et al. described a series of patients who ‫د‬lacked ‫د‬a ‫د‬history ‫د‬of ‫‘د‬significant’ ‫د‬alcohol ‫د‬intake ‫د‬ but ‫د‬in ‫د‬whom ‫د‬the ‫د‬liver ‫د‬histology ‫د‬resembled ‫د‬that ‫د‬of ‫د‬ alcoholic ‫د‬liver ‫د‬disease. ‫د‬They ‫د‬were ‫د‬the ‫د‬first ‫د د‬to ‫د‬use ‫د‬ the ‫د‬term ‫‘د‬nonalcoholic ‫د‬steatohepatitis’ ‫د‬for ‫د‬this ‫د‬ condition, ‫د‬the ‫د‬principal ‫د‬features ‫د‬of ‫د‬which ‫د‬were ‫د‬ hepatic ‫د‬steatosis ‫(د‬fatty ‫د‬change), ‫د‬inflammation ‫د‬and ‫د‬ exclusion ‫د‬of ‫د‬alcohol ‫د‬as ‫د‬an ‫د‬aetiological ‫د‬factor. ‫د‬Further ‫د‬small ‫د‬case ‫د‬series ‫د‬were ‫د‬published ‫د‬during ‫د‬ the ‫د‬next ‫د 51د‬years
  6. 6. • 1950 ‫د د‬Cirrhosis ‫د‬noted ‫د‬in ‫د‬diabetics • 1970 ‫د د‬Jejuno-ileal ‫د‬bypass ‫د‬liver ‫د‬disease ‫د‬resembles ‫د‬ alcoholic ‫د‬hepatitis • 1979/80 ‫د د‬Ludwig ‫د‬et al. Coined term NASH for steatohepatitis in non-drinkers ‫د 8~د‬papers/year ‫,د‬Small ‫د‬ series • 1990 ‫د‬Powell ‫د‬et al. ‫د‬NASH ‫د‬is ‫د‬benign ‫.د‬ • 1994 ‫د‬Bacon ‫د‬et al. 1994 ‫د‬Expanded ‫د‬scope ‫د‬of ‫د‬NASH ‫.د‬ • 1996 ‫د د‬CYP2E1 ‫د‬induced ‫د‬in ‫د‬rodent ‫د‬dietary ‫د‬model ‫د د د د د د د د د د د د‬ ‫د د د د د د د د د د د د د د د د د د د د د د د د د د د د د د د د د د د د د د د د د د د د د د د د د د د د د د د د د د د د د‬andEndotoxin ‫د‬ induces ‫د‬inflammation ‫د‬in ‫د‬steatotic ‫د‬liver • 1998 ‫د د‬CYP2E1 ‫د‬induced ‫د‬in ‫د‬human ‫د‬NASH,First ‫د‬NIH ‫د‬ conference ‫د‬on ‫د‬NASH, ‫د‬Pivotal ‫د‬importance ‫د‬of ‫د‬insulin ‫د‬ resistance
  7. 7. • • • • • • • 1999 ‫د د‬Several ‫د‬animal ‫د‬models First ‫د‬clinical ‫د‬trials 2002 ‫د 06~د د‬papers/year AASLD ‫د‬single ‫د‬topic ‫د‬conference First ‫د‬European ‫د‬and ‫د‬Japanese ‫د‬single ‫د‬topic ‫د‬conferences NASH ‫د‬established ‫د‬as ‫د‬part ‫د‬of ‫د‬insulin ‫د‬resistance ‫د‬syndrome 2004 ‫د‬Release ‫د‬of ‫د‬first ‫د‬book ‫د‬on ‫د‬NAFLD/NASH
  8. 8. Reasons why NAFLD/ NASH is important. • Possible ‫د‬role ‫د‬of ‫د‬NASH/hepatic ‫د‬steatosis ‫د‬in ‫د‬ hepatocarcinogenesis • Most ‫د‬common ‫د‬cause ‫د‬of ‫د‬abnormal ‫د‬liver ‫د‬tests ‫د‬in ‫د‬ community ‫د %8–2د‬of ‫د‬population ‫د‬have ‫د‬NAFLD – NASH ‫د‬now ‫د‬rivals ‫د‬alcoholic ‫د‬liver ‫د‬disease ‫د‬and ‫د‬chronic ‫د‬ hepatitis ‫د‬C ‫د‬as ‫د‬reason ‫د‬for ‫د‬referral ‫د‬to ‫د‬gastroenterologist ‫د‬or ‫د‬ liver ‫د‬clinic • NASH ‫د‬is ‫د‬a ‫د‬potential ‫د‬cause ‫د‬of ‫د‬cirrhosis, ‫د‬which ‫د‬may ‫د‬ be ‫‘د‬cryptogenic’, ‫د‬and ‫د‬lead ‫د‬to ‫د‬end-stage ‫د‬liver ‫د‬ disease • High ‫د‬prevalence ‫د‬of ‫د‬fatty ‫د‬liver ‫د‬disorders ‫د‬in ‫د‬ urbanized ‫د‬communities ‫د‬with ‫د‬affluent ‫‘(د‬Western’) ‫د‬ economies ‫د‬throughout ‫د‬the ‫د‬world
  9. 9. cont. • Liver ‫د‬failure ‫د‬is ‫د‬most ‫د‬common ‫د‬cause ‫د‬of ‫د‬death ‫د‬in ‫د‬ patients ‫د‬with ‫د‬cirrhosis ‫د‬resulting ‫د‬from ‫د‬NASH • Standardized ‫د‬mortality ‫د‬of ‫د‬liver ‫د‬disease ‫د‬in ‫د‬type ‫د 2د‬ diabetes ‫د‬greatly ‫د‬exceeds ‫د‬vascular ‫د‬disease • NASH ‫د‬recurs ‫د‬after ‫د‬liver ‫د‬transplantation • Hepatic ‫د‬steatosis ‫د‬as ‫د‬a ‫د‬cause ‫د‬of ‫د‬primary ‫د‬graft ‫د‬nonfunction ‫د‬after ‫د‬liver ‫د‬transplantation • Role ‫د‬of ‫د‬metabolic ‫د‬determinants ‫د‬of ‫د‬NASH ‫د‬in ‫د‬ pathogenesis ‫د‬of ‫د‬other ‫د‬liver ‫د‬diseases, ‫د‬particularly • hepatitis ‫د‬C ‫د‬and ‫د‬alcoholic ‫د‬cirrhosis
  10. 10. Causes of fatty liver in children are divided into • Hepatic ‫د‬causes. ‫د‬ • Non-hepatic ‫د‬causes. ‫د‬ • I- Hepatic causes:  – Over ‫د‬weight ‫د‬and ‫د‬obesity ‫د‬related. ‫د‬ – Metabolic ‫د‬liver ‫د‬disease ‫(د‬Wilson ‫د‬disease, ‫د‬glactosaemia, ‫د‬ hereditary ‫د‬fructose ‫د‬intolerance ‫د‬and ‫د‬glycogen ‫د‬storage ‫د‬ disease). ‫د‬ – Syndromes ‫(د‬schwachman-diamond ‫د‬syndromes, ‫د‬alastram ‫د‬ syndrome ‫د‬lipodystrophy ‫د‬syndrome ‫د‬and ‫د‬turner ‫د‬syndrome). ‫د‬ – Chronic ‫د‬hepatitis ‫د‬C. ‫د‬ – Autoimmune ‫د‬hepatitis. ‫د د‬ • II- Non-hepatic causes. 
  11. 11. • • • • • • • • • • • A) Nutritional: Protein ‫د‬caloric ‫د‬malnutrition. ‫د‬ Total ‫د‬parentral ‫د‬nutrition. ‫د‬ Starvation. ‫د‬ Intestinal ‫د‬bypass ‫د‬surgery. ‫د‬ Rapid ‫د‬weight ‫د‬loss. ‫د‬ Celiac ‫د‬disease B) Drugs: Glucocorticoid. ‫د‬ Hypervitaminosis ‫د‬A. ‫د‬ Toxins ‫(د‬mashrooms- ‫د‬Aminatta ‫د‬phalloid). ‫د‬
  12. 12. Risk Factors for NASH • Type ‫د 2د‬Diabetes ‫د د‬ • Hypertriglyceridemia • Obesity ‫د‬
  13. 13. The pathogenesis of NAFLD NASH • The ‫د‬pathogenesis ‫د‬of ‫د‬NAFLD ‫د د‬NASH ‫د‬ remain ‫د‬poorly ‫د‬defined. ‫د‬Current ‫د‬concept ‫د‬ suggest ‫د‬the ‫د‬development ‫د‬of ‫د‬NASH ‫د‬is ‫د‬a ‫د‬ Two ‫د‬hit ‫د‬process ‫د‬ * First hit. • Involve accumulation of Fat in hepatocytes.  * Second hit. • Oxidative ‫د‬stress ‫د‬is ‫د‬thought ‫د‬to ‫د‬be ‫د‬a ‫د‬key ‫د‬role ‫د‬ in ‫د‬the ‫د 2د‬nd ‫د‬hit ‫د‬
  14. 14. Diagnosis of NASH * Clinical diagnosis: • Clinical experience with pediatric NASH is limited, while there are no characteristic symptoms. • Children may complain of abdominal pain although they are often asymptomatic • Hepatomegaly can often detected on examination, however this physical finding may be missed in clinical practice. • Acanthosis nigricans, a black pigmentation found in skin fold and axilla associated with hyperinsulinaemia • Malaise or tiredness, history of drug ingestion may be elicited at time of presentation.
  15. 15. Pointers to NAFLD/ NASH in clinical practice • Unexplained elevation of ALT and GGT, typically minor, in a person with metabolic risk factors • ‘Rubbery’ hepatomegaly • Recent weight gain and expanding waistline • Lifestyle or medication changes favouring weight gain • Family history of type 2 diabetes, NAFLD, vascular disorders or hyperlipidaemia
  16. 16. cont. • Raised serum ferritin not attributable to iron storage disorder or alcohol • Abnormalities of hepatic imagingadiffuse echogenicity on ultrasonogram (‘bright liver’), radiolucency on CT • Patient with chronic HCV infection and diabetes and/or obesity, ‘rubbery’ hepatomegaly or steatosis with HCV genotype 1 infections • Patient with chronic HBV infection, raised ALT but nondetectable HBV DNA in presence of metabolic risk factors • ALT, alanine aminotransferase; CT, computerized tomography; GGT, gamma-glutamyl transpeptidase; HBV DNA, hepatitis B
  17. 17. • Imaging studies. – – – – – U/S. CT. MRI MRS Fibroscan (Transient elastography). • Non invasive biomarkers: – – – – – Liver enzyme. NASH fibro SURE. New generation of biomarker as FT, ST and NT. Breath test. Auto immune marker.
  18. 18. C.T of fatty liver
  19. 19. MRI
  20. 20. Liver enzymes: • Serum ALT was found to be reliable as screening tool for fatty liver. – Aminotramsferase: the ratio of AST/ALT is usually 1 – in NASH often 2 – Alkaline phosphatase: increase or may be normal. • GGT can be mildely elevated
  21. 21. NASH FibroSURE • NASH fibrosure is non invasive assessment of liver status for patient with NAFLD. • Quantitative results of to biochemical including. • α 2Macroglobulin. • Haptoglobulin. • Apolipoprotein A. • Bilirubin.
  22. 22. cont. • • • • • • • γ glutamyl transpeptides (GGT). Alanine aminotransferase (ALT). Asparatate aminotransferase (AST) Totoal cholesterol. Triglyceride. Fasting glucose. NASH fibro SURE should only be used for patient with suspected NAFLD, it is not recommended for patient with other liver disease.
  23. 23. Steatosis marker • Steatosis marker: has been studied in a variability of patient types including hepatitis C, alcoholic liver disease and NAFLD. Provide quantitative marker for hepatic steatosis grade • steatosis score 0.5 had sensitivity of 71% and specificity of 72% for identification of significant steatosis
  24. 24. • Biomarker to predict steatosis (Steatotest) fibrosis (fibrotest) among patient – NAFD, the diagnostic accuracy of all biomarker used to identify liver fibrosis seldom exceed 75-80%. These serum markers not available in all lab., may be expensive can't substitute liver biopsy
  25. 25. Breath test • Both microsomal and mitochondrial function are disturbed in NASH, • MBT for liver microsomal function • KBT for liver mitochondrial function. Liver breath test predirect higher state of NASH
  26. 26. Autoimmune Ab: (Auto immune marker). • In a pediatric study, seven of 14 children with NAFLD were found to be +ve for ANA or SMA in six and GPC in one, 4 of 6 children were be +ve for Ab.
  27. 27. Several NASH-specific biomarkers • Several NASH-specific biomarkers have recently been developed. The CK-18, a biomarker of apoptosis, was developed and tested in patients with NAFLD. Another non-invasive biomarker (NASH Diagnostics) is a simple panel that includes Cleaved CK-18, a product of the subtraction of Cleaved CK-18 level from intact CK-18, serum adiponectin
  28. 28. Liver Biopsy Liver biopsy is considered to be the gold standard for diagnosis of NASH
  29. 29. Category Pathology Clinicopathological correlation Type 1 Simple steatosis Known to be nonprogressive type2 Steatosis plus lobular inflammation Probably benign (not regarded as NASH Type3, Steatosis, lobular inflammation and ballooning degeneration NASH without fibrosis may progress to cirrhosis Type 4 Steatosis, ballooning degeneration and Mallory bodies, NASH with fibrosis may progress to cirrhosis and liver failure
  30. 30. —Natural history of nonalcoholic fatty liver disease. Small proportion of patients with fatty liver develop nonalcoholic steatohepatitis. Less than 10% of nonalcoholic steatohepatitis patients develop cirrhosis. Current research is aimed at detecting early stages of fibrosis that are potentially reversible. aProbable percentage of patients with hepatic steatosis progressing to nonalcoholic steatohepatitis. bDisease progression (%) of all nonalcoholic steatohepatitis patients.
  31. 31. Differential diagnosis of NASH In contrast to adults, with whom the major differential diagnosis is with alcoholic liver disease. In children the main considerations are metabolic or inflammatory disease that cause fatty liver in children. • Relatively common:– – – – – – Cystic fibrosis. Wilson disease. Hereditary fructose intolerance. Galactosaemia. Glycogen storage disease. Familial hyperlipidaemia.
  32. 32. Differential diagnosis of NASH • Less common: – – – – – – – – – Lipid storage disease. Cholesterol ester storage disease. Sialidosis. Hereditary tryrosinaemia type 1. A beta or hypo beta lipoprotienaemia. Tangier disease. argininaemia. Weber ehristian disease. Porphyria cutanea tarda .
  33. 33. Diseases Associated with NASH Established condition Emerging condition Obesity Obstructive steep apnea Type 2-diabetes/glucose intolerance Hypothyroidism Dyslipidaemia Polycystic ovary Metabolic Hypopitutrism.
  34. 34. Treatment of NASH in children The current best treatment of any form of NAFLD in children is life style modification in contrast to adult NAFLD. This is not centered around weight reduction programs, but directed towards increased physical activity promotion of healthy balanced diet to support normal growth and development. The success of this approach is variable and additional drug intervention might be needed.
  35. 35. Therapeutic option available for patient with NAFLD • • • • • • • • • • • Change in habit: diet physical exercise. Drugs that improve insulin sensitivity. Antioxidant. Lipid lowering agent. Usodeoxycolid acid. Antibiotics: lactobacillus prevent gut derived endotoxaemia. Anti TNF antibodies, TNF- receptor antagonist. Nutritional supplementation: Carnitine, choline. Therapeutic phelobotomies. Liver transplantation The main goal therapy for NAFLD should be to prevent progression of NAFLD to cirrhosis, un fortunately although a variety of treatment modalities have been proposed, none has proven efficacy in changing this end point
  36. 36. Role of nutrition in treatment of NASH • Nutritional recommendation for NASH focus on the underlying disease (Metabolic syndrome other secondary causes) • Diet composition: Dietary composition has an important consideration. There is some evidence that carbohydrate loading may be problematic, thus the food with high amount of corn syrup, product of high sugar content, high starch food may be particularly dangerous. It may not be just the total calorie intake that lead to NASH, but the types of calorie.
  37. 37. • Polyunsaturated fatty acid especially formulation rich in omega-3 are widely accepted in medical community for their beneficial affect on hyperlipidaemia • Recent studies ameliorate hepatic steatosis in human animal models of NASH by reducing hepatic fat content. One year course of omega-3 fatty acid (3gm/day) will produce improvement in NASH histological injury
  38. 38. Fiber in diet - • Children require help with appetite control. Food make individual feel full without delivering high amount of calories, in this regard fruits vegetables come to forfront of good selection. The most satisfying component of vegetable is dietary fiber in particular soluble fiber. • The most interesting of all soluble fiber is delivered from oats. Oat contain unique type of fiber hydrocolloid or oat-beta glycan it is proposed as fat substitute in foods
  39. 39. Cont. • This soluble fiber has an ability to smooth out blood sugar concentration following meals. This is called second meal effect of low glycaemic index food. • So soluble fiber is valuable in ↓ weight, ↓ IR control blood sugar • High fiber diet may tend to ↓ cholesterol
  40. 40. • Diet will therefore need to be tailored to individual needs. The inclusion of n-3 fatty acid, high MUFA foods, fruits, vegetables, low GI, high fiber foods reduced intake of saturated fat, simple carbohydrate sweetened drink may be universally recommended to NAFLD patient
  41. 41. Drug therapy of NASH • Although diet and exercise is the mainstay of treatment, medication might be warranted if an appropriate diet and regular physical activity don't improve biochemical markers and liver morphology
  42. 42. • Most attention of pediatric NAFLD is given to either vitamin E as antioxidant or to anti diabetic drugs, Metformin as an agent that counter IR • Antioxidant: the use of antioxidants for the treatment of NAFLD to protect cellular structures against damage from oxygen free radicals and from reactive products of lipid peroxidation
  43. 43. Antioxidant against oxidative stress • Metadoxine • Natural antioxidants (vitamin E, ubiquinone) • Synthetic antioxidants (including dihydroquinoline-type – only used experimentally) • Ursodeoxycholic acid • Lecithin • Selenium • Betaine • Silymarin
  44. 44. vitamin E • Oral vitamin E 400-1200 IU daily improves hepatic enzymes in patients with NAFLD • It might improve NASH by modulating cytokines and inhibiting the expression of intrahepatic TGF-ß, which is involved in fibrogenesis.
  45. 45. Lipid Lowering Drugs • As hypertriglyceridaemia and low HDL cholesterol levels are a manifestation of insulin resistance and common among subjects with NAFLD, several investigators have used lipid lowering drugs to treat NAFLD The use of statin drugs is currently contraindicated in the presence of active liver disease or persistent unexplained increases of aminotransaminases
  46. 46. Drug that protect hepatocyte • Several drugs believed to be hepatoprotective have been used in patient with NASH .these include UDCA, betain, vitamin E, lecithin, βcarotin ,and selenium and taurine
  47. 47. Nutritional supplementation • Dietary supplement of antioxidant as vitamin E ,selenium and restriction of iron intake may be beneficial for prevention of advanced disease, further regulation of bacterial flora in the gut using probiotic is promising for prevention and treatment of NASH.
  48. 48. Milk Thistle • Silymarin this is the active ingredient in the • • • • • milk thistle herb. It has a history of improving liver health. Many studies have shown that milk thistle might: Increase the speed of liver cell regeneration Restrain liver fibrosis Protect the liver from injury Decrease cholesterol absorption It is believed that it increase production of anti oxidant enzyme that help liver breakdown toxin,
  49. 49. Selenium • Selenium is a powerful anti oxidant that works synergistically to asses protection against further damage in liver injury. Selenium is a mineral that functions as a component of glutathione peroxidase, an essential antioxidant system. It is involved in metabolism of vitamin E. • Recommended daily intake in childhood (110 years): 40-50µg. • Selenium dietary source: Organ meat,fish,mashroom and selfish are generally selenium-rich.
  50. 50. Zinc • Many studies reported that zinc protected induced liver injury,not only reduction of oxidative stress in hepatocyte ,but also by prevention of intestinal permeability Recommended intake in children: 10mg • Zinc dietary source: zinc is found abundantly in shelfish,red meat,legumes and nuts
  51. 51. Prognosis and Prevention • Prognosis of NASH :Prognosis is dependant not only on the severity of the disease and number of risk factors, but also on the degree of histological damage. The presence of NASH Vs NAFLD and the stage of fibrosis provide a gradient for prognosis
  52. 52. Can NAFLD /NASH be prevented or reversed? • Because liver failure doesn't occur in NAFLD/ NASH unless cirrhosis has developed, reducing or reversing fibrotic progression must be of ultimate objective of treatment. • There is now compelling evidence that type 2 diabetes can be prevented or at least delayed in onset by life style intervention. NASH, a consequence of IR should also be prevented by change in diet physical activity
  53. 53. Summary • Summary: • Nonalcoholic fatty liver disease (NAFLD), a condition associated with obesity and diabetes, is increasingly being recognized in the western population. • Simple fatty liver is the most common form of NAFLD and seems to be a benign condition. In contrast, nonalcoholic steatohepatitis may progress to advanced fibrosis and cirrhosis.
  54. 54. • The diagnosis is often made after incidentally finding elevated liver enzyme levels or by clinical suspicion in patients with obesity or diabetes. Laboratory results or imaging examinations may confirm the diagnosis. However, at present, only a liver biopsy can differentiate simple steatosis from NASH. • There is no clear consensus on the effectiveness of the pharmacologic treatment of NAFLD. Several therapies, including insulin-sensitizing, antioxidant agents, and hepatoprotective medications, have been studied. Lifestyle modifications, particularly weight loss, have been shown to be particularly beneficial.
  55. 55. Conclusions • NAFLD affects a substantial portion of the general population and is associated with the metabolic syndrome, which includes obesity, insulin resistance, hyperlipidemia, and hypertension. Patients with NAFLD not only suffer from the metabolic sequlae of insulin resistance but have increased overall mortality.
  56. 56. • Although simple fatty liver seems to be a benign condition, some patients may progress to NASH and ultimately to cirrhosis. Because of the consequences of the disease, we emphasize the importance of the detection of NAFLD in high-risk groups, including obese patients, as well as those with evidence of insulin resistance or other components of the metabolic syndrome
  57. 57. • Screening and surveillance methods should be applied more uniformly from center to center, and reliable non invasive techniques are needed for the diagnosis of NAFLD and the detection of progressive liver disease. The diagnosis of NAFLD should prompt management of the metabolic risk factors.
  58. 58. • . Weight loss regimens are believed to be helpful, and numerous drugs have been investigated in small studies. Large, randomized, clinical trials are necessary to determine the real benefit of these agents. Finally, studies on the pathogenesis of NAFLD may not only improve our understanding of the mechanisms involved in NAFLD progression, but may lead to potentially novel therapeutic strategies to treat this condition.
  59. 59. Recommendation • We should screen all children at risk for development of NASH (obese diabetic children) by U/S laboratory investigation. • We should encourage our children to avoid unhealthy food which lead to obesity. • Encourage mother for exclusive breast feeding at 1st 6 month of life which proved to prevent obesity at childhood period adolescence.
  60. 60. Thank you