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home - Liver - Metabolic Conditions - NAFLD Written by Dr Sebastian Zeki

Recognises and appropriately investigates patients with auto-immune
liver diseases

Aware of management and complications of autoimmune liver
disease including extra-hepatic manifestations and associations
including malignant complications in PSC

Appreciates and understands that this range of liver disease is
frequently under-diagnosed and may have been inappropriately

Selects appropriate immunomodulatory therapy has awareness of
side effects and may well require specialist care

Responds urgently to the management challenge of these severe and
often acute diseases and involves more specialist services where
Maintains diagnostic vigilance as uncommon metabolic liver diseases
may go unrecognised and so retains awareness of them as
diagnostic possibilities

Recognises the potential need to screen relatives and keeps up to
date with contemporary developments of screening protocols

Liaises with clinical genetic unit where appropriate

Manages patients with steatohepatitis clearly and always


Stage IStage IIStage IIIStage IV (cirrhosis)67% 3 years survival(Death from co-morbidities mainly) Necro-inflammatoryGrade IGrade IIGrade III Types:Fatty liver alone (occurs in 37%).Fat accumulation with lobular inflammation (occurs in 7.5%).Fat accumulation with balloon in degeneration (occurs in 14%).Fat accumulation with balloon in degeneration and Mallory's high line or fibrosis (occurs in 41%). Prognostic factors in developing cirrhosis:Age.Obesity.Type II diabetes.Raised lipids.Female (?).AST to ALT ratio >1.Raised transferrin saturations. Biochemical features:AST/ALT <1 = NAFLD (>2 = ETOH).Bilirubin - normal, ALP - slightly raised.Some increased ANA/increased gammaglobulin.Raised lipids.Raised ferritin. Associations:Primary NAFLD.-Obesity.-NIDDM.-Raised lipids.-Metabolic syndrome.Secondary NAFLD.-PCOS.-short bowel syndrome.-TPN. Steatosis with no inflammation60% (of whole population) Cirrhosis NASH (steatosis with inflammation = steatohepatitis) -Jejuno-ileal and gastric bypass-Bacterial overgrowth-Hypertension (CFOBEN et al)Drug causes-Amiodarone-Gluco-corticoids-Diltiazem-Nifedipine-Tamoxifen and oestrogensGenetics (?undiscovered) Weight reduction should be gradual.Can lead to improved liver enzymesImprovement in steatosis (but not inflammation and fibrosis) 1yr following bariatric surgeryOrlistat-GI lipase inhibitor for obesity and T2DM.Pentoxifylline : Inhibits production of TNF alfa, which may contribute to NASH progression.Losartan: Angiotensin II is involved in the pathogenesis of hepatic fibrosis and enhances iron deposition and insulin resistance.Vitamin E and C Ursodeoxycholic acid: Pilot studies suggest potential benefit of ursodeoxycholic acid (UDCA)MetforminPioglitazone/ RosiglitazoneBetaine: Normal component of the metabolic cycle of methionine, which has a protective effect against steatosis in animal models. Pilot studies suggest benefit Probucol : Lipid lowering agent with antioxidant properties. NASH Treatment Hyperinsulinaemia Pathogenesis DefinitionThere should be no history of EtOH.Patients should be negative for hepatitis B and C. Primary non-alcoholic fatty liver disease Cause fibrosis Cytokine productionFas ligand induction Reactive oxygen species Lipid peroxidation Fatty acid Induce cytochrome P-450 2E1 and 4A Fatty acids accumulate in cell Mitochondrial overload Clinical features:Fat.Diabetic women.Some have RUQ pain.Some have hepatomegaly. Fibrosis Written by Dr Sebastian Zeki

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