Hepatology Guidelines for Primary Care November 2011

Size: px
Start display at page:

Download "Hepatology Guidelines for Primary Care November 2011"

Transcription

1 Common requests for hepatology opinion/advice 1. Abnormal LFTs (is this fatty liver?) 2. Fatty Liver Disease (is this serious liver disease?) 3. Abnormal liver ultrasound 4. Alcohol related liver disease 5. Raised ferritin 6. Incidental positive auto-immune serology 7. Chronic hepatitis B 8. Hepatitis C positive serology 9. Gall bladder polyps 10. Fast track referrals/advice/urgent clinic appointments (includes jaundice) 11. Haemochromatosis guidelines 12. Staff and contacts

2 1. Abnormal LFTs Commonest reason for abnormal LFTS is Non Alcoholic Fatty Liver Disease (NAFLD) ALT ALP GGT Suggests Action <100 normal NAFLD Follow algorithm >150 normal liver disease See map of medicine normal Biliary or intra-hepatic Arrange ultrasound focal disease normal normal Bone/joint disease or acute phase response Refer hepatology Consider checking CRP, Ca, Vitamin D, PSA etc. Map of medicine-management of abnormal LFT.-algorithms for isolated and combined abnormalities Includes Isolated hyperbilrubinaemia Isolated raised ALP Isolated raised GGT Isolated increase in transaminases Simultaneous abnormalities Causes of raised ALT Hepatic Hepatitis B Hepatitis C Haemochromatosis Auto immune chronic hepatitis Wilsons (if <50 or > 50 and neurological symptoms) α-1 antitrypsin Non-hepatic consider if not obese/no features of metabolic syndrome) Thyroid dysfunction Coeliac disease Drugs Tests HBsAg HCV antibody ferritin, transferrin saturation Immunoglobulins, ANA, SMA, AMA, anti-lkm1 Serum copper, caeruloplasmin TFT Anti-gliadin, anti-endomysial List on CATCH website

3 2. Fatty Liver Disease (Non Alcoholic Fatty Liver Disease NAFLD)

4 NAFLD Summary Fatty infiltration of liver No simple diagnostic test (histological diagnosis) Screen for other causes of raised ALT If results do not suggest other cause, consider NAFLD NAFLD has two major subsections a. Non Alcoholic Steatohepatitis (NASH) HIGH RISK FOR LIVER DISEASE/CIRRHOSIS inflammatory infiltration b. Hepatic steatosis LOW RISK non-inflammatory Risk factors for NASH type 2 DM Obesity Age >45 Metabolic Syndrome, hepatosplenomegaly, liver signs Pituitary/hypothalamic disease Primary Care Management Dietary changes (low saturated fat, low fructose) and treatment for metabolic syndrome features including, weight loss (not crash diet) and increased exercise. Medications to consider Hypertension-ACE inhibitors or ARA2A Dyslipidaemia-Statins (or fibrate for predominant hypertriglyceridaemia Diabetes-pioglitazone (some evidence for improving insulin resistance and removing fat from liver) Raised GGT or ALT predictor of diabetes Metabolic Syndrome NAFLD is best considered as the hepatic manifestation of the metabolic syndrome. Metabolic Syndrome-clustering of CVD risk factors Type 2 DM Hypertension Dyslipidaemia (low HDL, raised Triglycerides)

5 Obesity (increased waist circumference) Table 2: NCEP-ATPIII Criteria for Metabolic Syndrome Waist circumference Triglycerides >102cm (M) >88cm (F) 1.7 mmol/l Or On drug treatment for raised TG HDL-cholesterol Blood pressure <1.03 mmol/l (M) <1.30 mmol/l (F) Or On drug treatment for reduced HDL-C 130 or 85 mmhg Or On drug treatment for BP Fasting plasma glucose 5.6 mmol/l Or On drug treatment for elevated glucose Abnormal Liver Ultrasound Hepatomegaly usually merits referral to Hepatology Liver cysts Small simple cysts - common incidental finding. Thick walled or septated more significant-suggest refer Multiple cysts multiple cysts also require review, especially if family history of polycystic disease. Thick-walled or septated -more significant. Suggest refer. Haemangioma Small haemangiomata are common and usually incidental. Large or complex or atypical - require further clinical and radiological assessment.

6 4. Alcohol related liver disease No liver end-organ damage-community management including thiamine/vitamin B Chronic liver disease-abnormal LFT, enlarged liver/spleen-refer Jaundice/ascites-urgent referral 5. Raised Ferritin Ferritin is an acute phase reactant (raised with CRP) often elevated with insulin resistance (ie with metabolic syndrome) check transferrin saturation normal in acute-phase response or insulin resistance. Raised- refer for review/discussion about haemochromatosis (HFE) genotype testing 6. Incidental positive auto-immune serology smooth muscle antibody Normal LFT and IgG not raised monitor. If abnormal -REFER Antimichondrial antibody (AMA) (if positive will be sub-typed by immunology) M2 sub-type is diagnostic of Primary Biliary Cirrhosis. Refer for discussion of treatment, monitoring and prognosis, even if LFTs are normal.

7 7. Chronic Hepatitis B Map of medicine algorithms for hepatitis B includes management of acute and chronic hepatitis and advice. Hep B surface antigen (HBsAg) if positive refer hepatology Hepatitis B diagnosis. Serology Stage of infection Acute (early) Surface antigen (HBsAg) e antigen (HBeAg) IgM anticore antibody (antihbcab) IgG anticore antibody (antihbcab) Hepatitis B Virus DNA AntiHBe AntiHBs ALT + + +* Acute /- - (resolving) Chronic N** (immune tolerant) Chronic (immune active) Chronic /- - (eag Neg) Chronic N (inactive carrier) Resolved /- +/- N (immune)) Does not need referral Successful N vaccination *in very early infection the IgM anticore can be negative and by definition so can the IgG ** N=normal Taken from BASHH (2008) United Kingdom national guideline on the management of the viral hepatitides A, B & C British Association for Sexual Health and HIV Hepatitis C Positive Serology Confirm on repeat testing Refer hepatology for assessment of liver disease stage and treatment consideration If RNA negative will need annual monitoring

8 9. Gall bladder polyps Usually asymptomatic Can become malignant Risk increases with size Follow up with ultrasound When 7-10 cm refer hepatobiliary surgical team 10. Fast Track Referrals/advice/urgent clinic appointments eg jaundice, acute hepatitis, decompensated chronic liver disease, focal liver lesion on scan Jaundice often can be managed as an outpatient complete referral proforma and fax to (weblink) hepatology nurse specialists will 1. arrange urgent u/s 2. plan for urgent clinic review or CT or ERCP with MDT review as required If you feel a patient requires admission, please call Hepatology SpR ( ) who can advise/discuss the appropriate plan. Patients requiring urgent clinic appointment: Acute hepatitis, de-compensated chronic liver disease, focal liver lesion on scan often can be managed by urgent outpatient appointment Please fax referral to Referrals are triaged daily by a Consultant Hepatologist.

9 11. Haemochromatosis Management guidelines Why is it important? Hereditary haemochromatosis (HH) now easily screened for as most are homozygous for the C282Y mutation in the HFE gene 1 in 200 of Caucasian populations are homozygous There is variable expression ranging from asymptomatic (often just a raised transferrin saturation only) to those with bronze diabetes ; many will have subtle symptoms and modest elevation of ferritin Expression depends on age, iron losses (blood donation or menstruation lessen burden), alcohol use What to look for? Symptoms non-specific inc fatigue, arthralgia, loss of libido, abdominal pain Typical signs: hepatomegaly, diabetes, pigmentation, arthropathy (hips, knees and particularly 2 nd and 3 rd metacarpophalangeal joints) Check iron indices in anyone with raised ALT and in those with combination of above symptoms / signs Investigating suspected haemochromatosis If raised ferritin and transferrin saturation, send an EDTA sample for HFE genotyping to Molecular Genetics If unsure re genetic counselling or age of proband < 40yrs at diagnosis, refer to Medical Genetics for testing (box 134, Addenbrooke s Hospital) Genotypes compatible with HH: C282Y/C282Y (homozygous) or C282Y/H63D (compound heterozygote less common and milder) If homozygous then family screening as below When to refer to hepatology? HH with ferritin > 1000 or raised ALT, or non-hh iron overload: refer to Hepatology as may need liver biopsy HH with ferritin < 1000 and normal ALT: no biopsy as minimal risk of liver fibrosis but venesect if ferritin > 400 (refer Hepatology or local venesection service if available, aiming for ferritin of 50) NB non-hh genotype + mildly raised ferritin / ALT = likely fatty liver Family screening (C282Y homozygous index cases only) Refer to Medical Genetics Dept if: 1) index case genetics unknown 2) uncertain re counselling 3) index case not homozygous but family request

10 Siblings should have HFE / iron indices sent Children tested only when adult but can screen partner/spouse to see if carrier (children only at risk if spouse is carrier = 10% chance) Parents if symptoms suggestive of HH (homozygosity risk low otherwise) HH genotype + ferritin <200: reassure and monitor 2-5 yearly (less frequent if female, compound heterozygote, no evidence of iron accumulation) HH genotype + ferritin : reassure and suggest blood donation via NBS up to 4 x year max to prevent further iron overload (monitor annually) HH genotype + ferritin >400 see When to refer to hepatology? points 1 and 2 Useful info: British haemochromatosis society Staff and contacts Consultant Hepatologists Dr G Alexander Dr M Allison Dr A Gimson Dr B Griffiths Hepatology SpR Hepatology Clinical Nurse Specialists E Bateman and S Edwards Liver cancer and Fast Track Jaundice N Marsh Alcohol-related liver disease M Roat Non-alcoholic fatty liver disease F Smith/A Inte Ascites T Woodall Hepatitis C