KNOW ABOUT NEW SPECIALIZATION FAMILY MEDICINE
Posted by on Saturday, 1st November 2014
FAMILY MEDICINE – NEW SPECIALIZATION – MOST NEED FOR DEVELOPING COUNTRIES
Dr.S.ABBAS ALI
MD, DFM, DNB(FAM.MED)
MNAMS (Family Medicine)
FCGP, MCCP (Cardiology)
PGDHSc(Ultrasonography)
PGDHSc(Echocardiogram
Family medicine is defined as a field of specialization which provide comprehensive and holistic health care services centered on the family as the unit – from first contact to the ongoing care of chronic problems including promotive, preventive, curative and rehabilitative health care services. Family medicine is different from Community medicine. Community medicine specialists deals with populations and try to measure the needs of populations both sick and well and engaged in services to meet those needs. They do not provide comprehensive health services to individuals or Family. Family medicine is horizontal speciality like internal medicine and pediatrics, shares of large areas of content with other clinical disciplines. Family medicine is different from Internal medicine. The specialty of internal medicine is comprised of physicians trained in adult medicine who provide the majority of health care to adults in the hospital or clinic. The internist do not trained in maternity and child care and they do not treat children and neonates. In short, Family medicine specilist is specialist in internal medicine, paediatrics, Obs&gynae, surgery and community medicine. single specialization for all the problems of family and needed for developing nations.
Medicine has moved from organism to organ, from organ to cell and from cell to molecular properties. The vast increase of medical knowledge during the 20th century has contributed to increasing complexity of specialization with in the medical profession. There are at present 20 recognized specialties and many more subspecialties. Some specialties have emerged based on clearly defined skills such as surgery, radiology, and anesthesia, some based on parts of the body such as ENT ophthalmology, cardiology and gynecology and some based on particular age group such as pediatrics, geriatrics and obstetrics. Again in each speciality, there has been a growth of subspecialties as for example, neonatology, perinatology, pediatric cardiology, pediatric neurology, and pediatric surgery – all in pediatrics. A super specialist or sub specialist is one who learns more about less and less. He is concerned with particular organ or part of the body. The specialization and micro specialization contributed the mushrooming growth of large luxurious super speciality hospital. No doubt, specialization raised the standards of medical care but it favors high cost, low coverage, and elite oriented health services.
Despite spectacular advances in medical advances and massive expenditure, the death rates and life expectancy in the developed countries have remained unchanged. So the developed and developing countries needed a specialization which focuses on organism or specialization in general practice which give comprehensive and personalized health care. In 1966 two reports namely Mills commission report, Willard committee reporting United States made similar recommendations. In 1971 the American academy of general practice which began in 1947 changed its name to American academy of Family physicians. The emergence of new speciality family medicine has been hailed as a rediscovery of the human, social and cultural aspects of health and disease.
The American Academy of Family Practice (AAFP) defines family medicine as a “medical specialty which provides continuing, comprehensive health care for the individual and family. It is a specialty in breadth that integrates the biological, clinical and behavioral sciences. The scope of family medicine encompasses all ages, both sexes, each organ system and every disease entity.” Family medicine aims to provide initial, continuing and comprehensive care, while centering this process on the patient-physician relationship in the context of the family. These physicians emphasize disease prevention and health promotion, and when referral is indicated, the physician remains the coordinator of patient care.
In Family medicine referral system is not just sending patients to super speciality hospital or sub specialists but they consider it as two way exchange of information by referring to particular sub specialist and follow-up care of those who referred in consultation with sub specialist. It will ensure continuity of care and inspire confidence of the patients. The family doctor serves as a patient advocate in dealings with sub-specialists, third-party payers, employers and others. Ideally, this leads to decreased disintegration of patient care in inpatient settings, higher patient satisfaction, and increased cost-effectiveness.
National board of examinations, New Delhi requirements of family medicine specialization include after passing primary, 3 year mandatory training in the recognized centers of NBE, acceptance of thesis, pass in final examination. The training programmes address a large breadth of topics; general medicine, surgery, pediatrics, maternity care, gynecology, care of the surgical patient, musculoskeletal and sports medicine, emergency care, mental health, community medicine, skin, diagnostic imaging and nuclear medicine, and management of health systems
Rate It
APPROACH TO ABNORMAL LIVER FUNCTION TESTS
Posted by on Saturday, 1st November 2014
APPROACH TO ABNORMAL LIVER FUNCTION TESTS IN FAMILY PRACTICE
Dr.S.ABBAS ALI
MD, DFM, DNB(FAM.MED)
MNAMS (Family Medicine)
FCGP, MCCP (Cardiology)
PGDHSc(Ultrasonography)
PGDHSc(Echocardiogram)
Abnormal LFTs are common observation in family practice. It can be present in majority of patients with no symptoms and in some patients with minor symptoms like lethargy, pruritis, abdominal pain, low grade fever. An expert family physician with the help of detailed history and physical examination can suspect potentially fatal diseases like cirrhosis, primary biliary cirrhosis, primary sclerosing cholangitis, and liver tumors and by following cardinal principles of family practice like referral, sharing of responsibility and continued follow up may save patients lives with liver problems.
I. TEST FOR HEPATOCELLULAR INJURY
Aminotransferases: Alanine aminotransferase (ALT) and Aspartate Aminotransferase (AST) are released in blood stream after hepatocellular injury. Increased ALT activity reflects hepatic damage more specific.
II. TEST FOR CHOLESTASIS
Serum alkaline phosphatase: this enzyme situated in the canicular and sinusoidal membrane of liver cells. A greatly increased alkaline phosphatase activity is main biochemical indicator of biliary obstruction.
Gamma glutamyl transferase: increased plasma GGT occur in biliary obstruction and acute parenchymal damage from any cause
III. TEST FOR HEPATIC FUNCTION
They help in predicting prognosis
Serum albumin: decreasing levels indicate poor prognosis
Serum Bilirubin: increasing levels indicate poor prognosis
Prothrombin time (PT): increasing levels indicate poor prognosis
IV.CHOLESTASIS PREDOMINANT LIVER INJURY
ALT and AST levels are mildly elevated. Serum alkaline phosphatase and GGT levels are high.
Primary biliary cirrhosis: suspect if middle aged women of 50 years with autoimmune disorder like hypothyroidism, Rheumatoid arthritis etc with complaints of lethargy, pruritis, abdominal pain, low grade fever and increased serum alkaline phosphatase. Antimitochondrial antibody (AMA) positive. These patients should be referred to particular subspeciality for further evolution without delay. The definitive treatment was Liver transplantation. It should be considered as early as possible to minimize morbity and mortality. In PBC interlobular bile ducts are damaged by chronic granulomatous inflammation causing progressive cholestasis, cirrhosis and portal hypertension.
Primary sclerosing cholangitis: PSC is a disorder of unknown cause characterized by non malignant non bacterial inflammation, fibrosis and stricture of the intra and extra hepatic bile ducts.
Suspect if middle aged men with autoimmune disorder especially ulcerative colitis with elevated serum bilirubin and serum alkaline phosphatase with no symptoms or with fluctuating symptoms like lethargy, pruritis, abdominal pain and jaundice. P-ANCA is positive. There is no curative medical therapy and liver transplantation is the only option for survival and it should be considered early to minimize morbidity and mortality.
Secondary biliary cirrhosis:this develops after prolonged large duct biliary obstruction due to gall stones, bile duct strictures and sclerosing cholangitis.
Liver tumors: ultrasound of abdomen and abdominal CT are helpful. Alpha feto protein levels are increased in hepatocellular carcinoma.
Screening tests for chronic liver disease
HBV & HCV serology
Haemogram and iron studies for haemochromatosis: in Haemochromatosis ↑ferritin ↑iron ↓total iron binding capacity
Alpha 1 antitrypsin deficiency
Wilson diseases: serum copper low, serum ceruloplasmin low and urinary copper ↑
PBC: ↑AMA ( anti mitochondrial antibody)
PSC: ↑P-ANCA ↑ANA ↑AMA
AIH: ↑ANA ↑ASMA (anti smooth muscle antibody) ↑IgG
Immunoglobulins: ↑IgA in alcoholic liver disease ↑IgM in PBM and ↑IgG in autoimmune hepatitis (AIH)
Hepatocellular carcinoma: increased alpha fetoprotein
V.HEPATOCELLULAR PREDOMINANT LIVER INJURY
High levels of AST and ALT usually observed. If levels are high evaluate further by advising viral markers.
Acute viral hepatitis: AST and ALT raised. Serum bilirubin may be normal. Viral markers positive.
Chronic viral hepatitis: Hepatitis B & C are most common causes of abnormal LFT
Alcoholic liver disease: AST /ALT ratio is typically 2:1 or more. When the history is not reliable, normal serum alkaline phosphatase, ↑↑GGT and macrocytosis suggest this condition.
Fatty liver: is the most common cause mild abnormality of LFT in general population. Risk factors of nonalcoholic fatty liver include obesity, DM and ↑Lipids (triglycerides)
Autoimmune hepatitis: AIH occurs mainly in young and middle aged females with concomitant autoimmune disorders (eg. Rheumatological disorders, autoimmune thyroiditis)
Ischaemic hepatitis: can be seen in condition when effective circulatory volume is low (eg. MI, Hypotension, haemorrhage) AST, ALT and LDH raised.
Toxic hepatitis: paracetamol overdose is the main cause. History is vital.
Management and follow up
Manage according to specific diagnosis: If patient is asymptomatic and all the initial evaluation are negative then features of opportunistic health promotion and prevention are followed eg. life style modification, give help for reducing weight, alcohol, smoking, control DM, control hyperlipidaemia, and stop potentially hepatotoxic medication. Repeat test after 3 months, if abnormalities persists do an Ultrasound, abdominal CT has role. If the diagnosis is not apparent or the suspected diagnosis is beyond the reach of family practice then further testing is needed. In this cases cardinal principles of family practice like timely referral, sharing of responsibility, continued follow up are followed. This type of attitude may save patients lives with liver problems.
References
1. Fevery J: Bilirubin in clinical practice: A review. Liver Int 28:592, 2008
2. Laboratory tests, in Schiff's Diseases of the Liver, 10th ed, ER Schiff et al (eds). Philadelphia, Lippincott Williams & Wilkins, 2006
3. Navarro VJ, Senior JR: Drug-related hepatotoxicity. N Engl J Med 354:731, 2006
4. Pratt DS, Kaplan MM: Evaluation of abnormal liver-enzyme tests in the asymptomatic patient. N Engl J Med 342:1266, 2000.
5. Pietrangelo A: Hereditary hemochromatosis: Pathogenesis, diagnosis, and treatment. Gastroenterology 139:393, 2010.
6. Pietrangelo A: Hereditary hemochromatosis: Pathogenesis, diagnosis, and treatment. Gastroenterology 139:393, 2010.
7. Schmidt LE et al: Acute versus chronic alcohol consumption in acetaminophen-induced hepatotoxicity. Hepatology 35:876, 2002.
8. Silverman EK, SANDHAUS RA: Clinical practice. Alpha 1-antitrypsin deficiency. N Engl J Med 360:2749, 2009
9. Textbook of Liver Disease, 6th ed. Philadelphia, Saunders, 2011 totoxicity. N Engl J Med 349:474, 2003.
Rate It
ALCOHOLISM, ITS EFFECTS AND ROLE OF FAMILY PHYSICIAN
Posted by on Saturday, 25th October 2014
ALCOHOLISM, ITS PROBLEMS AND ROLE OF FAMILY PHYSICIAN
Dr.S.ABBAS ALI
MD, DFM, DNB (FAM.MED)
MNAMS (Family Medicine)
FCGP, MCCP (Cardiology)
PGDHSc (Ultrasonography)
PGDHSc (Echocardiogram)
Alcoholism is usually defined by the behavioral patterns and consequences of alcohol intake, not on the basis of the amount of alcohol intake. Abuse is defined by a repetitive pattern of drinking alcohol that has adverse effects on social, family, occupational, or health status. Dependence is defined by alcohol-seeking behavior, despite its adverse effects. Many alcoholics demonstrate both dependence and abuse, and dependence is considered the more serious and advanced form of alcoholism. A clinically helpful approach to diagnosis of alcohol dependence and abuse is the use of the CAGE or TWEAK questionnaire, which is recommended in all medical history-taking
CAGE Questions
Acronym Question
C Have you ever felt you ought to C ut down on your drinking?
A Have people Annoyed you by criticizing your drinking?
G Have you ever felt Guilty or bad about your drinking?
E Have you ever had a drink first thing in the morning to steady your nerves or get rid of a hangover (Eye-opener)?
TWEAK QUESTIONNAIRE
Acronym Questions points
T Have you an increased tolerance to alcohol 2
W Did you worry about your drinking 2
E have you ever had alcohol as an eye opener in the morning 2
A Do you ever get amnesia after drinking alcohol 2
K (C) Have you ever felt c(k)ut down on your drinking 2
A score of more than 2 suggests an alcohol problem. It may be more sensitive than the CAGE questionnaire in some populations (eg.pregnant women)
1. EPIDEMIOLOGY
World wide an estimated 2.3 million people die from alcohol related causes. This is 3.7% of all deaths. 6.1% among men and 1.1% among women. In India survey showed that around 20-30% of adult males and 5% of adult females use alcohol. While alcohol is used traditionally by men, its use by women is now on the increase. Over the past 30-40 years increasing percentages of young people have started to drink alcoholic beverages. Their alcohol consumption has increased in quantity and frequency and the age at which drinking starts has declined. This situation is disturbing because the young people concerned may run a greater risk of alcoholic problems in later life and also, in the short term because of increased rates of drunkenness and involvement in road accidents.
2. PROBLEMS OF DRINKING TOO MUCH ALCOHOL
Liver and body can usually cope with drinking a small amount of alcohol. Indeed, drinking a small amount of alcohol (1-2 units per day) may help to prevent heart disease and stroke. Heavy drinking has an increased risk of developing disturbance in function of many organs and in the long run organ damage with irreversible serious complications.
2.1. Liver problems: Drinking too much alcohol can lead to three types of liver conditions - fatty liver, hepatitis, and cirrhosis. Any, or all, of these conditions can occur at the same time in the same person.
2.1.1. Fatty liver
Drinking a large amount of alcohol, even for only a few days, can lead to a build-up of fats in the liver. This is called alcoholic fatty liver disease, and it's the first stage of ARLD. Fatty liver disease is not usually serious and rarely causes any symptoms but it is an important warning sign that you are drinking at a level harmful to your health. 90-100% of heavy drinkers have alcoholic fatty liver disease and it is reversible on abstinence of alcohol. If drinking of alcohol is continuous one in four drinkers with fatty liver disease will develop alcoholic hepatitis and one in five drinkers with fatty liver disease will develop cirrhosis.
HOW TO DIAGNOSE FATTY LIVER: Mild increase in Liver profile and increased serum triglyceride levels. Ultrasound of abdomen shows increased echogenicity of liver.
2.1.2. ALCOHOLIC HEPATITIS:
Hepatitis means inflammation of the liver. The inflammation can range from mild to severe. Alcoholic hepatitis is an acute form of alcohol-induced liver injury that occurs with the consumption of a large quantity of alcohol over a prolonged period of time; it encompasses a spectrum of severity ranging from asymptomatic derangement of biochemistries to fulminant liver failure and death
Mild hepatitis may not cause any symptoms. The only indication of inflammation may be an abnormal level of liver enzymes in the blood, which can be detected by a blood test. However, in some cases the hepatitis becomes persistent (chronic), which can gradually damage the liver and eventually cause cirrhosis.
A more severe hepatitis tends to cause symptoms such as feeling sick, jaundice (yellowing of the skin, caused by a high level of bilirubin - a chemical normally metabolized in the liver), generally feeling unwell and, sometimes, pain over the liver.
A very severe bout of alcoholic hepatitis can quickly lead to liver failure. This can cause deep jaundice, blood clotting problems, confusion, coma, and bleeding into the guts, and is often fatal.
The main treatment for alcoholic hepatitis is to provide adequate nutrition (this sometimes involves passing liquid feeds through a tube in the stomach) and steroids.
2.1.3. CIRRHOSIS: Cirrhosis is a condition where normal liver tissue is replaced by scar tissue (fibrosis). The scarring tends to be a gradual process. The scar tissue affects the normal structure and regrowth of liver cells. Liver cells become damaged and die as scar tissue gradually develops. So, the liver gradually loses its ability to function well. The scar tissue can also affect the blood flow through the liver which can cause back pressure in the blood vessels which bring blood to the liver. About 1 in 10 heavy drinkers will eventually develop cirrhosis. It tends to occur after 10 or more years of heavy drinking. The scarring and damage of cirrhosis is usually permanent. Early cirrhosis is compensated cirrhosis. Early symptoms of liver disease can include:
• fatigue
• nausea
• vomiting
• diarrhoea
• abdominal pains
Later stage cirrhosis (decompensated cirrhosis) symptoms are more serious – They can include:
• jaundice (yellow skin)
• vomiting blood
• fatigue
• weakness, loss of appetite
• itching
• easy bruising
• swelling of the legs ankles, or abdomen (ascitis)
• liver cancer
• bleeding in the gut
• increased sensitivity to alcohol and drugs, both medical and recreational (because the liver cannot process them)
In cirrhosis, complete abstinence of alcohol is essential to prevent more serious complications of liver failure. The treatment option of cirrhosis is Liver transplantation.
2.2.GI tract and stomach; obesity (alcohol has many calories)diarrhea, gastric erosions, peptic ulcer, varices (which results in haematemesis) carcinoma, oral mucosal lesions and pancreatitis (both acute and chronic)
2.3.CENTRAL NERVOUS SYSTEM: Stroke (CVA), poor memory (Problems with thinking, memory, mood) poor cognition, faintness and light headedness, cortical atrophy, retro bulbar neuropathy, fits, falls, wide based gait, neuropathy(numbness in legs and feet) , confabulation, korsokoff psychosis, wernicke’s encephalopathy. Mental health problems, including depression and anxiety, Jealousy, temper tantrums, vagrancy, auditory hallucinations, and paranoid delusions. Unintentional injuries, suicides, homicides, total social damage which includes family disorganization, domestic violence, wife battering, crime and loss of productivity.
2.4. Heart: arrhythmias, Hypertension, cardiomyopathy, sudden death in binge drinkers (Holiday heart syndrome)
2.5. GENITOURINARY SYSTEM: Sexual difficulties such as impotence, testicular atrophy, with shrinkage of seminiferous tubules, loss of sperm cells,
2.6. HAEMOPOITIC SYSTEM: leucopenia (decreased WBC) thrombocytopenia (decreased platelets), anemia, ↑MCV, sideroblastic anemia
2.7. VITAMIN DEFICIENCIES: alcoholism associated Vitamin B complex (thiamine) and Folate deficiency,
2.8. INCREASED CANCER RISK: Cancer is the second leading cause of death in alcoholics after cardiovascular disease. Common sites include head and neck, mouth, pharynx, larynx, oesophagus, cardia of stomach, colon, breast, Liver and pancreas.
2.9. Accidents - drinking alcohol is associated with a much increased risk of accidents. In a study in Bangalore, nearly 28% of traffic injuries were found directly attributable to alcohol.
2.10. High risk sexual behavior: Sexually transmitted diseases including HIV/AIDS, Hepatitis B and C: Alcohol use is considered a risk factor for high risk sexual behavior leading to STD including HIV/AIDS, Hepatitis B & C
2.11. Infections: pneumonia and tuberculosis are more common in alcoholics
2.12. FETAL ALCOHOL SYNDROME: Damage to an unborn baby in pregnant women. The baby has low IQ, short palpabral fissure, absent philtrum and small eyes.
2.13. ALCOHOL WITHDRAWAL: It starts after 10 to 72 hours after last drink characterized hypotension (↓BP) rapid pulse, tremor, confusion, fits, hallucinations (delirium tremens) may be visual or tactile eg. Animals are crawling on the skin. The alcohol withdrawal patients should be admitted in hospital
• give IV fluids and stabilize BP & pulse
• 25%Dextrose
• Inj. Thiamine
• Chlordiazapoxide 10-50mg 6 hourly etc.,
3. MANAGEMENT
3.1. The family physician should consider every consultation is an opportunity to detect early-warning signs that prevent illness and disease. Sensible, timely and appropriate interventions can help make people aware of the potential risks they are taking. Health promotion is not simply risk avoidance, rather than active encouragement of individuals to increase control over bad habits which are detrimental to health, to attain their best possible level of well being.
3.2. Opportunistic health promotion and disease prevention is defined as “an advice made more effective by being directly linked to the content of the preceding consultation”. For example, advice to stop alcoholism is proportionately more powerful when it is linked to an episode of acute vomiting, abdominal pain etc. Prevention: prevention is always better than cure because it reduces undue suffering from diseases. Promotion of health, preservation of health and restoration of health when it is impaired. Nowadays, however, the majority of mortality and disabling illness accounted for by ischemic heart disease, stroke, cancer, and chronic lung disease. These are principally affected by life styles and habits of individuals, alcoholism, smoking, diet and exercise. Consequently the role of the physicians has become more important and he/she must communicate this information more effectively to his/her patients. Helping patients to take responsibility of their own health must be the fundamental feature of opportunistic health promotion and disease prevention
3.3. Identity high risk factors: such as smoking, tobacco chewing, high risk sexual behaviour, physical inactivity, history of premature death or CHD, stress factors, contraceptive use and failure or inability to obtain preventive health services. If found provide promotive and preventive measures.
3.4. Identify co-morbid conditions: like Diabetes, obesity, hyperlipidaemia, hypertension. If found specific intervention and necessity of treatment should be carried out to control these conditions for preventing organ damage.
3.5. If alcoholic having liver problems, alcohol is contraindicated. The other conditions where alcohol contraindicated are pregnancy, carcinoid, peptic ulcer, and serious reactions will occur with drugs (antihistamines, metronidazole)
3.6. Psychological assessment of motivation: the patient should be psychologically motivated. Treating established alcoholic may be rewarding particularly if they want to change their life style. If so family therapy, group therapy or self help may be useful in self initiated and determined alcoholic. The family members and friends should encourage the alcoholic will to quit. Give and maintain follow up and encourage.
3.7. If patient is alcoholic with no evidence of liver disease advise measures for preventing alcohol-related liver disease. The most effective way to prevent ARLD is to stop drinking alcohol, or stick to the recommended daily limits and have at least two alcohol-free days a week.
3.8. .The recommended limits of alcohol consumption are:
Men should not regularly drink more than 3 units of alcohol a day.
Women should not regularly drink more than 2 units a day. One unit of alcohol is 10 ml (1 cl) by volume, or 8 g by weight, of pure alcohol. For example: One unit of alcohol is about equal to:
half a pint of ordinary strength beer or cider (3-4% alcohol by volume); or
a small pub measure (25 ml) of spirits (40% alcohol by volume);
A standard pub measure (50 ml) of fortified wine such as sherry or port (20% alcohol by volume).
There are one and a half units of alcohol in a small glass (125 ml) of ordinary strength wine (12% alcohol by volume) or a standard pub measure (35 ml) of spirits (40% alcohol by volume).
But remember, many wines and beers are stronger than the more traditional ordinary strengths. A more accurate way of calculating units is as follows. The percentage alcohol by volume (% abv) of a drink equals the number of units in o in one litre of that drink. For example:
Strong beer at 6% abv has six units in one litre. If you drink half a litre (500 ml) - just under a pint - then you have had three units.
Wine at 14% abv has 14 units in one litre. If you drink a quarter of a litre (250 ml) - two small glasses - then you have had three and a half units.
References
1. Savolainen VT, Liesto K. Männikkö A, et al: Alcohol consumption and alcoholic liver disease: Evidence of a threshold level of effects of ethanol. Alcohol Clin Exp Res 1993;17(5):1112-1117.
2. Lelbach WK: Cirrhosis in the alcoholic and its relation to the volume of alcohol abuse. Ann NY Acad Sci1975;252:85-105.
3. Grant BF, Dufour MC, Harford TC: Epidemiology of alcoholic liver disease. Semin Liver Dis 1988;8(1):12-25.
4. Stewart S, Jones D, Day CP: Alcoholic liver disease: New insights into mechanisms and preventative strategies. Trends Mol Med 2001;7(9):408-413.
5. Zhou Z, Wang L, Song Z, et al: A critical involvement of oxidative stress in acute alcohol-induced hepatic TNF-alpha production. Am J Pathol 2003;163(3):1137-1146.
6. Sorensen TIA, Orholm M, Bentsen KD, et al: Prospective evaluation of alcohol abuse and alcoholic liver injury in men as predictors of development of cirrhosis. Lancet 1984;2(8397):241-244.
7. Teli MR, Day CP, Burt AD, et al: Determinants of progression to cirrhosis and fibrosis in pure alcoholic fatty liver. Lancet 1995;356:987-990.
8. Maddrey WC: Alcoholic hepatitis. In Williams R, Maddrey WC (eds): Liver. London: Butterworths, 1984, pp 226-241.
9. Alexander JF, Lischner MW, Galambos JT: Natural history of alcoholic hepatitis II. Am J Gastroenterol1971;56:515-521.
10. Maddrey WC, Boitnott JK, Bedine MS, et al: Corticosteroid therapy of alcoholic hepatitis. Gastroenterology1978;75:193-199.
11. Sheth M, Riggs M, Patel T: Utility of the Mayo End-Stage Liver Disease (MELD) score in assessing prognosis of patients with alcoholic hepatitis. BMC Gastroenterology 2002;2:2.
12. U.S. Department of Health and Human Services. Organ Procurement and Transplantation Network. MELD Calculator. OPTN: Organ Procurement and Transplantation Network. Accessed November 6, 2012.
13. Louvet A, Naveau S, Abdelnour M, et al: The Lille Model: A New Tool for Therapeutic Strategy in Patients with Severe Alcoholic Hepatitis Treated with Steroids. Hepatology 2007;45:1348-1354.
14. Bonis PA, Friedman SL, Kaplan MM: Is liver fibrosis reversible? N Engl J Med 2001;344:452-454.
15. Romano DR, Jimenez C, Rodriguez F, et al: Orthotopic liver transplantation in alcoholic liver cirrhosis.Transplant Proc 1999;31:2491-2493.
16. Maddrey WC: Alcoholic hepatitis: Clinicopathologic features and therapy. Semin Liv Dis 1998;8(1):91-102.
17. International Group: Alcoholic liver diseases: morphological manifestations. Lancet 1981;1(8222):707-711.
18. Finlayson ND: Clinical features of alcoholic liver disease. Baillieres Clin Gastroenterol 1993;7(3):627-640.
19. O'Shea RS, Dasarathy S, McCullough AJ: Alcoholic Liver Disease. Hepatology 2010;51(1):307-328.
20. Mendenhall CL, Tosch T, Weesner RE, et al: VA cooperative study on alcoholic hepatitis II: Prognostic significance of protein-calorie malnutrition. Am J Clin Nutr 1986;43:213-218.
21. Schenker S, Halff GA: Nutritional therapy in alcoholic liver disease. Semin Liver Dis 1993;13(2):196-209.
22. Carithers RL, Herlong HF, Diehl AM, et al: Methylprednisolone therapy in patients with severe alcoholic hepatitis. Ann Intern Med 1989;110:685-690.
23. Ramond MJ, Poynard T, Rueff B, et al: A randomized trial of prednisolone in patients with severe alcoholic hepatitis. N Engl J Med 1992;326:507-512.
24. Depew W, Boyer T, Omata M, et al: Double-blind controlled trial of prednisolone therapy in patients with severe acute alcoholic hepatitis and spontaneous encephalopathy. Gastroenterol 1980;78(3):524-529.
25. Theodossi A, Eddleston ALWF, Williams R: Controlled trial of methylprednisolone therapy in severe acute alcoholic hepatitis. Gut 1982; 23(1):75-79.
26. mperiale TF, McCullough AJ: Do corticosteroids reduce mortality from alcoholic hepatitis? Ann Intern Med1990;113:299-307.
27. Christensen E, Gluud C: Glucocorticoids are ineffective in alcoholic hepatitis: A meta-analysis adjusting for confounding variables. Gut 1995;37(1):113-118.
28. Mathurin P, Mendenhall CL, Carithers RL, et al: Corticosteroids improve short-term survival in patients with severe alcoholic hepatitis (AH): Individual data analysis of the last three randomized placebo controlled double blind trials of corticosteroids in severe AH. J Hepatology 2002;36:480-487.
29. Hallé P, Paré P, Kaptein E, et al: Double-blind, controlled trial of propylthiouracil in patients with severe acute alcoholic hepatitis. Gastroenterology 1982;82:925-931.
30. Akriviadis E, Botla R, Briggs W, et al: Pentoxifylline improves short-term survival in severe acute alcoholic hepatitis: A double-blind, placebo-controlled trial. Gastroenterology 2000;119:1637-1648.
31. Rambaldi A, Gluud C: Meta-analysis of propylthiouracil for alcoholic liver disease—a Cochrane Hepato-Biliary Group Review. Liver 2001;21:398-404.
32. Naveau S, Chollet-Martin S, Dharancy S, et al: A double-blind randomized controlled trial of infliximab associated with prednisolone in acute alcoholic hepatitis. Hepatology 2004;39:1390-1397.
33. Bird G, Lau JYN, Koskinas J, et al: Insulin and glucagon infusion in acute alcoholic hepatitis: a prospective randomized controlled trial. Hepatology 1991:14(6):1097-1101.
34. Trinchet JC, Balkau B, Poupon RE, et al: Treatment of severe alcoholic hepatitis by infusion of insulin and glucagon: A multicenter sequential trial. Hepatology 1992;15(1):76-81.
35. Bird GLA, Prach AT, McMahon AD, et al: Randomised controlled double-blind trial of the calcium channel antagonist amlodipine in the treatment of acute alcoholic hepatitis. J Hepatol 1998;28:194-198.
36. Mezey E, Potter JJ, Rennie-Tankersley L, et al: A randomized placebo controlled trial of vitamin E for alcoholic hepatitis. J Hepatol 2004;40(1):40-46.
37. Rambaldi A, Gluud C: S-adenosyl-L-methionine for alcoholic liver diseases. Cochrane Database Syst Rev2006;CD002235.
38. Rambaldi A, Jacobs BP, Iaquinto G, et al: Milk thistle for alcoholic and/or hepatitis B or C liver diseases-a systematic cochrane hepato-biliary group review with meta-analyses of randomized clinical trials. Am J Gastroenterol 2005;100:2583-2591.
39. Tome S, Lucey MR: Timing of liver transplantation in alcoholic cirrhosis. J Hepatol 2003;39:302-307.
40. Aertgeerts B. Buntinx F, Kester A: The value of the CAGE in screening for alcohol abuse and alcohol dependence in general clinical populations: a diagnostic meta-analysis. J Clin Epidemiol 2004;57:30-39.
Rate It