Natural Cure for Liver Disease

Liver Disease Survivors Guide

Renowned Health Specialist experienced in working with numerous people with liver disorders share with you and: Explains how the liver works and how liver disorders develop in Simple English without Medical Jargon. Shares the facts about cirrhosis of the liver. Explains complications and treatments in simple language. Talks about Nutrition in Liver Disease. Explains Alternative Treatments available. Talks about the latest research developments in liver disease treatment. Shares resources for Liver disease forums and help-lines. Gives you the true in-depth stories from survivors and how they coped with the challenges of liver disorder. Shares touching stories of family members who had to cope with their loved ones suffering from cirrhosis of the liver, and the strategies they used to cope with them. With Liver Disease Survivors Guide, you will discover : Credible information on Liver disease obtained from detailed interviews with specialist doctors, explained in simple language. Healthy steps in dealing with liver disorders. What to do and what not to do while learning to adapt to the liver disorder. Remarkable stories in patients own words. It gives you a real emotional experience of a person with serious liver disorder and how they view the world. Latest research on liver disorders. Best resources and direct links to forums. Direct links to get professional help and identify the best experts in your area. Alternative treatments and therapies available for liver disorders. No medical jargon or difficult language, the book is written in simple and easy to understand language.

Liver Disease Survivors Guide Overview


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Postnecrotic cirrhosis

Postnecrotic cirrhosis is caused by hepatic necrosis and can be related to hepatitis, metabolic liver disease and infection. In patients with this type of cirrhosis, the liver can become smaller and distorted. Physical signs and symptoms of cirrhosis are weight loss, jaundice, anorexia, abdominal pain and bruising. Diagnosis of cirrhosis requires histological confirmation of altered hepatic architecture seen on liver biopsy. The only therapeutic option available for advanced cirrhosis is liver transplantation.

Complications of cirrhosis

Complications of liver cirrhosis include Although varices may present in other regions of the digestive tract, they develop most commonly in the submucosal veins of the distal oesophagus and in the stomach. Oesophageal varices are related to portal hypertension, often associated with alcoholic cirrhosis, but may also be seen in patients with chronic hepatitis and portal vein thrombosis. Although the presence of varices may be asymptomatic and variceal bleeding is painless, there is a high risk of rupture in the distal oesophageal veins, which causes potentially life-threatening bleeding. In an acute variceal bleed the patient vomits bright red blood and can develop signs and symptoms of hypovolaemia. Upper endoscopy is used to diagnose, evaluate and treat oesophageal varices (see Chapter 10).

Nutritional Management Acute Liver Failure

The nutritional status of someone with acute liver failure versus chronic liver failure can differ greatly. The primary goal of the nutritional management in acute liver failure is supportive. An increase in nausea, vomiting, and anorexia may be associated with acute liver disease, which may result in decreased oral intake. If normal nutritional status prior to the insult is assumed, the patient will have a much higher nutritional reserve than that of a patient in chronic liver failure. Energy needs can be met by providing the Dietary Reference Intakes for infants and children and approximately 30kcal kg for adults. The provision of adequate protein is crucial in fulminant hepatic failure and encephalopathy. Adequate protein must be provided to minimize catabolism, which may exacerbate any hyperammonemia present. Excessive protein intake should be avoided because it may increase ammonia levels. Protein recommendations for adults and teenagers are 0.5-1.0 g kg day and for infants and...

Cirrhosis of the liver

Cirrhosis refers to a distorted or scarred liver as a result of chronic inflammation. The functional liver cells are replaced by fibrous or adipose connective tissue. The symptoms of cirrhosis include jaundice, oedema in the legs, uncontrolled bleeding and sensitivity to drugs. Cirrhosis may be


Hepatic cirrhosis is a disease that leads to irreversible fibrosis of the parenchyma. It is localized in the spaces between the portal tracts and destroys the normal hepatic architecture. However, the development of cirrhosis in patients suffering from viral hepatitis is frequently inhibited by treatment with interferon 14 . Generally, diagnosis of liver cirrhosis is achieved by histological examination of a liver biopsy, whereas imaging is performed to determine the anatomical distribution of the disease. Typical features of advanced hepatic cirrhosis on diagnostic imaging are nodular contours and enlargement of the caudate lobe and lateral segment of the left lobe, combined with atrophy of the right lobe 26,59 . However, regional hypertrophy of certain liver segments, such as the caudate lobe, and atrophy of the right lobe are less likely to occur in alcohol-induced liver cirrhosis, which is one of the more frequent causes of cirrhosis 24 . As liver atrophy seems to be localized...

Liver Cirrhosis

It is now generally accepted that in alcoholic patients with advanced liver cirrhosis, hepatic SAMe concentration is greatly decreased (Lieber 2002). While transient SAMe depletion is necessary for the liver to regenerate, chronic hepatic SAMe depletion may lead to malignant transformation (Lu & Mato 2005). Studies with primates have found that the decreased hepatic SAMe concentrations and the associated liver lesions, including mitochondrial injury, can be corrected with SAMe supplementation (Lieber et al 1990).

Neuroendocrine Effects of Alcohol

The development of female secondary sexual characteristics in men (e.g., gynaecomastia and tes-ticular atrophy) generally only occurs after the development of cirrhosis. In women, the hormonal changes may reduce libido, disrupt menstruation, or even induce premature menopause. Sexual dysfunction is also common in men with reduced libido and impotence. Fertility may also be reduced, with decreased sperm counts and motility.

Alcohol and Nutrition

The nutritional status of alcoholics is often impaired. Some of the pathophysiological changes seen in alcoholics are direct consequences of malnutrition. However, in the 1960s, Charles Lieber demonstrated that many alcohol-induced pathologies, including alcoholic hepatitis, cirrhosis, and myopathy, are reproducible in animals fed a nutritionally adequate diet. Consequently, the concept that all alcohol-induced pathologies are due to nutritional deficiencies is outdated and incorrect.

Alcohol and Facial Flushing

This is similar to the disulfiram reaction due to the rise of acetaldehyde after inhibition of ALDH. Disulfiram is used therapeutically to encourage abstinence in alcohol rehabilitation programs. The aversive effects of acetaldehyde may reduce the development of alcoholism and the incidence of cirrhosis in 'flushers.' However, some alcoholics with ALDH2 deficiency and, presumably, higher hepatic acetaldehyde levels develop alcoholic liver disease at a lower intake of ethanol than controls.

Effects of Acetaldehyde

Adduct formation leads to retention of protein within hepatocytes, contributing to the hepatomegaly, and several toxic manifestations, including impairment of antioxidant mechanisms (e.g., decreased glutathione (GSH)). Acetaldehyde thereby promotes free radical-mediated toxicity and lipid peroxidation. Binding of acetaldehyde with cysteine (one of the three amino acids that comprise GSH) and or GSH also reduces liver GSH content. Chronic ethanol administration significantly increases rates of GSH turnover in rats. Acute ethanol administration inhibits GSH synthesis and increases losses from the liver. Furthermore, mitochondrial GSH is selectively depleted and this may contribute to the marked disruption of mitochondria in alcoholic cirrhosis.

Alcohol and Mortality Amount of Alcohol

Some have explained the J shape as an artefact due to misclassification or confounding. Prevailing beliefs among these researchers is that abstainers comprise a mix of former heavy drinkers, underreporting drinkers, ill people who have stopped drinking, and people with an especially unhealthy lifestyle apart from abstaining. However, most researchers attribute the 'J' to a combination of beneficial and harmful effects of ethanol. This is based on findings from population studies of alcohol-related morbidity and cause-specific mortality that show a decreased relative risk of coronary heart disease, and an increased risk of certain cancers and cirrhosis, with increased alcohol intake. Further evidence derives from studies in which people who were ill at baseline were excluded, and these confirmed the previously mentioned findings.

Risks Large Number of Somatic Diseases

At the other end of the range of intake, the ascending leg has been explained by the increased risk of cirrhosis and development of certain types of cancers with a high alcohol intake. The mechanisms by which alcohol induces cirrhosis have been intensively studied but sparsely enlightened. It is well documented that women, most likely due to smaller size and different distribution of body fat and water, are at higher risk of developing cirrhosis than men, but other risk factors for alcoholic cirrhosis are not well established (Figure 2). Figure 2 Relative risk of alcohol-induced cirrhosis according to sex and alcohol intake. Relative risk is set at 1.00 among nondrinkers (< 1 drink week). (Reproduced with permission from Becker U et al. (1996) Prediction of risk of liver disease in relation to alcohol intake, sex and age A prospective population study. Hepatology 23 1025-1029.) Figure 2 Relative risk of alcohol-induced cirrhosis according to sex and alcohol intake. Relative risk is...

Validity of Alcohol Intake

An invalid marker of self-reported alcohol intake in a general population. With regard to information on alcohol intake from the general population, the need for any such marker can further be questioned. First, participants in prospective cohort studies sampled from the general population have less reason to underreport, or deny, their alcohol intake than alcoholics or insurance populations. Second, in a study on alcoholic cirrhosis, it was found that self-reported alcohol intake in the questionnaire used in most of the studies included in the overview was a reliable measure of 'true alcohol intake' since self-reported alcohol intake is a valid predictor of this outcome (Figure 2).

Alcoholic Liver Disease

Alcoholic liver disease is among the top ten causes of mortality in the US with somewhat higher mortality rates in western European countries where wine is considered a dietary staple, and is a leading cause of death in Russia. Among the three stages of alcoholic liver disease, fatty liver is related to the acute effects of alcohol on hepatic lipid metabolism and is completely reversible. By contrast, alcoholic hepatitis usually occurs after a decade or more of chronic drinking, is associated with inflammation of the liver and necrosis of liver cells, and carries about a 40 mortality risk for each hospitalization. Alcoholic cirrhosis represents irreversible scarring of the liver with loss of liver cells, and may be associated with alcoholic hepatitis. The scarring process greatly alters the circulation of blood through the liver and is associated with increased blood pressure in the portal (visceral) circulation and shunting of blood flow away from the liver and through other organs...

Historical Background

More recently, 18-year-old Jesse Gelsinger died in 1999 from liver failure during a gene transfer trial at the University of Pennsylvania.2'3 In retrospect, investigators did not pay sufficient heed to animal data indicating the possibility of adenovirus-induced liver failure and overlooked abnormalities in Gelsinger's liver function tests. The principal investigator was also the founder of the biotechnology company that produced that adenovirus vector used in the study and thus had a significant financial interest in the success of the clinical trial. The researchers in this study also failed to use the consent form approved by the IRB and failed to report as adverse events instances of mild liver toxicity in previous participants. The tragic outcome in this highly publicized case led to additional federal regulations regarding conflicts of interest, training investigators in human participant's protection, and reporting adverse events.

Branched Chain Amino Acids Isoleucine Leucine Valine

In liver failure the plasma concentrations of the aromatic amino acids (AAAs) tyrosine, phenylala-nine, and tryptophan increase, probably because they are predominantly broken down in the liver, whereas the plasma levels of BCAAs decrease while they are degraded in excess in muscle as a consequence of hepatic failure-induced catabolism. As AAAs and BCAAs are all neutral amino acids and share a common transporter across the blood-brain barrier (system L carrier), changes in their plasma ratio are reflected in the brain, subsequently disrupting the neurotransmitter profile of

Alcohol And Its Complications In The Elderly

A number of studies have shown that alcohol in moderate amounts is actually a good medicine for the elderly (even the Prohibition Amendment permitted the sale of alcohol for medicinal purposes) and that it improves social interaction, mental alertness, and several signs of physical health. Alcohol is primarily a drug which depresses or deadens the central nervous system (CNS). Paradoxically, in moderate amounts it may seem to act as a stimulant with mood-elevating effects that account for its popularity. What it is actually doing in these cases is to depress or deaden inhibitions. The lack of inhibitions contributes to feelings of relaxation, confidence, and euphoria. However, alcohol abuse can result in serious damage to the brain and to the rest of the nervous system. It can cause brain tissue to shrink or waste away, unsteadiness and lack of coordination in movement, and damage to nerves throughout the body. Large doses of alcohol cause inflammation of the stomach, pancreas, and...

Underlying Chronic Diseases Liver disease

Cirrhosis is a well-established risk factor for gallstones particularly in the more advanced stages.54,55 The overall prevalence is much higher than the general population at 25 to 30 .56 Increasing Child-Pugh score and obesity are more likely associated with gallstones. Most stones in cirrhosis are of the black pigment type.57 The biologic mechanism likely relates to altered pigment secretion, abnormal gallbladder motility, or increased estrogen levels.1 The threat of these stones becoming symptomatic seems higher in women, those more advanced in age, and patients with viral hepatitis compared with alcohol-related cirrhosis.58 Gallstone disease is also associated with hepatitis C virus (even when not yet cirrhotic)59 and nonalcoholic fatty liver disease, the connection being the metabolic syndrome and obesity.60

Electroencephalographs Studies of Chronic Substance Abusers

It is a logical fallacy to unquestionably attribute an EEG EP ERP difference between one group of substance dependent patients and a group of healthy, non-drug-abusing volunteers to an effect of substance abuse. Collectively, substance-dependent patients are known to exhibit higher-than-normal rates of comorbid psychopathology, polydrug abuse, medical disorders (e.g., cirrhosis,

Segmental Hypertrophy

In conditions such as cirrhosis, Budd-Chiari syndrome or primary sclerosing cholangitis the liver may be dysmorphic in appearance. In the chronic phase of Budd-Chiari syndrome, the abnormal vascularization tends to be located more peripherally and to be most prominent around the caudate lobe due to its separate autonomous venous drainage. Consequently, this liver portion may increase in volume.

Notes Tragacanth Milkvetch

The taxonomic difficulties of this complex but useful genus. Hungry early man doubtless used traga-canth as a survival food, after seeing that ants, goats, and sheep relish the sweeter gums. Tragacanth gum is one of the oldest natural emulsifiers known to man, extensively used in vaginal jellies and creams, low-calorie syrups, toothpastes, and hand lotions. The gum is used in such foods as salad dressings, sauces, ice creams, confections, syrups, milk powder stabilizers, citrus oil emulsions, and cheeses. Together with guar, tragacanth may make the cheaper ice creams healthier, substituting soluble cholesterol-free polysaccharides for the unhealthy cream. Some of these polysaccharides are active against ascites tumor types in mice. Among the species taxonomically confused with or called tragacanth, or some derivative thereof, Hartwell notes folk-cancer remedies for chronic indurations of the liver (including, probably, cirrhosis), nasal polyps, non-ulcerated cancers, superfluous...

Arterioportal Fistulas

Arterioportal fistulas may be acquired or congenital, and may have an intra- or extrahepatic location. Common causes of acquired arterioportal fistulas are cirrhosis and hepatic neoplasms, blunt or penetrating trauma, percutaneous liver biopsy, gastrectomy, transhepatic cholangiography, and biliary surgery (Fig. 34). In the case of congenital arterioportal fistulas, these are typically associated with hereditary hemorrhagic teleangectasia, biliary atresia, and Ehlers-Danlos Syndrome. Often asymptomatic within the first year of life, the first symptom of arterioportal fistula is usually portal hypertension associated with splenomegaly, hy-persplenism, variceal formation, and ascites 2 .

Secondary Diabetes Mellitus Other Specific Types

Secondary diabetes can result from extreme insulin resistance induced by glucocorticoids (Cushing's syndrome) growth hormone (acromegaly) adrener-gic hormones (pheochromocytoma) other medical conditions, such as uremia, hepatic cirrhosis, or polycystic ovary syndrome or medications (diuretics or exogenous glucocorticoids).

Paul Devenyi Revised by Ralph Myerson

Acute toxicity results in the impairment of behavior leading to other complications (e.g., trauma) and, in the case of some drugs, high doses can decrease breathing (respiratory depression) or change the rhythm of the heart, leading to accidental or intentional death. Chronic use can result in organ damage, which may lead to chronic illness or death (as with alcoholic cirrhosis of the liver). Persistent use of many classes of drugs also leads to TOLERANCE (an increased amount is required to produce the same effects) and physiologic (physical) dependence, so that a WITHDRAWAL syndrome is associated with sudden cessation of drug use. Drug users who employ hypodermic needles and syringes (injecting drug users IDUs ) are at risk for blood-borne diseases associated with the use of unsterile equipment, such as hepatitis and human immunodeficiency virus (HIV 1 and 2 the viruses responsible for AIDS see ACQUIRED IMMUNODEFICIENCY Syndrome).

Alcohol And The Cardiovascular System

Ethanol has long been recognized as a toxic agent affecting different organ functions both acutely and chronically 6 , A prospective study of middle-aged Swedish males registered for alcohol addiction revealed a two-fold greater increase in the incidence of clinical cardiac events than for liver cirrhosis 7 , Several factors may be responsible for the deleterious effects of alcohol on the myocardium, including (i) a direct toxic effect of ethanol or its metabolites (ii) associated nutritional deficiencies (i.e., thiamine) or (iii) direct toxicity of additives in the alcoholic beverage (i.e., lead or cobalt) 8 ,

Hepatic Sarcomas 6141

40 of patients have hepatic fibrosis or cirrhosis at autopsy, the nature of the association between chronic liver disease and HAS is unknown. Further study is also required to delineate the cause of HAS in the remaining 60 of cases without a definitive etiologic association.

General Aspects Of Hgf And Met Structure And Activities

In parenchymal organs, HGF is expressed predominantly in mesenchymal or stromal cells while Met HGF receptor is expressed in epithelial cells (24, 27, 37, 38). HGF induces branching tubulogenesis of epithelial cells, as a mesenchymal-derived factor in several tissues, including kidney, lung, and mammary gland. Targeted mutation of HGF or the c-met gene results in impaired development of the liver, placenta, and skeletal muscles and diaphragm (39-41). HGF is essential for long-distance migration of myogenic precursor cells during development of skeletal muscles and the diaphragm. This is a pertinent example of the motogenic activity of HGF during normal biological processes. Physiologically, expression of HGF is regulated in response to tissue injuries and HGF supports regeneration of various organs such as the liver, kidney, lung, and vascular tissues (24, 26, 28). Thus, HGF exerts biological activities to construct or reconstruct normal tissue...

Approaches And Risks Of Cholecystectomy

Cholecystectomy can be performed by a key-hole operation (laparoscopic cholecystectomy), by a small-incision cholecystectomy (incision < 8 cm in length), or by traditional open operation (incision > 8 cm in length).16-18 The complications after cholecystectomy depend on the clinical presentation. The overall perioperative mortality varies between 0 and 0.3 .19-21 The overall incidence of bile duct injuries requiring corrective surgery varies between 0.1 and 0.3 .19-21 Corrective surgery for bile duct injury carries its own risks including perioperative mortality (1 to 4 ),22-24 secondary biliary cirrhosis (11 ),22 anastomotic stricture (9 to 20 ),22,24 and cholangitis (5 ).23 The quality of life can be poor several years after the corrective surgery.25 Apart from the serious complications of perioperative mortality and bile duct injury and its sequelae, other complications of cholecystectomy include

Contraindications And Precautions

Herbs with choleretic and cholagogue activity should be used with caution by people with bile duct obstruction (Blumenthal et al 2000), acute or severe hepatocellular disease (e.g. cirrhosis), septic cholecystitis, intestinal spasm or ileus, liver cancer or with unconjugated hyperbilirubinaemia (Mills & Bone 2005).

Pathophysiology of Stone Formation

There are three kinds of gall stone cholesterol, black pigment, or brown pigment stones. Cholesterol stones constitute 75-90 of all gall stones. They are composed purely of cholesterol or have cholesterol as the major chemical constituent. Most cholesterol gall stones are of mixed composition. Pigmented stones get their color and their name from precipitated bilirubin. Increased production of unconjugated bilirubin causes black pigmentation. Formation of black pigment stones is typically associated with chronic hemolysis, cirrhosis, and pancreatitis. Brown pigment stones are usually associated with infection. Cytoskeletons of bacteria can be seen microscopically in brown pigment stones, Rapid weight loss Total parenteral nutrition Diabetes Other conditions Immobility Cirrhosis Spinal cord injury Other conditions predisposing to gall bladder disease Insulin-resistant diabetes predisposes to cholelithiasis. A Swedish study showed that the prevalence of gall stones in Crohn's disease was...

Disorders of Fructose Metabolism

Hypoglycemia, hepatomegaly, growth retardation, proteinuria, lactic acidemia, hyperlipidemia, hyperuricemia (gout), hepatocellular carcinoma Cardiomyopathy, skeletal myopathy, cardiorespiratory failure Hypoglycemia (mild), hepatomegaly, myopathy, hyperlipidemia Hepatomegaly, cirrhosis, liver failure, myopathy

Portal Vein Thrombosis

The etiology of portal vein thrombosis falls into the Virchow trias, comprising reduced blood flow within the vessel, changes in the consistency of blood which affects flow properties, and pathologies of the vessel wall. Thus, etiological factors of portal vein thrombosis are slow flow secondary to cirrhosis, obstruction of the vessel by porto-hepatic lymphadenopathy, direct invasion by cancer, inflammatory changes secondary to pancreatitis, sclerosing cholangitis, abdominal infections, poly-cytemia vera and benign masses 1,45,51,75 .

Chronic Liver Disease

Table 4 Management of chronic liver failure in children Nutritional support From Kelly DA (2002) Managing liver failure. Postgraduate Medical Journal 78 660-667. promote hepatic cell growth. Recommendations for nutritional management of children with chronic liver disease are presented in Table 4. The energy need for adults with chronic liver disease is 30-35 kcal kg day. Energy requirements are increased to compensate for the weight loss that often occurs in cirrhosis. Protein should be provided as 0.8-1 g kg for adults unnecessary protein restriction should be avoided because it may only worsen total body protein losses. Energy from fat is best delivered as MCTs due to malabsorption of long-chain fatty acids. Several infant, pediatric, and adult formulas are available with a large percentage of fat in the form of MCTs. Supplementation with fat-soluble vitamins (A, D, E, and K) in water-miscible solutions is necessary due to the potential for deficiencies associated with fat...

Nutritional summary

Flushing (burning and itching of face, arms and chest) and stomach irritation arc the main side effects of moderately high supplemental niacin intake (more than 35 mg d). Liver damage that may culminate in irreversible liver failure is a risk associated with long-term use of very high doses (3000 and more mg dl as a cholesterol-lowering drug. Such high doses must never be used without close monitoring of liver function. High intakes of nicotinic acid may interfere with the effects of sulfinpyrazone (Anturane).

Treatment of liver tumours

The liver is one of the vital organs of the body, and while we are generally unaware of its function we are very soon aware of any dysfunction. Its importance as a synthetic and storage organ, in addition to its prime importance in producing body heat, is evident through its regenerative capacity. However, some infections and the abuse of some substances, principally alcohol, cannot be sustained indefinitely and ultimately liver failure will ensue. Cancer in the liver is often secondary to cancer elsewhere in the body and the liver's copious blood supplies (peripheral and portal circulations) and functional proximity to the lymphatic system mean that it is a prime site for metastases. These are invariably fatal. A patient with liver failure will feel very ill indeed and, due to poor prognosis from liver failure, will be very distressed. The patient may also be disfigured by jaundice, which can be quite frank and alarming in extreme liver failure, and by ascites. In addition to the...

Tissue Contents and Kinetics of Lycopene Turnover

Patients with alcoholic cirrhosis of the liver have greatly reduced hepatic lycopene concentrations indeed, hepatic lycopene seems to offer a sensitive index of hepatic health. Studies of organ concentrations (Table 3), suggest a gradient from circulating levels in plasma to different ones in specific tissues. The different carotenoid ratios between organs (not shown) also indicate selective transport and accumulation. However, the mechanisms involved are poorly understood. No lycopene is detectable in the retina or lens of the eye, where lutein and zeax-anthin are found however, lycopene is present in the ciliary body.

Alcoholic Liver Disease Role Of Free Radicals

Other hand, compounds which inhibit cytochrome P4502E1 such as chlomethiazol or diallyl sulfide 90,91 , also inhibit lipid peroxidation, radical production and result in an improvement ofhepatic morphology. Obviously, the degree of induction of cytochrome P4502E1 is of predominant importance with respect to ALD. It is, therefore, concluded that the ROS produced by this pathway may be especially important. This induction is diet dependent and enhanced with unsaturated fatty acids such as corn oil and low carbohydrates. In addition, iron, an important compound in the production ofROS, plays a significant role. Iron supplementation increases liver disease and administration of an iron chelator decreases ALD. Although, the administration of vitamin E to rodents inhibits ALD to some extent, data in humans are not very encouraging. The approach of administering vitamin E together with selenium and zinc to patients with alcoholic cirrhosis did show an improvement in mortality, but the number...

Assessment of Manganese Status

Slightly higher than normal in individuals consuming manganese supplements. Lymphocyte MnSOD activity and blood arginase activity are increased in individuals who consume manganese supplements however, their value as biomarkers for manganese status may be complicated due to the number of cytokines and disease states that may also increase their expression. Urinary manganese excretion has not been found to be sensitive to dietary manganese intake. With respect to the diagnosis of manganese toxicosis, the use of MRI appears to be promising because the images associated with manganese tox-icity are relatively specific. Whole blood manganese concentrations can be correlated with MRI intensity and Ti values in the globus pallidus even in the absence of symptoms of neurological damage. Thus, although it is relatively expensive, MRI may be particularly useful as a means of identifying susceptible individuals in, or around, manganese-emitting factories. In addition, the method may be useful...

Hepatocyte Injury Induced By Hcv Infection

During the course of a chronic HCV infection, hepatocytes are continuously damaged and replicated, and hepatic fibrosis appears to progress, whereas the frequencies of genetic alteration also probably increase. It is generally accepted that multiple genetic alteration, induced by mutations, is an important factor in carcinogenesis. Therefore, continuous cell death and replication and multiple genetic alteration may lead to the development of cirrhosis and HCC (Fig. 2). However, the mechanisms by which HCV induces liver injury and hepatocyte death remain, to a great extent, ambiguous.

Effects Of Shosaikoto On Hepatic Fibrosis

This is accompanied by a loss of cellular retinoid, and the synthesis of a-SMA and large quantities of the major components of the ECM, including collagen types I, III, and IV, fibronectin, laminin, and proteoglycans. a-SMA is an activation marker of HSCs. It has been shown that, in vivo, HSCs express the genes that encode for enzymes such as matrix metalloproteinase (MMP)-1, which catalyzes the digestion of native fibrillar collagen types I and III, and MMP-2, which acts on denatured collagen types I and III and native collagen type IV, as well as a tissue inhibitor of metalloproteinase (TIMP)-1 (34). The net effect of the production of proteins involved in matrix synthesis and degradation could be reduced matrix degradation, which could account for the marked increases in matrix deposition and nodule formation observed during hepatic fibrosis and cirrhosis (9,35). peroxidation (67). The antioxidant activity of Scutellaria root was due to the action of baicalin,...

Effects Of Shosaikoto On Hepatic Carcinogenesis

HCC is, worldwide, one of the most common malignancies, especially in Southeast Asia. Based on clinical information, as a causative agent, HCV is more common than HBV in both Japan and Western countries. The incidence of HCC has been shown to be higher in patients with chronic HCV infection than for those with chronic HBV infection (79). In chronic hepatitis B, a resolution of the disease can frequently be seen after the inactivation of viral replication (4), which probably contributes to a lower incidence of HCC. In contrast, HCV multiplication is sustained throughout the course of a typical infection (80,81). When hepatocytes are continuously damaged and replicated, as is the case for HCV-infected patients with cirrhosis, the frequencies of genetic alteration also probably increase along with hepatic fibrosis, leading to the development of cirrhosis and HCC (Fig. 2). It is generally accepted that multiple genetic alteration is important in carcinogenesis. The HCC occurrence rate in...

Presentday Cultivation And Usage

Milk thistle is indigenous to Kashmir, Southern Europe, Southern Russia, North Africa, and Asia Minor. It was introduced to most areas of Europe, North and South America, and Southern Australia, and is cultivated mainly in the dry rocky soils of European countries, Australia, Canada, China, North and South America as a medicinal plant. It is also grown as ornamental plant for its attractive foliage. The seeds are collected when ripe, during late summer. Presently, milk thistle seed, its purified extracts and its active constituents are mainly used in liver diseases. It is the most widely used hepatoprotective agent in chronic inflammatory hepatic disorders, including hepatitis, jaundice, alcohol abuse, fibrosis, cirrhosis, and fatty infiltration and in hepatotoxicity by mushroom poisoning and by industrial pollutants. It is also widely used as nutraceutical agent. In homoeopathy, the seed tincture is used in liver disorders, jaundice, gall stones, peritonitis, hemorrhage, bronchitis,...

Dangerous Supplements

The potential harmful effects of yohimbe, ephedra, and excessive caffeine intake have already been mentioned. Kava is an herb used to treat anxiety, but it may cause liver failure. In addition, individuals on prescription or over-the-counter medications should be wary of supplements, as there may be adverse interactions.

Prohibition Of Alcohol

Given the common belief that Prohibition failed utterly to alter the consumption of alcohol or its adverse effects on health, it is appropriate to ask, To what extent did the law reduce alcohol use in the United States First, there is no question that it succeeded in eliminating 170,000 saloons, even if it did not change the attitudes of most Americans about the morality of drinking. And, while some writers have asserted that drunkenness actually increased during Prohibition, most available records point to the opposite conclusion (Aaron & Musto, 1981 Lender & Martin, 1987). The most consistent findings on the impact of Prohibition come from statistics on medical problems known to be linked to alcohol consumption, especially excessive alcohol consumption. Among these problems were hospital admissions for alcoholism and admissions to state mental institutions for alcoholic dementia and alcoholic psychosis. Striking decreases were observed in New York and Massachusetts, two states...

Metabolic Complications Liver Disease

Although PN may be life sustaining, long-term use may be detrimental to the liver. The severity of injury ranges from reversible transaminase elevations to severe cholestasis and cirrhosis, especially in infants with short bowel syndrome. It is not clear whether this is due mainly to a nutrient deficiency, toxicity, or some physiological process missing because of the lack of enteral feeding. Prevention and treatment strategies continue to include minimizing or preventing episodes of sepsis, providing enteral feedings, moderating energy intake to provide for adequate growth but not to overfeed, cycling parenteral nutrition infusion, reduction of copper and manganese, use of an amino acid solution developed for infants, treatment prophylaxis for bacterial overgrowth, and the use of ursodeoxy-cholic acid. Another drug that has been studied but is not available for clinical use is cholecystokinin, which promotes gallbladder contraction. A recent and controversial recommendation is the...

Fibrolamellar Carcinoma FLC

FLC is a slow-growing neoplasm of unknown etiology with different clinical and pathological features of HCC and HB. It is frequently detected in patients of adolescent age and has no predilection for either gender 19 . It generally occurs in the non-cirrhotic liver with normal AFP levels. There are no known risk factors and the prognosis is better than for HCC due to the better chances of surgical resection.

Indications Milk Thistle

Acne (f MCK) Ague (f GMH) Allergy (f1 MCK ACT9 251) Amenorrhea (f MCK NP9(2) 6) Anorexia (2 FAD PHR) Anthrax (f BIB) Arthrosis (f ACT9 251) Asthma (f1 BIB ACT9 251) Atherosis (1 X15617879) Biliousness (f GMH WOI) Bleeding (f BIB HHB NP9(2) 6) Bron-chosis (f BIB BOU EB49 406) Calculus (f BIB WOI) Cancer (f JLH WOI NP9(2) 6) Cancer, bladder (f1 NP9(2) 6) Cancer, breast (f1 HHB JLH MAB) Cancer, cervix (f1 HC020444-262) Cancer, colon (f1 FNF JN133 3861S) Cancer, lung (f1 X15224346) Cancer, nose (f HHB JLH) Cancer, ovary (f1 HC020444-262) Cancer, prostate (f1 X15899838) Cancer, skin (f1 HC020444-262 NP9(2) 6 X15586237) Cancer, tongue (f1 HC020444-262) Cardiopathy (1 X15617879) Catarrh (f BIB GMH) Cerebrosis (f ACT9 251) Childbirth (f HHB) Cholecocystosis (2 APA BIB PHR PH2) Cholelithiasis (f MCK) Cirrhosis (2 BGB KOM PH2 SHT) Colic (f HH3 PH2) Colitis (f ACT9 251) Congestion (f MCK) Constipation (f MCK) Cough (f BIB) Cramp (f BIB) CTS (f1 ACT9 251 HC020444-262) Cystosis (f HH3) Depression...

Dietary Intake and Energy Expenditure

Energy expenditure is composed of the basal metabolic rate (BMR), the amount needed for growth and metabolism. Although clinical data are conflicting, some children with CLD have been shown to have an increased BMR. Shanbhogue et al. 9 reported a higher BMR, when related to lean tissue in patients with end-stage liver disease. In children with biliary atresia energy expenditure was 29 higher than healthy controls 10 . Also Shepherd 11 reported higher energy expenditure per unit body cell mass in children with biliary atresia. In contrast, Muller et al. 12 found that patients with cirrhosis

Jonathan Fryer Indications

Liver transplantation is indicated in circumstances where a life-threatening pathological process that involves the liver cannot be overcome, without replacing the entire liver. Most commonly, this occurs when end-stage liver disease (ESLD) has developed in a cirrhotic liver. Other situations where liver transplantation may be needed when cirrhosis is not present include acute liver failure, nonmetastatic tumors that are otherwise unresectable, polycystic liver disease, severe hepatic trauma, or acute failure of a transplanted liver. Disease entities that commonly cause cirrhosis in adults include hepatitis B and C, alcohol abuse, nonalcoholic steatohepatitis (NASH), primary biliary cirrhosis (PBC), and primary sclerosing cholangitis (PSC). In children common causes of cirrhosis include biliary atresia and metabolic liver diseases like Wilson's or alpha 1 antitrypsin deficiency. Other conditions, like acute liver failure and inborn errors of metabolism, may also necessitate...

The Two Frameworks Applied To Substance Abuse

About three quarters ( 107 billion) of the total cost in this tabulation is the value of labor Productivity lost as the result of illness, injury, or early death. The human capital lost as a result of alcohol-related mortality was computed for all those who died in 1992 from causes in which intoxication or chronic heavy drinking played a role. These include traffic fatalities and deaths from liver cirrhosis, among other causes. The lost human capital was valued by estimating how much the deceased would have earned if they had lived and worked until retirement age.

Secondary Deficiency

This may develop in conditions associated with diarrhoea, cirrhosis or malabsorption, as well as after extensive postoperative use of parenteral nutrition lacking adequate niacin. Pellagra may occur during prolonged isoniazid therapy (the drug replaces niacinamide in NAD), in malignant carcinoid tumour (tryptophan is diverted to form 5-hydroxytryptamine), and in Hartnup disease, an autosomal recessive disorder in which there is defective conversion of tryptophan to niacin (Beers & Berkow 2003). It has also been observed in Crohn's disease, most likely due to malnutrition and intestinal malabsorption (Abu-Qurshin et al 1997).

Special Syndromes Associated with Alcoholism

M., Van Thiel, D. H., Gavaler, J. S. and Schade, R. R., Hepatic dysfunction and neuropsychological test performance in alcoholics with cirrhosis. J. Stud. Alcohol 47 74-77, 1986. Tarter, R. E., Van Thiel, D. H., Arria, A. M., Carra, J. and Moss, H., Impact of cirrhosis on the neuropsychological test performance of alcoholics. Alcohol. Clin. Exp. Res. 12 619-621, 1988. Moore, J. W., Dunk, A. A., Crawford, J. R., Deans, H., Besson, J. A., De Lacey, G., Sinclair, T. S., Mowat, N. A. and Brunt, P. W., Neuropsychological deficits and morphological MRI brain scan abnormalities in apparently healthy non-encephalopathic patients with cirrhosis. A controlled study. J. Hepatology 9 319-325, 1989. Quero, J. C., Hartmann, I. J., Meulstee, J., Hop, W. C. and Schalm, S. W., The diagnosis of subclinical hepatic encephalopathy in patients with cirrhosis using neuropsychological tests and automated electroencephalogram analysis. Hepatology 24 556-560, 1996.

Primary Deficiency

This may result from malabsorption syndromes, cancer, liver cirrhosis and alcoholism, hyperthyroidism, congestive heart failure or medicine use, such as OCP, isoniazid, hydralazine, penicillamine, theophylline or MAO inhibitors (Beers & Berkow 2003, Bratman & Kroll 2000, Wardlaw et al 1997).

Management of Adcmrd for details see the guidelines of Peretti 2010 [29

Treatment consists primarily of a low fat diet, with the appropriate amounts of n-6 and n-3 fatty acids, supplemented with fat soluble vitamins. The failure to thrive of the children is the most important clinical feature and catch-up growth is not observed systematically 29 . The neurological and ophtamological complications may be less severe than in other familial hypocholesterolemias and may depend upon the levels of the fat soluble vitamins and when vitamin supplementation is instituted. Myolysis and cardiac abnormalities have been observed in some AD CMRD patients 23 and consequently, measurement of the serum CK level should be included in the evaluation and follow-up of the patients. A moderate degree of fat liver is common, but until now no case of cirrhosis has been published.

Hepatic And Renal Osteodystrophy

Both chronic liver disease and those conditions exhibiting end-stage renal disease result in compromised hydroxylation of vitamin D to produce its active metabolite. It has been reported that 50 of patients with chronic liver disease, especially those with primary or secondary biliary cirrhosis, present with associated osteodystrophy. This frequently leads to a vitamin D deficiency and manifests most commonly as metabolic bone disorders, hypocalcaemia and secondary hyperparathyroidism (Wills & Savory 1984). The resultant hypovitaminosis D can result in bone loss, cardiovascular disease, immune suppression and increased mortality in patients with end-stage kidney failure (Andress 2006). Consequently, correction of this deficiency has been one of many first line treatments in these situations.

Imaging of the Portal Venous System

The simultaneous availability of coronal source images permits demonstration of parenchymal lesions of the liver, pancreas, biliary tract and spleen. Precise and reliable assessment of the portal-venous system in patients with hepatic cirrhosis and portal hypertension is essential before liver transplantation, non-surgical transjugular shunting or surgical portosystemic shunting. In patients with portal hypertension and a history of gastro-esophageal bleeding, it is mandatory to ascertain whether the portal-venous system is patent or if the portal vein or its main branches are throm-bosed 28 .

Types of Hypertension

Hypertension is classified as either primary (or essential) hypertension or secondary hypertension. Primary hypertension has no specific origin but is strongly associated with lifestyle. It is responsible for 90 to 95 percent of diagnosed hypertension and is treated with stress management, changes in diet, increased physical activity, and medication (if needed). Secondary hypertension is responsible for 5 to 10 percent of diagnosed hypertension. It is caused by a preexisting medical condition such as congestive heart failure, kidney failure, liver failure, or damage to the endocrine (hormone) system.

Portal Vein Thrombosis and Cavernous Transformation

Thrombosis of the portal vein is a pathology that is frequently found in liver cirrhosis, pancreatitis, ascending portal thrombophlebitis or after scle-rotherapy of a gastroesophageal varix 1 . In this condition it is important to acquire accurate information regarding portal-venous patency (Fig. 16). 3D CE MR portography provides detailed information not only about the location and length of portal vein obstruction, but also about portal collateral pathways (Fig. 17). Over time, a network of small collateral vessels develops to bypass the portal-venous occlusion. This network of collaterals, known as a cavernous transformation, is identified by its characteristic enhancement pattern in the hepatic hilum during the portal-venous and equilibrium phases of imaging (Fig. 18).

Alcohol And The Immune System

Alterations of the immune system due to alcohol consumption have been a focus of multiple studies that have revealed impaired delayed-type hypersensitivity responses and ameliorated host defense against infections. Acute alcohol use has been associated with increased susceptibility to infections, posttrauma immunosuppression, and a decrease in antigen-specific T-cell proliferation response 13,16 , Malnutrition and cirrhosis are two of the conditions that develop with chronic ethanol consumption that affect the efficiency of the immune system to combat infections 11,12 , Ethanol influences the function of lymphocytes, monocytes and polymorphonuclear cells 13-15 ,

Malignant Focal Liver Lesions of Hepatocellular Origin

Nodular Enhancement Mri

Dysplastic nodules are commonly encountered pathologically in severe cirrhosis. However, only about 15 of such nodules are detected at MR imaging. When visualized, dysplastic nodules are typically hyperintense on T1-weighted images and hy-pointense on T2-weighted images 14 . However, since most are not seen, the most common appearance is therefore isointense compared to the surrounding liver parenchyma. Although arterial phase enhancement can increase the sensitivity for characterization of dysplastic nodules, this is at the expense of decreased specificity because of the overlap with the much more commonly seen arterial phase enhancement in HCC. The nature of nodular regeneration in cirrhosis, and the development of dysplastic nodules may lead to additional false-positive diagnoses of HCC. MR imaging is now widely considered the most successful imaging modality for differentiating regenerative and dysplastic nodules from HCC. Regenerating nodules may have altered SI depending on...

Pathophysiologic Background

The liver uniquely receives a dual blood supply approximately 1000-1200 ml min of blood arrives via the portal vein and approximately 400 ml min arrives via the hepatic artery. In a non-cirrhotic liver, blood perfusion occurs at pressures of approximately 7 mmHg and 100 mmHg, via the portal vein and hepatic artery, respectively. Arterio-portal parenchymal perfusion demonstrates the degree of reciprocity of the arterial and portal venous contributions by virtue of vascular flux through dynamic microcirculatory arterioportal shunts (APS), largely at the level of the portal triad by transplexal, transvasal, or even transtumoral routes 20,24 . These shunts can transiently open under the influence of angiogenic modulators but are frequently related to a pathology that either

Static Biochemical Tests

Iron status is assessed in relation to three stages of development of iron-deficiency anemia. In the first stage, to evaluate the size of body iron stores, serum or plasma ferritin can be measured by radiometric methods or using ELISA. Commercial kits are available. Confounding effects of infection, liver and malignant diseases, acute leukemia, Hodgkin's disease, rheumatoid arthritis, thalasse-mia major, alcohol consumption, age, and sex are reported. In the second stage, to determine the adequacy of iron supply to the erythroid marrow, serum iron (measured by the colorimetric method, available as commercial kits AAS is not recommended because it gives higher values), plasma or serum total iron binding capacity (TIBC by colo-rimetric or radioactive methods available as commercial kits), erythrocyte protoporphyrin (by specific hematofluorometer), and serum transferrin receptor (by ELISA using developed monoclonal antibodies) are measured. The percentage of trans-ferrin saturation is...

Techniques for Liver MR Imaging

Mrcp Images Setup

Valuable for sensitive evaluation of the acute and chronic changes of hepatitis, including cirrhosis. Dynamic perfusion analysis is obtained by the acquisition of a series of scans at multiple times (see Chapt. 3). No other imaging technique can provide the comprehensive evaluation of liver disease possible on MRI. Use of contrast-enhanced CT for multiphase examinations is associated with an ionizing radiation burden that is proportional to the number of scans obtained during the study. There are increasing concerns regarding the risks of radiation and the iodinated contrast agents associated with CT imaging of the abdomen. For example, the National Academy of Science has released BEIR VII, the seventh in a series of consensus reports on radiation risks, which includes a section on radiation from diagnostic CT. In brief, assuming the demographic distribution of the U.S. population, a single dose of 100 mSv is associated with an estimated lifetime attributable risk (LAR) for developing...

Confluent Hepatic Fibrosis

Confluent hepatic fibrosis is a mass-like fibrosis seen in approximately 15 of patients with advanced cirrhosis who are candidates for liver transplantation. The imaging findings of confluent fibrosis result in it being characterized due to its specific location in the liver, which is frequently the medial segment of the left and or right lobe. Calcifications or dilatation of the biliary ducts are very rare.

Pathogenic Autoantibodies

Majority of whom had SS and neurologic disease.83 The most common clinical presentation, based on retrospective review of 42 patients in whom clinical data was available, was neurologic in 33 (ataxia, motor, and sensory neuropathy). Interestingly, 44 of the patients with anti-GWB had reactivity to Ro52 as well. Other autoimmune diseases associated with GW P reactivity in less than 15 of the patients included SLE, primary biliary cirrhosis, RA, and MS.

Transient Hepatic Attenuation Differences THAD

Early enhancement of portal vein branches during the arterial phases of CT and MR dynamic studies is often indicative of APS. APS can sometimes be seen in association with small heman-giomas and seems to be related to the hyperdy-namic vasculature of this tumor. APS are common in liver cirrhosis, due to the damaged hepatic flow (Figs. 27,28), and can be a source of potential confusion with HCC, especially when they appear as small, round areas during the arterial phase (Figs. 29,30). Direct communication between the portal vein and systemic veins results in intrahepatic por-tosystemic venous shunts. These are frequent in the setting of liver cirrhosis with portal hypertension, and may be accompanied by extrahepatic portosystemic collateral circulation. THAD can be classified according to morphology (sectoral, segmental, and lobar), etiology (as a result of benign or malignant tumors, arteriopor-tal shunting, liver cirrhosis, or venous thrombosis), or pathogenesis (due to low portal...

The Effects Of Alcohol On Bodily Systems

Milder forms of these disorders are also detectable with neuropsychologic testing or brain IMAGING Techniques (CAT scans MRI). Studies of detoxified alcoholics (without other evidence of organic brain damage) reveal that 50 to 70 percent have impairments in neuropsychologic assessment (Eckardt & Martin, 1986). In most of these cases there is reversibility with abstinence from alcohol. Severe liver disease (e.g., advanced cirrhosis or Chronic alcohol consumption is associated with several pulmonary infectious diseases (in addition to risks associated with tobacco smoking). These include pneumonia, lung abscess, and tuberculosis. Aspiration pneumonia occurs in association with high levels of alcohol intoxication it is thought to be caused by the inhalation of bacteria caused by the impairment of the usual reflexes, such as coughing. Pancreatitis and alcoholic cirrhosis are associated with pulmonary effusions (build-up of fluid on the lung). Liver. Alcoholic liver disease is a major...

Indications Caper Bush

Adenopathy (f BIB JLH) Aging (f BIB) Allergy (1 X15799005) Amenorrhea (f DEP) Arteriosclerosis (f BIB BOU) Arthrosis (f BIB) Bleeding (f BOW) Cancer (f1 BIB) Cancer, abdomen (f1 FNF JLH) Cancer, bladder (f1 FNF JLH) Cancer, colon (f1 FNF JLH) Cancer, groin (f1 FNF JLH) Cancer, head (f1 FNF JLH) Cancer, kidney (f1 FNF JLH) Cancer, liver (f1 FNF JLH) Cancer, neck (f1 FNF JLH) Cancer, spleen (f1 FNF JLH) Cancer, uterus (f1 FNF JLH) Cataract (f BIB) Chill (f BIB BOU) Cirrhosis (f WO2) Cold (f BIB) Conjunctivosis (f BOW) Cough (f BOW GHA) Cramp (1 HOS) Cystosis (f JLH) Dengue (f BIB HJP) Diabetes (f GHA) Diarrhea (f BOW BOU) Dropsy (f BIB BOU DEP) Dysentery (f BIB) Dysmenorrhea (f BIB) Earache (f BI2 GHA) Enterosis (f BOW) Erythema (1 X15799005) Fever (f BOU) Fracture (f BIB) Ganglion (f BOU) Gastrosis (f BOW GHA) Gout (f DEP SKJ WO2) Headache (f BIB) Hepatosis (f1 JLH HOS WO2) Hyperacidity (f MKK) Impotence (f BOU) Induration (f JLH) Infection (f BOW BOU) Infertility (f BIB BOU)...

Comparing Single And Multiple Ring Enhancing Lesions Table

Weighted And Weighed

More, the use of SPIO in patients with cirrhosis is also challenging due to the diminished uptake and heterogeneous signal arising from fibrosis 24, 151 . However, in this regard a recent study has suggested a lower dose of SPIO agent might be useful in patients with cirrhotic liver 1 . In the dynamic phase of contrast enhancement after the administration of gadolinium-based contrast agents, lesions can be classified according to whether they demonstrate hypervascular or hypo-vascular enhancement patterns or delayed persistent enhancement on T1-weighted acquisitions during the arterial, portal-venous and equilibrium phases, respectively (Table 6). Within these three major groups of lesions, lesions can be classified further according to the presence or absence of certain characteristic features. For example, a central scar within a hypervascular lesion in a non-cirrhotic liver that shows low signal intensity on T1-weighted images and high signal intensity on T2-weighted images may be...

Alcoholic Liver Diseases

If a person stops drinking, the fat disappears from the liver cells, the swelling subsides and the AST and ALT levels become normal. The two-way arrow in the diagram of Figure 1 indicates that fatty liver is reversible with abstinence, and the condition may fluctuate back and forth between normal and fatty liver with abstinence and drinking, respectively. Thus, this, per se is not likely a serious situation it is an early warning that ''your liver does not like alcohol'' and that possibly worse things might yet come. There was a time when fatty liver was regarded as the precursor of the end-stage liver disease called cirrhosis (indicated by the broken arrow and question mark on Figure 1), but in the 1990s, most physicians do not believe that this direct connection exists. Thus, the outcome of alcoholic hepatitis can be death (worst scenario) or recovery (best scen-ario)-as shown on Figure 1. Repeated episodes of drinking and alcoholic hepatitis, however, even if the patient does not...

Histopathologic Classification of Liver Pathologies

Regenerative Liver Cells

2.8.6 Cirrhosis 2.8.7 Primary Biliary Cirrhosis 2.8.8 Secondary Biliary Cirrhosis Diffuse nodular hyperplasia can be subdivided into nodular regenerative hyperplasia in which no fibrous septa can be found, or diffuse nodular hy-perplasia containing fibrous septa or occuring in coexisting cirrhosis. Diffuse Nodular Hyperplasia with Fibrous Septa or in Cirrhosis As described above, this lesion corresponds to nodular regenerative hyperplasia with concomitant fibrous septa, or which is superimposed on a previous hepatic cirrhosis 177,184 . A regenerative nodule involving more than one solitary portal tract is called a multiacinar regenerative nodule. Normally, it presents in livers with pre-existing pathology such as cirrhosis, or in cases of severe disease of the portal veins, hepatic veins, or sinusoids. Usually, multiple nodules occur within the liver and these can correspond to cirrhotic nodules if they are surrounded by fibrous septa. If larger than most cirrhotic nodules of the same...

Leiomyosarcoma Malignant Fibrous Histiocytoma and Fibrosarcoma

These neoplasms are very rare tumors of the liver which usually occur in patients between 40 and 60 years of age, without gender predilection. Leiomyosarcoma is the most common of these lesions but to date only 54 cases have been described in the literature 29 . Microscopically, leiomyosarcomas originate from mesenchymal elements of the liver, and are composed of large smooth muscle spindle cells. Malignant fibrous histiocytoma was first described as a separate pathologic entity in the 1960s and 1970s. This lesion is composed of primitive cells that demonstrate partial histiocytic and fibroblastic differentiation. Finally, fibrosarco-ma is a malignant tumor of soft tissue that is composed of undifferentiated cells derived from collagen-producing fibroblasts 42,23 . Macroscopical-ly, each of these lesions appears as a large, typically solitary mass in a non-cirrhotic liver. Sometimes it is possible to find necrotic and hemorrhagic areas.

Images Anatomy For Mri Liver Contrast

Shunt Radiopaque Density

Patient with liver cirrhosis. On the pre-contrast CT scan (a) no focal lesions are visible. During the arterial phase (b) after contrast medium administration numerous, hyperdense areas (arrowheads) of variable size are appreciable. In the portal venous phase (c) these areas demonstrate rapid contrast medium wash-out resulting in isodensity. Unlike HCC, these lesions are not hypo-dense and there is no indication of a pseudocapsule on the portal venous phase scan Fig. 28a-c. Arterioportal shunts. Patient with liver cirrhosis. On the pre-contrast CT scan (a) the liver is homogeneous in density. On the dynamic study, a round, markedly hyperdense lesion (arrowhead) can be detected in the arterial phase (b). Rapid contrast medium wash-out occurs in the portal venous phase (c) but the lesion still appears slightly hyperdense compared to the surrounding liver parenchyma

Hepatocellular Carcinoma

Hepatocellular carcinoma (HCC) is the most common primary hepatic malignancy and one of the most prevalent visceral malignances worldwide 21 . HCC usually occurs in the setting of cirrhosis with a known cause, such as chronic viral hepatitis or alcoholism. Regarding alcoholism as a cause of cirrhosis, it is thought that alcoholism promotes hepatic malignancies indirectly via its immuno-suppressive effects. These effects facilitate the development of hepatitis B virus (HBV) and hepatitis C virus (HCV) infections. Furthermore, alcoholic cirrhosis is triggered by the well-known oxidative effects that deplete the anti-oxidative defense system 35 . Whereas in Asia HCC occurs almost exclusively in patients with chronic liver damage from hepatitis, in North America many patients develop HCC without cirrhosis or known risk factors 74 . In these latter patients it is possible that steroid hormones may play a role in carcinogene- sis, as tumors occurring in non-cirrhotic livers have been...

Biliary Atresia Triangular Cord Sign

Triangular Cord

Biliary atresia is an obliterative cholangiopathy that may affect not only the extrahepatic but also the intrahepatic bile duct system, with complete obliteration or discontinuity of the hepatic or common bile ducts at any point from the porta he-patis to the duodenum. Obstruction of bile flow leads to cholestasis, progressive fibrosis, and ultimately, cirrhosis. The disorder occurs once every 10,000-15,000 live births and is more common in girls than in boys 5 . It accounts for approximately one third of all cases of prolonged neonatal cholestatic jaundice (see Chapter 10,MR Imaging of the Liver in Pediatric Patients, Section 10.5.2, Biliary Atresia). The macroscopic aspect of the liver varies according to the stage of the disease. At first it enlarges and is dark green in color, becoming finely nodular as cirrhosis develops. In untreated cases cirrhosis may take between 1 and 6 months after birth to develop. Microscopically, cholestasis, periportal ductal proliferation, and the...

Hereditary Haemorrhagic Telangiectasia HHT

HHT, also called Rendu-Osler-Weber disease or Osler's disease, is a vascular, hereditary, autosomic dominant disorder that occurs with a frequency of approximately 10-20 cases 100,000 15 . HHT is characterized by the presence of mucocutaneous or visceral angiodysplastic lesions, the latter most frequently seen in the liver, lung, brain, and gastrointestinal tract. Hepatic involvement accounts for 10-40 of cases and is characterized by the presence of intrahepatic shunts (arterioportal, ar-teriosystemic, venous portosystemic), diffuse telangiectases, and vascular mass-forming lesions 3 . AVMs are usually distributed diffusely throughout the liver and may be associated with enlargement of the hepatic artery and increased tortuousity of vessels in the liver hilum and in the central portions of the liver lobes. In Osler's disease, increased arterial perfusion of the liver tissue frequently leads to secondary nodular hypertrophy, which may be misinterpreted as a malignant hepatic tumor....

Budd Chiari Syndrome Acute Chronic

Budd Chiarisyndrome

As a result of collateral venous drainage, Budd-Chiari syndrome is typically associated with peripheral hepatic atrophy and, conversely, caudate and central hypertrophy which, together, may lead to a displacement of the porta hepatis towards the anterior portion of the liver 20 . These morphological changes can be visualized on MRI, together with a clear depiction of the occluded liver veins. Other findings include regional differences in liver SI due to central lobular necrosis and hepatocellu-lar fat or iron content. Dynamic MR imaging of acute Budd-Chiari syndrome after bolus injection of extracellular contrast agents (Fig. 16) frequently reveals atypical parenchymal enhancement, which indirectly indicates the presence of increased vascular resistance. Unlike patients with liver cirrhosis, patients with acute Budd-Chiari syndrome demonstrate acute clinical symptoms and a large tender liver without signs of nodular changes. However, in chronic disease, nodular regenerative...

Thalassemia Macroscopic Image

Iron Liver Tabel

Dysplastic focus is defined as congeries of hepato-cytes, measuring less than 1 mm in diameter, which show dysplasia but no histological signs of malignancy. Dysplastic foci generally occur in cirrhosis of any origin and are extremely rare in non-cirrhotic livers. In addition, patients suffering from a-1-antitrypsin deficiency, tyrosinemia or chronic viral hepatitis B or C demonstrate a comparatively high prevalence of dysplastic foci. Usually, serum a-fetoprotein is normal or minimally increased. However, in patients with tyrosinemia, high levels of serum a-fetoprotein can be found even before nodules are macroscopically visible 12,181 . A dysplastic nodule is defined as a nodular region of hepatocytes, measuring at least 1 mm in diameter showing signs of dysplasia but no definite his-tological signs of malignancy. These nodules are usually found in cirrhotic livers. Dysplastic nodules may be differentiated into two subgroups on the basis of the degree of cellular dysplasia 59, 165 ....

Indications Dandelion

Abscess (f CRC MAD) Acne (f VAD) Adenopathy (f JLH) Ague (f BIB) Alactea (f LMP PH2) Alcoholism (f SKY) Alzheimer's (1 FNF) Anemia (f1 AAH DEM JFM WAM) Anorexia (12 APA KOM PH2 PIP VAD) Arthrosis (f BIB) Backache (f DEM) Bacteria (1 WOI) Biliary Dyskinesia (2 PIP) Biliousness (f BIB) Bladderstones (2 KOM) Boil (f CRC LMP) Bronchosis (f12 APA BIB LAF) Bruise (f BIB CRC) Cachexia (f NAD) Cancer (f CRC) Cancer, bladder (f JLH) Cancer, bowel (f JLH) Cancer, breast (f CRC JLH) Cancer, liver (f JLH) Cancer, spleen (f JLH) Caries (f CRC LMP) Cardiopathy (f APA BIB) Catarrh (f BIB CRC) Cellulite (1 FT71 S73) Chill (f HJP) Cholecystosis (2 BGB CRC HH3 KOM PH2) Cirrhosis (SKYf ) Cold (1 APA) Colic (1 PH2) Congestion (1 PH2) Conjunctivosis (f AAH AKT) Constipation (f1 FAD SKY FT71 S73) Consumption (f BIB) Cough (f MAD) Cramp (f DEM) Cystosis (1 WAM) Dermatosis (f APA BGB KAP KOM PH2) Diabetes (f1 BIB CRC JFM KOM MAD PH2 X15704495 X14750205) Dropsy (f1 BGB BIB DEM KAP MAD) Dysentery (f AKT)...

Dietary and Nutritional Management of Secondary Undernutrition

Acids or keto-analog amino acids has been devised to compensate for the metabolic defects of nitrogen handling in hepatic or renal failure states. The objective of nutritional support in patients with liver failure is to provide adequate macronutrients to ensure the specific substrates for energy and protein synthesis and integrity of normal hepatic tissue function, without inducing or accentuating encephalopathy or otherwise aggravating hepatic insufficiency.

Inflammatory Disorders

Polysaccharides extracted from G. lucidum were found by Park et al. (180) to have antifibrotic properties and to ameliorate cirrhosis induced by biliary ligation. The polysaccharides were given orally for 28 days postliga-tion, and this was found to lower collagen (hydroxyproline) content in rats liver and improved the liver morphology in comparison to control animals. The polysaccharide treatment also significantly decreased the ligation-in-duced increases in serum biochemical markers of liver damage (AST, ALT, alkaline phosphatase, and total bilirubin). These data suggest that polysac-charides from G. lucidum could be a promising antifibrotic therapy however, no mechanisms of this putative hepatoprotective action were described, and further study is needed (180).

Storage Disease Metabolic Diseases

In most cases, metabolic diseases affecting the liver ultimately lead to cirrhosis. Typically, the imaging findings in these cases are similar to those in adults in whom liver cirrhosis arises for other reasons. In other cases, however, the findings may be more subtle. Frequently hepatomegaly or fatty liver is the main finding during the early stages of disease. Glycogen Storage Disease. Another of the more common metabolic liver diseases is glycogen storage disease (GSD), a group of disorders that are associated with glycogen accumulation in the liver and other tissues due to specific defects in glycogenolysis. In this disease, mainly GSD type Ia is of interest with regard to imaging studies, since hepatomegaly with development of liver cell adenoma is a common finding. In GSD type Ia, there is developmental delay, hypoglycemia, metabolic aci-dosis, elevated triglycerides and uric acid levels in the blood, hepatomegaly, hepatic adenomas (Fig. 28), and HCC due to defects in the...

Kava Kava Piper Methysticum

A number of concerns have recently been raised about the safety of kava. In most studies, the number of adverse effects were similar to that of placebo (91). Undesired effects have usually consist of mild gastrointestinal upset and allergic skin reactions. Eye irritation and a yellow, scaly dry rash (kawaism) has been described with heavy, chronic use (87). Reports of extrapyramidal effects and exacerbation of Parkinson's disease do exist in the literature (93). The greatest concern regarding adverse effects has been over liver toxicity. Although rare, 25 cases of liver toxicity including hepatitis, cirrhosis, and fulminant hepatic failure have been reported in Europe (94). This has prompted the government of Switzerland to ban the sale of kava. The Food and Drug Administration is currently considering such actions in the United States.

Alcoholic versus viral or idiopathic chronic dilated cardiomyopathy DCM

Another clue to the possibility that alcoholics may have a viral pathogenesis for their chronic DCM is a little-known experiment on viral myocarditis in mice. Morin et al. 41 administered Coxsackie B virus to 48 mice. One half received laboratory chow and alcohol and the other half received laboratory chow and sweetened water. At the end of 5 weeks, 80 of the alcohol group showed microscopic cardiac involvement. Only 30 of the non-alcohol group had cardiac lesions (p 0.02). The cardiac involvement in the mice that received the alcohol was not only more frequent but also more severe than in the non-alcohol group 4T . How the damage of a viral attack on the myocardium can be augmented by alcohol is unknown, although there are many possibilities. It has been suggested, for example, that it may be due to the loss of potassium and magnesium from the myocardium or the ability of alcohol to inhibit the active transport of cations across the cell membrane 27,42 , An analogy may be made with...

Patient with jaundice

Jaundice results from an abnormally high bilirubin in the blood whose origin may be difficulty in eliminating it's then an obstructive jaundice. This is the most symptom in patients with periampullary cancer (located near the Vater's ampulla) or cancer of the pancreatic head. It can be considered a risk factor for postoperative complications. 8, 9 Many studies demonstrate that it could be associated with a higher incidence of insufficient postoperative renal function, but also of sepsis, haemorrhage, of liver failure and risk of mortality from about 16 (Jiang & Puntis, 1997). Jaundice causes a retention of acids and bile salts. In the long term, may cause ascending cholangitis and secondary hepatocellular damage. In case of interruption of bile flow, bile acids and salts can't inhibit the phenomenon of translocation and endotoxemia caused by gram-negative from the digestive tract. These bacteria will then multiply and, for a phenomenon of translocation, can contribute to the...

Using helpful alternative remedies

JflNG In late 2001, the Food and Drug Administration (FDA) issued a warning that some people in Europe who've used kava kava have experienced severe liver toxicity (damage to the liver, a crucial organ that you can't live without), suffering from such problems as hepatitis, cirrhosis, and even liver failure. In addition, the FDA also received reports on Americans experiencing liver problems with taking kava kava.

Effects of Alcohol on Liver Function

Continued alcohol consumption may lead to cirrhosis. However, not all alcoholics progress to cirrhosis. The reason for this is unclear. It has been suggested that genetic factors and differences in immune response may play a role. In alcoholic cirrhosis there is fibrocollagenous deposition, with scarring and disruption of surrounding hepatic architecture. There is ongoing necrosis with concurrent regeneration. Alcoholic cirrhosis is classically said to be micronodular, but often a mixed pattern is present. The underlying pathological mechanisms are complex and are the subject of debate. Induction of the MEOS and oxidation of ethanol by catalase result in free radical production. Glutathione (a free radical scavenger) is reduced in alcoholics, impairing the ability to dispose of free radicals. Mitochondrial damage occurs, limiting their capacity to oxidize fatty acids. Peroxisomal oxidation of fatty acids further increases free radical production. These changes eventually result in...

Liver in Specific Hepatobiliary Disorders Hepatocellular Diseases

Alcoholic liver disease The term 'alcoholic liver disease' refers to a spectrum of types of hepatic injury associated with continuous alcohol ingestion, ranging from alcoholic fatty liver to alcoholic stea-tohepatitis, fibrosis, and cirrhosis. Nutritional disturbances in alcoholics are an important cause of morbidity and mortality all classes of nutrients are affected. Anorexia leads to decreased food intake and subsequent protein-calorie malnutrition. Maldigestion and malabsorption can occur secondary to chronic alcohol injury to small intestinal mucosa. Alcohol consumption is often associated with chronic pancreatic insufficiency, which results in steatorrhea and decreased absorption of dietary protein, fat, and fat-soluble vitamins. Chronic alcohol ingestion also results in impaired hepatic amino acid uptake and protein synthesis. Many studies have examined the effect of oral or enteral nutritional supplementation in patients with alcoholic cirrhosis. Results are summarized in...


The liver not only processes nutrients but must detoxify all the harmful substances the villi were unable to prevent from being absorbed into the bloodstream. Other situations that can tax the liver considerably include overeating and eating foods that are refined. Refined foods are missing the nutrients they need to be properly metabolized. If the liver can no longer filter and cleanse the blood, or properly metabolize nutrients, or take care of its own health, it is because liver cells are damaged or begin to die. Liver damage is not easily detected by conventional testing and its condition may not be known until dysfunction becomes apparent through illness. Symptoms may range from headache, diarrhea, constipation, food sensitivities, flatulence, sleeplessness, and aching joints to cirrhosis and hepatitis.

Neurological Effects

The many neurological effects of acute and chronic alcohol abuse can be categorized as those related directly to alcohol, those secondary to chronic liver disease, and those mediated by thiamine deficiency. The stages of acute alcohol toxicity progress upward from legal intoxication with reduced reaction time and judgment, as occurs with blood levels greater than 0.08 g dl-1 that usually define legal intoxication, to coma and death with levels greater than 0.4 g dl-1. While mild intoxication is common with social drinking, coma and death have been described among college age males who consume excessive amounts of alcohol in a very short period of time. Automobile accidents, which account for a large portion of alcohol-related deaths, are more common in drunken pedestrians than drivers. Intoxication also leads to frequent falls and head trauma, and subdural hematoma can present with delayed but progressive loss of cognition, headaches, and eventual death. Chronic alcoholics are prone...


Chronic alcoholic patients are often iron deficient because of increased frequency of gastrointestinal bleeding, typically due to alcoholic gastritis or eso-phageal tears from frequent retching and vomiting, or from rupture of esophageal varices in patients with cirrhosis and portal hypertension. The major consequence of iron deficiency is anemia, which may be compounded by the concurrent effects of folate and pyridoxine deficiencies. Conversely, increased exposure to iron, e.g., from cooking in iron pots, increases the likelihood and severity of alcoholic liver disease, since the presence of iron in the liver promotes oxidative liver damage during the metabolism of alcohol.


Serotonin is synthesized in the central nervous system and is involved in the regulation of mood and sleep. In addition it is found in high quantities in neurons in the gastrointestinal tract where it is involved in regulation of gut motility. Tryptophan competes with BCAAs for transport across the blood-brain barrier and the ratio between trypto-phan and BCAAs therefore determines the uptake of both (groups of) amino acids by the brain (see section on BCAAs). Since albumin has a strong tryptophan-binding capacity, the plasma albumin concentration is inversely related to the plasma concentration of free tryptophan and as such influences the BCAA to tryp-tophan ratio and hence the brain uptake of both BCAAs and tryptophan. It has been suggested that increased plasma AAAs (tyrosine, phenylalanine, and tryptophan) levels in patients with liver failure are caused by the inability of the liver to degrade these amino acids. The resulting change in the ratio between AAA and BCAA plasma...

Toxic Effects

Chronic drinking also causes damage to a number of major organs. Permanent alterations in brain function have already been discussed. By far, one of the most important causes of death in alcoholics (other than by accidents) is liver damage. The liver is the organ that metabolizes ingested and body toxins it is essential for natural detoxification. Alcohol damage to the liver ranges from acute fatty liver to hepatitis, necrosis, and cirrhosis. Single doses of ethanol can deposit droplets of lipids, or fat, in the liver cells (called hepatocytes). With an accumulation of such lipid, the liver's ability to metabolize other body toxins is reduced. Even a weekend drinking binge can produce measurable increases in liver fat. It was found that liver fats doubled after only two days of drinking blood eth-anol levels ranged between twenty and eighty mg dl, suggesting that one need not be drunk in order to experience liver damage. Alcohol-induced hepatitis is an inflammatory condition of the...


A randomized, controlled clinical trial is the gold standard to reveal whether the beneficial effect of moderate alcohol intake is in fact due to this alcohol intake or results from some unknown confounding factor that no cohort study, however large, could discover. However, such a trial is unlikely to be performed to establish a direct link between alcohol consumption and health. Prospective observation of representative samples is the available method that comes closest to the ideal. A good start would be to design large cohort studies with the express aim of revealing the effects of alcohol intake on health. The studies presently available have not been designed primarily to this end. The problem of confounding, given the inter-correlation of many lifestyle practices and the imprecision with which they are measured, creates subtle and complex statistical challenges. Several guidelines for safe and sensible alcohol drinking have been suggested 60-62 , However, individual...

Arkshell See cockles

Ascaris lumbricoides. ascites Abnormal accumulation of fluid in the peritoneal cavity, occurring as a complication of cirrhosis of the liver, congestive heart failure, cancer and infectious diseases. Depending on the underlying cause, treatment may sometimes consist of a high-


Approximately two million Americans suffer from liver damage caused by alcohol abuse. About 10 to 20 percent of heavy drinkers will develop cirrhosis of the liver, which is characterized by scarring of the liver and causes irreversible damage. If heavy drinkers do not stop drinking, cirrhosis can cause poor health and, ultimately, death. In addition to cirrhosis, heavy drinkers may suffer from chronic liver disease or alcoholic hepatitis.

High Risk Groups

While alcohol abuse and alcoholism affect virtually every segment of the population, certain groups are at greater risk. Young adults between the ages of eighteen and twenty-nine have the highest prevalence of alcohol abuse, and persons who begin to drink at an early age, especially before the age of fourteen, have a greater risk for developing problems with alcohol. Persons with a family history of alcohol abuse or alcoholism are also more likely to experience alcohol-related problems. In the United States, American Indians and Alaska Natives (AI ANs) have the highest rates of current and heavy drinking of all racial or ethnic groups. Deaths from chronic liver disease and cirrhosis are nearly four times greater among AI ANs compared to the general U.S. population. They also have a higher prevalence of drunk driving compared to the general U.S. population. This illustration shows a healthy liver above, and a diseased liver below. Liver disease in alcoholics progresses from an...


If employed, the jejunal stent may be removed after a few weeks if the patient is well and a postoperative cholangiogram shows a patent anastomosis without narrowing. For patients with malignant disease, liver function tests and clinical status should be followed at regular intervals. A change in status or chemistries requires reevaluation with imaging to rule out tumor recurrence. For patients operated for benign strictures, regular lifelong surveillance of liver chemistries is indicated because of a significant rate of recurrent stricture formation, which may be asymptomatic but lead to secondary biliary cirrhosis if not corrected.

Extracts Garlic

Allicin mean MIC 4.1 pg ml mean MBC 7.9 pg ml) were lower than those for the Gram-positive strains tested (garlic MIC range 142.7-35.7 mg ml allicin mean MIC 27.5 pg ml mean MBC 91.9 pg ml). The putative periodontal pathogens had among the lowest MICs (17.8-1.1 mg ml garlic) and MBCs (35.7-1.1 mg ml garlic) (X15892950). Verma et al. (2005) demonstrated adapotogenic activity of garlic oil on exercise tolerance in coronary patients. Thirty patients were given garlic oil for 6 weeks. The 6-week treatment reduced heart rate at peak exercise and resultant workload on the heart (X15881870). Kim et al. (2005) showed that too much diallyl disulfide could be cytotoxic to neuronal cells. Levels of free radicals and membrane lipid peroxidation increased dose dependently at levels higher than 25 pM (X 15950962). Chang et al. (2005) found that sodium 2-propenyl thiosulfate had cyclooxygenase inhibitory as well as antiaggregant activity in canine platelets (X15850716). Akyuz and Kaymakoglu (2005)...

Adverse Effects

Benzodiazepines have proven to be exceptionally safe agents. The dose at which these agents are lethal tends to be exceedingly high. Fatalities are more apt to occur when these drugs are taken in combination with other central nervous system depressant agents such as ethanol. Sedation is a common adverse effect associated with benzodiazepine use. Light-headedness, confusion, and loss of motor coordination may all result following the administration of benzodiazepines. MEMORY impairment may be detected in individuals treated with benzodiazepines, and this effect may prove to be particularly troublesome to ELDERLY patients who are experiencing memory-related problems. PSYCHOMOTOR impairment can be hazardous to individuals when they are driving. This problem can be exacerbated in individuals who consume ethanol while they are being treated with benzodiazepines. Hypnotic agents that are converted into active metabolites that are slowly eliminated from the body, such as flurazepam, may...