Aetiologies
Primary aetiology of malnutrition is poor oral intake, stemming form multiple factors such as altered sense of taste, early satiety due to mechanical compression from massive ascites, dietary restrictions, weakness, fatigue and low-grade encephalopathy. Malabsorption, increased energy expenditure and altered fuel consumption are other important factors that lead to malnutrition.

Treatment

The goals of nutitional therapy are to improve PEM and correct nutrient deficiencies. This can be accomplished via oral, enteral or parenteral methods, or combination of these modalities. Intervention in the early stage of malnutrition can improve the outcome. As a guideline oral intake should be encouraged; if patients are unable to maintain adequate intake orally, a nasogastric tube should be inserted for enteral feeding. Cabre et al found that, in severely malnourished patients with cirrhosis, enteral feeding improved serum albumin levels and Child-Turcotte-Pugh scores, and decreased in-hospital mortality rates compared with standard oral diet.
Parenteral nutrition is the less desirable option than enteral nutrition and should be reserved for patients in whom enteral feeding cannot be achieved.

In 1997, ESPEN (European Society for Clinical Nutrition and Metabolism) created a guideline for meeting nutritional goals in patients with enteral feeding when oral intake is inadequate. In patient with compensated cirrhosis, guidelines recommend that the patient consume 25-35 kcal/kg body weight per day of non-protein energy and 1-1.2 g/kg body weight per day of protein or amino acids. In patient with complicated cirrhosis associated with malnutrition, non-protein energy should be increased to 35-40 kcal/kg body weight per day and protein intake should increased to 1.5 g/kg body weight per day. According to the guidelines, protein intake should decrease to 0.5 to 1.5 g/kg body weight per day if stage I or II encephalopathy is present and to 0.5 to 1.5 g/kg body weight per day if stage III and IV encephalopathy is present.

Supplementation with BCAA
The usefulness of branched-chain amino acid (BCAA) supplementation in patient with cirrhosis has long been debated. It was proposed that depletion of BCAAs, as seen in many patients with advanced liver disease, might promote the development of hepatic encephalopathy by enhancing the passage of aromatic amino acids across the blood- brain barrier, resulting in synthesis of false neurotransmitters. Early investigations, therefore, focused on BCAAs as a potential treatment for hepatic encephalopathy. Recent studies advocate the use of nocturnal BCAA administration. It is believed that BCAAs that are consumed during the day are primarily used as a source of energy for physical exercise, whereas when administered at night, BCAAs might be preferentially used for protein synthesis.


Otsuka Philippines Liver Nutrition Advocacy Campaign

After twelve years of exposure in the Philippine pharmaceutical market, Otsuka products showed great potential and that expansion was imminent. Thus, in 1997, Otsuka (Philippines) Pharmaceutical, Inc. (OPPI) was established. Official operations of Otsuka (Philippines) Pharmaceutical, Inc. (OPPI) began January, 1998 with sixty-five employees, composed mainly of Medical Representatives deployed nationwide promoting Otsuka products one of which was Aminoleban Injection (launched May 1989) and Aminoleban EN (launched May 1993) for the treatment of hepatic encephalopathy and nutritional supplement for liver failure patients.

Over the years of its incorporation, OPPI continues to grow despite many economic and political issues. To address the concerns of many patients taking Aminoleban EN, Aminoleban ORAL was launched last October 2004. Aminoleban Oral offers the same nutritional value as the Aminoleban EN, more affordable with palatable taste amino acid enteral formula.

Now, Aminoleban leading the Liver Cirrhosis market, is expanding its perspective to help more patients with liver impairment through the establishment of PEM Pal Club (Protein-Energy Malnutrition Patient Support Program), a patient support system that aims to provide patient education through lay-forums which will be conducted on different “Bantay Atay Centers” nationwide. Lectures will be presented by local Medical Doctors and Nutritionist to ensure ethical and accurate information. The PEM Pal hotline and website will serve as communication medium to all patients and their caregivers who wished to learn more about liver disease prevention and management. Lastly, Aminoleban Oral discounts will be provided to all patients registered by their attending physicians to PEM Pal Club.

Zeroing in on Liver Cirrhosis
Jaime G. Ignacio, MD, FPCP, FPSG, FPSDE


Like all organs, the liver can be affected by various disease processes. Of all the disease conditions affecting the liver, cirrhosis is one of the most important. Most Filipinos have only a vague idea as to what cirrhosis exactly is and what it can lead to, and oftentimes equate it with liver cancer. More importantly, most do not know how to avoid developing liver cirrhosis.

The liver is considered to be the largest gland in the body. It lies a little bit to the right-hand side of the upper abdomen and is concerned with various vital bodily functions. These include: production of vital blood proteins, enzymes and certain substances that make blood clotting possible, energy storage to fuel muscles, maintenance of normal blood sugar levels, hormonal regulation and metabolism of cholesterol. Much of the blood leaving the intestines passes through the liver before reaching the rest of the body.

Cirrhosis is a condition where the normal liver tissue is almost completely replaced by scar tissue which occurs as a result of continuous long-term liver damage by some offending agent. This scar tissue forms despite the liver’s ability to heal and regenerate itself and interferes with the normal blood circulation within the liver and may also seriously impair its normal functions. It is, therefore, a late complication rather than an early consequence. More importantly, it is also known to lead to the development of liver cancer. Individuals with early cirrhosis may experience very trivial symptoms or sometimes no symptoms at all. However, in more advanced stages symptoms may include loss of appetite and weight, abdominal enlargement due to fluid accumulation in the abdominal cavity, yellowing of the eyes and skin, vomiting of blood due to ruptured blood vessels in the stomach and esophagus, coma and often death. Needless to say, this stage is often punctuated by frequent expensive hospitalizations and treatments.

There are quite a number of causes of cirrhosis. In the Philippines, the most common causes include long standing hepatitis B (and to a lesser extent hepatitis C), prolonged excessive alcohol intake and possibly non-alcoholic fatty liver disease (NAFLD). The country is particularly endemic for hepatitis B and prolonged untreated infection with this virus poses a very significant risk. Persons consuming more than 20 grams of ethanol (e.g.: more than 2 bottles of beer) daily for at least 15 years likewise have a significant risk of developing liver cirrhosis. There is emerging evidence that a variant of NAFLD called non-alcoholic steato-hepatitis (NASH) may be a risk factor for cirrhosis among overweight diabetic individuals. Occasionally, prolonged exposure to certain toxic chemicals like certain insecticides and solvents may also lead to its development.

The best way to avoid developing cirrhosis is by avoiding viral hepatitis through vaccination against hepatitis B and by not drinking alcohol excessively. There is also convincing evidence that correctly treating hepatitis B and C with the available scientifically validated medications may prevent cirrhosis in infected individuals. There is no medication definitely proven effective for NAFLD/NASH at this time. The best recommendation for these patients would be to maintain good control of their weight and blood sugar levels through regular exercise and proper diet. There is no definite evidence that certain concoctions, herbal preparations or liver-protecting agents can prevent cirrhosis among those who are at risk. Self-medication with these substances without regard for the risk factors should be strongly discouraged and high-risk individuals should be advised to consult a qualified physician. What the patient can do is eat a well-balanced nutritious diet appropriately rich in important proteins and low in salt. Protein restriction in the stable cirrhotic should not anymore be advised as this will further worsen the already malnourished state of these patients. Once cirrhosis reaches an advanced stage, cure is very unlikely and liver transplantation may oftentimes be the only option for these very sick patients.

It also pays to be well-informed about one’s condition. While books and the internet may be very important tools to obtain information, nothing beats an experienced physician when it comes to answering one’s questions about health and disease and giving sound advice.

FATTY LIVER: SOUNDS FAMILIAR?

FOIE GRAS… tastes good, isn’t it? But do you know what it means? That’s French for “Fatty liver”. Do you know how it is made? Goose are forced fed with large amounts of fat, making the liver grow twice its normal size, and before that goose becomes a patient of the French healthcare system, it is boxed up by some French Pate house for your consumption. Are you turning yourself into a human pate?

Though fatty liver is commonly seen among heavy alcoholics and in patients with chronic viral hepatitis, its presence in diabetics, in patients with high cholesterol and triglycerides, and in overweight or obese individuals, adults and kids alike, makes it a growing concern of the new millennium. What is indeed alarming is that, according to Dr. Joel Lavine, University of California, San Diego, fatty liver has been found in obese children as young as three years old and its complication of cirrhosis as young as age seven (www.passporthealthaustin.com).

Excessive alcohol intake of more than 3 bottles of beer, one shot (30 cc.) of whisky, or a 100 cc of wine daily may lead to fatty liver. Prolonged alcohol intake may then cause liver inflammation and later cirrhosis. If the fatty liver is not associated with alcohol intake, it is called non-alcoholic fatty liver disease.

Fatty liver is simply a condition of excessive accumulation of fat in the liver cells. Most of individuals with fatty liver have no symptoms though some individuals may have non-specific symptoms of abdominal pains or enlargement of the abdomen and skin yellowing, depending on the severity of the disease. Simple non-alcoholic fatty liver (or steatosis) usually does not damage the liver, but its more severe form, non-alcoholic steatohepatitis (NASH), which is associated with inflammation of the liver, may lead to complications of liver cirrhosis and even liver cancer.

Fatty liver disease and NASH are usually detected only because of abnormal laboratory examinations, more specifically an elevated liver enzyme (AST/ALT) or an abnormal ultrasound result. Blood sugar levels and cholesterol and triglycerides may also be elevated depending on the cause. A CT scan or MRI may also detect fatty liver with better accuracy than ultrasound. To differentiate simple fatty liver and NASH, however, a liver biopsy may have to be done.

Presently there is no standard medical treatment specific for non-alcoholic fatty liver disease. Treatment basically consists of treatment of the underlying cause. In its early stages, fatty liver may be reversible, but once cirrhosis and even liver cancer sets in, liver transplantation may be necessary.

A healthy diet, however, is basic in the treatment of fatty liver. Diet and an exercise program may reduce the amount of accumulated fat in the liver. The most effective diet is rich in fiber and low in calories and saturated fat, with total fat accounting for no more than 30 percent of total calories. Weight reduction, however, should be gradual at 1-2 lbs a week. And even if you are not overweight, a healthy diet and daily physical activity may reduce liver inflammation, lower elevated levels of liver enzymes and decrease insulin resistance.

For diabetics, strict blood sugar control with diet exercise and medications or insulin, may reduce the amount of fat in the liver and prevent further liver damage. Control of elevated cholesterol and triglycerides also with diet, exercise and the use of cholesterol lowering drugs may stabilize or reverse non-alcoholic fatty liver disease. Alcoholic drinks and drugs causing liver injuries should be avoided.

Prevention of fatty liver should be one’s goal. Your best defense against nonalcoholic fatty liver disease is to maintain a healthy body through a balanced diet, regular exercise and avoidance of excess alcohol.

 
 
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