Diet in the patient with liver disease

  1. Gastroepato
  2. Gastroenterology
  3. Diet in the patient with liver disease
  4. The diet in diarrheal syndrome


Every day I see numerous liver patients who ask me what foods they should consume to avoid water retention and weight gain. In fact they are followed for cirrhosis having to weigh every morning, being treated for ascites (ascites cure). My teacher comes to me, when one day he saw a bottle of mineral water in the hands of a cirrhotic and, reading the composition of the water and the fixed residue at 180 degrees, ie the salts that remain after having evaporated the water for boiling , reading that this value was 1.3 g / liter, he was seized with such an annoyance that he scolded us and removed the bottle.
In the age of fast-food and the problems associated with the wrong diet of adolescents who are sedentary and obese and suffering from Mody type diabetes or early type 2 diabetes, as for adults, the rediscovery of simple food and campagnolo is a panacea for our nutrition of the future.

This report to tell you that a diet in the cirrhotic patient is not a trivial matter! We read and try to understand why some foods should be preferred and others abolished, including alcohol! Finally, we remind our kind Navigators that this page alone scientific information, can not be used any diet to cure themselves, without first having consulted their personal doctor who is responsible for the care of their client. First of all, let's say that the right diet for the liver is divided into two distinct phases:dieta e steatosi

- Preventive topic, ie the right diet that prevents liver steatosis and the consequent cirrhosis
- Dietotherapeutic topic, ie the right diet that can be useful to the patient with liver disease, for example the patient with hepatic insufficiency and ascites.

Diet to prevent liver damage: the preventive moment


Today's life imposes frenetic rhythms and meals outside the home; I remember what a friend of mine told me the other night and that is, that he had lunched out with his wife for two whole years, causing acute gastritis and fatty liver, eating in the fry and fast-food, with sandwiches consumed on the fly, washed down with various fizzy drinks. This condition is called steatosis, better known as fatty liver. The excess of lipids, saturated fats, especially saturated and hydrogenated fats, overloads the liver, which is the key organ of lipid metabolism, whereby the disturbed hepatobiliary system is charged with triglycerides and meets the NAFLD syndrome, especially if it is abused of alcohol.


There are other conditions that can lead to NAFLD syndrome and are:

- Diabetes
- L'obesità
- Diplipidemias (lipids and atheromatous plaque)

In all these diseases, a proper diet is at the base of the prevention of the liver pathologies already described at the reported links and also of cardiovascular diseases, since it is known that an excess of lipids in the circulation is responsible for the formation of atheromatous plaques in the overlapping trunks. aortic and coronary arteries, with possible cerebral stroke and myocardial infarction, also limiting the cholesterol intake avoids the formation of cholesterol stones in the gallbladder (see gallbladder stones, calculi of the bile duct). Furthermore, a right amount of fiber allows a modification of the bile salts pool, in the sense that the deoxycholic acid pool is reduced while that of the chenodeoxycholic acid is increased, with a reduction in the bile saturation index in gallbladder and, therefore, reduction of the risk of forming calculations in the gallbladder and biliary tract. If we then add the polyunsaturated fats, ie the extra virgin Sicilian corn or olive oil in the diet, then we will have a further strengthening of the hypocholesterolemic effect and a further reduction in the risk of calculosis.

And we come to our right diet. We told you about the calculation of the appropriate diet in this website and the proper diet and modern food pyramid that requires an adequate consumption of fruit and vegetables at the expense of saturated fat and red meat, but here we want to talk about the diet to prevent damage to the liver.

Diet to prevent liver disease

  
Calories 1806 (take into account that the amount of calories is very high, possibly the portions should be reduced): Protidi g 105 - 24% of total calories - Lipids g 70 - 35% - Glucidi g 181 - 41%


Breakfast:
Before breakfast at least 60 minutes of good walking, that is 5 km / h, you do not have to run like crazy!
200 grams of skimmed milk-colored coffee without sugar
20 g of bread or wholemeal rusks


Lunch:
70 g of pasta with 50 g of peeled tomatoes and a tablespoon of oil
150 grams of lean meat, but better skinny fish, seasoned with raw oil, a spoon
200 grams of green salad and / or various boiled vegetables
40 g of bread
200 g of fruit, e.g. emperor apples, little sweet pears, no figs, bananas, sweet table grapes, melon and sugary fruit etc.


Dinner:
gr 50 of cheese (eg provolone, emmenthal) or better white meat or boiled fish, exchanging the dish with lunch
g 350 vegetables, ex. escarole, or boiled beets etc., seasoned with very little raw oil
250 gr of fruit (as above)

Diet and sick liver

The diet therapy to be implemented in the patient with cirrhosis with encephalopathy.

The hepatopathic patient must reduce the protein intake to about 40-50 grams, since an excess of proteins is responsible for the onset of hepatic encephalopathy, a condition in which the liver can not detoxify the body from the ammonia produced in the intestine starting from the catabolism of the amino acids, and that contributes to the synthesis of the false neurotransmitters, which in poor words means that the patient presents itself to your eyes drowsy or even in a hepatic coma. Most doctors advise their patients with this condition to eat only about 40 gr. of proteins a day, and prescribe Lactulose or Neomycin or Paromomycin or Rifaximin to lower the production of ammonia. Non-meat proteins are also recommended, but the "less noble" ones usually found in legumes or milk (see group IV food). The cirrhotic hepatopatiative diet should be supplemented with oral or intravenous branched amino acids, depending on whether the patient is or is not in a coma. In general, the diet must be high-calorie, that is, provide 35-40 kcal / kg weight, while the proteins must be calculated between 1 and maximum 1.5 g / kg ideal weight of the patient, but as we said, sometimes drastically reduced if the doctor considers it appropriate. The appearance of ascites (cf. ascites care) involves the drastic reduction of sodium intake in the feed, including water

Diet in the hepatopathy with water retention

Calories 2029 (take into account that the amount of calories is very high, possibly the portions are reduced)
Protidi g 95 - Lipids g 86 - Glucides g 208 - Sodium 500 mg


Breakfast:
150 gr of coffee-stained latté and 15 g of sugar
an egg
30 g of bread or slices


Lunch:
50 g of pasta with 50 g of peeled tomatoes and a tablespoon of oil
150 grams of lean meat, but better skinny fish, seasoned with raw oil, a spoon
150 grams of green salad
40 g of bread
250 g of fruit, e.g. apples, pears


Dinner:
30 grams of rice
150 g of minced meat (eg grilled burgers
200 grams of potatoes
30 g of bread without salt
230 g of pears

An association with celiac disease is reported in patients with PBC. In fact, the malabsorption of magnesium or iron is always to be related to celiac disease. An important malabsorption of fats in patients with cholestasis can be treated with the administration of medium-chain triglycerides.

Vitamin A is available from animal diet sources such as retinol and from plants such as P-carotene. Retinol uptake by intestinal cells is regulated by the retinol binding protein. Absorption of B-carotene depends on the availability of bile acids in the small intestine. In addition to the poor absorption secondary to bile acid deficiency, the decreased availability of retinol binding protein, resulting from chronic hepatobiliary disease, contributes to vitamin A deficiency. Vitamin A deficiency leads to impaired adaptation in the dark, which the patient may not even be aware of; therefore, an ophthalmologic consultation is generally necessary for a complete examination in patients at risk for this deficiency. The activation of retinol in photochemical compound and the hepatic secretion of retinol binding protein depend on zinc; therefore, it is necessary to monitor zinc levels and correct deficiency if present. Oral doses of 25,000 Ul / d to 30000 Ul are recommended 3 times a week for vitamin A supplementation. Vitamin A can be toxic to the liver and other organs; therefore, it must be administered under strict control so as not to exceed those considered normal levels.

The most important source of vitamin D in men is endogenous production. The metabolism of vitamin D is normal even in patients with PBC. This has suggested that low cholesterol exposure due to chronic debilitating disease is the major cause of vitamin deficiency in cholestasis, in addition to decreased absorption and renal losses of its metabolites, which may be increased in PBC. . Vitamin D, parathormone and calcitonin regulate the homeostasis of phosphorus and calcium, therefore, the levels of the latter can be abnormal in cases of vitamin D deficiency. The recommended doses for vitamin D supplementation range from 400 to 4000 Ul orally daily or 50,000 Ul oral 3 times a week. Chronic vitamin D supplementation may result in hypocalcemia and soft tissue calcifications. Natural tocopherols that require micellar solubilization for absorption are the most abundant source of vitamin E. Vitamin E inhibits the oxidation of unsaturated fatty acids, prevents lipid peroxidation and eliminates free radicals.

Vitamin E deficiency manifests with a neurological syndrome characterized by peripheral neuropathy, cerebellar degeneration and abnormal eye movements. Retinal degeneration can be attributed to the deficiency of vitamins E and A alone or combined. Complications of vitamin E deficiency are much more severe in children than in adults with cholestasis. It is recommended to treat viticular deficiency. And with doses of α-tocopherol from 2 to 20 μl per os per day, 100 μg twice a day or from 10 to 25 μl / kg / day. Two forms of vitamin K contribute to its activity; K1, or phytonadione, which is found in most plants and K2, a series of menachinones, which is produced by gram-positive bacteria in the intestine.

Vitamin K deficiency manifests with coagulopathy, as can be seen from a prolonged PT secondary to the deficiency of vitamin K dependent coagulation factors, or it may be asymptomatic. Vitamin K deficiency coagulopathy secondary to cholestasis resolves with the administration of the missing vitamin subcutaneously. Vitamin K deficiency can be corrected with 1 to 10 mg of vitamin K, subcutaneously daily for three consecutive days. In patients with chronic cholestasis, vitamin K deficiency can be prevented by monthly administration of 10 mg of vitamin K. Intramuscular administration of vitamin K, or other drugs, should be avoided in patients with coagulopathy due to the risk of intramuscular bleeding . If the coagulopathy is caused by the damage of the hepatocytes, it will not be resolved with treatment with vitamin K.

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