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.
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.