Cirrhosis of the liver is a chronic IRREVERSIBLE disease characterized by degeneration, hardening, scarring and functional loss of liver cells.
The onset of liver cirrhosis is potentially influenced by diet.
Causes of liver cirrhosis
Cirrhosis of the liver can have multifactorial causes and based on them, diet plays a more or less important role in the pathological course:
- HBV (hepatitis B virus) or HCV (hepatitis C virus) infection *
- Alcohol abuse *
- Autoimmune diseases (autoimmune cirrhosis and primary biliary cirrhosis)
- Metabolic disorders (Wilson's disease and Hemochromatosis)
- Vascular diseases (which cause blood stasis or stagnation in the liver)
- External toxic agents and / or drugs
* overall cause of 90% of cases of liver cirrhosis in Italy
Symptoms and complications
Initially, liver cirrhosis is an asymptomatic disease; early diagnosis of this stage, otherwise defined compensated cirrhosis, is fundamental to the success of the therapy. The removal of etiological agents and the adoption of a diet for cirrhosis are fundamental, even if the hypertension of the portal vein (pathological modification from which all the others subsequently originate) is modest, and the portion of active hepatocytes manages to comply to the functions of those definitively dead.
In the event that no therapy or diet is implemented for liver cirrhosis, the pressure of the portal vein would continue to increase and the active hepatocytes would decrease in number until they are insufficient; The first symptoms of advanced liver cirrhosis are:
- Anorexia
- Weight loss
- Loss of muscle mass
In the event that the degeneration becomes complicated, the next stage is called decompensated cirrhosis; the symptoms are:
- Jaundice and itching
- Increased abdominal volume (ascites)
- Edema in the lower limbs
- Changes in coagulation, easy bleeding (ecchymosis and petechiae).
The most serious complications of liver cirrhosis mainly concern the accumulation of intraperitoneal fluid (ascites) due to the reduction of the osmolar protein portion of the blood and possible infection (peritonitis), formation of varices and possible rupture with gastro-intestinal haemorrhage, hepatic encephalopathy (due to alteration blood composition), hepatorenal syndrome (renal failure secondary to cirrhosis), hepatocellular carcinoma (liver cancer) and portal thrombosis.
Liver cirrhosis therapy
Therapeutic treatment of liver cirrhosis includes:
- Removal of the patient from risk and etiological factors
- Balanced and specific diet (right protein / amino acid and dietary sodium intake)
- Use of drugs to reduce complications of cirrhosis (eg diuretics for ascites)
- Bed rest (which facilitates venous return)
- Evacuative paracentesis (procedure through which, through the use of a syringe and a needle, the ascitic fluid contained in the abdominal cavity is taken; when only a few cubic centimeters of fluid are taken in order to analyze it, the paracentesis is called exploratory. If the abdominal fluid is abundant and creates a sense of swelling, larger quantities can be taken and the procedure is called paracentesis evacuative).
Although liver cirrhosis is a disease with an irreversible and often fatal course (high correlation between liver cirrhosis and hepatocarcinoma), if well treated, it is possible to drastically slow down its degenerative progress and promote the indispensable regeneration of the liver; obviously, this depends on the state of the disease, therapy and primary causative agent. In the case of alcoholic cirrhosis, the definitive suspension of the abuse involves a GREATER restoration of liver function compared to the treatment of the other forms of cirrhosis.
In a state of cirrhosis compensated it is sufficient to eliminate the etiological agent (antiviral treatment, elimination of alcohol, elimination of toxic or drugs) and restore a balanced diet.
The diet for compensated cirrhosis, in addition to scrupulously respecting all the requirements for a healthy and correct diet, must be particularly careful to ensure a protein intake of about 1.2g / kg of body weight; in case of inappetence it can be useful "integration. On the contrary, the diet for decompensated cirrhosis depends very much on the clinical condition of the subject; secondary complications significantly affect the state of health and often require the adoption of artificial nutrition. This is the case of encephalopathy, which requires protein reduction up to 0.5g / kg in order to improve the nitrogen balance, or the syndrome hepatorenal, which on the contrary increases its requirement as it favors the plasma protein excretion with the urine. In the absence of encephalopathy it is recommended to maintain a protein intake of about 1.5g / kg.
Curiosity
It has been shown that the diet for liver cirrhosis can significantly improve the symptoms of encephalopathy following the replacement of AROMATIC amino acids with branched chain amino acids, thanks to the reduction of nitrogenous waste and the improvement of the overall nitrogen balance. This determines a potential increase in the amino acid ration essential to meet the greater plastic needs of the cirrhotic with encephalopathy and secondary renal insufficiency.
Another fundamental precaution to follow in the preparation of the diet for liver cirrhosis is the restriction of dietary sodium. The excess of this trace element promotes the worsening of ascites and in 10-20% of patients the dietary correction allows the disappearance of the effusion; on the contrary, the sodium defect can negatively affect renal function. Ultimately, in the diet for liver cirrhosis it is strongly recommended to limit the intake of dietary sodium to no more than 40mEq / day (920 mg / day = 2.3 grams of sodium chloride) but not to fall below the 20mEq / day (which would also significantly affect the cost of the special diet).
Bibliography:
- SINPE Guidelines for Hospital Artificial Nutrition 2002
- Cirrhosis of the liver in clinical practice - G. Laffi, G. La Villa - SEE Florence - pages 184; 391
- Complete treatise on abuse and addiction - U. Nizzoli, M. Pissacroia - Piccin - page 984
