Io

Large Waist

High Glucose

Low HDL

High High Triglycerides Pressure

Figure 1 Prevalence of metabolic alterations fitting the criteria of the metabolic syndrome in patients with NAFLD according to classes of body mass index. (Reproduced with permission from Marchesini G, Buigianesi E, Forlani G et al. (2003) Nonalcoholic fatty liver, steatohepatitis, and the metabolic syndrome. Hepatology 37: 917-923.)

Large Waist

High Glucose

Low HDL

High High Triglycerides Pressure

Figure 1 Prevalence of metabolic alterations fitting the criteria of the metabolic syndrome in patients with NAFLD according to classes of body mass index. (Reproduced with permission from Marchesini G, Buigianesi E, Forlani G et al. (2003) Nonalcoholic fatty liver, steatohepatitis, and the metabolic syndrome. Hepatology 37: 917-923.)

Table 3 Daily intake of main dietary constituents in NASH patients and controlsa

NASH patients (n = 25)

Controls (n = 25)

p value

Total energy intake (kcal)

2638 i 444

2510 i 139

0.695

kcal/kg body weight

33 i 5

32 i 6

0.580

Dietary fat (g)

102.8 i 31.6

92.1 i 35.2

0.264

Dietary carbohydrate (g)

295.1 i 53.l

315.2 i 101.9

0.381

Dietary protein (g)

121.2 i 25.2

101.2 i 32.1

0.096

Alcohol (g)

13.3 i l.3

13.5 i 8.9

0.105

Dietary fat (% kcal)

35.1 i l.1

32.3 i 6.1

0.158

Dietary carbohydrate (% kcal)

44.l i 8.l

48.6 i 9.1

0.128

Simple carbohydrate (% total carbohydrate)

30.3 i 6.4

32.5 i 5.1

0.185

Fiber (g)

12.9 i 4.1

23.2 i 1.8

0.000

Dietary protein (% kcal)

20.2 i 3.l

16.1 i 4.3

0.003

SFA (g)

40.2 i 12.l

28.1 i 11.1

0.001

MUFA (g)

52.1 i 1l.4

41.8 i 16.1

0.311

PUFA (g)

103.9 i 4.9

13.4 i 4.1

0.019

Cholesterol (mg)

506 i 108

405 i 111

0.002

SFA (% total kcal)

13.l i 3.1

10.0 i 2.1

0.000

MUFA (% total kcal)

1l.l i 4.4

16.1 i 5.1

0.462

PUFA (% total kcal)

3.5 i 1.3

4.1 i 2.0

0.015

SFA (% total fat)

39.1 i 4.8

31.1 i 5.2

0.000

MUFA (% total fat)

50.9 i 6.5

51.9 i 5.9

0.512

PUFA (% total fat)

10.0 i 3.5

14.5 i 4.0

0.000

(P:S ratio)

0.24 i 0.10

0.46 i 0.12

0.000

Vitamin A (mg)

582.6 i 383.1

641.1 i 501.3

0.614

Vitamin C (mg)

84.3 i 43.1

144.2 i 63.1

0.000

Vitamin E (mg)

5.4 i 1.9

8.1 i 2.9

0.000

Iron (mg)

12.1 i 2.3

14.5 i 3.9

0.011

aData are presented as mean ± SD.

SFA, saturated fat intake; PUFA, polyunsaturated fat intake; MUFA, monounsaturated fat intake; P:S ratio, polyunsaturated to saturated fat.

From Musso R, Gambino R, DeMichiele F et al. (2003) Dietary habits and their relations to insulin resistance and postprandial lipemia in nonalcoholic steatohepatitis. Hepatology 37(4): 909-915.

aData are presented as mean ± SD.

SFA, saturated fat intake; PUFA, polyunsaturated fat intake; MUFA, monounsaturated fat intake; P:S ratio, polyunsaturated to saturated fat.

From Musso R, Gambino R, DeMichiele F et al. (2003) Dietary habits and their relations to insulin resistance and postprandial lipemia in nonalcoholic steatohepatitis. Hepatology 37(4): 909-915.

saturated fatty acids, total fat, and cholesterol and a lower intake of polyunsaturated fat, fiber, and the antioxidant vitamins C and E. These findings provide a strong rationale for specific dietary modifications in NASH patients.

Pregnancy and liver disease Liver diseases that predominantly affect females, such as PBC and autoimmune hepatitis, decrease the chances of conception and demand that pregnant women with these disorders should be managed in high-risk obstetric facilities. Liver diseases that can evolve as a consequence of pregnancy include intrahepatic cholestasis of pregnancy, acute fatty liver of pregnancy, and HELLP (hemolysis, elevated liver enzymes, and low platelets syndrome). The latter has been associated with disorders of fatty acid oxidation in offspring. Successful pregnancies are the rule for women who have undergone liver transplantation, but preterm delivery and low-birth-weight infants are common. Careful attention to the nutritional management of the pregnant female with liver disease is necessary to ensure the best outcome for the fetus.

Total parenteral nutrition-associated liver disease

Premature infants and children with short gut syndrome are particularly prone to develop this disorder, and in the pediatric age group total parenteral nutrition (TPN) liver disease is usually cholestatic. The cholestasis can be solely intrahepatic or can be associated with cholelithiasis. TPN liver disease can be seen at any age and with any disease etiology resulting in long-term dependence on parenteral nutrition; in older children and adults, steatosis is more common as an initial presentation rather than cholestasis. Potential pathogenetic mechanisms include the gastrointestinal dysfunction associated with the lack of enteral nutrients as well as components of the parenteral nutrition solutions as potential hepatotoxins, including amino acids, glucose, lipids (particularly peroxidizable lipids), and photoexposed multivitamins. The most effective management is aggressive administration of enteral nutrients and a decrease and/or discontinuation of parenteral nutrition as early as possible.

Viral hepatitis Hepatitis A virus infection never results in chronic liver disease, so there are no specific nutritional recommendations for patients with this disorder. Hepatitis B virus infection evolves to chronic hepatitis in ^95% of neonates who acquire the infection perinatally but only ~5% of adults. Hepatitis C virus (HCV) infection has a much higher rate of chronicity in adults—up to 80% of those infected will develop chronic infection. Approximately 20-30% of those will progress to cirrhosis over 10-20 years and a smaller proportion of those will develop hepatocellular carcinoma. There is much less information about nutritional disturbances and nutritional management of patients with chronic viral hepatitis than there is for patients with alcoholic liver disease.

In general, the nutritional recommendations for management of alcoholic hepatitis, cirrhosis, or cho-lestasis detailed previously can be applied to patients with these various manifestations of chronic viral hepatitis. For example, it has been shown that thia-mine deficiency is common in patients with cirrhosis secondary to either chronic alcohol consumption or chronic HCV and thiamine supplementation is indicated for patients with either type of liver disease.

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