ABSTRACT
Development of ALD........................................................................ 166 11.3.3 Correction of Abnormal Methionine Metabolism as a Therapy ...... 168
11.3.3.1 SAM Therapy..................................................................... 168 11.3.3.2 Folate Therapy ................................................................... 169 11.3.3.3 Betaine Therapy ................................................................. 169
11.4 Selected Other Vitamin and Mineral Deciencies as Related to ALD ........ 169 11.4.1 Vitamins ........................................................................................... 169
11.4.1.1 Vitamin B1/Thiamine ......................................................... 169 11.4.1.2 Vitamin B2/Riboavin ....................................................... 170 11.4.1.3 Vitamin B3/Niacin ............................................................. 170 11.4.1.4 Vitamin B6/Pyridoxine ...................................................... 170 11.4.1.5 Vitamin D .......................................................................... 171 11.4.1.6 Vitamin A/Retinol ............................................................. 171
11.4.2 Minerals ............................................................................................ 172 11.4.2.1 Magnesium ......................................................................... 172 11.4.2.2 Selenium ............................................................................ 172
11.5 Overall Nutritional Intervention ................................................................... 173 11.6 Summary ...................................................................................................... 175 References .............................................................................................................. 175
Malnutrition is common in most forms of cirrhosis including alcohol-induced cirrhosis. Moreover, virtually all patients with alcoholic hepatitis have some evidence of malnutrition. Patients may have global protein calorie malnutrition and/or isolated nutrient deciencies, such as zinc deciency. Nutritional deciencies in alcoholic liver disease (ALD) may be caused by inadequate intake/anorexia, malabsorption, decreased nutrient storage, increased nutrient need, increased excretion, or decreased ability to metabolize nutrients into their active forms. Malnutrition may play a mechanistic role in the development of ALD, either directly or indirectly by modifying factors such as gut permeability, oxidative stress, or cytokine production (Figure 11.1). This chapter will review (1) two major nutritional abnormalities (alterations in zinc and methionine metabolism) of major research interest to our research group and of major importance in the pathogenesis and treatment of ALD; (2) selected other nutrient abnormalities; and (3) overall nutritional therapy in ALD. Because the role of lipids/fatty acids and iron is covered in other chapters, it will not be discussed here.
