The Authors determined zinc (Zn) and magnesium (Mg) in the plasma, urine, erythrocytes (RBCs), mono- and polymorphonuclear cells (MNCs and PMNs) of patients with overt alcoholic and nonalcoholic liver cirrhosis. In order to obtain a clearer clinical picture, biochemical and nutritional parameters (retinol, tocopherol, six different carotenoids, creatinine-height index and tricipital skinfold), as well as markers of portal hypertension (spleno-portal size and platelet count) were also evaluated.The plasma levels of Zn and Mg were found to be reduced, as were the urine levels of Mg. Urine Zn, on the other hand, was higher than normal. Plasma Zn correlated inversely, and urine Zn directly, with the severity of the disease, rather than with alcohol consumption or treatment with diuretics. Protein metabolism impairment would appear to affect the plasma transport of Zn rather than its overall availability in the organism; the opposite was found in the case of Mg, the availability of which appeared to be reduced. Determination of the two elements in RBCs, MNCs and PMNs suggested that a true nutritional deficit cannot be demonstrated. MNCs, rather than RBCs or PMNs seem better to reflect tissue status of trace elements.

The ingestion of an amino acid mixture lacking tryptophan causes a rapid fall of plasma tryptophan in healthy subjects. This is because amino acids elicit protein synthesis and endogenous tryptophan is incorporated into new proteins. If protein synthesis is the mechanism through which tryptophan-free solution decrease blood tryptophan, it may be interesting to study tryptophan levels after a tryptophan-free mixture in subjects with impaired protein synthesis. In the present paper we show that in 27 cirrhotics the administration of a tryptophan-free solution caused a fall of total plasma tryptophan that began significantly later than in 14 control subjects, the delay being significantly proportional to the severity of the disease. The difference between control and cirrhotic subjects was due to the bound fraction of plasma tryptophan. The diagnostic and clinical usefulness of our findings are discussed.

The role played by carotenoids, retinol and tocopherol in quencing oxidative cellular damage and combatting tumor growth is well documented, but little is known about their activity in human liver cirrhosis (LC), where oxidative damage and tumoral complications are common-place. We investigated 59 patients with LC of different etiology on admission to hospital and compared them with 32 healthy controls, matched for age and sex. Nutritional (cutaneous skinfolds, creatinine-height index) and serum parameters were determined; of these, alpha- and beta-carotene, cryptoxanthin, lycopene, retinol and alpha-tocopherol were detected by an high-performance liquid chromatographic (HPLC) technique, devised in our laboratory, which afforded an accurate and simultaneous resolution of all six compounds. The results point to a significant reduction in almost all the vitamin factors in LC, as well as in total serum lipids. In consequence, the ratio tocopherol/total serum lipids remains almost unchanged: 2.45 +/- 0.08 (m +/- se) in controls and 2.34 +/- 0.16 in patients. The effects of age, sex, nutritional habits, alcohol, malnutrition and the severity of the disease were also evaluated in relation to the vitamin-factor levels. It is suggested that the reduced levels observed in LC patients are due to a number of factors including portal hypertension and lymphatic circulation impairment, and it is concluded that thorough screening and improved diet are beneficial in the follow-up of LC.