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.

Serum ferritin, an index of iron stores, was studied in 60 patients with porphyria cutanea tarda (PCT), in 21 patients who had other liver diseases without siderosis (cirrhosis [LC] and chronic active hepatitis [CAH]), and in 32 patients with associated liver siderosis (alcoholic LC, LC and CAH in minor thalassemia). Ferritin levels were higher in patients with porphyria than in healthy controls and patients without liver siderosis (P less than 0.001), whereas no statistical difference was observed between patients with porphyria and those with liver siderosis. Because iron removal is considered the treatment of choice for PCT, some patients with PCT underwent phlebotomy and others received chelating therapy with subcutaneous infusion of deferoxamine. Follow-up of the patients showed a correlation between serum ferritin level and urinary porphyrin excretion; when the clinical and biochemical syndrome became normal, serum iron and ferritin had fallen to normal values (t test pair data analysis before and after: P less than 0.001 in each group). No appreciable difference was found between controls and patients with PCT whose conditions had been normalized, irrespective of the chronic liver damage always present in PCT. Our results suggest that serum ferritin increase in PCT is related more to liver iron overload than to liver damage, and ferritin follow-up is recommended to indicate the exhaustion of hepatic iron stores during iron depletion therapy, as well as to detect an early replenishment after remission.

Twenty-five patients with overt clinical and biochemical findings of porphyria cutanea tarda took part in a study comparing intensive phlebotomy with slow subcutaneous desferrioxamine treatment. Fifteen male patients (Group A) had intensive venesection therapy. Ten patients (Group B) with associated diseases (minor thalassemia, cardiovascular impairment, pulmonary tuberculosis or severe liver cirrhosis) received 1.5 g of desferrioxamine by slow subcutaneous infusion using an automatic syringe pump 5 days a week. No patient complained of appreciable side effects. Serum iron, ferritin and uroporphyrins were normalized in all subjects by the end of treatment. The mean time necessary for complete recovery was 13.8 months (range 9-19) and 11.2 months (range 6-14) in Groups A and B, respectively. Liver function significantly improved during and after the treatments in both groups. We conclude that recovery from porphyria cutanea tarda can be achieved equally well using phlebotomy or desferrioxamine subcutaneous infusion. Phlebotomy is easily performed and remains the treatment of choice; slow subcutaneous desferrioxamine treatment, although expensive, is recommended when severe associated diseases contra-indicate venesection.