[Hyperoctanoatemia and the hepatic encephalopathy of cirrhosis. 150 dosages in 61 patients (author's transl)]. / Hyperoctanoatémie de l'encéphalopathie hépatique des cirrhoses. 150 dosages chez 61 malades.

A new and sensitive method for determination of octanoate in serum by gas-liquid chromatography is described. It was validated by mass spectrometry. Octanoate concentrations were determined in the serum of 61 fasting cirrhotic patients of which 47 also had hepatic encephalopathy. Concentrations in arterial and venous blood were higher in cirrhotic patients with encephalopathy than in those without and higher in the latter than in controls. Arterial concentrations were higher than venous concentrations and octanoate and ammonia varied independently. A predominant endogenous origin is likely. Data obtained from studies using palmitic acid labeled at different loci suggest that recovered serum octanoate was formed mostly by incomplete oxidation of long chain fatty acids. Sodium octanoate infusion to rhesus monkeys studied polygraphically induces a temporary coma.

Sources of serum [14C]-octanoate in cirrhosis of the liver and hepatic encephalopathy.

Serum octanoate levels of patients with liver cirrhosis and hepatic encephalopathy have been shown to be three to 15 times higher than those of controls. Assays for octanoate have been modified to permit isolation of pure octanoate after GLC. Patients with these conditions were given intravenously differently labeled [14C]-palmitates; serum [14C]-octanoate was isolated in each case and shown by mass spectrometry to be authentic octanoate. [1-14C]-oleate and [1-14C]-stereate were also shown to serve as precursors of serum [14C]-octanoate. When differently labeled palmitates (1-[14C]; omega [14C]; and [14C]-uniformly labeled) were used, different yields of serum [14C]-octanoate were recovered. Octanoate samples were chemically degraded to yield individual carbons or groups of carbons. In this manner it was possible to determine the percentage distribution of the [14C] label within the octanoate carbon chain. The data obtained from these studies suggest that 60% to 80% of the serum octanoate was obtained from the incomplete beta-oxidation of long-chain fatty acids and that 20% to 40% of the octanoate may have been formed de novo.

Relapsing polyradiculitis after portocaval anastomosis.

A case of relapsing polyneuritis in a cirrhotic woman with a surgical splenorenal shunt is reported. The ultrastructural study of the nerve biopsy shows widespread segmental demyelinization with total myelin breakdown in most fibers; some Schwann cells are invaded by mononuclear cell processes. Such histological changes are characteristic of the Guillain-Barré syndrome. Alcohol and diabetes are unlikely to be the causative factors of the nerve damage. The possible role of unidentified toxic metabolites such as those which cause portosystemic encephalopathy, also present in our patient, is discussed.

A method for serum octanoate in hepatic cirrhosis and hepatic encephalopathy.

We describe a new, more efficient, and more reproducible method for determination of octanoate in serum. This method involves ethanol extraction, followed immediately by alkali addition before concentration of the extract. The concentrate is made acidic only before it is to be steam distilled (in a special all-glass apparatus with an alkali trap). The material is acidified again just before separation by gas-liquid chromatography. The yield is 89-107%. When assayed by mass spectrometry, only octanoate was found in the fraction from chromatography. Previous methods yielded only 30-55% of the expected octanoate value and the recovered materials showed impurities by mass spectrometry. Octanoate concentrations were determined in the serum of 24 fasting controls and that of 85 fasting cirrhotic patients, of whom 50 had encephalopathy. Concentrations in arterial and venous blood were significantly higher in cirrhotic patients in coma than in those not in coma, and arterial concentrations were statistically higher than venous concentrations in the cirrhotic patients.

[Quantitative study of multimolecular forms of serum gamma glutamyl transferase by polyacrylamide gel electrophoresis]. / Etude quantitative des formes multimoléculaires de la gamma-glutamyl-transférase du sérum par électrophorèse en gel de polyacrylamide

The quantitative distribution of the multimolecular forms of serum gamma-glutamyl-transferase is studied in 286 sera by acrylamide gel electrophoresis, incubation, coloration in situ, photography, slide reading and integration. In 43 normal sera, the fast fraction represents 66% of the total activity; the ratio of the mean fast fraction to the medium and slow fraction was 2. During pregnancy (53 cases), in cord blood (54 cases), in hepatic cytolysis or cholestasis (55 cases), and in secondary liver carcinoma (21 cases), this ratio is considerably lower, demonstrating the predominance of medium and slow fractions. A similar decrease in the ratio, with predominance of the medium and slow fractions was seen in 22 cases of advanced cancer without metastases in the liver.