Assessment of diazepam loading dose therapy of delirium tremens.

The efficacy of the diazepam loading dose method of treatment of delirium tremens was assessed in comparison with the traditional therapy. The experimental group and the control group comprised 51 and 45 patients respectively. The clinical institute withdrawal assessment for alcohol (CIWA-A) scale was applied to assess the intensity of the symptoms. Diazepam doses in the experimental group oscillated from 40 to 210 mg (mean 86.9 +/- 47.2 mg). The control group was receiving diazepam and other psychotropic drugs in divided doses. In the experimental group deliric symptoms were present from 2 to 24 h (mean 6.9 +/- 4.8 h), and in the control group from 2 to 123 h (mean 33.8 +/- 25.7 h). The results show a large efficacy of the loading dose method corresponding to substantial reduction of the psychosis duration (fivefold in comparison to the control group). The method proved to be safe, with no significant complications.

[Treatment of delirium tremens with quick administration of diazepam]. / Terapia majaczenia alkoholowego metoda szybkiego nasycania diazepamem.

In this efficacy the study of diazepam loading-dose treatment of delirium tremens was evaluated in comparison with traditional therapeutic methods. Experimental and control groups consisted of 42 and 40 patients respectively. The severity of the withdrawal symptoms was evaluated from clinical status, in the experimental group CIWA-A score was also employed. Study results suggest high efficacy of the loading-dose method, which was characterized by significant shortening of psychosis duration (five times shorter in experimental vs. control group). The method turned out to be safe, no complications were observed during and after the treatment.

The effect of thermally oxidized soya bean oil on metabolism of chylomicrons. Increased uptake and degradation of oxidized chylomicrons in cultured mouse macrophages.

Oral administration of thermally oxidized soya bean oil (TO) increased the level of lipid peroxides in human plasma, mainly in chylomicrons. No changes were observed after fresh oil (FO) intake. Human chylomicrons obtained after TO ingestion were rich in lipid peroxides and degraded more rapidly by cultured mouse macrophages than chylomicrons after FO. The uptake of TO chylomicrons by macrophages occurred via a saturable process and was partially inhibited by beta-very low density lipoprotein as well as by acetyl-low density lipoprotein and fucoidin. A 48-h incubation of macrophages with TO chylomicrons caused a 10-fold higher accumulation of cholesterol ester mass in the cells than the incubation with FO chylomicrons. These studies suggest that chylomicrons containing lipid peroxides may be taken up by mouse macrophages by mediation of beta-VLDL receptor as well as by acetyl-LDL receptor, and show a potential pathway by which chylomicrons obtained after ingestion of heated oil could contribute to accumulation of cholesterol esters in macrophages.

Serum lipoproteins, lipid peroxides and prostacyclin biosynthesis in patients with coronary heart disease.

Serum low-density lipoproteins (LDL) and high-density lipoproteins (HDL) were prepared by gradient ultracentrifugation and dialysis from 12 healthy subjects and 15 patients with coronary heart disease and hyperlipoproteinemia. In both lipoprotein fractions cholesterol and lipid peroxides were determined. The effect of these lipoproteins on spontaneous prostacyclin biosynthesis in rat aortic slices was studied. Serum lipoproteins were susceptible to peroxidation during the preparation procedure. LDL were more prone to peroxidation than HDL. Little lipid peroxides were formed in lipoproteins when calcium ions had been removed by EDTA, and when butylated hydroxytoluene (BHT) was present at all stages of their preparation. LDL when prepared without these precautions either from healthy subjects or from patients with coronary heart disease markedly suppressed prostacyclin generation by rat aortic slices. This inhibition was unrelated to LDL-cholesterol, but was due to LDL-lipid peroxides. Peroxide-low LDL prepared from most of the healthy subjects and patients with coronary heart disease and concomitant hyperlipoproteinemia, did not inhibit prostacyclin biosynthesis. However, in one quarter of the patients, LDL was inhibitory. Consequently, in some patients with coronary heart disease, there operate unknown mechanisms which are responsible for the inhibitory activity of LDL on prostacyclin generation.

Serum cobalt-activated acylase and gamma-glutamyl transpeptidase activities in toxic hepatitis.

Marked activity of cobalt-activated acylase was found in the sera of 33 of 37 patients with acute toxic hepatitis due to poisoning with either amanita mushrooms or chemicals. The activity of the enzyme showed a positive correlation with that of serum transaminases, reached the highest levels on the patient's admission to hospital and within a few days fell rapidly to undetectable levels. Slight acylase activity was observed in the majority of patients intoxicated with drugs or carbon monoxide but was not seen in sera of those poisoned with non-amanita mushrooms who showed no signs of liver injury. Unlike acylase, the serum activity of gamma-glutamyl transpeptidase remained unchanged over the first days of acute toxic hepatitis. The determination of serum cobalt-activated acylase might be of value in the diagnosis of acute liver injury.