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PubMedDate not supplied

[Metabolism of essential fatty acids and prostaglandins in the rat liver in chronic alcoholic intoxication].

Patterns of essential fatty acids and of prostaglandins metabolism were studied in liver tissue of rats which consumed 5% solution of ethanol as a single source of drinking material within 3, 6 and 9 months. Deficiency of essential fatty acids and a decrease in the content of prostaglandins occurred during development of chronic alcohol intoxication. Activity of PGE2 synthetase was decreased within 3 and 9 months and the activity of PGF2 alpha synthetase--within 9 months of the experiment. Activity of linoleyl-CoA-desaturase was decreased similarly in all the systems studied. The decrease in prostaglandins content found in liver tissue after long-term consumption of ethanol was due both to a deterioration in accessibility of the substrate for prostaglandin synthetase and to the decrease in activity of prostaglandin synthetases.

Alcoholism↗
PubMed1986

Scald burns complicated by isopropyl alcohol intoxication. A case of fatal child abuse.

Scald burns are the most common type of thermal injury in child abuse. Death associated with nonaccidental burns, however, is uncommon. We recently investigated the case of a 4-year-old child who died from extensive body burns due to scalding. A contributory cause of death was isopropyl alcohol intoxication resulting from application of this chemical to the burns.

1-Propanol↗
PubMed1982

The decrease of the non secretory phospholipase A in rat pancreas during a chronic alcohol intoxication.

It is known that ethanol induces morphological lesions in the exocrine pancreas of man and of experimental animals. We showed recently that ethanol is metabolized by the rat pancreas. It has also been demonstrated that ethanol acts on the lipid metabolism of the pancreas by stimulating the lipid biosynthesis and by inhibiting fatty acids oxidation. We recently characterised a non secretory phospholipase A in the rat pancreas, probably involved in the intracellular phospholipid turnover. The actions of chronic alcoholic intoxication on the level of this enzyme is investigated in this paper. The ethanol intoxication was prolonged for two years and resulted in a progressive decrease in the level of the pancreatic non secretory phospholipase (p less than 0.01). This result confirms the chronic metabolic modifications induced by alcohol on the pancreas and emphasizes its metabolic participation in chronic alcoholic pancreatitis.

Alcoholism↗
PubMed2006

Alcohol intoxication and post-burn complications.

Results from the studies discussed in this article suggest that alcohol (EtOH) intoxication is a major public health problem. While the effects of injury and EtOH intoxication independent of each other have been studied in detail, only few studies have evaluated the effect of a combined insult of EtOH intoxication and burn injury on host defense. An analysis of the studies conducted in the clinical setting suggests that intoxicated patients require frequent intubations, experience delayed wound healing and longer hospital stay. Furthermore, there is a greater risk of mortality in these patients compared to those who sustained injuries in the absence of EtOH intoxication. On the other hand, there are a few studies that do not support this notion. The results obtained in experimental models clearly suggest that acute EtOH intoxication before burn injury impairs host defense and increases susceptibility to infection. Additionally, experimental data from our laboratory also indicate that EtOH intoxication before burn injury suppresses intestinal immune defense, impairs gut barrier functions and increases bacterial growth. This results in increased bacterial translocation in EtOH and burn injury. In addition, a decrease in cardiac function is also reported following a combined insult of EtOH intoxication and burn injury. Altogether, these findings suggest that EtOH intoxication before burn injury diminishes host resistance resulting in increased susceptibility to infection. Moreover, the findings of a higher incidence of infectious complications in burn and trauma patients who sustained injury in the presence of EtOH compared to those in its absence suggest that EtOH intoxication at the time of injury is a risk factor. Therefore blood EtOH should be monitored in burn/trauma patients at the time of admission in the emergency room.

Accidents↗
PubMed1994

Isopropyl alcohol intoxication in a neonate through chronic dermal exposure: a complication of a culturally-based umbilical care practice.

A 21-day-old boy presented to our emergency department hypotonic, lethargic, and intermittently unresponsive to pain. A workup for ketoacidosis, sepsis, and central nervous system hemorrhage was negative. A urine drug screen collected eight hours after hospitalization showed 39 mg/dl of isopropyl alcohol and 76 mg/dl of acetone. The first serum drug analysis was not performed until 18 hours after admission, at a time when there had been clinical improvement. The isopropyl alcohol concentration was 8 mg/dl, and the acetone concentration was 203 mg/dl. Management was supportive, and the patient stabilized. He was discharged from the hospital in good health in three days. A further review of the history showed no evidence for an oral exposure to isopropyl alcohol. However, since leaving the maternity hospital the mother had been applying gauze pads or cotton balls soaked with isopropyl alcohol to the umbilicus with every diaper change. We conclude that the child suffered from an isopropyl alcohol intoxication that occurred by absorption through the umbilical area.

1-Propanol↗
PubMedDate not supplied

[Features of lipid metabolism impairment in chronic alcoholic intoxication].

Long-term administration of ethanol into animals within 1-6 months resulted in distinct alterations of blood serum fatty acid composition as well as in elevation of the saturation rate simultaneously with a decrease of fatty acid polyunsaturation. Calculated coefficients, which included ratios between fatty acid with various rates of unsaturation, were highly informative. Alterations of fatty acid composition in blood serum, registered during observations, reflected the state of fatty acid metabolism in tissues. Analysis of fatty acid spectrum in blood serum enabled to evaluate the severity of impairments in liver tissue and pancreas under conditions of alcohol intoxication: increase in the rate of phospholipid catabolism, in content of cholesterol, triglycerides and total lipids was observed both in blood serum and liver tissue. These impairments of lipid metabolism may produce alcohol hepatitis, which is the basis for liver tissue alcohol cirrhosis.

Alcoholism↗
PubMed1988

[The osmotic gap in the diagnosis of alcoholic intoxication].

Sodium, urea, glucose and osmolality were determined in 50 hospitalized patients. Osmolality was calculated according to two different methods and compared with measured osmolality. Both methods showed equally close correlations (r = 0.87), and for clinical use we recommend the following simple formula: osmolality = 2 x sodium + glucose + urea. The two formulas studied were then used to calculate the osmolal gap (difference between measured and calculated osmolality) in 30 patients with ethanol intoxication, in order to estimate the blood alcohol concentration. For the equation: blood ethanol concentration (g/L) = osmolal gap/27 we found a very good correlation between calculated and measured ethanol levels (r = 0.95). Our data confirm previous reports that blood ethanol can be quickly and fairly exactly estimated by using the osmolal gap.

Alcoholic Intoxication↗