Thyrotoxic periodic paralysis in a Caucasian man in treatment for Graves' disease.

Thyrotoxic periodic paralysis (TPP) is the main secondary form of hypokalemic periodic paralysis and is mostly associated with Graves' disease. Initially diagnosed in Asian countries, TPP has been sporadically reported in different populations of the Western World. Increased Na+/K(+)-ATPase activity seems to be responsible for the marked hypokalemia observed during the transient paralysis attacks. We report on a 35-year-old Italian man without history of hypokalemic periodic paralysis and hyperthyroidism, in treatment for Graves' disease, who suffered episodes of flaccid paralysis even with normal thyroid hormone levels. An insulin-glucose provocation test confirmed our diagnosis. Oral and parenteral potassium reverse the symptoms. Monitoring of thyroid function is also important to prevent further attacks.

Early acute cellular rejection: no effect on late hepatic allograft function in man.

Whereas early acute cellular rejection, even if successfully treated, seems to have an impact on late function and survival of kidney and heart transplants, little quantitative data are available on its effect(s) on liver transplants. Routine liver function tests, the functioning liver cell mass (galactose elimination capacity) and microsomal metabolic capacity (aminopyrine breath test) were determined prospectively in 37 consecutive patients 1 year after liver transplantation. Of these, 19 (7 females and 12 males, 32-69 years of age) had previously required treatment for at least one biopsy proven acute cellular rejection episode occuring a median 7 days after grafting, while 18 (6 females and 12 males, 30-67 years of age) had not. The functioning liver cell mass and microsomal metabolic capacity were both within normal limits for the majority of patients and did not differ significantly between patients with and without previous acute cellular rejection episodes. In contrast to other solid organ transplants, early acute cellular rejection episodes do not affect late function of liver allografts in man.

Gastric and intestinal ethanol toxicity in the rat. Effect on glutathione level and role of alcohol and acetaldehyde metabolisms.

BACKGROUND/AIMS: This study investigated the dose- and time-dependent effect of ethanol on gastric and intestinal glutathione and protein oxidative state in the rat. METHODS: Rats received 1 or 4 g/kg of 25% ethanol solution orally or isocaloric glucose. Some rats received diethylmaleate, cimetidine or cyanamide before ethanol (1 g/kg). Glutathione, carbonyl proteins and histological damage were evaluated in the gastric and intestinal mucosa 6 hours after treatment. RESULTS: An increase in glutathione was observed 2 to 6 hours after 1 g/kg of ethanol both in the gastric and intestinal mucosa, whereas 4 g/kg decreased glutathione. The rise in glutathione after ethanol was associated with increased levels of its oxidized form; however, the total/oxidized ratio was significantly decreased only in the intestinal tract. Diethylmaleate depleted mucosal glutathione, while the subsequent ingestion of ethanol increased it. Unlike stomach, intestine showed a significant increase in carbonyl proteins and marked histological lesions after ethanol ingestion. Cimetidine and cyanamide inhibited by 50% the activity of alcohol dehydrogenase and by 80% aldehyde dehydrogenase, respectively, in the gastric and intestinal mucosa. Cyanamide significantly enhanced ethanol-induced protein oxidation and mucosal injury in the stomach. No such effect was observed in the intestine. CONCLUSIONS: The increase of glutathione after ingestion of low amounts of ethanol appears to be an adaptive mechanism against ethanol toxicity. Depletion of glutathione increased protein oxidation and the extent of histological damage in ethanol-treated rats. At gastric level, the effects of ethanol are exaggerated by the inhibition of acetaldehyde metabolism; while intestinal damages appear to be ascribed to ethanol itself.

Nursing role innovations: improved outcomes in a trauma center.

Trauma systems operate on the principle that people with severe injuries require special medical capabilities if they are to have their best chance of recovery. However, optimal trauma care is threatened by the problems of inadequate financial reimbursement. This threatens the ability to deliver trauma patient care. A variety of strategies is necessary to continue to provide care. Two specific nursing role innovations provide the opportunity to improve the ability to provide coordinated, efficient, and cost-effective quality care.

Oxidative modification of proteins in chronic alcoholics.

Oxidative modification of proteins is of great importance because of their biological role in transport, enzyme activity, immune response and membrane fluidity. This study investigated the redox status of proteins in plasma, erythrocyte and erythrocyte ghosts of chronic alcoholics; a comparison with subjects affected by chronic viral hepatitis and healthy controls was also performed. Compared to the other groups, chronic active alcoholics showed significant increase of plasma, erythrocyte and erythrocyte ghost concentrations of carbonyl proteins, marker of protein oxidative damage. Also, a significant correlation was noted between daily alcohol intake and plasma levels of carbonyl proteins. The incubation of fresh human plasma with acetaldehyde, but not with ethanol, led to a significant increase of the carbonyl protein production. In conclusion, plasma, erythrocyte and membrane proteins are oxidatively modified in active chronic alcoholics; these changes seem to be related to acetaldehyde rather than ethanol toxicity.

Mitochondrial oxidative phosphorylation and intracellular glutathione compartmentation during rat liver regeneration.

The rate of mitochondrial oxidative phosphorylation and the cytosolic and mitochondrial total and oxidized glutathione concentrations were studied in regenerating rat livers after partial (70%) hepatectomy. The rate of mitochondrial oxidative phosphorylation progressively decreased during the early prereplicative phase of liver regeneration. This was accompanied by a progressive decrease in mitochondrial, but not cytosolic, glutathione concentration. Twenty-four hours after partial hepatectomy, both the rate of adenosine triphosphate (ATP) synthesis and the amount of mitochondrial glutathione were depressed by 50% with respect to controls (sham-operated animals). During the second replicative phase, both the oxidative phosphorylation rate and mitochondrial glutathione concentration were recovered; however, the kinetics of the recovery were different, being the total amount of mitochondrial glutathione completely restored 48 hours after partial hepatectomy, whereas 72 hours were needed for the recovery of oxidative phosphorylation. The decrease in the rate of oxidative phosphorylation, during the early phase of liver regeneration, appeared to be secondary to the decreased content of the catalytic subunit beta-F1 of the ATP synthase complex, which in turn was shown to be linearly related to the decrease of intramitochondrial glutathione. These observations suggest that the two phenomena may be due to the previously reported increased free radical production during the early phase of liver regeneration. The depression of mitochondrial glutathione after partial hepatectomy may play a contributory role in structural and functional alterations of mitochondria occurring in the first retrodifferential phase of liver regeneration.