[Neuroleptic malignant syndrome in the elderly: description of 4 patients]. / Síndrome maligno por neurolépticos en el anciano: descripción de cuatro pacientes.

The neuroleptic malignant syndrome is a fulminant, life-threatening reaction to neuroleptic medication. It is characterized by fever, rigidity, autonomic disfunction and fluctuating consciousness. Usually described in young adults with psychiatry illnesses, its presentation in an elderly population has received scant attention in medical literature. We describe the clinics and evolutive characteristics of 4 cases of this syndrome in elderly which a mean age of 78 years. We emphasise about the existence of a brain organic illness with dementia as a predisposing factor, and the correct evolution of the showed cases in probably relation with measures and drug therapy.

Nifedipine in rat liver cirrhosis.

Rat liver cirrhosis induced by CCl4+ethanol was employed to assess the effectiveness of nifedipine in reducing liver injury. Nifedipine reduced the severity of hepatocellular necrosis, significantly decreased Mallory bodies (p < 0.01), decreased polymorphonuclear inflammatory infiltrate (p < 0.05) and reduced perivenular fibrosis. Plasma lactic acid levels were significantly increased in the CCl4+ethanol group (p < 0.01). Lactacidaemia remained at normal values when the calcium antagonist blocker was employed. Nifedipine did not significantly alter the incidence of cirrhosis in this experimental model.

Effect of colchicine on lactate production by isolated hepatocytes in rats treated with carbon tetrachloride and ethanol.

This study was designed to evaluate the lactate production by isolated hepatocytes in rats with cirrhosis induced by means CCl4 + ethanol and the effect of colchicine in this experimental model of fibrosis. The effect of colchicine on lactate metabolism may be important in explaining the beneficial mechanism of this therapy on liver cirrhosis. Colchicine treatment produced a decrease in perivenular fibrosis and a descense in the degrees of this histological lesion. Colchicine treatment ameliorated the subsequent further development of cirrhosis. Lactate production in colchicine groups were higher than the carbon tetrachloride groups. By contrast, a priori, we observed a decrease in lactacidaemia and a lesser lactate utilization in colchicine groups comparison with CCl4 + ethanol groups. Our results suggest that colchicine improves the fibrosis by a mechanism independent of hepatic lactate metabolism.

Colchicine alters lactate utilization in isolated hepatocytes of rats treated with CCl4 and ethanol.

Lactic acidosis has been described in patients with liver disease. Hyperlactacidaemia results from an imbalance in lactate production versus lactate utilization. It is estimated that the liver utilizes approximately 30 percent of the total lactate produced in the body under basal conditions, primarily by gluconeogenesis. The gluconeogenesis from lactate 10 mM and lactacidaemia were determined in order to investigate the effects of CCl4+ethanol administration in liver injury and, the possible effect of colchicine in our experimental fibrosis model. The tests were determined after 15, 30 or 45 days of treatment. The results indicate that the gluconeogenesis was significantly inhibited in both CCl4+ethanol groups and CCl4+ethanol+colchicine groups. By contrast, the lactacidaemia levels were much higher in the CCl4+ethanol groups than the colchicine groups. Summarising, we have documented that hyperlactacidaemia is due to the inhibition of lactate utilization by the isolated hepatocytes in experimental cirrhosis, and that the improvement in lactacidaemia caused by colchicine is not primarily due to an increase in hepatic lactate utilization.

Comparative effect of nifedipine and S-adenosylmethionine, singly and in combination on experimental rat liver cirrhosis.

An experimental rat liver cirrhosis, by means of carbon tetrachloride and ethanol during 8 weeks, was employed to assay the effect of Nifedipine (a calcium antagonist blocker), S-Adenosylmethionine (a precursor of glutathione); singly and in combination on rat liver cirrhosis. A slight decrease of cirrhosis (N.S.) was observed with the pharmacological therapy employed singly. The combination therapy (Nifedipine+S-Adenosylmethionine) significantly inhibited liver cirrhosis (p < 0.01).

Effect of nifedipine and S-adenosylmethionine in the liver of rats treated with CCl4 and ethanol for one month.

An experimental model of toxic liver injury in rats was employed to assay the effect of Nifedipine (a calcium antagonist blocker) and S-Adenosylmethionine (a precursor of glutathione). An important decrease in both perivenular fibrosis and cirrhosis was found. Furthermore, a significant decrease in lactic acid levels was found in the group of animals treated with pharmacologic therapy, although no correlation was seen between lactic acid levels and the different degrees of perivenular fibrosis. No significant variations in ALT and AST enzymes were observed between both groups, as opposed to a significant decrease in LDH enzyme in the Nifedipine+S-Adenosylmethionine group. The results indicate an improvement in the histologic picture of the liver in rats treated by means of pharmacological association, without any change in inflammatory infiltrate and with a slight decrease in necrosis, indicating an action mechanism via creeping fibrosis (instead of a hepatitis pathway).