High levels of plasma FVIII and vWF in the toxic epidemic syndrome patients.

Factor VIII and von Willebrand factor proteins were evaluated in 115 patients having the chronic phase of the Toxic Epidemic Syndrome (TES), a new multisystemic disease probably caused by the ingestion of denatured rapeseed oil, and in 50 control volunteers. Higher circulating levels of factor VIII procoagulant activity (VIII:C) (158 +/- 58.4 U/dl), von Willebrand factor antigen (vWF:Ag) (166.1 +/- 55.5 U/dl) and von Willebrand factor ristocetin cofactor activity (vWF:RCo) (178.7 +/- 55.2 U/dl) were seen in TES patients (p less than 0.001, TES patients versus control subjects, for each parameter). The increased levels of vWF:Ag and vWF:RCo observed in TES patients correlated with the scleroderma like lesion of the skin, with the sicca syndrome and with Raynaud's phenomenon (p less than 0.01), but not with other clinical manifestations. The multimeric analysis of vWF in 92% of the TES patients was similar to that found in normal plasma, but in the remaining 8% a very slight increase of larger vWF multimers in plasma were observed. The raised levels of vWF found in TES patients in the chronic phase may reflect an "in vivo" vascular injury.

Epilepsy and neurocysticercosis in an Andean community.

BACKGROUND: Taenia solium neurocysticercosis (NCC) has been documented as one of the major causes of epilepsy in developing countries. However, methodological limitations have hindered the evaluation of the epidemiological relationship between cysticercosis and epilepsy at the community level. METHODS: We used the WHO protocol for epidemiological evaluation of neurological disorders to conduct a door-to-door survey among 2723 residents of San Pablo del Lago, an Ecuadorean rural community in which T. solium taeniasis/cysticercosis was known to be endemic. The WHO protocol was complemented by neuroimaging and immunological tests to confirm the diagnosis of this infection. RESULTS: In all 31 people suffering from active epilepsy were detected (prevalence 11.4 per 1000, 95% CI:7.7-15.4); 26 agreed to undergo a computer tomography (CT) examination, and 28 agreed to have blood drawn for serodiagnosis. Fourteen of the 26 (53.8%) had CT changes compatible with NCC and six of the 28 (21.4%) tested positive in the enzyme-linked immunoelectro-transfer blot (EITB) assay. In a seizure-free random sample of this population, 17 of 118 (144 per 1000) subjects examined by CT and 10 out of 96 (104 per 1000) examined by EITB had evidence of this infection. The differences between the epilepsy group and the random sample of the population were statistically significant (OR = 6.93, 95% CI: 2.7-17.5, P < 0.001) for CT diagnosis, but not for EITB results (OR = 2.75, 95% CI: 0.8-7.1, P > 0.12, NS). CONCLUSIONS: These findings confirm that T. solium NCC is a significant cause of epilepsy at the community level in Andean villages of Ecuador. It is important to initiate effective public health interventions to eliminate this infection, which may be responsible for at least half of the cases of reported epilepsy in Ecuador.

Changes in hepatic and serum gamma-glutamyltransferase activities following chronic ethanol intake in rats.

The effect of chronic ethanol consumption on serum and liver gamma-glutamyltransferase (GGT) activities was studied in male Wistar rats. Animals were fed for 1-9 weeks a liquid diet containing 36% of total energy as ethanol or isocaloric carbohydrates. Compared to control diet, chronic ethanol significantly and progressively increased serum activity from 3 weeks of treatment. Liver GGT activity was also enhanced although changes were not parallel to those found in serum. Chronic ethanol intake led to an enhancement of liver glutathione concentration with a 45% increase at 3 weeks of treatment and a decrease thereafter. It is suggested that the increased hepatic GGT activity is not the only determinant of the enhanced serum levels of the enzyme and that it is not related to the modifications of liver glutathione content induced by ethanol consumption.

Effect of chronic ethanol feeding on glutathione and glutathione-related enzyme activities in rat liver.

The effects of chronic ethanol consumption on liver glutathione concentrations and glutathione-related enzyme activities were studied in rats over a period of 1-9 weeks. The animals received a liquid diet containing 36% of calories as ethanol or isocaloric carbohydrate. Glutathione concentrations were significantly enhanced following ethanol intake with increases of 99% after 3 weeks and a progressive decrease thereafter. Glutathione S-transferase activity reached a maximum increase of 36% after 2 weeks of ethanol feeding. Glutathione peroxidase activity remained unchanged for the first 6 weeks of treatment, with a tendency to decrease in the last weeks of ethanol consumption. Our findings indicate that chronic ethanol administration profoundly modifies the hepatic metabolism of glutathione and may thus have important effects on the detoxification of xenobiotics by the liver.

Possible role of prolactin in the induction of hypogonadism by chronic alcohol treatment in the male rat.

Treatment of adult male rats with ethanol for a period of six weeks resulted in a numerical but not significant increase in plasma prolactin levels together with a reduction in plasma luteinizing hormone (LH) levels. Although basal plasma testosterone (T) levels were not affected in ethanol-treated animals, testicular weight was reduced and seminiferous tubules exhibited signs of atrophy. The responses of LH to luteinizing hormone releasing hormone (LHRH) and T to hCG were significantly impaired in ethanol-treated rats (p less than 0.01). Treatment with bromocriptine (1 mg/kg body weight/day), resulted in the expected decrease in plasma levels of prolactin and an increase in basal plasma LH levels to the levels found in control groups. Basal plasma T levels were not affected by bromocriptine. However, both plasma LH responses to LHRH and plasma T responses to hCG were significantly improved by bromocriptine treatment in alcoholic rats and became similar to the responses measured in control animals. The results suggest that bromocriptine-induced suppression of prolactin release has a beneficial effect on ethanol-induced hypogonadism.

Influence of acute ethanol administration on hepatic glutathione metabolism in the rat.

The effect of acute ethanol administration on the hepatic metabolism of glutathione was studied in male Wistar rats. Animals fasted for 18 hr received ethanol (5 g/kg body wt.) through a gastric tube as a 20% (w/v) solution in 0.154 NaCl. Four hours after administration of ethanol liver glutathione content was decreased by 21% when compared to saline-treated controls. A significant reduction (28%) was also found in gamma-glutamylcysteine synthetase activity and plasma glutathione levels were increased non significantly by 17% with respect to control rats. Glutathione S-transferase activity in the liver of ethanol-treated animals was decreased by 28% but no change was found in total glutathione peroxidase activity. The results indicate that the lowered glutathione synthesis could be an important factor contributing to the reduction of hepatic glutathione concentration following the acute ingestion of ethanol.

[Liver disease in toxic oil syndrome. Clinical and enzymatic course]. / Hépatopathie de la maladie par huile toxique. Evolution clinique et enzymatique.

One-hundred and fifty-nine patients intoxicated with adulterated oil in the province of Salamanca, Spain, were followed-up for 2 years from the onset of the syndrome, in 1981. Four alcoholic patients were excluded from the study. In the remaining 155 patients the liver involvement at the onset took different forms. It was acute in 12 (7%), with jaundice and/or hepatomegaly associated with cytolysis and/or cholestasis; 21 patients (13%) had evidence of cytolysis and/or cholestasis without clinical symptoms, and 29 (18%) only showed a rise in gamma-glutamyltranspeptidase with normal transaminase and alkaline phosphatase levels. Liver enlargement and/or jaundice subsided within 1 month in the 12 patients with clinical symptoms. However, high gamma-glutamyltranspeptidase levels persisted in 4 of them and in 5 of the 21 patients with laboratory abnormalities only. At the end of the study, this enzyme remained elevated in 6 and 7 patients respectively of these two groups and in 5 of the 29 patients with no other abnormality than a rise in gamma-glutamyltranspeptidase.

[Triple association of mesencephalic syndromes]. / Triple asociación de síndromes mesencefálicos.

INTRODUCTION: The mesencephalic alternating syndromes or syndromes of Weber, Benedikt and Claude are uncommon in clinical practice. They are caused by a lesion in the mesencephalus which affects the third cranial nerve bundle, together with the corticospinal pathway, subthalamic nucleus and the dentato-rubric path. CLINICAL CASE: We present the case of a normotensive patient who, as a consequence of a hematoma in the mesencephalic tegmentum, had the association of these three syndromes consecutively. The clinical course was favorable, so that after three months of follow-up only paralysis of the third cranial nerve bundle persisted. DISCUSSION: In the syndromes of Weber, Benedikt and Claude there is the association of ophthalmoplegia with hemiplegia, or a cerebellar hemisyndrome or contralateral abnormal movements compatible with hemiballismus, respectively. Amongst the commonest causes are expansive processes, tumors and arteriovenous malformations. More rarely they are due to cerebrovascular accidents, which are usually ischemic and occasionally hemorrhagic in aetiology. CONCLUSIONS: Spontaneous mesencephalic hematomas are infrequent. They make up approximately 1% of all intracranial hematomas. The commonest site is the tegmentum followed by the peduncle and tectum. They have better prognosis than other hematomas of the brainstem.

[Multiple cranial neuropathy: an atypical variant of the Guillain-Barre syndrome?]. / Neuropatía craneal múltiple: una variante atípica del síndrome de Guillain-Barré?

INTRODUCTION: Multiple cranial neuropathy or polineuritis cranealis is rarely seen in everyday clinical practice. It is considered to be a topographically circumscribed form of the Guillain-Barré syndrome. The cases described have a wide range of clinical and biological characteristics. Some of these may be due to infectious agents. CLINICAL CASE: We present the case of a 50 year old man with acute onset of diplopia, dysphagia, anarthria, cervical and right arm flexor-extensor muscle weakness due to involvement of many motor cranial nerves and superior cervical nerve roots. On neurological examination there was mixed involvement, mainly of the axons of the nerve trunks involved. Studies to determine aetiology did not show any demonstrable agent. DISCUSSION AND CONCLUSIONS: Different topographical varieties of the Guillain-Barré syndrome have been described, including: Fisher's syndrome, pharyngo-cervico-brachial paralysis, arreflexive paraparesia, bilateral facial paralysis with paraesthesias, hyporeflexia and bilateral lumbar polyradiculopathy. We compare the clinical characteristics of our patient with those described in the literature. We found a degree of heterogenicity in the clinical and biological characteristics of the cases described, which may mean that they had different aetiologies. Therefore, we consider that before labelling these conditions as atypical variants of the Guillain-Barré syndrome, a thorough search should be made for a precise aetiology.

Co-gasification of different rank coals with biomass and petroleum coke in a high-pressure reactor for H(2)-rich gas production.

Four coals of different rank were gasified, using a steam/oxygen mixture as gasifying agent, at atmospheric and elevated pressure in a fixed bed reactor fitted with a solids feeding system in continuous mode. Independently of coal rank, an increase in gasification pressure led to a decrease in H(2) + CO production and carbon conversion. Gasification of the different rank coals revealed that the higher the carbon content and reactivity, the greater the hydrogen production. Co-gasification experiments of binary (coal-biomass) and ternary blends (coal-petcoke-biomass) were conducted at high pressure to study possible synergetic effects. Interactions between the blend components were found to modify the gas production. An improvement in hydrogen production and cold gas efficiency was achieved when the coal was gasified with biomass.

[Hypothalamic-hypophyseal-gonadal axis in chronic alcoholic patients]. / Estudio del eje hipotálamo-hipofisario-gonadal en pacientes alcohólicos cronicos.

Eleven male chronic alcoholics without cirrhosis but with clinical features of alcoholism were studied. Ten healthy men of similar age served as controls. After suppressing hormone (FSH), luteinizing hormone (LH), 17-beta-oestradiol (E2) and testosterone were determined in basal conditions and after administration of clomiphene citrate in each case. Basal levels of FSH, LH and E2 were higher and the testosterone level lower in the alcoholic group. After stimulation, there was no difference in gonadal hormone levels between both groups, suggesting a normal hypothalamic-pituitary axis with an adequate gonadal response.

[Hypothalamic-hypophyseal-gonadal axis in patients with liver cirrhosis of alcoholic origin]. / Estudio del eje hipotálamo-hipofisario-gonadal en pacientes con cirrosis hepática de etiología alcohólica.

Plasma levels of testosterone, 17-beta-oestradiol (E2), follicle stimulating hormone (FSH) and luteinizing hormone were estimated in 19 males with alcoholic cirrhosis and in 10 healthy age matched controls in basal conditions and after administration of clomiphene citrate. The gonadal hormone response is normal in the cirrhotic group after stimulation with clomiphene citrate, suggesting a normal functional reserve of the gonad of the cirrhotic patients. It is emphasized the direct damage that the alcohol produces in the Leydig cell.

Time-dependent effects of alcohol on the hypothalamic-hypophyseal-testicular function in the rat.

Adult male rats were followed throughout ethanol administration, in order to examine the time-dependent effects of ethanol on the hypothalamic-pituitary-gonadal axis. The results indicate that there is an increase in plasma prolactin levels together with a reduction in basal plasma luteinizing hormone (LH) levels, which are evident from the beginning of the intoxication period. An exaggerated response of LH to luteinizing hormone-releasing hormone was also evident from 2nd week on, in ethanol-treated rats. Basal and human chorionic gonadotropin-stimulated plasma testosterone levels were decreased in alcohol-treated as compared to control rats, at all time points studied. In addition, plasma estradiol levels were increased in ethanol-fed rats. These data suggest a direct suppressive effect of ethanol on LH release in the beginning of the intoxication period. Subsequent elevations of plasma estradiol and prolactin levels may have contributed to the maintenance of hypogonadism at the end of the intoxication period.

Influence of a single dose of ethanol on the kinetics of valproic acid in rats.

A study was made of the influence of ethanol on the kinetics of valproic acid (VPA) in rats that received single doses of both compounds. Three groups of animals received a single dose of VPA (100 mg/kg) through a gastric tube, alone (Group I: controls) or together with ethanol at doses of 2.5 mg/kg (Group IIa) and 5 mg/kg (Group IIb). VPA was determined using the homogeneous immunoassay EMIT. VPA kinetics were fitted to an open two-compartment model with a first order two phase absorption process defined by the constants Ka1 and Ka2, where Ka1 would reflect the rate of gastric emptying, and Ka2 could express the true absorption constant. The groups of animals receiving ethanol showed a statistically significant decrease (p less than 0.05) in plasma concentrations of VPA compared with the control group. Ka2 increased in groups IIa and IIb compared with the control group (35.79 hr-1 and 36.61 hr-1 vs. 28.18 hr-1). However, Ka1 decreased in group IIb as compared with the control rats (2.34 hr-1 vs. 4.18 hr-1), whereas no modifications were seen in group IIa (4.35 hr-1). The t1/2 beta was greater in groups IIa and IIb than in the controls (8.77 hr and 7.78 hr vs. 4.55 hr), and Ke was lower in those groups than in the controls (0.86 hr-1 and 0.48 hr-1 vs. 0.98 hr-1), suggesting a decrease in the elimination of VPA following administration of a single dose of ethanol.

Effect of ethanol consumption on adult rat liver mitochondrial populations analyzed by flow cytometry.

In the present study, the effects of administering ethanol to adult male rats on the distribution of the low fluorescence population (LFP) and high fluorescence population (HFP), and the rhodamine-123 fluorescence intensity of these groups of mitochondria are analyzed by flow cytometry. Our results show that ethanol administration to adult male rats induces a redistribution of the HFP and LFP mitochondrial populations leading to an increase of the less functional HFP mitochondria. In addition, ethanol induced an increase in the mean intensity of green fluorescence of the HFP that is probably related to an increased number of rhodamine-123 binding sites per mitochondria resulting from mitochondria enlargement.

[Effect of chronic consumption of alcohol on the hypothalamo-pituitary-testicular axis in the rat]. / Efecto del consumo crónico de alcohol sobre el eje hipotálamo-hipofiso-testicular en la rata.

An experimental model of chronic alcohol abuse is developed, in order to study the hypothalamic-pituitary testicular axis in the rat. For this purpose basal plasma prolactin, gonadotropins, testosterone and estradiol have been measured. Also these hormones were studied after LHRH or hCG stimulation. This experimental model allows us to study the role of alcohol in hypogonadism induction. Chronic alcohol administration resulted in an inconstant decrease in plasma testosterone levels and very diminished response of it to hCG. Along with these modifications, there was an increase in basal plasma estrogen levels, as has been shown in the human. The decrease in plasma LH levels in alcoholic rats together with a normal response to LHRH suggest a toxic role of alcohol at higher levels than the pituitary. The existence of a hyperprolactinemic state under chronic alcohol ingestion is confirmed. The decrease in plasma prolactin levels after LHRH administration suggests that prolactin and gonadotropin secretion are very closely related.