Resolución de un síndrome de Youssef mediante tratamiento con análogos de GnRh. Caso clínico

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Fístula vesicouterina: análisis de seis casos de una rara entidad / Vesicouterine fistula: analisys of six cases of a rare entity

Objetivo: Valorar los aspectos etiológicos, diagnósticos y terapéuticos de las fístulas vesicouterinas.Material y métodos: Estudio retrospectivo de las fístulas vesicouterinas observadas en el Hospital Son Dureta entre 1982 y 1999.Resultados: Seis casos con una edad media de 36,6 años. El antecedente de cesárea se dio en cinco ocasiones. Dos pacientes tenían tres cesáreas. Otras dos tenían una cesárea y debutaron clínicamente tras un segundo embarazo que terminó en parto vaginal. Una fístula se observó tras cesárea histerectomía en la que se conservó el cuello. La clínica consistió en la incontinencia urinaria, la hematuria y la menuria. El diagnóstico se basó en la cistoscopìa y uretrocistografía. El tratamiento fue quirúrgico mediante la reparación de la fístula por vía abdominal y los resultados fueron siempre satisfactorios.Conclusiones: Las fístulas vesicouterinas son muy poco frecuentes, pero deben considerarse ante una paciente con antecedente de cesárea y que presente incontinencia de orina combinada o no con hematuria (AU)

Effects of clenbuterol and salbutamol on tissue rubidium uptake in vivo.

In anesthetized rats, injection of the beta 2-adrenoceptor (beta 2-AR) agonist clenbuterol (0.45 mumol/kg) caused a marked stimulation of 86RbCl (Rb) uptake by skeletal muscle, but had no effect on other tissues; soleus muscle showed the largest (144% increase) response. Injection of another beta 2-AR agonist (salbutamol 0.45 mumol/kg) had no effect on Rb uptake by any tissue except soleus muscle (83%). Both agonists increased body (colonic) temperature to the same extent. A 3-day treatment with salbutamol as a dietary admixture had no effect on body weight, muscle mass, or tissue Rb uptake, whereas the same treatment using clenbuterol produced significant increases in body weight and muscle mass and significant decreases in Rb uptake in three of the four muscle groups studied; Rb uptake in soleus was not affected. In another experiment, the short-term effect of clenbuterol injection on muscle Rb uptake was found to be resistant to a high dose (20 mg/kg) of the selective beta 2-AR antagonist ICI 118551. It was concluded that the selective effects of short-term administration of clenbuterol on muscle Rb uptake, coupled with its effects over 3 days on Rb uptake and muscle hypertrophy, implicate beta-AR modulation of cation transport (possibly via Na,K-adenosine triphosphatase [ATPase] activity) in the anabolic effects of clenbuterol on muscle protein deposition. Since the stimulation of Rb uptake by clenbuterol was resistant to high doses of a selective beta 2-AR antagonist and since salbutamol had little or no effect on muscle hypertrophy or Rb uptake, it is suggested that clenbuterol may exert its effects via an atypical beta-AR.

Anabolic effects of clenbuterol after long-term treatment and withdrawal in t the rat.

Injection of rats with the beta 2-adrenoceptor agonist clenbuterol (1 mg/kg/d for 15 days) stimulated an increase in body weight (9%) and protein (8%) and water (7%) content, but reduced food intake (4%) and epididymal fat pad mass (39%). Nine days after termination of treatment, ex-clenbuterol rats were heavier (5%) and had a greater protein (7%) and water (6%) content and lower fat pad mass (32%) than controls. Clenbuterol-fed rats (2 mg/kg diet for 10 days, providing an average of 0.04 mg clenbuterol/kg/d) increased body weight (7%), muscle mass (15% to 21%), and muscle protein content (9% to 26%), whereas epididymal fat pad weight and muscle glycogen content were reduced. During the withdrawal period, the greater body weight of ex-clenbuterol rats was sustained overall (ANOVA, P < .00005), but by day 10 this difference was no longer significant. At this point, gastrocnemius muscle mass was still higher (11%) when compared with that of control animals, but soleus muscle mass, muscle glycogen concentration, and epididymal fat pad weight had reverted to control values. These results were corroborated in a subsequent experiment using older rats. It was concluded that, unlike other beta-adrenoceptor-mediated effects, muscle protein accumulated during clenbuterol treatment can be maintained in certain muscles after removal of the drug for a period of time that is at least equivalent to the duration of treatment. This could have implications for the potential therapeutic use of this class of compound, and differences in the response observed between muscle types may help to elucidate the mechanisms responsible for the muscle protein deposition induced by clenbuterol.

Effects of digoxin on the anabolic response to clenbuterol.

The possible involvement of increased cation exchange in the anabolic response to the beta 2-selective adrenergic agonist clenbuterol was investigated using dietary admixtures of clenbuterol and the Na,K-adenosine triphosphatase (ATPase) inhibitor digoxin. In a rat feeding trial to assess the effects on body composition, it was found that the higher of two levels (5 and 30 mg/kg diet) of digoxin had an inhibitory effect on the repartitioning effects (ie, increased body weight and fat-free mass) of clenbuterol (2 mg/kg diet). In two further experiments using 30 and 60 mg digoxin/kg diet, it was found that the anabolic effects of clenbuterol on gastrocnemius muscle protein deposition were inhibited by digoxin, but the effects of clenbuterol on soleus muscle protein were more resistant to inhibition. Given the observed dose-dependent inhibition by digoxin of gastrocnemius muscle protein deposition in the three experiments, it was concluded that at least part of clenbuterol's anabolic actions on skeletal muscle may depend on increased Na,K-ATPase activity. However, different mechanisms or a different time course of Na,K-ATPase activation may occur in different muscle fiber types.

Antibiotic prophylaxis in Wertheim-Meigs surgery. A single dose vs three doses.

A prospective, randomized study to compare the prophylactic efficacy of a single dose of piperacillin with that of a three doses, was carried out with patients undergoing Wertheim-Meigs surgery. The results demonstrate that in this case three doses of piperacillin have a higher efficacy than one dose in the prevention of febrile complications and post-operative infections.

Alpha 2-adrenergic blockade prevents hyperglycemia and hepatic glutathione depletion in nickel-injected rats.

To study the involvement of the adrenergic system in nickel-induced hyperglycemia and hepatic glutathione depletion in rats, several adrenergic antagonists (phentolamine, prazosin, yohimbine, and propranolol) were administered in a single ip injection before acute nickel treatment (ip injection). Moreover, the effects of nickel on adrenalectomized rats were investigated. Hyperglycemia was suppressed by either alpha-antagonist phentolamine or alpha 2-antagonist yohimbine. Such blockade coincided with the prevention of the hypoinsulinemic response to nickel, which occurred simultaneously to hyperglycemia. Nickel-induced hyperglucagonemia remained almost unaltered by pretreatment with adrenergic antagonists. In adrenalectomized animals treated with nickel, hyperglycemia was attenuated, whereas hypoinsulinemia still persisted. Therefore, catecholamines seemed to participate in nickel-induced hyperglycemia, directly, i.e., stimulating glucose output from liver, or by modulating insulin secretion throughout alpha 2-adrenoreceptor stimulation in pancreatic islets. Hepatic glutathione depletion caused by nickel was prevented by either alpha 1-antagonist prazosin or alpha 2-antagonist yohimbine. Interestingly, adrenalectomy did not alter the drop in hepatic GSH induced by nickel treatment. Overall results suggest that the effects observed after acute nickel exposure were caused by a combined action of catecholamines released from the adrenal glands and those released at the efferent nerves. Such events have been found to be mediated by alpha 2-adrenergic receptors.

Nickel effects on hepatic amino acids.

Female Wistar rats were treated with nickel (single i.p. injection of 6 mg Ni(II)/kg body weight) and twenty amino acids and glutathione (GSH) concentrations were determined in liver 90 minutes later. Hepatic GSH content dramatically diminished after nickel injection. Glycine and glutamate levels, precursor amino acids of GSH, were not affected by nickel treatment, whereas cysteine level, the third precursor, was drastically increased in comparison with control rats. These findings showed that hepatic GSH depletion, caused by acute nickel exposure, was not due to a reduction in the availability of precursor amino acids. Nickel treatment also induced a 2-fold increase in phenylalanine and a decrease in taurine to one fifth. Therefore, the role of taurine in protecting membranes was clearly jeopardized in liver after nickel exposure, which could account for some of the toxicologic actions of this metal. However, further research is needed to explore such suggestion.

Effects of copper, cadmium and nickel on liver and kidney glutathione redox cycle of rats (Rattus sp.).

1. Glutathione redox cycle alterations induced by acute treatment of nickel, cadmium and copper, have been investigated in liver and kidney of adult male rats. 2. In liver, nickel treatment decreased GSH and GSSG levels, followed by a significant rebound in GSH content. Copper produced drastic reduction in the GSH/GSSG ratio, while cadmium treatment altered GSSG concentrations. 3. In kidney, the glutathione redox cycle remained unaltered after cadmium or nickel exposure, whereas copper caused similar changes to those observed in liver. 4. Hepatic glucose-6-P dehydrogenase and GSSG-reductase activities decreased after copper or nickel injection. GSH-S-transferase activity was altered in various ways, depending on the organ and the metal.

Nickel-induced hyperglycaemia: the role of insulin and glucagon.

Glucagon and insulin changes were measured in acute nickel-treated rats. Also, several parameters related to glucose homeostasis were evaluated. Nickel treatment caused an important and transitory rise in plasma glucose levels. These changes occurred simultaneously to hyperglucagonemia and hypoinsulinemia, leading to a drastic drop in the insulin/glucagon plasma ratio. In such a catabolic situation, hepatic and muscular glycogen levels remained almost unaltered. Hepatic fructose-2,6-bisphosphate (an indicator of gluconeogenic/glycolytic state) was drastically reduced a short time after nickel injection. Such events suggested that it was mainly gluconeogenesis and not glycogenolysis, which contributes to enhanced plasma glucose. Animals treated with large doses of glucagon did not mimic the hyperglycaemic responses induced by nickel, due to counteracting effects of insulin on plasma glucose. When diabetic rats were treated with nickel, the hyperglucagonemic response still remained, but plasma glucose levels did not increase at the same extent as when nickel was applied to control animals. Overall results suggest that both, glucagon and insulin changes are essential in the development of nickel-induced hyperglycaemia. Also, the lack of glycogenolytic response insinuates a direct or indirect inhibition of this process mediated by nickel and will need further investigation.

Effects of acute nickel toxicity upon plasma and liver metal homeostasis as a function of sex.

The effects of an acute dose of nickel chloride (4 mg Ni/kg body wt) upon liver and plasma essential metal homoeostasis were studied in male and female rats. Total levels of copper and zinc in the tissues and in the fractions of chromatographic profiles (Sephadex G-100 and G-150) were determined. Plasma and liver levels of both metals rose significantly. The higher levels of copper in plasma are associated with increased ceruloplasmin activity and the initial increase of zinc in plasma is due to higher zinc content in the plasma albumin fraction. In the liver, the higher levels of both metals similarly affected all the metal-containing chromatographic fractions, although a significant increase is only observed in metallothionein-containing fractions, which agrees with previous reports on increased levels of metallothionein after nickel treatment. Regarding the sex-dependent changes, both sexes showed the same alterations, yet males recovered faster than females from all the nickel-induced changes in metal homoeostasis.

[Antibiotic prophylaxis with piperacillin in vaginal hysterectomy. Study of 1 dose versus 3 doses]. / Profilaxis antibiótica con piperacilina en la histerectomiá vaginal. Estudio de una dosis frente a tres.

A homogeneous and consecutive series of 93 patients treated with vaginal hysterectomy is studied in a controlled, randomized clinical essay. The patients were divided in two groups. One of the groups received one single dose of 49 of piperacillin 30 minutes before surgery; the other, three doses of 4 g of the same antibiotic 30 minutes before surgery and 6 & 12 hours after it. No significant difference was found between both groups and therefore it is fair to suppose that one single preoperative dose of piperacillin shows similar efficacy to the usually used three doses, one preoperative and two postoperative.

Immature teratoma primary of the uterine cervix. First case report.

The extragonadal germ cell tumours represent 1-2% out of all the germ cell tumors. The retroperitoneal and the mediastinic spaces are the most common localizations. Visceral localizations are very infrequent. We present a case, the first described in literature, of immature teratoma of the uterine cervix in a 13 year old girl.

Effects of a high lipidic diet on murine energetic reserves in food deprivation.

Female mice were fed for one month either control or cafeteria diets. Then they were subjected to food deprivation for up to 36 hours and their weight loss, tissue lipid, glycogen and protein were determined together with their plasma glycose, amino acids, urea, lipoproteins and ketone bodies. Cafeteria mice were able to cope with prolonged starvation with altered plasma composition and important loss of lipids and protein, sparing to a certain degree their glucose and amino acids. Control-fed mice, however, showed a intense ketosis and significant losses of nitrogen. The results obtained showed a higher ability of cafeteria mice to handle and use lipids, that evolves in a better suitability to resist food deprivation with less extensive alterations in their fuel and nitrogen homeostasis.

Alterations of energy metabolism induced by hexadecane in mice.

Two groups of young male OF-1 mice were fed for 60 days with cafeteria or, as controls, with standard pellet diet respectively. At that time, both groups were daily treated with hexadecane (HDK) on the skin. HDK induced a drastic body weight loss much higher in cafeteria than control mice. White adipose tissue were exhausted after 4 days of treatment in controls but not after 10 days in cafeteria ones. HDK resulted in mobilization of liver glycogen in both groups while muscle glycogen decreased slightly in the end. Hexadecane treatment did not result in massively enhanced nitrogen metabolism, as the actual oxidation of amino acids decreased considerably as indicated by the low levels of plasma urea. The results could be explained by powerful and lasting effects of hexadecane on thermogenesis and metabolic reserve balance. The use of this material for pharmacological manipulation of body weight appeared difficult.

Characterization of the inhibition effect induced by nickel on glucose-6-phosphate dehydrogenase and glutathione reductase.

Kinetic characterization of the inhibition effect of nickel on glucose-6-phosphate dehydrogenase (EC 1.1.1.49) (G-6-PD) and glutathione reductase (GR; EC 1.6.4.2) from Saccharomyces cerevisiae was made. The effect of nickel on G-6-PD activity is consistent with a mixed-type inhibition pattern, with a competitive character, since the inequality ki,int greater than ki,slope shows an inverse relation between varied substrate concentrations and fractional inhibition. An inhibition effect of nickel on GR activity, when NADPH is the varied substrate, is also consistent with a mixed-type inhibition pattern. However, pure competitive inhibition is found on GR reaction when oxidized glutathione is the varied substrate. This investigation shows the highest sensibility of GR before the inhibitory effect of nickel, in agreement with the experimental values of inhibition constants found in this study, where constants related to the GR system are lower than the ones of the G-6-PD system.

Serum protein changes in cafeteria mice induced by starvation.

Serum protein changes in cafeteria and control mice induced by starvation have been studied. Animals were subjected to food deprivation at 0, 3, 6, 9, 12, 18, 24 or 36 hours. Results show a more stabilized situation in cafeteria mice than controls particularly in protein metabolism. Serum protein composition changed very little during starvation, suggests a lower protein and amino acid catabolism induced by the high adaptation to consume lipids.