Síndrome de Sweet de localización atípica en pierna izquierda / Sweet syndrome atipical located in left leg

El Síndrome de Sweet (SS) es una enfermedad de la piel recidivante y poco frecuente, caracterizado por la aparición de pápulas inflamatorias dolorosas que se convierten en placas, acompañadas de fiebre, artralgias y leucocitosis periférica. La mayoría de los casos se presentan entre los 30 y los 60 años de edad, siendo la etiología desconocida, posiblemente por una reacción de hipersensibilidad de tipo III, una activación de linfocitos T por antígenos o una alteración de la función de los neutrófilos, sin embargo ninguno de estos 3 mecanismos se ha demostrado de manera consistente. Esta enfermedad afecta normalmente: cara, cuello, tronco y extremidades superiores y en algunos casos está asociado con infección por Yersinia. Se presenta el caso de un paciente masculino de 74 años transferido al Policlínico N°32 de la Caja Nacional de Salud (CNS) por un cuadro de celulitis en la pierna izquierda, misma que no respondió al tratamiento inicial con Cefotaxima, Ciprofloxacina, Ranitidina e Ibuprofeno, por lo cual se pide biopsia donde se reporta compatibilidad con una dermatosis de causa vascular la cual sugiere Síndrome de Sweet y se procede a administrar Dapsona e Indometacina.

Sweet's Syndrome (SS) is a relapsing and rare skin disease, characterized by the appearance of painful inflammatory papules that become plates, accompanied by fever, arthralgia and peripheral leukocytosis. Most cases occur between 30 and 60 years old, being the unknown etiology, possibly by a hypersensitivity reaction type III, T cell activation by antigens or impaired neutrophil function without But none of these three mechanisms has been consistently demonstrated, This disease usually affects: face, neck, trunk and upper extremities and in some cases is associated with Yersinia infection. It presents a male patient of 74 years old transferred to Polyclinic No. 32 of the Caja Nacional de Salud (CNS) with symptoms of cellulitis in his left leg, it did not respond to initial treatment with Cefotaxime, Ciprofloxacin, Ranitidine and Ibuprofen, a biopsy is requested which has reported compatibility with Vascular dermatoses suggesting Sweet Syndrome and it's treated with Dapsone and Indomethacin.

Dynamic and spatial features of the inhibitory pallidal GABAergic synapses.

The globus pallidus, one of the basal ganglia nuclei, plays a major role in both basal ganglia physiology and pathophysiology. The globus pallidus is innervated mainly by striatal spiny neurons and globus pallidus collaterals. These GABAergic synapses constitute 90% of the input to globus pallidus cells. Despite the dominance of this inhibitory GABAergic input, globus pallidus cells are spontaneously active and most of them increase their firing rate in a task related manner. To explain this apparent inconsistency, we studied the dynamic and spatial effects of GABAergic inputs to globus pallidus neurons. To this end, we used intra-cellular recording from globus pallidus neurons in rat brain slices, investigating the effect of bath and local GABA application, as well as the responses to electrical stimulation of the striatum. We showed that the properties of the responses to either local or global GABA applications are similar to the responses of globus pallidus cells to GABA release from nerve terminals. Since the stimulus-evoked responses have been shown to be inhibitory in nature, we concluded that GABAergic inputs to globus pallidus both at soma and dendrite level are inhibitory. Furthermore, we showed that GABA can promote globus pallidus synchronization by affecting the timing of globus pallidus spiking, and that the globus pallidus GABAergic synapse undergoes rapid frequency-dependent depression. This prominent synaptic depression can account for the ability of globus pallidus neurons to fire in the presence of a majority of inhibitory inputs and might indicate that globus pallidus neurons are tuned to detect frequency changes. Furthermore, globus pallidus synaptic depression rules out the possibility of activation of GABAeregic afferents as the main mechanisms of high-frequency deep brain stimulation, used for treatment of severe parkinsonian patients.

[Budd-Chiari syndrome: updated treatment modalities].

Budd-Chiari Syndrome (BCS) refers to hepatic venous outflow obstruction, resulting in simultaneous occurrence of hepatic congestion and portal hypertension, leading to a typical clinical triad consisting of right upper quadrant pain, hepatomegaly and ascites. Contrary to Asia and Africa, where BCS is caused primarily by an obstructing membranous web, BCS in the western world is considered a thrombotic complication of an underlying hypercoagulable state. Recognition of the contribution of hypercoagulability as a causative factor in BCS, has led to acknowledgement of the importance of anti-coagulant therapy in BCS. Indeed, a conservative approach consisting of diuretics and anti-coagulant therapy is considered an appropriate treatment strategy for the BCS patient, in the absence of significant hepatic insult. However, once disease progression is noted, based on clinical symptoms, hepatic laboratory disturbance or histological evidence of irreversible hepatic damage, a definite invasive treatment should be applied. The specific procedure to be used is dependent upon the extent of hepatic insult and the anatomical characteristics of the venous obstruction in any individual patient. In the absence of significant hepatic damage, one may employ surgical shunting or invasive roentgenic measures, such as TransJugular Intrahepatic Porto-Systemic Shunt procedure, for the decompression of the portal system. Alternatively, in cases of a single localized obstruction, one may use balloon angioplasty with stent insertion. In contrast, upon evidence of significant hepatic damage, liver transplantation becomes necessary. To date, numerous studies report excellent results regarding the success of liver transplantation for patients with advanced BCS disease accompanied by significant hepatic damage.

[Etiopathogenesis of giant cell arteritis]. / Etiopatogenia de la arteritis de células gigantes.

Giant cell arteritis is a vasculitis of large and medium size arteries, especially those of the aortic arch with an extracranial distribution, but also the aorta and some of its larger branches. It is characterised by the presence of mononuclear inflammatory infiltrates close to the internal elastic lamina formed by lymphocytes and macrophages, which in slightly more than 50% of the cases contain multinucleate giant cells. The morbidity associated with this disease is related to phenomena of distal ischemia to the luminal stenosis of the inflamed arteries, and to a lesser extent to the formation of aneurisms due to the weakening of the arterial wall. With an unknown aetiology, its pathogenesis is immune through the migration and location of gamma-INF -producing T cells in the adventitia of the inflamed arteries, it being assumed that this is the place of immune stimulation by a still unidentified antigen. The recruitment and activation of macrophages by this cytokine is one of the most important points of its pathogenesis. The destruction by these of the arterial elastic tissue is a relevant phenomenon, as is the production of other factors promoting neoangiogenesis and a proliferation of neointime, responsible through obliterating light for the ischemic manifestations of the disease. The process is accompanied by an important systemic repercussion characterised by a strong reaction of acute phase and general but barely specific symptoms of disease. On the other hand, an important percentage of patients show a clinical picture of polymyalgia rheumatica, an entity that has a historical and controversial relationship to this arteritis. In recent years important contributions have been made to the understanding of the immune mechanisms involved in its pathogenesis.

[Core body temperature monitoring using the telemetric pill].

Exposure to extreme weather or physical work conditions can lead to dangerous core temperature changes, and to the clinical syndromes accompanying them. Core temperature measurement is the main tool for diagnosing these syndromes. Recent technological advances particularly NASA's telemetry and miniaturizing technologies, have led to the development of a CorTemp Ingestible Temperature Sensor, or "pill". The pill is a small electronic device, which senses the body's temperature and transmits it through a radio wave signal to an external receiver. The advantage of the pill over other temperature measurement devices is that it is a simple device that enables core temperature measurement for many hours without the need of any wire connections or other cumbersome instruments. For this reason, the pill is an ideal tool for core temperature measurements in field locales or for continuous long duration temperature monitoring of ambulatory patients. The following study reviews available literature concerning the use of the pill and the validity of its measurements. A high correlation has been revealed between pill temperature measurements and rectal or esophageal measurements. Pill temperature values usually fall between the high rectal and the low esophageal measurements, considered the gold standard for core temperature measurement. A number of studies emphasizing the advantage of the pill are presented in this review.

In vitro lithotripsy with the Alexandrite laser.

The Alexandrite laser system has proven to be an effective and safe method of ureteral lithotripsy. Some authors have recently reported the risk of interspersion of fiber splinters into tissue during lithotripsy, when short pulses and high power densities are employed. In vitro lithotripsy on renal calculi artificially placed in human ureters was realized under the parameters of a manufactured model (Alexantriptor, HMT). We have observed neither interspersion of fragments nor ureteral damage. These in vitro experiments and our clinical experience confirm that Alexandrite laser lithotripsy is reliable and safe.

[Usefulness of warning flags in the handling of biological samples in an emergency room]. / Utilidad de los distintivos de precaución en el manejo de muestras biológicas en un servicio de urgencias.

The present study evaluates the utility of biohazard precautions labels for identifying biological samples of patients with probable severe transmissible infectious diseases. The study was performed in a total of 633 patients in the emergency department of a General Hospital. In an anonymous way we determine the presence or absence of serological markers of HIV and hepatitis B infection (HBsAg) and we evaluated the labeling of the sample. Our results demonstrate the very low usefulness of this common procedure: a total of 54.5% of HIV positive patients and 87.5% of those positive to HBsAg were not marked correctly. We discuss the necessity of using universal precautions instead of labeling samples in the current way.

Lithotripsy with the alexandrite laser: our initial 100 clinical cases.

The alexandrite laser system has proven to be an effective and safe method of treating ureteral stones. When the electromagnetic energy of a laser light pulse is selectively absorbed by the stone, a plasma forms at the surface. This plasma, which is composed of ions and electrons, continues to absorb laser energy, reaching very high pressure and generating a shock wave that fragments the stone. The degree of stone fragmentation is directly related to the composition and crystal lattice structure of the calculus. 112 calculi have been treated, and laser lithotripsy was successful in 87.5%. 6% of the stones were inadvertently flushed back into the kidney. No patient required an open ureterolithotomy. Guidance of the laser fiber onto the stone was performed by rigid ureteroscopy. There were no troublesome complications, and in a 3-month follow-up, no sequelae were reported.

Chlortetracycline and aflatoxin interaction in two lines of chicks.

To determine if feed contaminants and feed additives interact, day-old chicks from lines bred for high and low antibody response to sheep erythrocytes were fed aflatoxin at a level of 3,000 ppb, chlortetracycline at a level of 550 ppm, or a combination of aflatoxin and chlortetracycline for a period of 6 wk. Weight gain in both lines of chicks was adversely affected by the aflatoxin treatment. There was a synergistic adverse effect in chicks of the low antibody response line when given chlortetracycline as well as aflatoxin, an effect not noted in chicks of the high antibody response line. Chlortetracycline alone had no effect on weight gain of low antibody response birds but increased the weight gain of chicks from the high antibody response line. Bursa to body weight ratios were adversely affected by aflatoxin in both lines of chicks, but chlortetracycline further adversely affected this parameter only in the low antibody response line. These results indicate that adverse effects of aflatoxin may be enhanced by addition of antibiotics to feed.

Interactions of aflatoxin and the antioxidant butylated hydroxytoluene in two-week-old chicks.

Two-week dietary administration of 2500 ppb aflatoxin was sufficient to cause a decrease in bursal weights and a reduction in the number of splenic leukocytes in chicks. No significant effects on weight gain or feed efficiency were evident. The chicks also had elevated heterophil-to-lymphocyte ratios, suggesting a heightened reaction to stress. This effect could be blocked by dietary administration of the antioxidant butylated hydroxytoluene (BHT) at a concentration eight-fold over that normally present to preserve control feed. The BHT treatment increased the activities of the enzymes glutathione-S-transferase, aniline hydroxylase and O-demethylase, which metabolize aflatoxins in the liver.