Vasculitis in patients with the myelodysplastic syndrome (MDS) is a rare phenomenon. We describe a patient who presented with necrotic lesions of his toes, which proved to be the result of immune complex mediated vasculitis. This unusual combination of vasculitis and MDS prompted us to review the literature. Forty-four cases of vasculitis in association with MDS were found. The pathogenesis of the vasculitis in MDS remains speculative, although several reports suggest an immunological mechanism. The temporal relationship could not be determined in 20 (45%) of reported cases. The prognosis of these patients appears to be worse than in patients with MDS without vasculitis. Steroids were used in 41 (93%) of the reported cases. Our patient did not receive any drug therapy, nevertheless his necrotic lesions improved within a few weeks.
These results indicate that free MDA was formed artifactually during tissue homogenization in the absence of butylated hydroxytoluene. Furthermore, free MDA could not be detected in perfused rat hearts after control perfusion, or 20 min of ischemia, or 20 min of ischemia followed by 5 or 30 min of reperfusion.
Intoxication with Aconitum napellus is rare in our regions. Aconite alkaloids can cause ventricular arrhythmia by a prolonged activation of sodium channels. Because the margin of safety is low between the analgesic and toxic dose, intoxication is not rare when Aconite is used in herbal medicine. We present a case in which a 39-year-old male was accidentally intoxicated with Aconite. Even though no antidote or adequate therapy is available he was successfully resuscitated. (Neth Heart J 2008;16: 96-9.) Keywords: intoxication, aconite, aconitum, cardiotoxic, resuscitation A conitum napellus, commonly known as Aconite, Monkshood or Wolfsbane, is a herb with bluishpurple flowers (figure 1). It can be found throughout the world and is notorious for its toxicity. Most notably, the Roman emperor Claudius (41 to 54 AD) was murdered by his spouse Agrippina so her son Nero could then ascend the throne. It is thought that he was poisoned with Aconite. Even though it has known toxicity, Aconite roots are often sold freely and are commonly used in herbal medicine for treating musculoskeletal pain. However, the margin of safety between analgesic and toxic doses is very low. Therefore, intoxications are not extremely rare, especially in Southeast Asia. The most important cause of death due to an intoxication with Aconite is malignant ventricular tachyarrhythmia. We report an extraordinary case in which an accidental but life-threatening intoxication with Aconite occurred. Our patient recovered completely after prolonged resuscitation. Case reportA 39-year-old male with no medical history was admitted to our emergency department with collapse and signs of food intoxication. Less than two hours before, he had eaten a homemade salad of canned tuna and herbs from his own garden. After ingestion he became unwell with sweating and he developed paresthesiae in both his hands and tongue. Later he experienced nausea, vomited and had profound diarrhoea. Shortly before his admission he had collapsed once, and spontaneously regained consciousness. When he was first seen by paramedics, his blood pressure was unrecordable and ECG showed a broad complex tachycardia.When admitted to our emergency department we saw an ill, sweaty man who was still conscious. He told us that he had ingested more than 100 g of a kind of herb, which our patient believed to be celery. He had never eaten this before and it was unclear whether the ingested herb could be digitalis. At this moment he experienced dizziness and nausea. He had no complaints of chest pain. There was no history of intoxication with either nicotine, alcohol or any drugs. In his family there were no cases of sudden cardiac death; his father had undergone a percutaneous coronary intervention at the age of 64 years.The ECG showed a monomorphic ventricular tachycardia with a frequency of 220 beats/min (figure 2). After five minutes this rhythm evolved into a polymorphic ventricular tachycardia and subsequently ventricular fibrillation. Resuscitation was initiated immediately including intubatio...
The objectives of this study were to determine 1) whether reactive oxygen species generated upon postischemic reperfusion lead to oxidative stress in rat hearts, and 2) whether an exogenous prooxidant present in the early phase of reperfusion causes additional injury. Isolated buffer-perfused rat hearts were subjected to 30 min of hypothermic no-flow ischemia followed by 30 min of reperfusion. Increased myocardial content of glutathione disulfide (GSSG) and increased active transport of GSSG were used as indices of oxidative stress. To impose a prooxidant load, cumene hydroperoxide (20 microM) was administered during the first 10 min of reperfusion to a separate group of postischemic hearts. Reperfusion after 30 min of hypothermic ischemia resulted in a recovery of myocardial ATP from 28% at end-ischemia to 50-60%, a release of 5% of total myocardial LDH, and an almost complete recovery of both coronary flow rate and left ventricular developed pressure. After 5 and 30 min of reperfusion, neither myocardial content of GSSG nor active transport of GSSG were increased. These indices were increased, however, if cumene hydroperoxide was administered during early reperfusion. After stopping the administration of cumene hydroperoxide, myocardial GSSG content returned to control values and GSH content increased, indicating an unimpaired glutathione reductase reaction. Despite the induction of oxidative stress, reperfusion with cumene hydroperoxide did not cause additional metabolic, structural, or functional injury when compared to reperfusion without cumene hydroperoxide. We conclude that reactive oxygen species generated upon postischemic reperfusion did not lead to oxidative stress in isolated rat hearts. Moreover, even a superimposed prooxidant load during early reperfusion did not cause additional injury.
The aim of this study was to test the hypothesis that a decreased myocardial concentration of reduced glutathione (GSH) during ischemia renders the myocardium more susceptible to injury by reactive oxygen species generated during early reperfusion. To this end, rats were pretreated with L-buthionine-S,R-sulfoximine (2 mmol/kg), which depleted myocardial GSH by 55%. Isolated buffer-perfused hearts were subjected to 30 min of either hypothermic or normothermic no-flow ischemia followed by reperfusion. Prior depletion of myocardial GSH did not lead to oxidative stress during reperfusion, as myocardial concentration of glutathione disulfide (GSSG) was not increased after 5 and 30 min of reperfusion. In addition, prior depletion of GSH did not exacerbate myocardial enzyme release, nor did it impair the recoveries of tissue ATP, coronary flow rate and left ventricular developed pressure during reperfusion after either hypothermic or normothermic ischemia. Even administration of the prooxidant cumene hydroperoxide (20 microM) to postischemic GSH-depleted hearts during the first 10 min of reperfusion did not aggravate postischemic injury, although this prooxidant load induced oxidative stress, as indicated by an increased myocardial concentration of GSSG. These results do not support the hypothesis that a reduced myocardial concentration of GSH during ischemia increases the susceptibility to injury mediated by reactive oxygen species generated during reperfusion. Apparently, myocardial tissue possesses a large excess of GSH compared to the quantity of reactive oxygen species generated upon reperfusion.
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