PubMed · 15399562
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S KARELITZ. 1949-12-26. Serum sickness.. https://doi.org/10.1111/j.1749-6632.1949.tb39877.x
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The pathophysiological responses to immune stress (IS) include activation of several processes which are dependent on cytosolic Ca2+ elevation. Magnesium frequently acts as a natural Ca2+ antagonist. In this study we have observed that Mg2+ can protect guinea-pigs against IS. Antigen-sensitized guinea-pigs, which had been fed a magnesium-deficient diet, were given a single dose (15 mg) of MgCl2 intraperitoneally 1 h before antigen challenge. The development of anaphylactic shock (AS) was observed during the next 2 h, and the hearts were subsequently examined histologically for signs of cardiac myolysis (CM). Magnesium (i) reduced the incidence of CM from 40% to 10% (p < 0.05); (ii) reduced the incidence of AS from 61% to 35% (p < 0.05); (iii) attenuated the severity of the AS; and (iv) lowered mortality from 39% in the control to 19% in the Mg(2+)-treated group (p = 0.1). Serum and tissue total [Mg2+] were not affected by the administration of MgCl2. Also, the serum and heart Mg2+ levels were the same whether or not the guinea-pigs developed AS or CM. In cell culture we demonstrated that by elevating the [Mg2+] in the medium bathing sensitized rat basophilic leukemia (RBL) cells, the increase in cytosolic [Ca2+] subsequent to antigen challenge was reduced from 174 +/- 23.28% (1 mM) to 82.74 +/- 13.22% (3 mM). We conclude that a single treatment with Mg2+ can considerably diminish damage induced by immune stress, probably by its altering the Ca2+: Mg2+ ratio. Since the physiological reaction to different types of stress is similar, Mg2+ could prove beneficial in preventing stress-induced shock in general. Studies examining the mechanisms by which Mg2+ exerts its effects thus provide a scientific basis for the current clinical use of Mg2+ in acute myocardial infarction (AMI) and asthma.
OBJECTIVE: To provide information on morbidity and ethical questions associated with learning of invasive techniques (tracheal intubation, positioning of central venous or epidural catheters) and management of anaphylactic shock. STUDY DESIGN: Retrospective survey. METHODS: Written questionnaire to 54 anaesthesiologists and 55 residents. RESULTS: Training was primarily performed by residents having a 6 months-experience for general anaesthesia and by more experienced residents for epidural analgesia. Residents observed first two or three procedures performed by seniors, but did not have theoretical lectures in 30 to 50% of cases. Dead bodies or manikins were rarely used. Despite the presence of experienced anaesthesiologists during the first attempts, there was a high morbidity rate which was considered by 22 to 37% of the interviewed anaesthesiologists a loss of benefit for the patients. Despite a high level of coaching, a high morbidity rate was associated with the first attempts. However, only few residents explicitly stated to be concerned by ethical questions. Among anaesthesiologists, who had yet to manage anaphylactic shock, 21 and 35% of them reported that diagnostic and treatment could have been performed faster. Virtual learning was misunderstood but 46% of anaesthesiologist described numerous advantages in using simulator of anaesthesia. CONCLUSION: Despite an apparent morbidity with a loss of benefit, informed consent of the patients were rarely obtained.
A case of a girl who presented at age 12 years with idiopathic cold urticaria is described. Her reactions to the cold became progressively more severe over a period of approximately 2 years, despite therapy with H1 antagonists and a type 1 receptor for cysteinyl leukotrienes receptor antagonist. She began to experience systemic symptoms on immersion in ocean water. She was atopic and had moderate persistent asthma. A trial of anti-IgE resulted in complete resolution of her urticaria and its associated manifestations. These findings should prompt a reexamination of the potential pathogenetic role played by IgE and its high-affinity receptor on mast cells in idiopathic cold urticaria.