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  • Serum soluble sCD is a

    2024-04-12

    Serum soluble sCD21 is a shedding product from the ectodomain of membrane CD21 after B cell activation (Masilamani et al., 2003, Masilamani et al., 2004a, Masilamani et al., 2004b, Grottenthaler et al., 2006, Hoefer et al., 2008), which resembles the ligand-binding capacity of intact CD21 (Wu et al., 2001). Previous studies have shown that sCD21 can combine with CD23, C3, IgG or IgE in serum to mediate the activation of monocytes and other immunocytes (Masilamani et al., 2004a, Masilamani et al., 2004b, Grottenthaler et al., 2006, Hoefer et al., 2008). The reason why sCD21 decreased in autoimmune disease still remains unclear. Theoretically, several evidence could explain the mechanisms of sCD21 decreased in vivo of MG patients. First, following immunoactivation, more and more complement activated fragments were generated, which consumed CD21 for the subsequent function or were just in an attempt to facilitate negative feedback effect to avoid excessive immune stimulation. Second, during the course of immunoactivation, a large number of proteins were released into serum, together with protease inhibitors, such as alpha 1-protease inhibitor. CD21 shedding might be inhibited by those protease inhibitors. Third, even if CD21 was shed into serum, the sCD21 shedding product might be digested by proteolytic enzymes. In our study, the level of sCD21 correlated negatively with anti-AchR IgG, which at least indicated that the decreased level of sCD21 was due to binding of anti-AchR IgG.
    Acknowledgments This work was supported by the National Nature Science Foundation of China (No. 81070962), MDA, and innovation project for postgraduate of central south university (No. 2010ssxt058).
    Introduction Snake bites due to Elapidae (neurotoxic family) have inadequate signs of Cilomilast and are easily missed (Kularatne, 2002). Myasthenic crisis, on the other hand, could be the first sign of myasthenia gravis in up to 20% of patients (Wendell and Levine, 2011). Both neurotoxic envenomation and myasthenic crisis present with ptosis, diplopia, dysphagia, weakness of neck muscles and respiratory failure. Both respond to acetyl choline esterase inhibitors and both can show decremental response on repetitive nerve stimulation tests (Sanmuganathan, 1998). When a good clinical history is unavailable, we might have to rely on ancillary tests to differentiate these two clinical conditions- or so we thought. In this article we describe two such patients, whose clinical presentation resulted in a diagnostic dilemma, and the ancillary testing made it even worse.
    Clinical vignette Our first patient was a 30year old male, who was normal when he went to sleep, but woke up with bilateral ptosis. As the day progressed he complained of breathing difficulty and was taken to a primary health care centre. He was intubated there and was referred to us. On examination patient had bilateral ophthalmoplegia with pupils being spared. He had a flaccid quadriparesis with preserved reflexes and normal plantar response. There was also a small erythematous lesion over plantar aspect of his right great toe but rest of the examination was normal. Repetitive nerve stimulation (RNS) of nasalis and abductor pollicis brevis (stimulation @ 5 hertz) revealed a decremental response of >10%. The possibility of neurotoxic envenomation or myasthenic crisis was suspected. 20 vials (200mL) of polyvalent anti-snake venom (ASV) were administered. Patient's serum was sent for Anti-AChR Ab testing and he was started on T. Pyridostigmine at 30mg 4 times a day. The next day patient's ptosis had improved and he was breathing spontaneously. The following day he was extubated and he was mobilized. After recovery, patient denied previous history of ptosis, diplopia, bulbar weakness or fluctuating weakness. He also denied history of snake bite, but had observed snakes near the vicinity of his house. His serum sample for Anti-AChR Ab was positive (1.1nmol/L). CT thorax did not show any evidence of thymoma. He was discharged with a possible diagnosis of myasthenic crisis. Pyridostigmine was continued and prednisone was added to his drug regimen.