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25 In contrast, as the normal function of LPR4 involves interaction with MuSK in AChR clustering during synaptogenesis, one would predict a disease mechanism similar to MuSK MG in which complement-mediated end plate destruction does not appear to have a role

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Existem relatos em estudos, mas bastante raro

If the above measures are not as efficient as expected, either a decrease in GLP-1 RA dose or a temporary interruption of the treatment may be considered [35]