Myasthenia Gravis

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Retrieved

2022-04-26

Source

Gard

Trials

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Genes

CFB, HLA-B, MUSK, HLA-DPB1, POMC, FAS, HLA-DRB1, HLA-DQA1, PTPN22, HLA-A, TNIP1, C2, IL10, NFKBIL1, ZNRD1, MUC21, SFTA2, HCG9, PSORS1C1, CTLA4, NOTCH4, MUCL3, CYP21A2, RBM45, BTNL2, GPSM3, MSH5, TSBP1, MICB, LRP4, TRIM31, POU5F1, HLA-DQA2, RNF39, GABBR1, VARS2, LINC00243, ABCF1, IFNG, MSH5-SAPCD1, HCG17, TNFRSF11A, TCF19, BCHE, ATP6V1G2, STK19, TNF, HCG18, GPANK1, SEMA5A, TTN, TSBP1-AS1, RBBP8, ACHE, PRRC2A, CXCL13, IL17A, IL2RA, IL6, ISG20, EIF3K, IL2, FOXP3, AIRE, IL4, CHRNA1, TRBV20OR9-2, HLA-DQB1, THM, LTA, IL1B, CD274, IL22, PDCD1, IL21, TLR9, CHRNE, IL1A, MIR150, AQP4, HT, TGFB1, CDR3, ECD, MIR21, DOK7, TLR4, CD40, TLR3, MBP, CCL21, CHRNA4, TAP2, CXCR4, IGHG3, IFNB1, MAPK1, PDLIM7, IL18R1, IL15, EBI3, IL4R, SMN1, CXCL10, IFNA13, TLR7, TNFRSF13C, FGFR3, MIR146A, ESR1, TSLP, CD40LG, GNAO1, DNMT3B, HLA-DQB2, CAV3, IL23A, MIR125A, ADRB2, IFNA1, IFN1@, HMGB1, C4orf3, DIPK1A, SOCS3, LGI1, MSC, SCO2, CD83, GRAP2, MIR145, MIRLET7C, NTN1, MIR155, PPP6R2, MIR143, MBTPS1, MIR15B, SCFV, LOC102723407, IFNG-AS1, LINC-ROR, C4B_2, C20orf181, TEC, CCR2, DDX39B, MIR653, MIR323B, MIR19B1, MIR338, AIMP2, FOSL1, MIR320A, USO1, TNFRSF25, MIR30E, MALAT1, TNFSF10, DDX39A, RMDN2, MYAS1, CCAR2, RNF19A, CNTNAP2, HIF3A, ROBO3, POLDIP2, IFIH1, IGAN1, B3GAT1, DPYSL5, PART1, RETN, IGHV3-52, TWNK, MSL2, KRT20, ICOS, SLC25A37, VAV1, TMEM109, PPP1R15A, PRSS16, UNC5A, CLEC4C, CDIPT, NXF1, MZB1, TRIM9, AHSA1, IL17F, IL33, TNFSF13B, DDX58, CCR9, FHDC1, LILRB1, FAM136A, SLC7A9, TBC1D9, ICOSLG, SEC14L2, VIP, RAF1, UTRN, CNTFR, CRK, MAPK14, CSF1, CCN2, CTSV, CTSS, CYP3A5, CD55, BRINP1, DCC, DNMT3A, ATN1, TYMP, CTTN, ERBB4, ESR2, FCGR2A, FLNB, FOS, FOSB, CXCR3, GRIA2, GRM2, CXCL1, GZMB, HLA-C, HLA-DOA, HLA-DPA1, HLA-DRB3, CR2, CCR7, HNMT, CCR5, ADCYAP1, AGER, ALB, APOE, APRT, ABCC6, BCL2, TNFRSF17, BDNF, C4A, C4B, C5, CA3, CACNA1S, CALCA, CALCR, CAMP, CASP1, CASP3, CD19, MS4A1, CD28, CD86, CD69, CDS1, CHRNB1, CHRND, CLC, CCR4, HLA-G, HOXD13, TYMS, NTRK1, P2RX7, PAM, PAX7, ABCB1, PMP22, MAPK3, PTPRC, PLAAT4, RELB, S100A8, S100A11, S100B, SCN4A, SCO1, CCL5, CCL17, CCL22, CXCL12, SGCA, SLAMF1, SMN2, SPP1, STAT3, STAT4, TAP1, THBS1, TNFAIP3, TNFSF4, TNFRSF4, OSM, NCAM1, HSPA5, MYOG, IRF8, IFNA2, IFNA17, IFNGR1, IGF1, IGF1R, IGFBP1, IGL, IL1RN, IL2RB, IL7R, IL9, IL12B, IL12RB2, INS, IRF4, ITGAX, JUN, JUNB, JUND, KIT, KRT5, LDLR, LGALS1, LGALS8, LIF, MEFV, MFAP1, MMP10, LOC102724971

Drugs

5'-CTG CCA CGT TCT CCT GC-(2' methoxy)A-(2' methoxy)C-(2' methoxy)C-3', Eculizumab ( SOLIRIS ), Efgartigimod alfa

5'-CTG CCA CGT TCT CCT GC-(2' methoxy)A-(2' methoxy)C-(2' methoxy)C-3', Eculizumab ( SOLIRIS ), Efgartigimod alfa, Fusion proteins composed by a genetically modified cholera toxin subunit A1, peptides from the acetylcholine receptor alpha chain and a dimer of the D fragment from Staphylococcus aureus protein A, H-Val-Ile-Val-Lys-Leu-Ile-Pro-Ser-Thr-Ser-Ser-Ala-Val-Asp-Thr-Pro-Tyr-Leu-Asp-Ile-Thr-Tyr-His-Phe-Val-Ala-Gln-Arg-Leu-Pro-Leu-OH, Methotrexate ( LEDERTREXATE, NORDIMET, METHOTREXATE WYETH LEDERLE ), Monarsen, Peptides mimicking antigen receptors on autoimmune B cells and autoimmune T cells associated with myasthenia gravis, Recombinant Human Alpha-Fetoprotein (Rhafp), Rozanolixizumab, recombinant mutated extracellular domain of the human acetylcholine receptor subunit alpha1

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Myasthenia gravis (MG) is a chronic autoimmune neuromuscular disease characterized by weakness of the skeletal muscles. Common symptoms include weakness of the muscles that control the eye and eyelid, facial expressions, chewing, talking, and swallowing. Weakness tends to increase during periods of activity and improve after periods of rest. The condition results from a defect in the transmission of nerve impulses to muscles, which is due to the presence of antibodies against acetylcholine. The exact reason this occurs is not known. Some cases have been linked to tumors in the thymus gland. Researchers believe that variations in certain genes may increase a person's risk to develop MG, but other factors likely also play a role. There is no cure for MG at this time, but treatment can significantly improve muscle weakness. Some cases may go into remission temporarily, and muscle weakness may disappear so that medications can be discontinued.