Table 1.
Clinical characteristics and demographics of MG patients.
Fig 1.
Complement activity in AChR MG does not associate with clinical status or autoantibody titer.
Complement activity in the serum of AChR MG patients was measured by CH50 hemolysis assay. The assay measures the activation of the classical complement pathway by testing the ability of the complement components of sera samples to lyse antibody-sensitized sheep erythrocytes. The CH50 values are given as the percentage (%) of serum needed to lyse 50% of sheep erythrocytes. (A) AChR MG patients (N = 51) and healthy controls (N = 20) were measured by CH50 hemolysis assay. (B) Comparison of the complement activity between immunotherapy naïve (N = 22) vs non-immunotherapy naïve (N = 29) AChR MG patients. (C) Comparison of the complement activity between AChR MG patients 60 years of age and older (N = 29) vs AChR MG patients younger than 60 years of age (N = 22). (D) Serial samples of patient 5 (Table 3) were measured by CH50 hemolysis assay and compared to the corresponding disease burden (MGC score) at the time of each collection. The X axis shows the time in months since the first sample collection, the left Y axis shows the CH50 values (%) and the right Y axis shows the Myasthenia Gravis Composite (MGC) score. (E) Correlation of complement activity with the MGC score. The MGC score values were available for 33 of the 51 patients. (F) Correlation of complement activity with the AChR antibody titer (N = 51). The linear regression is shown with Spearman correlation values. Patients 1–6 (Table 2) are individually illustrated (see legend) with their corresponding MGC score (E) or antibody titer (F) if values were available. Values higher than the mean + 2SD of the HC controls (indicated by the horizontal dotted line) were considered reduced (A-C).
Table 2.
Characteristics of six AChR MG patients with reduced complement activity.
Fig 2.
Correlation between complement activity and MG patient subcohort demographics.
Correlation tests between complement activity to clinical status and autoantibody titer in different MG patient subcohorts defined by complement activity, age of disease onset, treatment status, and thymoma. (A-H) Correlation of complement activity with MGC score (first and third columns) and AChR antibody titer (second and fourth columns). The subcohorts are defined by complement activity (A and B), age of disease onset (early onset MG (EOMG; C); late onset MG (LOMG; D)), treatment status (E and F) and thymoma status (G and H). Limited specimens (n = 1) in the thymoma category with matching MGC scores prohibited correlative analysis (G left panel). The linear regression is shown with Spearman correlation values. The Bonferroni correction was used to adjust for multiple tests. Patient 1–6 (Table 2) are individually illustrated (see legend) for each panel.
Table 3.
Patient characteristics during longitudinal sample collection.