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Table 4 CgA peptides according to the presence of arterial wall enhancement, of active TA and of vascular progression

From: Chromogranin-A production and fragmentation in patients with Takayasu arteritis

Whole TA sample

No arterial wall enhancement (N = 25)

Arterial wall enhancement (N = 5)

p value

 CgA439 (nM)

0.06 (0–0.62)

0.00 (0–0.78)

n.s.

 CgA-FRs (nM)

1.85 (0.39–5.03)

1.41 (0.32–3.93)

n.s.

 VS-1 (nM)

0.25 (0.02–1.15)

0.23 (0.10–0.79)

n.s.

 Rank CgA439 + rank VS-1

38 (5–83)

36 (24–80)

n.s.

Patients on PPIs

No arterial wall enhancement (N = 20)

Arterial wall enhancement (N = 4)

p value

 CgA439 (nM)

0.07 (0–0.62)

0.00 (0–0.78)

n.s.

 CgA-FRs (nM)

2.45 (0.41–5.03)

2.60 (1.25–3.93)

n.s.

 VS-1 (nM)

0.27 (0.06-1.15)

0.48 (0.22–0.79)

n.s.

 Rank CgA439 + rank VS-1

44 (29–83)

32 (24–80)

n.s.

Hypertensive patients

No arterial wall enhancement (N = 13)

Arterial wall enhancement (N = 2)

p value

 CgA439 (nM)

0.06 (0–0.62)

0.43 (0.09–0.78)

n.s.

 CgA-FRs (nM)

2.76 (0.77–5.03)

2.06 (0.32–3.8)

n.s.

 VS-1 (nM)

0.38 (0.17–1.15)

0.42 (0.10–0.74)

n.s.

 Rank CgA439 + rank VS-1

50 (28–83)

58 (36–80)

n.s.

Whole TA sample

Inactive TA (N = 30)

Active TA (N = 12)

p value

 CgA439 (nM)

0.05 (0–0.62)

0.03 (0–0.78)

n.s.

 CgA-FRs (nM)

1.37 (0.22–6.68)

1.80 (0.28–5.03)

n.s.

 VS-1 (nM)

0.19 (0.02–1.15)

0.21 (0.09–0.79)

n.s.

 Rank CgA439 + rank VS-1

37 (5–83)

35 (18–80)

n.s.

Patients on PPIs

Inactive TA (N = 18)

Active TA (N = 12)

p value

 CgA439 (nM)

0.08 (0–0.62)

0.03 (0–0.78)

n.s.

 CgA-FRs (nM)

2.55 (0.41–6.68)

1.80 (0.28–5.03)

n.s.

 VS-1 (nM)

0.32 (0.06–1.15)

0.21 (0.09–0.79)

n.s.

 Rank CgA439 + rank VS-1

52 (24–83)

35 (18–80)

0.072

Hypertensive patients

Inactive TA (N = 15)

Active TA (N = 7)

p value

 CgA439 (nM)

0.08 (0–0.62)

0.06 (0–0.78)

n.s.

 CgA-FRs (nM)

2.50 (0.22–6.68)

1.85 (0.28–5.03)

n.s.

 VS-1 (nM)

0.39 (0.05–1.15)

0.20 (0.09–0.74)

n.s.

 Rank CgA439 + rank VS-1

50 (8–83)

39 (18–80)

n.s.

Whole TA sample

No vascular progression (N = 31)

Vascular progression (N = 9)

p value

 CgA439 (nM)

0.06 (0–0.78)

0 (0–0.14)

n.s.

 CgA-FRs (nM)

1.49 (0.22–5.03)

1.76 (0.32–4.24)

n.s.

 VS-1 (nM)

0.20 (0.02–1.15)

0.20 (0.09–0.79)

n.s.

 Rank CgA439+ rank VS-1

42 (5–83)

36 (22–40)

n.s.

Patients on PPIs

No vascular progression (N = 20)

Vascular progression (N = 8)

p value

 CgA439 (nM)

0.09 (0–0.78)

0 (0–0.14)

0.063

 CgA-FRs (nM)

2.45 (0.41–5.03)

1.81 (0.46–4.24)

n.s.

 VS-1 (nM)

0.27 (0.06–1.15)

0.21 (0.09–0.79)

n.s.

 Rank CgA439 + rank VS-1

52 (24–83)

34.5 (22–40)

0.010

Hypertensive patients

No vascular progression (N = 16)

Vascular progression (N = 4)

p value

 CgA439 (nM)

0.08 (0–0.78)

0.05 (0–0.14)

n.s.

 CgA-FRs (nM)

2.63 (0.22–5.03)

1.40 (0.32–4.24)

n.s.

 VS-1 (nM)

0.39 (0.05–1.15)

0.15 (0.09–0.37)

n.s.

 Rank CgA439 + rank VS-1

52 (8–83)

33 (22–39)

0.050

  1. Levels of CgA439, CgA-FRS, VS-1 and the sum of the ranks of CgA439 and of VS-1 are compared according to the presence of arterial wall enhancement, of active disease and of vascular progression. The impact of PPI therapy or arterial hypertension is also considered
  2. CgA chromogranin-A, TA Takayasu arteritis, CgA 439 full-length CgA (residues 1–439), n.s. not significant, CgA-FRs fragments of CgA spanning from the N-terminus to the central region but lacking the C-terminal region, VS-1 vasostatin-1, PPI proton-pump inhibitor