Figure 1
Figure 1. Clinical applications of circulating CD34− c-Kit+ population rate. (A-B) Correlation of Valent stage disease with the rate of circulating CD34−c-Kit+ population and the rate of serum tryptase. (A) The rate of the circulating CD34−c-Kit+ is shown for each patient along with disease stage, indicating the aggressiveness of their disease, and compared with healthy controls. All mastocytosis patients with systemic forms had a significantly higher rate of CD34−c-Kit+ cells than the controls: ISM (P = .0007), ASM (P = .0031), and SM-AHNMD (P = .0005). This association was not found for cutaneous forms, which were comparable with the healthy controls (P = .5). (B) The serum rate of tryptase was always elevated among patients with mastocytosis, independently from the stage of the disease: cutaneous as well as systemic forms had an elevated serum tryptase. Indeed, serum tryptase levels among controls were always lower than patients with CM (P = .0385), ISM (P = .0242), ASM (P = .0005), or SM-AHNMD (P = .0012). (C-E) Clinical and biologic follow-up of 3 patients with aggressive systemic mastocytosis until death. (C) Patient 42. (D) Patient 32. (E) Patient 38. The clinical evolution and treatment are mentioned as well as the rate of the circulating CD34−c-Kit+ population. It shows that, when patients present aggressive disease with massive mast cell infiltration, the rate of the circulating CD34−c-Kit+ population is a good tool to quickly follow (within 24-48 hours) the clinical evolution of the disease and to determine the efficiency of the treatments. CT indicates healthy control; 2CDA, Leustatin, Zenapax, daclizumab; and C1 to C4, cure number.

Clinical applications of circulating CD34 c-Kit+ population rate. (A-B) Correlation of Valent stage disease with the rate of circulating CD34c-Kit+ population and the rate of serum tryptase. (A) The rate of the circulating CD34c-Kit+ is shown for each patient along with disease stage, indicating the aggressiveness of their disease, and compared with healthy controls. All mastocytosis patients with systemic forms had a significantly higher rate of CD34c-Kit+ cells than the controls: ISM (P = .0007), ASM (P = .0031), and SM-AHNMD (P = .0005). This association was not found for cutaneous forms, which were comparable with the healthy controls (P = .5). (B) The serum rate of tryptase was always elevated among patients with mastocytosis, independently from the stage of the disease: cutaneous as well as systemic forms had an elevated serum tryptase. Indeed, serum tryptase levels among controls were always lower than patients with CM (P = .0385), ISM (P = .0242), ASM (P = .0005), or SM-AHNMD (P = .0012). (C-E) Clinical and biologic follow-up of 3 patients with aggressive systemic mastocytosis until death. (C) Patient 42. (D) Patient 32. (E) Patient 38. The clinical evolution and treatment are mentioned as well as the rate of the circulating CD34c-Kit+ population. It shows that, when patients present aggressive disease with massive mast cell infiltration, the rate of the circulating CD34c-Kit+ population is a good tool to quickly follow (within 24-48 hours) the clinical evolution of the disease and to determine the efficiency of the treatments. CT indicates healthy control; 2CDA, Leustatin, Zenapax, daclizumab; and C1 to C4, cure number.

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