Table 1 Clinical and laboratory characteristics of 270 Mayo Clinic patients and 232 University of Florence patients with essential thrombocythemia (ET) (total n = 502).

From: Mutations and thrombosis in essential thrombocythemia

Variables

Mayo Clinic (n = 270)

Florence (n = 232)

Age in years; median (range)

57 (18–92)

54 (13–85)

Males; n (%)

108 (40)

96 (41)

Hemoglobin, g/dl; median (range)

“N” evaluable = 382 (92%)

13.7 (6.9–17.9)a

14.1 (12–17.0)a

Platelets, ×109/L; median (range)

“N” evaluable = 407 (98%)

844 (451–3330)

739 (451–2000)

Platelets > 1000 × 109/l; n (%)

“N” evaluable = 407 (98%)

82 (31)

33 (16)

Leukocytes, ×109/L; median (range)

“N” evaluable = 399 (96%)

8.7 (2.7–70.7)

8.5 (3.8–26)

Leukocytes ≥ 11 × 109/l; n (%)

“N” evaluable = 399 (96%)

64 (25)

36 (19)

Palpable splenomegaly

“N” evaluable = 412 (99%)

48 (18)

45 (21)

Karyotype “N” evaluable = 345 (83%)

Abnormal; n (%)

20 (9)

15 (10)

Fibrotic progression; n (%)

44 (16)

76 (33)b

Leukemic transformations; n (%)

12 (4)

15 (6.5)

Follow up in years;

median (range)

9.9 (0–34.6)

12.9 (1–36.3)

Deaths; n (%)

104 (39)

87 (38)

Mutationsc

JAK2 mutated; n (%)

146 (54)

129 (56)

CALR mutated; n (%)

79 (29)

59 (25)

TET2 mutated; n (%)

25 (9)

28 (11)

ASXL1 mutated; n (%)

18 (7)

47 (20)b

DNMT3A mutated; n (%)

19 (7)

14 (7)

SF3B1 mutated; n (%)

14 (5)

12 (5)

SH2B3 mutated; n (%)

3 (1)

6 (3)

SRSF2 mutated; n (%)

6 (2)

6 (3)

MPL mutated; n (%)

11 (4)

17 (7)

KIT mutated; n (%)

5 (2)

2 (1)

IDH2 mutated; n (%)

4 (1)

2 (1)

TP53 mutated; n (%)

5 (2)

9 (4)

U2AF1 mutated; n (%)

3 (1)

6 (2.5)

RUNX1 mutated; n (%)

4 (1)

5 (2)

EZH2 mutated; n (%)

5 (2)

9 (4)

CBL mutated; n (%)

3 (1)

3 (2)

  1. aET patients who had low hemoglobin, presented with concomitant bleeding disorders, iron deficiency anemia, chronic renal insufficiency, or other rare disorders such as sickle cell anemia and Osler-Weber-Rendu disease.
  2. bThe difference in the frequency of ASXL1 mutation and fibrotic transformation in the two patient cohorts is explained by the intentional enrichment of the Florence cohort with patients who had transformed to myelofibrosis for the purposes of a prior project examining the predictive value of mutations for post-ET fibrotic transformation.
  3. cIncluded mutations with frequency of at least 1%. Also, the denominator for the percentages in parenthesis is the number of evaluable cases.