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Prolactin is a hormone and cytokine secreted from the anterior pituitary gland, that is best known for its role in stimulating milk production. However, it is also produced by other cells such as neurons, epithelium, and immune cells influencing Th1 and Th2 immune responses, and modulating the function of B cells and T cells by acting as a growth and survival factor. Prolactin can enhance immunoglobulin production by B lymphocytes, and dysregulation of prolactin can promote autoimmunity. Hyperprolactinemia has previously been reported in patients with graft-versus-host disease (GvHD); however, its correlation with GvHD activity has not been explored in detail.1
Maria Queralt Salas and colleagues investigated if prolactin can be used as a biomarker for chronic GvHD (cGvHD) activity. The results of this retrospective analysis were recently published in the European Journal of Haematology.1
Table 1. Baseline patient characteristics1
ALL, acute lymphoblastic leukemia; AML, acute myeloid leukemia; CLL, chronic lymphocytic leukemia; CML, chronic myelomonocytic leukemia; GvHD, graft-versus-host disease; MDS, myelodysplastic syndrome; MPN, myeloproliferative neoplasm; MRD, matched related donor; MUD, matched unrelated donor. |
|
Characteristic |
% of patients (N = 316) |
Median age (range) |
53 (19–71) |
Sex, male/female |
51.3/48.7 |
Diagnosis |
|
AML |
42.7 |
ALL |
10.7 |
MDS |
12.6 |
MPN |
10.1 |
CML |
5.4 |
CLL |
10.7 |
T-prolymphocytic leukemia |
0.6 |
Severe aplastic anemia |
2.9 |
Other |
1.2 |
Donor type |
|
10/10 MRD |
44.9 |
10/10 MUD |
41.8 |
9/10 MUD |
12.0 |
Haploidentical donor |
1.3 |
Intensity of conditioning regimen |
|
Myeloablative |
60.1 |
Reduced intensity |
39.9 |
GvHD prophylaxis |
|
T-cell depletion |
47.5 |
No T-cell depletion |
52.5 |
Source of graft |
|
Bone Marrow |
5.7 |
Peripheral Blood |
94.3 |
As primary hypothyroidism and renal impairment can influence prolactin levels, thyroid stimulating hormone (TSH) levels and kidney function were assessed in this patient population.
Table 2. Prolactin and TSH assessment 1 year after allo-HSCT1
allo-HSCT, allogeneic hematopoietic stem cell transplant; cGvHD, chronic graft-versus-host disease; TSH, thyroid stimulating hormone. |
||||
Result |
Total population (N = 316) |
Active cGvHD (n = 65) |
Non-active cGvHD (n = 251) |
p value |
Prolactin level, % |
|
|
|
|
Normal |
80.1 |
49.2 |
88 |
< 0.001 |
Elevated |
19.9 |
50.8 |
12 |
|
TSH level, % |
|
|
|
|
Normal |
89.9 |
86.2 |
91.2 |
0.224 |
Elevated |
10.0 |
13.8 |
8.8 |
Table 3. Multivariate analysis of characteristics associated with active cGvHD1
cGvHD, chronic GvHD; CI, confidence interval; TSH, thyroid stimulating hormone; GvHD, graft-versus-host disease. |
|||
Variable |
Odds ratio |
95% CI |
p value |
Prolactin levels (elevated vs normal) |
6.94 |
3.6–13.1 |
< 0.001 |
TSH levels (elevated vs normal) |
1.51 |
0.58–3.90 |
0.389 |
T-cell depletion for GvHD prophylaxis (with vs without) |
0.34 |
0.18–0.66 |
0.001 |
Prolactin may serve as a biomarker for activity of cGvHD as patients with hyperprolactinemia were ~7 times more likely to have active cGvHD compared with those with normal levels of prolactin. However, further studies are needed to confirm these findings and explore if prolactin has a role in regulating Th1 and Th2 immune responses in the development of GvHD or is simply a consequence of B-cell and T-cell activation.
This study is limited by its retrospective nature and because prolactin levels were only analyzed annually. Therefore, prospective studies assessing prolactin levels during the development and resolution of cGvHD are required to confirm if prolactin can be used as a biomarker for active cGvHD.
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