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Cancer. 2019 May 15;125(10):1748-1755. doi: 10.1002/cncr.31975. Epub 2019 Jan 28.

Growth hormone deficiency and neurocognitive function in adult survivors of childhood acute lymphoblastic leukemia.

Author information

1
Department of Epidemiology and Cancer Control, St. Jude Children's Research Hospital, Memphis, Tennessee.
2
Department of Psychology, St. Jude Children's Research Hospital, Memphis, Tennessee.
3
Department of Biostatistics, St. Jude Children's Research Hospital, Memphis, Tennessee.
4
School of Pharmacy, Faculty of Medicine, The Chinese University of Hong Kong, Shatin, Hong Kong SAR, China.
5
Department of Pediatric Medicine, Division of Neurology, St. Jude Children's Research Hospital, Memphis, Tennessee.
6
Department of Radiation Oncology, St. Jude Children's Research Hospital, Memphis, Tennessee.
7
Department of Diagnostic Imaging, St. Jude Children's Research Hospital, Memphis, Tennessee.
8
Department of Oncology, St. Jude Children's Research Hospital, Memphis, Tennessee.
9
Department of Pediatrics, Memorial Sloan Kettering Cancer Center, New York, New York.
10
Department of Pediatric Medicine, Division of Endocrinology, St. Jude Children's Research Hospital, Memphis, Tennessee.

Abstract

BACKGROUND:

The impact of growth hormone deficiency (GHD) on neurocognitive function is poorly understood in survivors of childhood acute lymphoblastic leukemia (ALL). This study examined the contribution of GHD to functional outcomes while adjusting for cranial radiation therapy (CRT).

METHODS:

Adult survivors of ALL (N = 571; 49% female; mean age, 37.4 years; age range, 19.4-62.2 years) completed neurocognitive tests and self-reported neurocognitive symptoms, emotional distress, and quality of life. GHD was defined as a previous diagnosis of GHD or a plasma insulin-like growth factor1 level less than -2.0 standard deviations for sex and age at the time of neurocognitive testing. Hypothyroidism, hypogonadism, sex, age at diagnosis, CRT dose, and intrathecal and high-dose intravenous methotrexate were included as covariates in multivariable linear regression models.

RESULTS:

Of the 571 survivors, 298 (52%) had GHD, and those with GHD received higher doses of CRT (P = .002). Survivors who had GHD, irrespective of prior growth hormone treatment, demonstrated poorer vocabulary (z-score, -0.84 vs -0.61; P = .02), processing speed (z-score, -0.49 vs -0.30; P = .04), cognitive flexibility (z-score, -1.37 vs -0.94; P = .01), and verbal fluency (z-score, -0.74 vs -0.44; P = .001), and they self-reported more neurocognitive problems and poorer quality of life compared with survivors who did not have GHD. Multivariable and mediation models revealed that GHD was associated with small effects on quality of life (general health, P = .01; vitality, P = .01; mental health, P = .01); and CRT dose accounted for the lower neurocognitive outcomes.

CONCLUSIONS:

Adult survivors of childhood ALL who receive CRT are at risk for GHD, although poor neurocognitive outcomes are determined by CRT dose and not by the presence of GHD.

KEYWORDS:

growth hormone deficiency; leukemia; neurocognitive; survivors

PMID:
30690723
PMCID:
PMC6486430
[Available on 2020-05-15]
DOI:
10.1002/cncr.31975

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