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Response of preterm infants with transient hypothyroxinaemia of prematurity to the thyrotropin-releasing hormone
Akane Yamamoto1, Kogoro Iwanaga1, Takashi Matsukura1
1Department of Pediatrics, Graduate School of Medicine, Kyoto University, Kyoto, Japan.
Insights
Transient hypothyroxinaemia of prematurity (THOP) in very low-birth weight infants is primarily caused by hypothalamic suppression, not peripheral hormone inactivation. This is indicated by delayed TSH response and lower reverse T3 levels in THOP infants.
Area of Science:
- Neonatal endocrinology
- Pediatric thyroid disorders
- Prematurity research
Background:
- Transient hypothyroxinaemia of prematurity (THOP) is a common condition in very low-birth weight (VLBW) infants.
- The exact etiology of THOP remains incompletely understood, impacting neonatal care and outcomes.
Purpose of the Study:
- To investigate the underlying causes of THOP in VLBW infants.
- To differentiate between hypothalamic-pituitary and peripheral factors contributing to THOP.
Main Methods:
- Thyrotropin-releasing hormone (TRH) stimulation tests were performed on 43 VLBW infants, divided into THOP and non-THOP groups.
- Measurements included basal free thyroxine (FT4), free triiodothyronine (FT3), reverse triiodothyronine (rT3), and serial thyroid-stimulating hormone (TSH) levels post-TRH administration.
- The primary outcome was the ratio of TSH at 180 minutes to TSH at 0 minutes.
Main Results:
- Infants with THOP showed a significantly higher TSH 180min/0min ratio compared to non-THOP infants (3.0 vs 1.3, P < .01).
- No significant difference in FT3 levels was observed between groups (P = .06).
- Reverse T3 (rT3) levels were significantly lower in the THOP group (92.9 pg/mL) than in the non-THOP group (168.0 pg/mL, P < .01).
Conclusions:
- The findings suggest that hypothalamic suppression is the primary driver of THOP in VLBW infants.
- The data indicate that peripheral thyroid hormone metabolism is not the main factor in THOP.
- TRH stimulation tests and rT3 levels are valuable in elucidating THOP etiology.
Objectives:
We evaluated the response to the thyrotropin-releasing hormone (TRH) stimulation test in very low-birth weight (VLBW) infants to elucidate the aetiology of transient hypothyroxinaemia of prematurity (THOP).
Design And Methods:
We performed TRH stimulation tests on 43 VLBW infants. Subjects were divided into two groups; a THOP group (N = 11; basal TSH < 15 mU/L and basal FT4 ≤ 0.8 ng/dL) and a non-THOP group (N = 32; basal TSH < 15 mU/L and basal FT4 > 0.8 ng/dL). Basal FT4 and FT3 were measured before, and TSH (0, 30, 60, 90, 120 and 180 minutes) was measured after, the administration of TRH (7 µg/kg). We calculated the ratio of TSH 180 minutes to THS 0 minute as the primary outcome. We also collected data on T3 and rT3 in this study.
Results:
In both groups, TSH 30 minutes values were the highest. However, the ratios of TSH 180 minutes to THS 0 minutes in the non-THOP group and the THOP group were (median [IQR]) 1.3 [1.0-1.7] and 3.0 [1.5-5.3] (P < .01). No significant differences were observed in T3 (1.0 [0.8-1.3] and 0.7 [0.4-0.7] ng/mL, P = .06). However, in the THOP group, rT3 was significantly lower than that of the non-THOP group (168.0 [148.1-197.0] and 92.9 [74.7-101.6] pg/mL, P < .01).
Conclusions:
The delayed decrease in the TSH concentration after the peak for the TRH tests and decreased levels of rT3 suggest that the main aetiology for THOP is suppression at the level of the hypothalamus, but not inactivation of peripheral thyroid hormone metabolism.
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