Robustness of the male lactotropic axis to the hyperprolactinemic stimulus of primary thyroidal failure

Ali Iranmanesh, German Lizarralde, Johannes D Veldhuis

Research output: Contribution to journalArticle

8 Citations (Scopus)

Abstract

Primary hypothyroidism is a presumptive proximate basis for increased serum PRL concentrations. However, most studies to date have been performed in females and do not address the possible effect of sex differences. In the present study we investigated the 24-h patterns of pulsatile PRL release in 10 hypothyroid men (24-h mean ± SEM: total T4, 35 ± 8 nmol/ L; TSH, 55 ± 10 mU/L) by sampling blood at 10-min intervals for 24 h. The study was repeated in 5 men, 5-7 months and again 14-36 months after treatment with levothyroxine. The control group consisted of 7 normal age-matched euthyroid men. The mean 24-h serum PRL concentration of 4.9 ± 0.6 μg/L in 10 hypothyroid men was not significantly different from the value of 4.9 ± 0.5 μg/L found in the normal group (P > 0.5). Pulsatile features of PRL release were evaluated by Cluster analysis, which revealed normal mean PRL peak frequency (12.6 ± 0.7 vs. 13.4 ± 0.6 pulses/24 h; P > 0.5), maximal peak amplitude (6.1 ± 0.7 vs. 6.7 ± 0.6 μg/L; P > 0.5), peak increment (2.2 ± 0.3 vs. 2.6 ± 0.3 μg/L; P = 0.3), mean valley (4.2 ±0.6 vs. 4.4 ± 0.4 μg/L; P > 0.5), and prepeak nadir (3.6 ± 0.5 vs. 3.6 ± 0.4 μg/L; P > 0.5) PRL concentrations. Five to 7 months of T4 therapy in 5 hypothyroid men caused significant decreases in the mean 24-h (2.9 ± 0.5 vs. 6.1 ± 1.2 μg/L; P < 0.05), interpulse valley (2.5 ± 0.4 vs. 5.2 ± 1.1 μg/L; P < 0.05), and prepeak nadir (2.3 ± 0.3 vs. 4.6 ± 1.0 μg/L; P < 0.05) PRL concentrations. These values returned to normal after 14-36 months of treatment. Cosinor analysis revealed preserved circadian PRL rhythmicity during hypothyroidism, with a normal circadian mesor (mean), amplitude, and acrophase. In summary, we have demonstrated normal mean 24-h serum PRL concentrations as well as normal pulsatile and circadian patterns of PRL release in men with primary hypothyroidism. These results stand in contrast to previous reports of increased serum PRL concentrations observed predominantly in hypothyroid premenopausal women. The foregoing disparity suggests the possibility of a role for estrogen in enhancing the effect of hypothyroidism on PRL release. Decreased serum PRL concentrations after 5-7 months of T4 replacement, but not at later follow-up, indicate one or more transient alterations in the secretion and/or clearance of PRL during the early phases of thyroid hormone replacement.

Original languageEnglish (US)
Pages (from-to)559-564
Number of pages6
JournalJournal of Clinical Endocrinology and Metabolism
Volume74
Issue number3
StatePublished - Mar 1992
Externally publishedYes

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Cluster analysis
Thyroxine
Thyroid Hormones
Estrogens
Blood
Sampling
Hypothyroidism
Scanning electron microscopy
Serum
Periodicity
Sex Characteristics
Cluster Analysis
Therapeutics
Control Groups

ASJC Scopus subject areas

  • Biochemistry
  • Endocrinology, Diabetes and Metabolism

Cite this

Robustness of the male lactotropic axis to the hyperprolactinemic stimulus of primary thyroidal failure. / Iranmanesh, Ali; Lizarralde, German; Veldhuis, Johannes D.

In: Journal of Clinical Endocrinology and Metabolism, Vol. 74, No. 3, 03.1992, p. 559-564.

Research output: Contribution to journalArticle

Iranmanesh, Ali ; Lizarralde, German ; Veldhuis, Johannes D. / Robustness of the male lactotropic axis to the hyperprolactinemic stimulus of primary thyroidal failure. In: Journal of Clinical Endocrinology and Metabolism. 1992 ; Vol. 74, No. 3. pp. 559-564.
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title = "Robustness of the male lactotropic axis to the hyperprolactinemic stimulus of primary thyroidal failure",
abstract = "Primary hypothyroidism is a presumptive proximate basis for increased serum PRL concentrations. However, most studies to date have been performed in females and do not address the possible effect of sex differences. In the present study we investigated the 24-h patterns of pulsatile PRL release in 10 hypothyroid men (24-h mean ± SEM: total T4, 35 ± 8 nmol/ L; TSH, 55 ± 10 mU/L) by sampling blood at 10-min intervals for 24 h. The study was repeated in 5 men, 5-7 months and again 14-36 months after treatment with levothyroxine. The control group consisted of 7 normal age-matched euthyroid men. The mean 24-h serum PRL concentration of 4.9 ± 0.6 μg/L in 10 hypothyroid men was not significantly different from the value of 4.9 ± 0.5 μg/L found in the normal group (P > 0.5). Pulsatile features of PRL release were evaluated by Cluster analysis, which revealed normal mean PRL peak frequency (12.6 ± 0.7 vs. 13.4 ± 0.6 pulses/24 h; P > 0.5), maximal peak amplitude (6.1 ± 0.7 vs. 6.7 ± 0.6 μg/L; P > 0.5), peak increment (2.2 ± 0.3 vs. 2.6 ± 0.3 μg/L; P = 0.3), mean valley (4.2 ±0.6 vs. 4.4 ± 0.4 μg/L; P > 0.5), and prepeak nadir (3.6 ± 0.5 vs. 3.6 ± 0.4 μg/L; P > 0.5) PRL concentrations. Five to 7 months of T4 therapy in 5 hypothyroid men caused significant decreases in the mean 24-h (2.9 ± 0.5 vs. 6.1 ± 1.2 μg/L; P < 0.05), interpulse valley (2.5 ± 0.4 vs. 5.2 ± 1.1 μg/L; P < 0.05), and prepeak nadir (2.3 ± 0.3 vs. 4.6 ± 1.0 μg/L; P < 0.05) PRL concentrations. These values returned to normal after 14-36 months of treatment. Cosinor analysis revealed preserved circadian PRL rhythmicity during hypothyroidism, with a normal circadian mesor (mean), amplitude, and acrophase. In summary, we have demonstrated normal mean 24-h serum PRL concentrations as well as normal pulsatile and circadian patterns of PRL release in men with primary hypothyroidism. These results stand in contrast to previous reports of increased serum PRL concentrations observed predominantly in hypothyroid premenopausal women. The foregoing disparity suggests the possibility of a role for estrogen in enhancing the effect of hypothyroidism on PRL release. Decreased serum PRL concentrations after 5-7 months of T4 replacement, but not at later follow-up, indicate one or more transient alterations in the secretion and/or clearance of PRL during the early phases of thyroid hormone replacement.",
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N2 - Primary hypothyroidism is a presumptive proximate basis for increased serum PRL concentrations. However, most studies to date have been performed in females and do not address the possible effect of sex differences. In the present study we investigated the 24-h patterns of pulsatile PRL release in 10 hypothyroid men (24-h mean ± SEM: total T4, 35 ± 8 nmol/ L; TSH, 55 ± 10 mU/L) by sampling blood at 10-min intervals for 24 h. The study was repeated in 5 men, 5-7 months and again 14-36 months after treatment with levothyroxine. The control group consisted of 7 normal age-matched euthyroid men. The mean 24-h serum PRL concentration of 4.9 ± 0.6 μg/L in 10 hypothyroid men was not significantly different from the value of 4.9 ± 0.5 μg/L found in the normal group (P > 0.5). Pulsatile features of PRL release were evaluated by Cluster analysis, which revealed normal mean PRL peak frequency (12.6 ± 0.7 vs. 13.4 ± 0.6 pulses/24 h; P > 0.5), maximal peak amplitude (6.1 ± 0.7 vs. 6.7 ± 0.6 μg/L; P > 0.5), peak increment (2.2 ± 0.3 vs. 2.6 ± 0.3 μg/L; P = 0.3), mean valley (4.2 ±0.6 vs. 4.4 ± 0.4 μg/L; P > 0.5), and prepeak nadir (3.6 ± 0.5 vs. 3.6 ± 0.4 μg/L; P > 0.5) PRL concentrations. Five to 7 months of T4 therapy in 5 hypothyroid men caused significant decreases in the mean 24-h (2.9 ± 0.5 vs. 6.1 ± 1.2 μg/L; P < 0.05), interpulse valley (2.5 ± 0.4 vs. 5.2 ± 1.1 μg/L; P < 0.05), and prepeak nadir (2.3 ± 0.3 vs. 4.6 ± 1.0 μg/L; P < 0.05) PRL concentrations. These values returned to normal after 14-36 months of treatment. Cosinor analysis revealed preserved circadian PRL rhythmicity during hypothyroidism, with a normal circadian mesor (mean), amplitude, and acrophase. In summary, we have demonstrated normal mean 24-h serum PRL concentrations as well as normal pulsatile and circadian patterns of PRL release in men with primary hypothyroidism. These results stand in contrast to previous reports of increased serum PRL concentrations observed predominantly in hypothyroid premenopausal women. The foregoing disparity suggests the possibility of a role for estrogen in enhancing the effect of hypothyroidism on PRL release. Decreased serum PRL concentrations after 5-7 months of T4 replacement, but not at later follow-up, indicate one or more transient alterations in the secretion and/or clearance of PRL during the early phases of thyroid hormone replacement.

AB - Primary hypothyroidism is a presumptive proximate basis for increased serum PRL concentrations. However, most studies to date have been performed in females and do not address the possible effect of sex differences. In the present study we investigated the 24-h patterns of pulsatile PRL release in 10 hypothyroid men (24-h mean ± SEM: total T4, 35 ± 8 nmol/ L; TSH, 55 ± 10 mU/L) by sampling blood at 10-min intervals for 24 h. The study was repeated in 5 men, 5-7 months and again 14-36 months after treatment with levothyroxine. The control group consisted of 7 normal age-matched euthyroid men. The mean 24-h serum PRL concentration of 4.9 ± 0.6 μg/L in 10 hypothyroid men was not significantly different from the value of 4.9 ± 0.5 μg/L found in the normal group (P > 0.5). Pulsatile features of PRL release were evaluated by Cluster analysis, which revealed normal mean PRL peak frequency (12.6 ± 0.7 vs. 13.4 ± 0.6 pulses/24 h; P > 0.5), maximal peak amplitude (6.1 ± 0.7 vs. 6.7 ± 0.6 μg/L; P > 0.5), peak increment (2.2 ± 0.3 vs. 2.6 ± 0.3 μg/L; P = 0.3), mean valley (4.2 ±0.6 vs. 4.4 ± 0.4 μg/L; P > 0.5), and prepeak nadir (3.6 ± 0.5 vs. 3.6 ± 0.4 μg/L; P > 0.5) PRL concentrations. Five to 7 months of T4 therapy in 5 hypothyroid men caused significant decreases in the mean 24-h (2.9 ± 0.5 vs. 6.1 ± 1.2 μg/L; P < 0.05), interpulse valley (2.5 ± 0.4 vs. 5.2 ± 1.1 μg/L; P < 0.05), and prepeak nadir (2.3 ± 0.3 vs. 4.6 ± 1.0 μg/L; P < 0.05) PRL concentrations. These values returned to normal after 14-36 months of treatment. Cosinor analysis revealed preserved circadian PRL rhythmicity during hypothyroidism, with a normal circadian mesor (mean), amplitude, and acrophase. In summary, we have demonstrated normal mean 24-h serum PRL concentrations as well as normal pulsatile and circadian patterns of PRL release in men with primary hypothyroidism. These results stand in contrast to previous reports of increased serum PRL concentrations observed predominantly in hypothyroid premenopausal women. The foregoing disparity suggests the possibility of a role for estrogen in enhancing the effect of hypothyroidism on PRL release. Decreased serum PRL concentrations after 5-7 months of T4 replacement, but not at later follow-up, indicate one or more transient alterations in the secretion and/or clearance of PRL during the early phases of thyroid hormone replacement.

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