INFLUENCE OF THYROID STATUS ON THE PARADOXICAL GROWTH-HORMONE RESPONSE TO THYROTROPIN-RELEASING-HORMONE IN HUMAN OBESITY

被引:7
作者
COIRO, V
VOLPI, R
CAPRETTI, L
SPERONI, G
MARCHESI, C
VESCOVI, PP
CAFFARRI, G
COLLA, R
ROSSI, G
DAVOLI, C
CHIODERA, P
机构
[1] UNIV PARMA,SCH MED,INTERNAL MED CLIN,I-43100 PARMA,ITALY
[2] UNIV PARMA,SCH MED,ENDOCRINOL CLIN,I-43100 PARMA,ITALY
[3] UNIV PARMA,SCH MED,PSYCHIAT CLIN,I-43100 PARMA,ITALY
[4] HOSP CREMONA,DIV INTERNAL MED,CREMONA,ITALY
[5] HOSP CODOGNO,ENDOCRINE UNIT,CODOGNO,ITALY
[6] HOSP GUASTALLA,RIA LAB,GUASTALLA,ITALY
来源
METABOLISM-CLINICAL AND EXPERIMENTAL | 1994年 / 43卷 / 04期
关键词
D O I
10.1016/0026-0495(94)90086-8
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
Thyrotropin-releasing hormone (TRH) tests were performed in 38 age- and weight-matched obese but otherwise healthy men. In all subjects, total thyroxine (T4) and triiodothyronine (T3) concentrations were in the normal range. According to basal and TRH-stimulated serum thyrotropin (TSH) levels, subjects were divided into the following three groups: group I (n = 14), euthyroid subjects; group II (n = 11), euthyroid subjects with normal basal but abnormally elevated TSH responses to TRH; group III (n = 13), subjects with elevated basal and TRH-induced TSH levels (subclinical hypothroidism). Basal TSH levels were 1.8 ± 0.4 mU/L in group I, 1.7 ± 0.3 in group II, and 6.0 ± 0.7 in group III. In both groups II and III, TRH-induced TSH increments were above the normal range (maximal increment >14 mU/L) and were significantly higher than in group I. The definition of euthyroidism for groups I and II and of subclinical hypothyroidism for group III according to the basal levels of TSH was confirmed by clinical (Billewicz index), hormonal (serum free-T4 levels), and metabolic (serum apoprotein [apo] AI levels) parameters. Basal concentrations of growth hormone (GH) were similar in all groups. When GH levels after TRH stimulation were measured, significant increments (peak minus baseline >5 μg/L) were observed in nine of 13 hypothyroid obese men. The overall mean peak GH increase in group III was 4.5 times higher than baseline and was observed at 45 minutes. None of the euthyroid obese subjects of groups I and II showed any significant change in GH levels in response to TRH. These data show a paradoxical GH response to TRH in most obese men when they are affected by subclinical hypothyroidism, suggesting that this abnormality is related to hypothyroidism and not to obesity. The finding of an abnormal GH responsiveness to TRH in obese men with subclinical hypothyroidism but not in euthyroid obese men with elevated TSH responses to TRH suggests that these subjects are affected by different neuroendocrine alterations. The GH response to TRH may contribute to distinguish clinical conditions that are similar but require different therapeutic attention. © 1994.
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收藏
页码:514 / 517
页数:4
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