A sensitive immunoradiometric assay for serum thyroid stimulating hormone: a replacement for the thyrotrophin releasing hormone test?

The value as a thyroid function test of a new, rapid, and highly sensitive immunoradiometric assay for thyroid stimulating hormone (TSH) was assessed in 188 consecutive new patients with suspected hyperthyroidism. The diagnosis was made on clinical grounds and on the basis of serum total triiodothyronine and thyroxine concentrations and the response of TSH to thyrotrophin releasing hormone (TRH) as measured by radioimmunoassay. In all except one patient the basal TSH concentration by immunoradiometric assay predicted the response of TSH by radioimmunoassay to TRH, an undetectable value being recorded in patients with a subnormal response and a measurable value in those with a normal test result. This clear relation was not observed for basal TSH concentrations as measured by radioimmunoassay. In a series of 39 hospital inpatients with acute or chronic non-thyroidal illness, of whom 11 had low concentrations of total thyroxine or triiodothyronine, or both, basal TSH concentrations were detectable by both radioimmunoassay and immunoradiometric assay in all cases and were associated with normal responses to TRH. The immunoradiometric assay for TSH, which is commercially available, may therefore obviate the need for the more time consuming TRH test and simplify the approach to thyroid function testing in patients with suspected hyperthyroidism.     

Diagnostic value of thyrotrophin releasing hormone tests in elderly patients with atrial fibrillation

A prospective study was carried out to compare clinical and biochemical thyroid states with responses of thyroid stimulating hormone (TSH) to thyrotrophin releasing hormone (TRH) in elderly patients with either atrial fibrillation (n = 75; mean age (SD) 79.3 (6.0) years) or sinus rhythm (n = 73; mean age 78.4 (5.6) years) admitted consecutively to the department of geriatric medicine. No patient in either group had symptoms or signs of hyperthyroidism. Overall, the TSH responses to TRH did not differ significantly between the two groups. Ten (13%) of the patients with atrial fibrillation (of whom four had raised thyroid hormone concentrations) and five (7%) of the patients with sinus rhythm showed no TSH response to TRH while 26% of each group (20 and 19 patients, respectively) showed a much reduced response. Only one of 13 patients with apparently isolated atrial fibrillation showed no TSH response to TRH, and none of these 13 patients was hyperthyroid. In particular, three patients (two with atrial fibrillation and one with sinus rhythm) who showed no TSH response to TRH at presentation exhibited a return of TSH response to TRH at follow up six weeks later. In conclusion, reduced or absent TSH responses to TRH are common in sick elderly patients whether they have atrial fibrillation or sinus rhythm and whether they are euthyroid or hyperthyroid biochemically. An absence of response is therefore an uncertain marker of hyperthyroidism in these groups of patients, and diagnosis and ablative treatment should be based at least on the presence of raised circulating free triiodothyronine or free thyroxine concentrations, or both.     

Growth hormone, prolactin and thyrotrophin responses to thyrotrophin-releasing hormone in diabetic patients.

Growth hormone (GH), prolactin (PRL) and thyrotrophin (TSH) responses to thyrotrophin-releasing hormone (TRH) were studied in 15 insulin-dependent diabetic patients. Basal plasma GH levels were raised above 5 mu./l in 6 patients and following the injection of TRH there was a significant rise in plasma GH levels in 9. The mean rise in plasma GH from basal to peak values was significant in the group as a whole (P < 0.01). Basal PRL and TSH levels were normal and rose normally in response to TRH. GH release may be qualitatively abnormal in some diabetics and any such loss of specificity of GH-releasing mechanisms would further contribute to the raised GH levels found in many diabetics which would be of importance if GH is a factor in the aetiology of diabetic microangiopathy.     

Hyperthyroidism due to inappropriate TSH secretion with associated hyperprolactinaemia--a case report and review of the literature.

A patient with inappropriate thyrotrophin (TSH) secretion is described. She initially presented with classical hyperthyroidism during pregnancy, responded to propylthiouracil and, subsequently, had a normal delivery. Hyperthyroidism persisted and 7.5 months later a subtotal thyroidectomy was performed. After a further 16 months, mild symptoms of hyperthyroidism recurred. She again responded to propylthiouracil, but developed galactorrhoea. At that stage, it was noted that she had persistently elevated circulating TSH in the presence of elevated T4 and T3 levels. Her symptomatology was mild, although objective indices of thyroid activity, including pulse rate, BMR, sex hormone binding globulin and cholesterol, were indicative of hyperthyroidism. CT scan and tomography of the sella were normal. She had a markedly exaggerated TSH response to thyrotrophin releasing hormone (TRH). Basal TSH and responsiveness to TRH was suppressed by high dose dexamethasone. The TSH response to TRH was partially suppressed by exogenous T3, but there was no effect on basal TSH levels. TSH also decreased slightly with L-dopa and bromocriptine. Circulating TSH rose markedly during methimazole administration. TSH alpha and beta subunits were elevated and appropriate for the high TSH. In addition, both subunits increased following TRH. The patient had basal hyperprolactinaemia with an impaired prolactin (PRL) response to TRH and metoclopramide. PRL suppressed with L-dopa and bromocriptine. The remaining anterior pituitary function was intact. Most of the laboratory findings argue against the presence of a TSH producing pituitary tumour and the most likely cause for inappropriate TSH secretion in this patient is selective resistance of the thyrotroph to thyroid hormones. A mild element of peripheral resistance might also be present. The hyperprolactinaemia could be related to lactotroph resistance to thyroid hormone. The complexities of treatment in this patient are stressed. Therapy was initially attempted with low dose dexamethasone, but this had no effect. T3 treatment produced an exacerbation of her symptomatology and did not influence basal TSH, thyroid hormones, or 131I uptake. Bromocriptine administration for 11 months partially suppressed basal TSH without influencing T3 and there was an increase in T4. Methimazole did decrease her T4 and T3, but TSH and PRL rose to even greater levels. Her hyperthyroidism was eventually controlled with an ablative dose of 131I. Thyroid hormone will be given in an attempt to suppress her TSH.     

EFFECT OF THYROID HORMONE DOSAGE ON THYROID FUNCTION TESTS IN T4-REPLACED HYPOTHYROID PATIENTS

To examine the relative importance of serum thyroxine (T4), free thyroxine (fT4) and triiodo thyronine (T3) in monitoring adequate T4 dose in patients on T4-replacement therapy, the effect of T4 dose on total T4, fT4 and T3, basal thyroid stimulat- ing hormone (TSH) and TSH-response to thyrotropin releasing hormone (TRI'I) were investigated in 33 patients taking T4 doses of 50-200\µg/day. The T4- treated patients had highly elevated mean T4 (total and free) and lower basal TSH levels compared to the mean values in normal subjects. But serum T3 was not significantly different. The patients on T4 doses greater than 150Ug/day frequently had more suppressed TSH response tol TRH than those on T4 doses less than 150µg/day. Total T4 and T4, but not serum T3 levels, cerrelated significantly with T4 dosage. Changes in T4 dosage led to concomi tant changes in total T4 and fT4 and inverse changes in TSH-response to TRH. The study also revealed a high incidence (33%) of elevated serum fT4 (hyperthyroxinemia) dLtring therapy. The hyperthyroxinemic group was characterised by clevated serum T4 (total ancl free), T3 and T4 dose, and suppressed TSH-response to TRH compared to the T4-treated group with normal serum T4 Ievels. These findings may be indicative of excessive T4 treatment iri these patients and suggest serum T4 may be more useful than T3 in monitoring T4 dosage in T4-replacement therapy. The discrepancy between normal serum T4 levels and TSH-response to TRH may reflect hetero- geneity in returning normal function of the pituitary- thyroid axis. Clearly, measurement of TSH or TRH test can ~ot be used alone in assessing thyroid status iki these patients, particularly when serum T4 is in normal'range.     

Effect of a sensitive thyrotropin-stimulating hormone assay on dosing of L-thyroxine

The Wisconsin Veterans Home has had a special interest in thyroid disease since 1986. Until recently, dosage adjustment of L-thyroxine in residents with primary hypothyroidism was accomplished by individual physicians guided by standard thyroid function tests. A shift to a sensitive thyrotropin-stimulating hormone (TSH) assay provided an opportunity to assess the frequency of sensitive TSH suppression secondary to excessive doses of L-thyroxine which would not be recognized by the standard TSH assay. We reviewed the charts of 46 residents who were not acutely ill and had been in the facility at least 6 months. Sensitive TSH was determined while on a stable dose of L-thyroxine for a minimum of 6 weeks. Six residents (13%) had low sensitive TSH levels indicating an excessive dose of L-thyroxine. The application of the sensitive TSH assay resulted in dose reduction.     

Long-term L-thyroxine therapy is associated with decreased hip bone density in premenopausal women

The effect of long-term L-thyroxine (L-T4) therapy on axial skeleton bone density was studied in 31 premenopausal women; the bone densities of these women were compared with the bone densities of 31 age- and weight-matched women without thyroid or bone abnormalities. The women receiving L-T4 therapy had been receiving the medication for a minimum of five years. There was no difference in calcium intake or excretion between the L-T4-treated women and the controls. Women receiving L-T4 had increased serum thyroxine concentrations (134 +/- 5 vs 95 +/- 3 nmol/L [10.4 +/- 0.4 vs 7.4 +/- 0.2 micrograms/dL]), an increased free thyroxine index (9.4 +/- 0.4 vs 6.8 +/- 0.2), and decreased serum thyroid-stimulating hormone concentrations (0.9 +/- 0.2 mU/L vs 2.1 +/- 0.3 mU/L [0.9 +/- 0.2 vs 2.1 +/- 0.3 microU/mL]). Serum triiodothyronine concentrations were normal and were similar in both groups. Women treated with L-T4 had a 12.8% lower bone density at the femoral neck and a 10.1% lower bone density at the femoral trochanter compared with matched controls. In contrast, lumbar spine bone density was similar in the two groups. The data suggest that long-term L-T4 therapy, which is often given at supraphysiologic dosages, may predispose patients to decreased bone density in the hip and may increase the risk of age-related bone loss. It is advisable, therefore, to employ a dosage of L-T4 that is carefully monitored to avoid the long-term use of dosages that are excessive for the thyroid condition being treated.     

妊娠期亚临床甲状腺功能减退症左甲状腺素治疗剂量探讨

目的：探讨影响妊娠期亚临床甲状腺机能减退（SCH）患者左甲状腺素（L-T4）治疗剂量的因素。方法：42例妊娠期SCH患者,每4周监测甲状腺功能,根据促甲状腺激素（TSH）水平调整L-T4剂量,使每次TSH值均达标。记录首诊时患者体质量、TSH值、甲状腺过氧化物酶抗体（TPO-Ab）水平、产前体质量和新生儿体质量等。使用SPSS17.0对产前L-T4剂量进行多元线性回归分析。结果：产前L-T4剂量与患者体质量及体质量增加值、首诊时TSH值、TPO-Ab水平、新生儿体质量等无明显关系（P〉0.05）。结论：患者首诊时TSH值、体质量、孕期体质量增加值、TPO-Ab水平、新生儿体质量等不能预测产前L-T4剂量,TSH全程控制达标有赖于规律的监测和随访。     

Impaired thyrotrophin secretion following the administration of thyrotrophin-releasing hormone in type II diabetes mellitus

Serum thyrotrophin has been measured before and after the intravenous administration of 200 micrograms of thyrotrophin-releasing hormone in 91 white subjects (33 stable diabetic patients and 58 healthy controls), none of whom had any clinical evidence of thyroid or pituitary dysfunction. Seven of the diabetic subjects failed to achieve a rise of serum thyrotrophin of greater than 2 mU/l above basal concentrations, as compared with only one of the control subjects (P = 0.006). The difference in response between diabetics and controls was confined to patients with Type II (non-insulin-dependent) diabetes: thus 5 of 13 Type II patients and 2 of 20 Type I (insulin-dependent) patients failed to show a normal response to thyrotrophin releasing hormone injection. No significant effect of glycaemic control on thyrotrophin responses was noted. These results suggest that Type II diabetes mellitus may be a cause of impaired thyrotrophin secretion in patients with no clinical evidence of pituitary disease. The mechanism for this impaired pituitary hormone release remains to be clarified.     

THYROTROPIN RELEASING HORMONE STIMULATION TEST ANID ITS CLINICAL SIGNIFICANCE

This article summa.rizes the results of thyrotropin releasing hormone (TRH) stimula- tion test done on 118 subjects since 1976. The relsponses are cla.ssified int.0 4 groups: normal, active, low and no response. 30 no.rmal medical workers recelive;d 2 doses of TRH 0.5 and LO mg, and 17 cases of untreat- ed Grave s disease all showed no response. Four cases treated with antithyroid drugs gave active responses, 2 0f them presenting manifes- tations of hypothyroidism, but in the other 2 no response was seen during the test. One case of autonomo,us hyperfunctional adenoma with T- 3-hypertoxicosis gave a low response. 12 0f the 13 untreated cases of primary hypothyroidism gave active responses, 1 ha.d normal response. 2 0f primary hypothyroidism with desiccated thyroid during substitution therapy gave no rersponses. In 13 secondary hypothyroidism cases, 3 gave normal response:s, 1 low re.sponse and the remaining 9 no response. E.ffect of TRH test of various drugs was also observed. Among the 14 cases treated with adrenal glucooorticoids 6 gave no responses and 4 each gave normal and low response. 6 0f 9 cases of parkinsonism treat.ed with L-dopa showed no response, 2 normal respon.se and 1 low response. Among 15 women receiving steroid cointraceptives (compound quinoestrol) 10 showed active response and 5 norma.l response. Clinical significance, dosage and side effects of TRH test and factors influencing it are discusseld.     

Thyrotropin-and prolactin--secreting pituitary tumor dissociated hormonal response to bromocriptine

A 41-year-old male with recurrent hyperthyroidism resulting from pituitary tumor was studied. Because of recurrent hyperthyroidism, he had been treated with propylthiouracil for four years and had been operated. At the time of high serum thyroid hormone (T4: 20 micrograms/dl; T3:502 ng/dl), there was also elevated basal serum TSH level (55 microU/ml) which could not be suppressed by exogenous thyroid hormone administration. In addition, the serum TSH showed blunt response to intravenous TRH infusion. An elevated serum prolactin level was also observed (111 ng/ml). After bromocriptine administration (2.5 mg daily), the suppressibility of serum TSH level was found better than that of prolactin level. The existence of a TSH- and PRL-secreting pituitary tumor in this patient exhibited a dissociated hormonal response to low doses of dopaminergic agents.     

Congenital hypothyroidism from complete iodide transport defect: long-term evolution with iodide treatment

Hypothyroidism from iodide transport deficiency is a rare disease, especially when found in two affected siblings. Treatment with high doses of iodide has been recommended, but no long term results have been reported. Two siblings with congenital hypothyroidism due to total failure to transport iodide have been followed up during twelve and a half years of treatment with oral potassium iodide. Iodine doses varied between 10.3 and 22 mg/day, and serum total iodine concentrations between 100 and 210 micrograms/dl. Total triiodothyronine (T3), thyroxine (T4) and free T4 were in the normal range during the time of study. Basal thyroid stimulating hormones (TSH) and maximum TSH response to thyrotrophin releasing hormone (TRH) were also in the range of normal values. These data along with clinical findings confirmed the potential usefulness of iodine in hypothyroidism due to complete iodide transport defect.     

Clinical hyperthyroidism due to non-neoplastic inappropriate thyrotrophin secretion

We report a case of hyperthyroidism due to inappropriate thyrotrophin (TSH) secretion in a patient with selective pituitary resistance to thyroid hormone action. Symptoms of hyperthyroidism in patients with this disorder are usually mild, implying some peripheral tissue resistance to the metabolic effects of thyroid hormone. Our patient had unusually severe symptoms, including marked weight loss and cardiac arrythmias which required carbimazole and beta-blocker therapy for control. Somatostatin was ineffective in suppressing TSH secretion. The introduction of sensitive thyrotrophin assays should facilitate the accurate diagnosis of TSH-induced hyperthyroidism and avoid inappropriate treatment.     

Clinical significance of multiple hypothalamic-pituitary functions assessment in patients with Turner’s syndrome

Summary Hypothalamic-pituitary functions in 26 cases of Turner syndrome were assessed with a combined stimulation test. The results showed that the peak GH levels of 12 cases were less than 10 μg/L; 3 patients were demonstrated as having an even TSH response, while another one with a delayed TSH peak, and other 4 had high basal values and consistent exaggerated TSH responses to TRH; all patients showed increased basal and peak LH and FSH levels but 5, whose LH and FSH secretion patterns were similar to normal. 12 cases have been treated with individualized protocols and followed up for 12 months or more, of them the growth velocity all increased, especially those with hypothyroidism or with a BA less than 13. It is suggested that multiple functions of hypothalamic-pituitary axis in Turner patients be evaluated as early as possible, in order that proper treatment could be adopted and their growth and development improved.     

The effective evaluation of thyroid status in patients on phenytoin, carbamazepine or sodium valproate attending an epilepsy clinic

To assess the most efficient means of monitoring thyroid status in an epilepsy clinic, total thyroxine (T4), free thyroxine stimulating hormone (TSH) were measured in 71 adult patients treated long-term with either phenytoin (DPH), carbamazepine (CBZ) or sodium valproate (VAL). Twenty-seven patients with one or more abnormal thyroid hormone results were further investigated by a thyrotrophin releasing hormone (TRH) test and clinical assessment. T4 was found to be normal in 85% on VAL, 40% on CBZ and 39% on DPH. FT4 was normal in more patients, namely 95% on VAL, 70% on CBZ and 65% on DPH. The TRH tests indicated that FT4 was the most efficient screening test for hypothyroidism in this epileptic population. We estimate that the use of FT4 alone as a screening test would have reduced by 60% the number of TRH tests required.     

甲状腺素联合多奈哌齐对成年期甲状腺功能减退症大鼠额叶乙酰胆碱、munc-18的影响

目的：观察甲状腺素联合多奈哌齐对成年期甲状腺功能减退症(简称甲减)大鼠额叶内乙酰胆碱含量以及munc-18表达的影响,探讨甲减脑额叶损伤及恢复的可能分子机制。方法采用给予含0．05%丙基硫氧嘧啶的饮用水6周建立大鼠甲减模型。自第5周起,给予多奈哌齐、甲状腺素或甲状腺素联合多奈哌齐治疗2周,采用放射免疫法检测血清甲状腺激素水平,碱性羟胺比色法测定额叶内乙酰胆碱含量,免疫组化法检测额叶内munc-18的分布与表达。结果甲减组、多奈哌齐治疗组大鼠血清三碘甲状腺原氨酸(T3)、四碘甲状腺原氨酸(T4)水平显著减低、促甲状腺激素( TSH)水平明显增加( P<0．01),甲状腺素治疗组、联合治疗组T3、T4、TSH水平与正常对照组相比差异无统计学意义;甲减组大鼠额叶内乙酰胆碱含量下降(P<0．05),多奈哌齐治疗组、甲状腺素治疗组、联合治疗组乙酰胆碱含量均恢复至正常水平,其中联合治疗组有进一步恢复趋势;甲减组、多奈哌齐治疗组大鼠munc-18在额叶内Ⅱ、Ⅲ、Ⅳ、Ⅴ层表达下降(P<0．05)。其中,以Ⅲ/Ⅴ层下降最为显著(P<0．01),甲状腺素治疗组munc-18表达仍下降(P<0．05),联合治疗组额叶内munc-18表达正常。结论多奈哌齐可以改善甲状腺功能减退引起的额叶内乙酰胆碱含量改变;甲状腺素联合多奈哌齐治疗有利于成年期甲状腺功能减退造成的额叶内胆碱含量改变和突触蛋白损伤的恢复。     

Do acute diseases transiently impair anterior pituitary function in patients over the age of 75? A longitudinal study of the TRH test and basal gonadotrophin levels.

Several studies have shown that anterior pituitary function is affected by the ageing process. Little is known, however, about the effect acute diseases have on the anterior pituitary. Should they be associated with a disturbance of anterior pituitary hormone production, they might make anterior pituitary function tests difficult to interpret when they are most needed. To test this hypothesis, we studied the thyrotrophin (TSH) releasing hormone (TRH) test and basal plasma gonadotrophins, taken as indicators of anterior pituitary function and reserve, in 74 consecutive patients (49 women) mean age 82 +/- 5.1 suffering from acute diseases soon after admission to hospital. A total of 44 (30 women) were followed up and retested after 3 disease-free months following recovery and discharge home. Seventy-one age- and sex-matched healthy controls (47 women), mean age 82 +/- 5.0 living in the community were also studied. The mean peak TSH increment after TRH (mean delta max TSH) increased from 5.7 soon after admission, to 7.7 U/l at follow-up (P = 0.01). The mean plasma LH increased from 25 to 35 U/l in women (P = 0.0004) and from 9.7 to 14 U/l in men (P = 0.03). The mean plasma FSH increased from 21 to 25 U/l in women (P = 0.04) and from 7.5 to 9.4 U/l in men (P = 0.01). Controls had greater TSH responses to TRH and higher plasma gonadotrophins levels when compared with acute patients (LH women P = 0.17, for all other tests P < 0.05). We conclude that a transient reduction of anterior pituitary function is a common occurrence in patients over the age of 75 suffering from acute diseases. This has diagnostic relevance and therapeutic implications.     

Effect of somatostatin on thyrotropin, prolactin, growth hormone and insulin responses to thyrotropin releasing hormone and arginine in healthy, hypothyroid and acromegalic subjects.

The effect of somatostatin on the thyrotropin (TSH), prolactin, growth hormone (GH) and insulin responses to the combined administration of thyrotropin releasing hormone (TRH) and arginine was studied in six healthy subjects, three hypothyroid patients and three acromegalic patients. Similar inhibition by somatostatin of the TSH and insulin responses was observed in the three groups. While the tetradecapeptide had no significant effect on the prolactin response in the healthy and acromegalic subjects, it caused an unexpected inhibition of the prolactin response in two of the hypothyroid subjects. Contrary to the findings in the healthy and hypothyroid subjects, somatostatin did not inhibit the GH response in the acromegalic patients. Normal inhibition by somatostatin of the insulin response, followed by a rebound in insulin secretion, was observed in all subjects. These preliminary data indicate increased sensitivity of the prolactin-secreting cells to somatostatin in hypothyroidism and suggest that decreased responsiveness of the somatotrophs to somatostatin could play a role in the pathogenesis of acromegaly.     

Primary hypothyroidism presenting as a pituitary mass

Pituitary enlargement secondary to primary hypothyroidism is a known but uncommon occurrence, which can be difficult to distinguish on computerized tomography (CT) and magnetic resonance imaging (MRI) from primary pituitary tumors. We describe a 33 year old female who was referred to a neurosurgeon for removal of a pituitary mass. The markedly elevated thyrotrophin stimulating hormone (TSH), absence of clinical features of hyperthyroidism, and low thyroid hormone values led to a diagnosis of pituitary enlargement secondary to primary hypothyroidism. The pituitary gland returned to normal size with thyroxine replacement therapy. Surgery was not indicated.     

L-T4 替代治疗对妊娠期亚临床甲状腺功能减退 孕妇血清抵抗素、同型半胱氨酸的影响

目的 探讨左旋甲状腺激素替代治疗（L-T4）对妊娠期亚临床甲状腺功能减退（SCH）孕妇血清抵 抗素（RE）、同型半胱氨酸（HCY）的影响。方法 选取2014 年1 月-2016 年1 月该院收治的90 例SCH 患者， 依据随机数字表法将其分为两组：观察组接受L-T4 替代治疗，每隔4 周复查甲状腺激素（TSH）水平，治疗目 标为妊娠早期TSH 水平在0.3 ～ 2.5 mIU/L，中期和晚期为0.3 ～ 3.0 mIU/L，直到治疗达标为止；对照组不接 受治疗，每隔4 周复查TSH 水平。所有患者入院次日及复查TSH 当日取空腹肘静脉血，测定血清HCY 和RE 水平，记录妊娠结局和子代发育12 个月的智力情况。结果 观察组治疗8 周后，血清TSH 达到0.3 ～ 3.0 mIU/L， 达到治疗目标，故将治疗8 周的时间点定义为治疗后。观察组治疗后，血清TSH、HCY 水平降低（P <0.05）， 游离甲状腺素（FT4）、RE 水平升高（P <0.05），对照组各指标无变化（P >0.05）；观察组治疗后的TSH 较对照组 低（P <0.05），FT4 指标较对照组高（P <0.05）；观察组不良妊娠结局发生率（10.3%）低于对照组（28.1%）（P <0.05）； 两组子代发育12 个月时的精细动作发育商（FMQ）、大运动发育商（GMQ）、个人社交发育商（ISBQ）及语言发 育商（LQ）评分比较，差异均有统计学意义（P <0.05）。结论 妊娠早期行左旋甲状腺激素替代治疗有助于降低 SCH 患者血清TSH、HCY 水平，升高抵抗素水平，改善母体状态和妊娠结局，并促进子代智力发育，具有一定的 临床意义。