Prolactin levels before and after stimulation with thyroliberin in primary hypothyroidism

The authors examined the concentration of thyrotropic hormone (TSH) and prolactin (PRL) before and after stimulation with synthetic thyroliberine (0.2 mg TRH i.v.) in a group of 72 women with primary hypothyroidism (mean age 45 years, range 17-69 years) and 12 controls (mean age 35 years, range 17-49 years). According to the total thyroxin concentrations (TT4) and TSH they divided the group into three smaller subgroups: developed primary hypothyroidism (n = 8, mean age 50 years, TT4 < 65 nmol/l, basal TSH concentration > 15.0 mIU/l nmol/l), subclinical hypothyroidism, severe grade (n = 23, mean age 36 years, TT4 > 65 nmol/l, basal TSH concentration < 4.5 mIU/l), subclinical hypothyroidism mild degree (n = 39, mean age 42 years, TT4 > 65 nmol/l, basal TSH concentration < 4.5 mIU/l, TSH after TRH stimulation > 25 mIU/l). Mean basal PRL concentrations were in all three patient groups significantly higher than in the control group (P < 0.01) but mutually they did not differ significantly. Poststimulation PRL concentrations were also significantly higher than in controls however the values in developed hypothyroidism were significantly higher than in subclinical patients. No correlation was found between TSH and PRL concentrations.     

The reaction of the hypophysis to thyroliberin and metoclopramide in women with hyperprolactinemia

Functional tests with i.v. injection of metoclopramide (10 mg) and thyroliberin (200 micrograms) with a record of PRL and TSH levels for 120 min. were performed in 87 women of reproductive age (19 healthy nonpregnant women, 9 women in the early postnatal period, 10 patients with primary hypothyroidism, and 30 patients with PRL secreting chromophobe adenomas). Hyperprolactinemic anovulation was noted in 35 examinees. Comparison of the results of thyroliberin and metoclopramide tests in different groups of examinees was suggestive of a decrease in dopaminergic inhibition of the hypophysis in postnatal and adenomatous hyperprolactinemia. The presence and a degree of hyperprolactinemia in patients with primary hypothyroidism depends, probably, on the ratio of a stimulating effect of endogenous thyroliberin and inhibitory action of dopamine on hypophyseal lactotrophs.     

Prolactin and thyrotrophin responses to thyroliberin (TRH) in patients with growth hormone deficiency: study in 167 patients

Both thyrotrophin (TSH) and prolactin (Prl) were studied under thyroliberin (TRH) stimulation tests in 167 hypopituitary dwarfs out of GH or T4 treatment. TSH and/or Prl responses were either low, normal or exaggerated and/or protracted. Various abnormal patterns were observed in most of the patients with low T4 but also in many patients with normal T4. The TSH response should be considered together with the value of T4. A normal response of TSH with a low T4 reflects a relative TSH deficiency from pituitary or hypothalamic origin. There was no clear relationship between the cause or type of hypopituitarism and the pattern of the responses of either TSH or Prl. The abnormalities of TSH and Prl were not related to each other except in patients with a past history of breech delivery. Then both TSH and Prl have to be measured after TRH in order to obtain full information from the test about hypothalamo-pituitary function. The frequency of the exaggerated and/or delayed or protracted responses of TSH and Prl with normal or low T4 is probably mostly related to hypothalamo-pituitary dysfunction. Abnormal responses of TSH or Prl, seldom of both hormones, were observed in otherwise isolated growth hormone (GH) deficiency, leading to a modification of such a diagnosis after the TRH test. Actually, the TRH test may be useful to ascertain the diagnosis of GH deficiency when the GH responses to provocative tests are borderline.     

Comparative analysis in assessing the thyroliberin test in thyroid function disorders

The thyroliberine test was performed in 128 subjects with euthyroidism, thyrotoxicosis and initial hypothyrosis, using a "Hoechst" (FRG) drug in a dose of 200 micrograms, injected intravenously before and 30 minutes after thyroliberine administration, followed by radioimmunoassay of thyreotropic hormone. The test results were evaluated according to the difference and ratio of stimulated basal thyrotropin levels. Distribution of random errors of these findings was studied. Examination of a statistical hypothesis on the normal law of propagation of errors was realized according to the X2 criterion. It was detected that the introduction of a new index for the test evaluation is of interest, i.e. logarithm of ratio between stimulated and basal thyrotropin levels, which was the best one in the thyroid function increase. In initial hypothyrosis the use of the difference between stimulated and basal thyrotropin levels is more informative.     

甲状腺过氧化物酶及其抗体与甲状腺疾病

在自身免疫性甲状腺疾病（AITD）中,甲状腺过氧化物酶抗体（TPOAb）滴度有不同程度的升高,这对AITD的分类及预后有指导意义。最近研究表明,甲状腺组织甲状腺过氧化物酶（TPO）的异常表达或者血清中TPO含量的变化为甲状腺肿瘤的诊断提供了一种新的途径。另外,部分先天性甲状腺疾病的发生也与TPO基因突变相关。进一步研究TPO及TPOAb,有助于对甲状腺疾病病因的探讨并加深对甲状腺疾病诊断及治疗的认识。     

Prolactin, immunoregulation, and autoimmune diseases

Cells of the immune system synthesize prolactin and express mRNA and receptors for that hormone. Interleukin 1, interleukin 6, gamma interferon, tumor necrosis factor, platelet activator factor, and substance P participate in the release of prolactin. This hormone is involved in the pathogenesis of adjuvant arthritis and restores immunocompetence in experimental models. In vitro studies suggest that lymphocytes are an important target tissue for circulating prolactin. Prolactin antibodies inhibit lymphocyte proliferation. Prolactin is comitogenic with concanavalin A and induces interleukin 2 receptors on the surface of lymphocytes. Prolactin stimulates ornithine decarboxylase and activates protein kinase C, which are pivotal enzymes in the differentiation, proliferation, and function of lymphocytes. Cyclosporine A interferes with prolactin binding to its receptors on lymphocytes. Hyperprolactinemia has been found in patients with systemic lupus erythematosus. Fibromyalgia, rheumatoid arthritis, and low back pain patients present a hyperprolactinemic response to thyrotropin-releasing hormone. Experimental autoimmune uveitis, as well as patients with uveitis whether or not associated with spondyloarthropathies, and patients with psoriatic arthritis may respond to bromocriptine treatment. Suppression of circulating prolactin by bromocriptine appears to improve the immunosuppressive effect of cyclosporine A with significantly less toxicity. Prolactin may also be a new marker of rejection in heart-transplant patients. This body of evidence may have an impact in the study of rheumatic disorders, especially connective tissue diseases. A role for prolactin in autoimmune diseases remains to be demonstrated.     

Sialic acid level reflects the disturbances of glycosylation and acute-phase reaction in rheumatic diseases

In the rheumatic diseases, the changes in the carbohydrate part of serum glycoproteins occur and these abnormalities can be monitored by serum level of total and free sialic acid. The aim of this study was to evaluate the total and free sialic acid level as a marker of inflammation activity (TSA) and the changes in glycosylation of blood glycoproteins (FSA) in rheumatoid arthritis (RA), systemic sclerosis (SSc) and systemic lupus erythematosus (SLE). Studies were carried out in 50 patients with RA, 24 with SLE and 32 with SSc. TSA concentration was measured with an enzymatic, colorimetric method and FSA with a thiobarbituric method. The serum levels of TSA in RA and SLE patients were significantly increased compared to controls and in RA patients were higher than that in SSc patients. The mean serum level of FSA in RA patients was significantly higher, but in SSc patients significantly lower than that in the controls, and in RA patients was significantly higher than in SLE and in SSc patients. All acute-phase proteins were changed: Positive acute-phase proteins were elevated, and the negative protein was decreased. The positive acute-phase proteins positively correlated with the levels of TSA and FSA in RA and SSc patients. In SLE patients, TSA positively correlated with haptoglobin and α1-antitrypsin. In RA patients, there was the positive correlation of TSA and FSA with DAS 28. The changes in the serum levels of TSA and FSA in the course of rheumatic diseases could reflect the abnormalities in glycosylation/sialylation patterns of glycoproteins induced by acute-phase response.     

Detection of autoantibodies to thyroid peroxidase in autoimmune thyroid diseases by micro-ELISA and immunoblotting

Serum autoantibodies to thyroid peroxidase (TPO) in patients with thyroid autoimmune diseases were studied by micro-ELISA and immunoblotting. Twenty-four patients, 15 with Graves' disease and 9 with Hashimoto's thyroiditis, whose serum titers were greater than 3200 on the microsomal hemagglutination test (except for 1 patient with a titer of 800) had autoantibodies to TPO. Both immunoglobulin G and M classes of autoantibodies were detected, with the former being more prominent. When TPO and thyroid microsomes were used as a target in a competitive binding inhibition test, the results suggested that TPO was a major thyroid microsomal antigen. On the other hand, immunoblotting analysis showed 3-4 bands in the 45-60K region stained by patients' sera in addition to human TPO with mol wt of 100K and 107K; only the latter 2 bands stained with antiporcine TPO antibody. In the majority of sera, TPO bands were clearer than others, although some sera showed the clearest band with a mol wt of 55K. These results indicate that patients with autoimmune thyroid disease often have autoantibodies to TPO that can be detected by micro-ELISA and immunoblotting, and that TPO is a major component of the thyroid microsomal antigen.     

碘与甲状腺疾病

微量元素碘摄入过低或过高均可诱发各种甲状腺疾病。碘摄入量过低与结节性甲状腺肿以及甲状腺恶性肿瘤的患病率有一定的联系,而碘摄入量过高与多种甲状腺疾病（包括结节性甲状腺肿、甲状腺功能亢进症、甲状腺功能减退、自身免疫性甲状腺疾病、甲状腺肿瘤等）的相关性已经得到不同文献的证实。为防治缺碘性甲状腺疾病推行补碘策略后,某些地区在碘摄入量增加的情况下却发现一些甲状腺疾病的患病率也有所增加。现对近年来流行病学、临床研究、分子生物学等领域的相关研究进展进行归纳与总结,并探讨碘摄入量对甲状腺疾病的影响及其相应作用机制。     

碘与甲状腺疾病

微量元素碘摄入过低或过高均可诱发各种甲状腺疾病.碘摄入量过低与结节性甲状腺肿以及甲状腺恶性肿瘤的患病率有一定的联系,而碘摄入量过高与多种甲状腺疾病(包括结节性甲状腺肿、甲状腺功能亢进症、甲状腺功能减退、自身免疫性甲状腺疾病、甲状腺肿瘤等)的相关性已经得到不同文献的证实.为防治缺碘性甲状腺疾病推行补碘策略后,某些地区在碘摄入量增加的情况下却发现一些甲状腺疾病的患病率也有所增加.现对近年来流行病学、临床研究、分子生物学等领域的相关研究进展进行归纳与总结,并探讨碘摄入量对甲状腺疾病的影响及其相应作用机制.     

碘与甲状腺疾病

碘是合成甲状腺激素的主要原料,同时也是影响甲状腺疾病的重要环境因素.明确碘在体内的代谢过程、碘与甲状腺功能的关系,以及碘对甲状腺疾病的影响是指导甲状腺疾病防治工作的理论基础.以下就碘与甲状腺疾病的关系进行综述.     

硒与甲状腺疾病

硒是人体所必需的一种微量元素,在机体中发挥多种生物学作用,如抗氧化、提高免疫功能、抗肿瘤等。硒和碘一样,参与甲状腺激素的合成、活化及代谢过程,从而影响甲状腺功能。在甲状腺肿、自身免疫性甲状腺疾病、甲状腺癌等患者中,血清硒的水平都存在异常。后者可能通过影响甲状腺滤泡上皮细胞内多种含硒基蛋白酶和(或)影响机体的免疫功能而导致甲状腺疾病的发生与发展。给与某些甲状腺疾病患者含硒制剂可以改善甲状腺功能,这为甲状腺疾病的治疗另辟蹊径。