In 1972 it was reported that in some euthyroid depressed patients the serum thyrotropin (TSH) response to thyrotropin-releasing hormone (TRH) was deficient. Since then, 41 reports describing 917 depressed patients have confirmed this finding. Although it is useful to report differences between mean response values of patient populations, it is necessary to identify those individuals in whom the fault occurs so that sensitivity, specificity, state-trait distribution, and clinical correlates can be determined. Present data allow some tentative conclusions: 1) the fault usually reflects a defect in central regulation of the pituitary-thyroid axis, 2) in some patients the fault may be a trait marker, and 3) it may represent a biological bridge between some depressed patients and some patients with other mental disorders.

Serum thyrotropin response to thyrotropin-releasing hormone in psychiatric patients: a review.

Subclinical hypothyroidism is a frequent syndrome affecting about 10 million people in the United States. The management of such patients is open to debate. In a long-term prospective study we analyzed the spontaneous course and the value of predictive factors in the development of overt thyroid failure. We studied 82 female patients with subclinical hypothyroidism prospectively over a mean observation period of 9.2 yr. TSH, thyroid hormones, thyroid reserve after TRH administration, thyroid antibodies, and clinical parameters were assessed at yearly intervals. The cumulative incidence of overt hypothyroidism was calculated using life-table analysis and Kaplan-Meier curves. According to the initial serum TSH concentrations (TSH, 4–6/>6–12/>12 mU/liter), Kaplan-Meier estimates of the incidence of overt hypothyroidism were 0%, 42.8%, and 76.9%, respectively, after 10 yr (P < 0.0001). When only patients with TSH levels greater than 6 mU/liter were analyzed, the cumulative incidence was 55.3%. The incidence o...

Prospective Study of the Spontaneous Course of Subclinical Hypothyroidism: Prognostic Value of Thyrotropin, Thyroid Reserve, and Thyroid Antibodies

Previous studies have suggested that certain cases of idiopathic central hypothyroidism of hypothalamic origin may result from the secretion of biologically inactive thyrotropin. To investigate this possibility and to define the mechanism of defective hormone action, we measured the adenylate cyclase-stimulating bioactivity (B) and receptor-binding (R) activity of purified immunoreactive serum thyrotropin (I) from seven patients with hypothalamic hypothyroidism. We found a strikingly decreased R/I ratio (less than 0.15) in patients as compared with controls (0.6 to 2.7) and a similarly decreased B/I ratio (less than 0.2 vs 2.8 to 5.6). After acute injection of thyrotropin-releasing hormone (TRH, 200 micrograms intravenously), the R/I ratio increased in two of three patients, but the B/I ratio became normal in only one. After administration of TRH for 20 to 30 days, an increase in immunoreactive serum thyrotropin was observed in all patients. Moreover, both ratios returned to normal in all but one patient, who had apparent desensitization. The increase in the amount and bioactivity of secreted thyrotropin after long-term TRH therapy resulted in enhanced secretion of serum thyroid hormones in all patients studied. We conclude that in certain cases of hypothalamic hypothyroidism, secreted thyrotropin lacks biologic activity because of impaired binding to its receptor; TRH treatment can correct both defects. These data suggest that TRH regulates not only the secretion of thyrotropin but also its specific molecular and conformational features required for hormone action.

https://www.nejm.org/doi/pdf/10.1056/NEJM198504253121703?listPDF=true

Decreased receptor binding of biologically inactive thyrotropin in central hypothyroidism. Effect of treatment with thyrotropin-releasing hormone.

The aim of the present study was to evaluate the lipid profiles (total cholesterol, triglycerides, low-density lipoprotein-cholesterol, high-density lipoprotein-cholesterol, and the electrophoretic low-density lipoproteins and high-density lipoproteins) in patients with subclinical (n = 52) and overt hypothyroidism (n = 18) in comparison to normal controls (28 and 18, respectively), matched for age, sex and body mass index. Subclinical hypothyroidism was defined as a syndrome with normal free thyroxine and total thyroxine but elevated basal thyrotrophin levels and/or an exaggerated TSH response to oral thyrotrophin releasing hormone. In subclinical hypothyroidism there was an elevated LDL concentration (P less than 0.01), a diminished HDL fraction (P less than 0.05) and a borderline elevated LDL-C (not reaching the limit of significance, P = 0.07). Total cholesterol and triglyceride concentrations remained unaltered. For the whole group of patients and controls significant negative correlations were found between LDL-C and T4 (P less than 0.04), total cholesterol and free thyroxine-index (P less than 0.01); positive correlations could be demonstrated between LDL-C and basal TSH (P less than 0.03), the ratio total cholesterol/HDL-C and basal TSH (P less than 0.03), and triglycerides and basal TSH (P less than 0.01). Our data provide a possible explanation for the higher prevalence of coronary heart disease reported in subclinical hypothyroidism. There may well be a case for the detection and early treatment of such individuals.

Ldl/hdl‐changes in subclinical hypothyroidism: possible risk factors for coronary heart disease

Publisher Summary This chapter discusses the regulatory pathways, the targets, the functions, and the interactions among the corticotropic, melanotropic, and thyrotropic axes, and the evidence that implicates each axis in the stress response. Multiple hypothalamic factors are involved in the regulation of the secretions from the corticotrope, melanotrope, and thyrotrope pituitary cells in fishes. Among these factors, corticotropin‐releasing factor (CRF) and thyrotropin‐releasing hormone (TRH) stimulate, and dopamine generally inhibits the secretions from all three hypothalamo–pituitary axes. The CRF system also plays a master role in the regulation of the endocrine response to stressors. In general, the contributions of the corticotropic, melanotropic, and thyrotropic axes to the stress response are species‐specific and depend on the challenge imposed on the system, its duration, and the homeostatic resilience of the fish. Multiple interactions and feedback effects have been identified among these endocrine axes. In the chapter it has been postulated that the extensive multidirectional communication as well as the cross‐talk among the corticotropic, melanotropic, and thyrotropic axes forms a “stress web” that exerts well‐concerted actions on energy metabolism as its prime task.

Chapter 6 Regulation And Contribution Of The Corticotropic, Melanotropic And Thyrotropic Axes To The Stress Response In Fishes

In euthyroid subjects, repeated oral doses of TRH produced a greater increase of plasma levels of thyroxine (T4) and triiodothyronine (T3) than did a single dose. The TSH response, in contrast, was diminished. To determine if this blunting of the response was mediated by a negative feedback mechanism, we compared the effects of single and repeated oral doses of TRH on TSH, T3, and T4 responses in euthyroid subjects and in patients with primary thyroid failure. Thirty-five euthyroid subjects were given 3 oral doses of 40 mg TRH over a period of 26 h. The mean TSH peak declined from 13.0 µU/ml after the 1st dose to 5,9 µU/ml after the 3rd dose (P < 0.0005). T4 concentrations increased from basal 7.5 to 10.2 µg/100 ml 3 h after the 3rd dose of TRH and T3 from 1.52 to 2.19 ng/ml. Repeated oral doses of TRH were also given to 9 patients with primary hypothyroidism and 9 patients after total thyroid ablation for thyroid carcinoma. The same significant blunting of the TSH response after the 3rd oral dose of TRH ...

Blunting of TSH response after repeated oral administration of TRH in normal and hypothyroid subjects.

Popular Tasks used by Researchers

How can I help with your research?

Get more enhanced response by uploading the PDFs you want me to reference.

No relevant PDFs in your library

SciSpace is the AI research assistant for academics. Run systematic literature reviews on 280M+ papers, and write papers with cited sources. Trusted by 1M+ students, PhDs & researchers.

SciSpace | AI for Research

We encountered an error while loading the panel. Please try refreshing the page.

Something went wrong

Analyze PDFs

Code & Manuscripts

Funding & Grants

Literature & Patents

Medical & Clinical Data

Systematic Review

Visualize & Present

Web & Data

Build a Google Scholar-like website for your research.

Build a website

Create charts and images for your research

Create a Chart

Write a paper for submission to a journal

Draft a manuscript

Patent Search

Design eye-catching scientific posters in minutes.

Scientific Poster Generation

Systematic Literature Review

Anyone with the link can view this chat. You can switch it back to private anytime.

One task is running at the moment. Your messages will be shown right after.

Drag and drop or click here to browse

Loved by <highlight>1 million+</highlight> researchers

Extract a list of specific topics and their sources from unstructured text

Topics

Compare and analyze relevant papers that matches with your search

Papers

Get insights from PDFs and bookmarked papers from your library

My library

Recent searches

Try searching for:

Catch AI-generated content in scholarly and non-scholarly content

{ai} Detector

Ai Writer

Get PDF Summaries, highlighted text explanations 

Chat with PDF

Effortlessly create in-text citations and bibliographies in APA and 2,500 other formats

Citation generator

Get explanations, summaries, and answers on academic papers

Ease up your research workflow with {scispace}'s cohort of exciting AI tools

Elevate your academic writing skills and convey your ideas the way you want

Paraphraser

Explore our range of reading and writing tools

Your file is being prepared and should be ready in a few minutes. If it's a large file, it might take a bit longer. You can close this window, and we'll email you the file when it's done.

You have reached a maximum limit of <strong>{limit}</strong> columns in the table. Remove at least <strong>1</strong> column to add or create another one.

Baur U

Author Tools

Chat about Author

Papers

Blunting of TSH response after repeated oral administration of TRH in normal and hypothyroid subjects.