PubMed Health⌕ Search
Home/Archive/PubMed

PubMed · 414050

Parameters of thyroid function in patients with active acromegaly.

D F Corrigan·L Wartofsky·R C Dimond·M Schaaf·J M Earll·J E Rogers·F D Wright·K D Burman
View original source ↗Export metadata ↓

Abstract

In order to determine if acromegaly per se may be associated with abnormalities in thyroidal economy, serum thyroxine-binding globulin (TBG), resin T3 uptake, total and free T4, T3, and reverse T3 concentrations were measured in 21 patients with active acromegaly. Mean (+/- SE) total T4, T3, and reverse T3 levels were 7.1 +/- 0.2 microgram/dl, 111 +/- 4 ng/dl, and 45 +/- 2 ng/dl, respectively, and the mean TBG concentration was 3.6 +/- 0.2 mg/dl. Similarly, mean free T4, T3, and reverse T3 concentrations were 2.4 +/- 0.09 ng/dl, 383 +/- 22 pg/dl, and 118 +/- 7 pg/dl, respectively. None of these values is significantly different from normal and the thyrotropin response to thyrotropin-releasing hormone was also normal. In contrast to several earlier reports, these data suggest that parameters of thyroid function are generally normal in patients with active acromegaly.

Explore related subjects

AcromegalyAdultFemaleGrowth HormoneHumansMaleMiddle AgedPostoperative ComplicationsThyroid Function TestsThyrotropinThyrotropin-Releasing HormoneThyroxineThyroxine-Binding ProteinsTriiodothyronineJournal Article

Keep this discovery

Explore connections, maps & timelines

BibTeXRIS

D F Corrigan, L Wartofsky, R C Dimond, M Schaaf, J M Earll, J E Rogers, F D Wright, K D Burman. 1978. Parameters of thyroid function in patients with active acromegaly.. https://doi.org/10.1016/0026-0495(78)90166-x

Cite the original work for its findings. Save a collection to share your selection of sources.

KEEP EXPLORING

Related citations

PubMed2007

Protein metabolism in acromegaly: differential effects of short- and long-term treatment.

CONTEXT: GH acutely increases body protein by stimulating protein synthesis and reducing protein oxidation. OBJECTIVE: The objective of the study was to determine whether these changes in protein metabolism are sustained in long-term GH excess and reversed by correction. DESIGN: We conducted a cross-sectional study in 16 acromegalic and 18 normal subjects and a longitudinal study in which acromegalic subjects were studied before and after short-term (n=8) or long-term (n=10) treatment. SETTING: The study was conducted at a clinical research center. MAIN OUTCOME MEASURES: Whole-body rates of leucine appearance (leucine Ra; an index of protein breakdown), leucine oxidation, and nonoxidative leucine disposal (NOLD; an index of protein synthesis) estimated using infusion of 1-[13C] leucine were measured. RESULTS: Leucine Ra and NOLD were greater (P<0.01) in acromegalic compared with normal subjects, whereas leucine oxidation did not differ. Leucine oxidation increased significantly (P<0.05) after short-term treatment but returned to baseline after long-term treatment. Both leucine Ra and NOLD decreased significantly (P<0.05) after short- and long-term treatment. Adjustment for body composition did not affect results. CONCLUSIONS: In acromegalic subjects, protein breakdown and synthesis are increased, whereas protein oxidation does not differ from normal subjects. Protein oxidation increases transiently, whereas protein breakdown and synthesis are stably reduced after treatment. Because protein oxidation represents irreversible loss, we conclude that the normal state of protein oxidation found in acromegaly and after long-term treatment represents metabolic adaptation, which maintains protein mass at a steady state after stable changes in GH status.

Acromegaly↗
PubMed2007

Acromegaly.

Explore the source record for details and available documents.

Acromegaly↗
PubMed2007

Carney complex: the first 20 years.

PURPOSE OF REVIEW: The purpose of this review is to comment on the current findings on Carney complex, a dominantly inherited disease and a unique multiple endocrine neoplasia syndrome. RECENT FINDINGS: Sequencing of the PRKAR1A gene in more than 150 kindreds has revealed a number of pathogenic mutations; in more than 90% of the cases, the sequence change was predicted to lead to a premature stop codon and, thus, mutant mRNAs were subject to nonsense-mediated mRNA decay. In Carney complex syndrome cells carrying these mutations, protein kinase A activity is irregularly stimulated by cAMP. Mutations that did not lead to a premature stop codon have also been described; these were also associated with abnormal protein kinase A activity. Animal models of the disease have been recently developed; they reproduced some of the stigmata of Carney complex syndrome but not all. Genetic testing of patients' family members has been introduced in recent years, leading to early detection and a better overall prognosis. SUMMARY: New treatments have yet to be applied; the elucidation of the molecular pathways regulated by PRKAR1A holds the promise of leading to molecularly designed therapies.

Acromegaly↗