The DOI matches its Crossref record; 40 of the 40 references it cites were found in a registry or an index; 8 of the 29 sources its claims cite were checked for support.
The Role of Thyroid Hormone in Blood Pressure Homeostasis: Evidence from Short-Term Hypothyroidism in Humans
Open accessAbstract
Arterial hypertension is known to be frequently associated with thyroid dysfunction, with a particularly high prevalence in chronic hypothyroidism. However, to our knowledge no comprehensive study addressed causal mechanisms possibly involved in this association. We here report the physiological relationships between blood pressure and neuro-humoral modifications induced by acute hypothyroidism in normotensive subjects. Twelve normotensive patients with previous total thyroidectomy were studied. Ambulatory 24-h blood pressure monitoring was performed, and free T3, free T4, TSH, PRA, aldosterone, cortisol, adrenaline, and noradrenaline were assayed 6 wk after oral l-T4 withdrawal (phase 1) and 2 months after resumption of treatment (phase 2). During the hypothyroid state (TSH, 68.1 ± 27.7 μIU/ml; mean ± sd), daytime arterial systolic levels slightly, but significantly, increased (125.5 ± 9.7 vs. 120.4 ± 10.8 mm Hg; P < 0.05), and daytime diastolic levels (84.6 ± 7.9 vs. 76.4 ± 6.8 mm Hg; P < 0.001), noradrenaline (2954 ± 1578 vs. 1574 ± 962 pmol/liter; P < 0.001), and adrenaline (228.4 ± 160 vs. 111.3 ± 46.1 pmol/liter; P < 0.05) also increased. PRA remained unchanged (0.49 ± 0.37 vs. 0.35 ± 0.21 ng/ml·h; P = NS), whereas both aldosterone (310.3 ± 151 vs. 156.9 ± 67.5 pmol/liter; P < 0.005) and cortisol (409.2 ± 239 vs. 250.9 ± 113 pmol/liter; P < 0.02) significantly increased. By using univariate logistic regression daytime arterial diastolic values, noradrenaline and aldosterone were found to be significantly related to the hypothyroid state (P < 0.02, P < 0.036, and P < 0.024, respectively). In conclusion, our data show that thyroid hormones participate in the control of systemic arterial blood pressure homeostasis in normotensive subjects. The observed sympathetic and adrenal activation in hypothyroidism, which is reversible with thyroid hormone treatment, may also contribute to the development of arterial hypertension in human hypothyroidism.
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Written from the paper’s full text.
TL;DR
In 12 normotensive patients after total thyroidectomy, short-term L-T4 withdrawal-induced hypothyroidism raised daytime systolic and diastolic blood pressure and increased noradrenaline, adrenaline, aldosterone, and cortisol, while PRA did not change. These changes reversed with L-T4 replacement, suggesting thyroid hormone contributes to blood pressure homeostasis and that sympatho-adrenal activation may contribute to hypothyroid hypertension.
Key findings
- During hypothyroidism (TSH 68.1 ± 27.7 IU/ml), daytime systolic BP increased from 120.4 ± 10.8 to 125.5 ± 9.7 mm Hg (P < 0.05) and daytime diastolic BP increased from 76.4 ± 6.8 to 84.6 ± 7.9 mm Hg (P < 0.001); nighttime BP changes were not significant.
- Noradrenaline rose from 1574 ± 977 to 2954 ± 1578 pmol/liter (P = 0.001), adrenaline from 111.3 ± 46.1 to 228.6 ± 159.6 pmol/liter (P = 0.05), aldosterone from 156.8 ± 67.4 to 310.3 ± 151.3 pmol/liter (P < 0.005), and cortisol from 251.0 ± 113 to 409.11 ± 239 pmol/liter (P < 0.02).
- PRA remained unchanged (0.35 ± 0.21 vs. 0.49 ± 0.38 ng/ml·h; NS).
- In univariate logistic regression, daytime diastolic BP, noradrenaline, and aldosterone were significantly related to the hypothyroid state (P < 0.02, P < 0.036, and P < 0.024, respectively). The paper also reports that BP increased into the hypertensive range in one third of patients when hypothyroidism was induced.
Methods
- Twelve normotensive patients (9 women, 3 men; mean age 50.7 ± 8.4 yr) with previous total thyroidectomy and radioiodine ablation for stage I differentiated thyroid cancer were studied in two phases: 6 wk after L-T4 withdrawal (hypothyroid phase 1) and 2 months after resumption of oral L-T4 replacement (phase 2).
- At both time points, 24-h ambulatory BP monitoring was performed with a SPACE-LABS 90207 device, and plasma free T3, free T4, TSH, PRA, aldosterone, cortisol, adrenaline, and noradrenaline were assayed.
- Continuous variables were compared by paired t test or Wilcoxon test; relationships were assessed by linear regression and univariate logistic regression, with P < 0.05 considered significant.
Limitations
- Stated: the authors caution that results from this unique short-term human model may not transfer directly to long-term thyroid function abnormalities.
- Stated: changes in catecholamines, aldosterone, and cortisol are difficult to interpret per se because hypothyroidism may alter intravascular volume, hormone clearance, salt sensitivity, vasopressin, and atrial natriuretic peptide.
- Evident from the text: the sample is small (n = 12) and highly selected (normotensive patients with treated thyroid cancer and no other disease or pharmacological treatment), and the study lacks a separate control group, so generalizability is limited.
Model-written summary. Check it against the paper before relying on it.
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Claims the paper makes
8 of 29 cited sources checked · 2 supported · 0 flagged · accuracy not yet measured
The sources with a verdict support this claim; the rest weren’t checked yet, have no full text we could read, or their verdicts aren’t rated yet.
In the paper
“In the presence of a reduced PRA, ALDO secretion could be sustained by the pituitary hormone ACTH; according to this finding, recent studies have reported a reactive increase in ACTH secretion in response to adrenal cortex dysfunction induced by acute hypothyroidism in experimental animals (33,34).”
§ The Role of Thyroid Hormone in Blood Pressure Homeostasis: Evidence from Short-Term Hypothyroidism in Humans > Discussion
What the sources say
- Not checked — no full text of the sourcecites [33] Tohei, 1997, Adrenal and gonadal function in hypothyroid adult male rats., J Endocrinol source
- Supportedcites [34] Tohei, 1998, Hypersecretion of corticotrophin-releasing hormone and arginine vasopressin in hypothyroid male rats as estimated with push-pull perfusion., J Endocrinol source
The citation follows the sentence’s second clause, about increased ACTH in response to adrenal dysfunction in hypothyroid experimental animals. The Discussion reports lower adrenal weights and corticosterone, higher ACTH, and concludes that hypothyroidism causes adrenal dysfunction and ACTH hypersecretion in male rats after two weeks of thiouracil treatment. The preceding PRA/ALDO proposition is not the point attributed to this citation. (LLM, conf=0.91)
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesThe cited sources that could be checked couldn’t confirm or dispute this claim.
In the paper
“in the hyperthyroid state the increase in renin release secondary to the hormone-dependent decrease in systemic vascular resistance may stimulate the angiotensin-aldosterone axis and consequently sodium reabsorption (13)(14)(15)(16)(17)(18)(19)(20)(21)(22)(23).”
§ The Role of Thyroid Hormone in Blood Pressure Homeostasis: Evidence from Short-Term Hypothyroidism in Humans > Abstract
What the sources say
- Not checked — no full text of the sourcecites [13] Klein, 2001, Thyroid hormone and the cardiovascular system., N Engl J Med source
- Could not verifycites [14] Levey, 1971, Catecholamine sensitivity, thyroid hormone and the heart: a reevaluation., Am J Med sourceExperimental — accuracy not yet measured
The Physiologic and Pharmacologic Studies section describes hyperthyroidism’s hyperdynamic circulation and thyroid hormone’s effects on the heart, but does not address the proposed renal mechanism. Searches for renin release, systemic vascular resistance, aldosterone, and sodium reabsorption found no passage supporting that chain; page numbers were unavailable in our copy. (LLM, conf=0.76)
- Not checked — no full text of the sourcecites [15] Polikar, 1993, The thyroid and the heart: a reevaluation., Circulation source
Strength:hedged· not yet calibratedCausal:conditional· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes? Load-bearing: unclear✓ Based: passesThe cited sources support only part of this claim — read each source’s verdict below.
In the paper
“Sympatho-adrenal stimulation could thus contribute to sustain BP levels during acute hypothyroidism as a possible mechanism counteracting the decrease in myocardial inotropism and cardiac output (4,14,15).”
§ The Role of Thyroid Hormone in Blood Pressure Homeostasis: Evidence from Short-Term Hypothyroidism in Humans > Discussion
What the sources say
- Not checked — no full text of the sourcecites [4] Klein, 1990, Thyroid hormone and the cardiovascular system., Am J Med source
- Partly supportedcites [14] Levey, 1971, Catecholamine sensitivity, thyroid hormone and the heart: a reevaluation., Am J Med sourceExperimental — accuracy not yet measured
The Physiologic and Pharmacologic Studies section (page unavailable) reports reduced intrinsic contractility in hypothyroid cat heart muscle but unaltered responsiveness to catecholamines and sympathetic nerve stimulation. This supports the possibility of an adrenergic response despite reduced contractility, but the paper does not say that sympatho-adrenal stimulation sustains blood pressure or offsets reduced cardiac output during acute hypothyroidism. (LLM, conf=0.84)
- Not checked — no full text of the sourcecites [15] Polikar, 1993, The thyroid and the heart: a reevaluation., Circulation source
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesThe cited sources support only part of this claim — read each source’s verdict below.
In the paper
“Observational studies in the literature have pointed out a high prevalence of hypertension, particularly in chronic hypothyroidism (1)(2)(3)(4)(5)”
§ The Role of Thyroid Hormone in Blood Pressure Homeostasis: Evidence from Short-Term Hypothyroidism in Humans > Abstract
What the sources say
- Not checked — no full text of the sourcecites [1] Endo, 1979, Re-evaluation of a possible high incidence of hypertension in hypothyroid patients., Am Heart J source
- Partly supportedcites [2] Saito, 1983, Hypothyroidism as a cause of hypertension., Hypertension sourceExperimental — accuracy not yet measured
The Summary (pp. 112–115) reports a higher prevalence of hypertension in hypothyroid than euthyroid patients with chronic thyroiditis (14.8% versus 5.5%). The Discussion emphasizes the finding in patients over 50, but the paper does not establish that hypertension is particularly prevalent in chronic, as opposed to other, hypothyroidism. (LLM, conf=0.82)
- Not checked yetcites [3] Klein, 1989, Thyroid hormone and high blood pressure. In: Laragh JH, Brenner BM, Kaplan NM, eds. Endocrine mechanisms in hypertension., New York: Raven Press; vol
Strength:plain· not yet calibratedCausal:correlational· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes? Load-bearing: unclear✓ Based: passesThe cited sources support only part of this claim — read each source’s verdict below.
In the paper
“In animal models T 3 has a positive direct inotropic effect by inducing a predominant synthesis of fast ␣-isoforms of heavy myosin chains and by increasing calcium-adenosine triphosphatase and cAMP levels, together with the number and sensitivity of -adrenergic receptors (6 -10).”
§ The Role of Thyroid Hormone in Blood Pressure Homeostasis: Evidence from Short-Term Hypothyroidism in Humans > Abstract
What the sources say
- Not checked — no full text of the sourcecites [6] Dilmann, 1990, Biochemical basis of thyroid hormone action in the heart., Am J Med source
- Partly supportedcites [7] Morkin, 1993, Regulation of myosin heavy chain genes in the heart., Circulation sourceExperimental — accuracy not yet measured
In Regulatory Factors (page not provided), the paper describes an inotropic action of thyroid hormone, T3 stimulation of calcium uptake, and thyroid-hormone-induced fast myosin isoforms in rabbits and rats. It also says an isoform switch is unlikely to be the major mechanism of that inotropic action. The cited passages do not establish the claimed increases in cAMP or in the number and sensitivity of β-adrenergic receptors. (LLM, conf=0.88)
- Supportedcites [8] Kiss, 1994, Thyroid hormone-induced alterations in phospholamban protein expression. Regulatory effects on sarcoplasmic reticulum Ca2+ transport and myocardial relaxation., Circ Res source
The Animals section reports T3 treatment of rats. In the left-ventricular-function Results (page not available), basal contractility (+dP/dt) was significantly higher in isolated, perfused hearts from hyperthyroid rats than in hearts from euthyroid rats, supporting a positive inotropic effect in this animal model. (LLM, conf=0.88)
Strength:plain· not yet calibratedCausal:direct· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes? Load-bearing: unclear✓ Based: passesA result the paper reports from its own data — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“daytime arterial systolic levels slightly, but significantly, increased (125.5 ؎ 9.7 vs. 120.4؎ 10.8 mm Hg; P < 0.05)”
- Also stated in: § BP · plain
“A significant decrement was observed in daytime SBP (P Ͻ 0.05)”
§ The Role of Thyroid Hormone in Blood Pressure Homeostasis: Evidence from Short-Term Hypothyroidism in Humans > Abstract
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passes- Also stated in: § BP · plain
A result the paper reports from its own data — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“noradrenaline (2954 ؎ 1578 vs. 1574 ؎ 962 pmol/liter;”
§ The Role of Thyroid Hormone in Blood Pressure Homeostasis: Evidence from Short-Term Hypothyroidism in Humans > Abstract
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesA result the paper reports from its own data — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“After l-T 4 treatment, BP was in the normotensive range, except for one subject with 146 mm Hg systolic levels.”
§ The Role of Thyroid Hormone in Blood Pressure Homeostasis: Evidence from Short-Term Hypothyroidism in Humans > BP
Load-bearingStrength:plain· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesA result the paper reports from its own data — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“cortisol (409.2 ؎ 239 vs. 250.9؎ 113 pmol/liter; P < 0.02) significantly increased.”
§ The Role of Thyroid Hormone in Blood Pressure Homeostasis: Evidence from Short-Term Hypothyroidism in Humans > Discussion
Strength:plain· not yet calibratedCausal:direct· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes? Load-bearing: unclear✓ Based: passesA result the paper reports from its own data — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“PRA remained unchanged (0.49 ؎ 0.37 vs. 0.35 ؎ 0.21 ng/ml⅐h; P ؍ NS)”
§ The Role of Thyroid Hormone in Blood Pressure Homeostasis: Evidence from Short-Term Hypothyroidism in Humans > Discussion
Strength:plain· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes? Load-bearing: unclear✓ Based: passes
- Probably not a substantial claim. 3
- It may state two separate claims as one. 7
- The quote only partly states this claim. 1
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“the consistent prevalence (3-4%) of hypothyroidism in the general nonselected hypertensive population (1,2,36)”
§ The Role of Thyroid Hormone in Blood Pressure Homeostasis: Evidence from Short-Term Hypothyroidism in Humans > Discussion
What the sources say
- Not checked — no full text of the sourcecites [1] Endo, 1979, Re-evaluation of a possible high incidence of hypertension in hypothyroid patients., Am Heart J source
- Could not verifycites [2] Saito, 1983, Hypothyroidism as a cause of hypertension., Hypertension sourceExperimental — accuracy not yet measured
The Patient Population section describes women with chronic thyroiditis, not a general nonselected hypertensive population. The Age-Matched Comparisons section reports the prevalence of hypertension among hypothyroid patients (14.8%), which reverses the direction of the claimed prevalence. A search for the 3–4% estimate and for unselected hypertensive patients found neither in our copy. (LLM, conf=0.78)
- Partly supportedcites [36] Streeten, Hypertension sourceExperimental — accuracy not yet measured
The Results report hypothyroidism in 25 of 688 hypertensive patients (3.6%), supporting the 3–4% figure for this study's patients. But these were patients referred for hypertension evaluation, and the authors explicitly say their prevalence cannot be taken to represent the entire hypertensive population. The claim's extension to a general, nonselected population is therefore unsupported. (LLM, conf=0.90)
Strength:boosted· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes✗ Load-bearing: fails✓ Based: passesProbably not a substantial claim. The paper’s conclusions may not depend on it.
A result the paper reports from its own data — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“In the hypothyroid state mean 24 h systolic BP (SBP) was less than 140 mm Hg in all patients; in four cases the mean diastolic BP (DBP) was 90 mm Hg or higher (see Fig. 2).”
§ The Role of Thyroid Hormone in Blood Pressure Homeostasis: Evidence from Short-Term Hypothyroidism in Humans > BP
Strength:plain· not yet calibratedn = 4Tests✓ Asserted: passes✓ Checkable: passes? Load-bearing: unclear✓ Based: passesIt may state two separate claims as one.
A result the paper reports from its own data — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“Nighttime systolic BP was inversely related to morning CORT levels as well as DBP.”
§ The Role of Thyroid Hormone in Blood Pressure Homeostasis: Evidence from Short-Term Hypothyroidism in Humans > Linear regression analysis (Table 2)
Strength:plain· not yet calibratedCausal:correlational· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes? Load-bearing: unclear✓ Based: passesIt may state two separate claims as one.
A result the paper reports from its own data — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“During hypothyroidism, PRA was at the lower normal limit in nine patients and was almost suppressed in the remaining three (Ͻ0.20 ng/ml⅐h).”
§ The Role of Thyroid Hormone in Blood Pressure Homeostasis: Evidence from Short-Term Hypothyroidism in Humans > Adreno-cortical steroids and PRA
Strength:plain· not yet calibratedn = 9Tests✓ Asserted: passes✓ Checkable: passes? Load-bearing: unclear✓ Based: passesIt may state two separate claims as one.
A result the paper reports from its own data — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“During hypothyroidism, fT 3 and TSH correlated with NA levels; the regressions was negative for fT 3 and positive for TSH, respectively.”
§ The Role of Thyroid Hormone in Blood Pressure Homeostasis: Evidence from Short-Term Hypothyroidism in Humans > Linear regression analysis (Table 2)
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIt may state two separate claims as one.
In the paper
“To improve the reliability of measurements and to reduce the effects of interassay variability, we assayed each serum sample on several occasions in the same experiment and in different sessions (at least three times) (24).”
§ The Role of Thyroid Hormone in Blood Pressure Homeostasis: Evidence from Short-Term Hypothyroidism in Humans > Materials and Methods
What the sources say
- Not checked — no full text of the sourcecites [24] Iervasi, 1996, Normalization of peripheral thyroid hormone metabolism induced by successful chronic amiodarone treatment in patients with ventricular arrhythmias., Eur J Clin Invest source
Strength:plain· not yet calibratedCausal:direct· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes✗ Load-bearing: fails✓ Based: passesProbably not a substantial claim. The paper’s conclusions may not depend on it.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“our data indicate that thyroid hormone deprivation promotes an increase in BP as well as activation of the sympathetic/adrenal systems.”
§ The Role of Thyroid Hormone in Blood Pressure Homeostasis: Evidence from Short-Term Hypothyroidism in Humans > Discussion
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIt may state two separate claims as one.
- Rests on an assumption: The short-term hypothyroid state induced by 6-week L-T4 withdrawal is a valid model for studying the physiological role of thyroid hormone in BP homeostasis.
In the paper
“that of renovascular hypertension (ϳ1%), one of the most investigated forms of secondary hypertension (37).”
§ The Role of Thyroid Hormone in Blood Pressure Homeostasis: Evidence from Short-Term Hypothyroidism in Humans > Discussion
What the sources say
- Not checked yetcites [37] Kaplan, 1998, Renal vascular hypertension, In: Pine Jr JW, ed. Clinical hypertension. Baltimore: Williams & Wilkins;
Strength:plain· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes✗ Load-bearing: fails✓ Based: passesProbably not a substantial claim. The paper’s conclusions may not depend on it.
What the paper did — it cites no source for this, so there is none to check. The quote shows it is in the paper.
In the paper
“For this reason we selected a group of normotensive patients, all of them free from any pharmacological treatment.”
§ The Role of Thyroid Hormone in Blood Pressure Homeostasis: Evidence from Short-Term Hypothyroidism in Humans > Discussion
Load-bearingStrength:plain· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIt may state two separate claims as one. The quote only partly states this claim.
A claim is checked only against the cited paper’s full text, never its abstract, and none is available for its sources.
In the paper
“thyroid hormone can increase angiotensinogen (16) and atrial natriuretic peptide levels (17,18) and respectively decrease vasopressin levels (19,20).”
§ The Role of Thyroid Hormone in Blood Pressure Homeostasis: Evidence from Short-Term Hypothyroidism in Humans > Abstract
What the sources say
- Not checked — no full text of the sourcecites [16] Dzau, 1982, Hormonal control of angiotensinogen production., Life Sci source
- Not checked — no full text of the sourcecites [17] Zamir, 1993, Thyroid hormone restores atrial stretch-induced secretion of atrial natriuretic peptide in hypophysectomized rats., Horm Metab Res source
- Not checked — no full text of the sourcecites [18] Sergev, 1990, Thyrotropin-releasing hormone increases plasma atrial natriuretic peptide levels in humans., J Endocrinol Invest source
Strength:plain· not yet calibratedCausal:direct· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes? Load-bearing: unclear✓ Based: passesIt may state two separate claims as one.
The paper relies on this without support.
There are no prior studies on normotensive subjects showing the effect of short-term thyroid hormone variation on both blood pressure and its regulatory mechanisms.
“To our knowledge, there are no studies carried out on normotensive subjects showing the effect of a short-term variation in thyroid hormone levels on both blood pressure and some of its important regulatory mechanisms represented by renin, sympathetic, and adrenal systems.”
The paper relies on this without support.
The short-term hypothyroid state induced by 6-week L-T4 withdrawal is a valid model for studying the physiological role of thyroid hormone in BP homeostasis.
“We addressed this issue by the use of a unique clinical model encompassing a short-term variation from a state of acute hypothyroidism to one of restoration of normal thyroid function in normotensive patients.”
Self-check
Percentages, sums and reported differences re-computed from the paper’s own numbers.
Each contradiction between two passages listed here was confirmed by an independent check.
Several abstract hormone values differ from Table 1
MinorThe abstract and Table 1 give different values for the hypothyroid-state adrenaline mean (228.4 versus 228.6), hypothyroid-state PRA SD (0.37 versus 0.38), and treated-state aldosterone mean (156.9 versus 156.8). These differences are not attributable to rounding the tabulated values to the abstract's printed precision.
“adrenaline (228.4 ؎ 160 vs. 111.3؎ 46.1 pmol/ liter; P < 0.05) also increased.PRA remained unchanged (0.49 ؎ 0.37 vs. 0.35 ؎ 0.21 ng/ml⅐h; P ؍ NS), whereas both aldosterone (310.3 ؎ 151 vs. 156.9؎ 67.5 pmol/liter; P < 0.005)”
“| Adrenaline (pmol/liter) | 228.6 Ϯ 159.6 | 111.3 Ϯ 46.1 | 0.05 | | PRA (ng/ml⅐h) | 0.49 Ϯ 0.38 | 0.35 Ϯ 0.21 | NS | | Aldosterone (pmol/liter) | 310.3 Ϯ 151.3 | 156.8 Ϯ 67.4 | Ͻ0.005 |”
Noradrenaline SD differs between abstract and Table 1
MinorThe abstract gives the treated-state noradrenaline SD as 962 pmol/liter, whereas Table 1 gives 977 pmol/liter for the same mean.
“noradrenaline (2954 ؎ 1578 vs. 1574 ؎ 962 pmol/liter;”
“| Noradrenaline (pmol/liter) | 2954 Ϯ 1578 | 1574 Ϯ 977 | 0.001 |”
Daytime DBP logistic-regression P value differs from Table 3
MinorThe abstract reports P < 0.02 for daytime diastolic blood pressure, but Table 3 gives P = 0.0287. Both values indicate significance at 0.05, but the tabulated value does not meet the abstract's stated threshold.
“daytime arterial diastolic values, noradrenaline and aldosterone were found to be significantly related to the hypothyroid state (P < 0.02, P < 0.036, and P < 0.024, respectively).”
“| Daytime DBP | 0.152 | 1.0160 -1.3341 | 0.0287 | 0.2894 |”
Citations
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Metadata
- Authors
- Fommei, E., & Iervasi, G.
- Affiliations
- University of Pisa (IT)
- Venue
- The Journal of Clinical Endocrinology & Metabolism
- Publisher
- The Endocrine Society
- Published
- 2002-05-01
- Volume
- 87
- Issue
- 5
- Pages
- 1996-2000
- ISSN
- 0021-972X (ISSN-L)
- 1945-7197
- OpenAlex
- W2050166046
- Cited by
- 172
- References
- 37
- Citations by year
- 2026: 1 · 2025: 4 · 2024: 6 · 2023: 5 · 2022: 6 · 2021: 4 · 2020: 6 · 2019: 5 · 2018: 8 · 2017: 8 · 2016: 9 · 2015: 16 · 2014: 11 · 2013: 9 · 2012: 7
- FWCI
- 3.26
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- The Journal of Clinical Endocrinology & Metabolism (publishedVersion)
- PubMed (publishedVersion)
- CINECA IRIS Institutial research information system (University of Pisa) (submittedVersion)
- Topics
- Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Thyroid Disorders and Treatments
- Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Blood Pressure and Hypertension Studies
- Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Hormonal Regulation and Hypertension
- Keywords
- thyroid hormones, hypothyroidism, blood pressure, hypertension, thyroidectomy, levothyroxine withdrawal, norepinephrine, epinephrine, aldosterone, cortisol, renin-angiotensin system, sympathetic nervous system, thyroid-stimulating hormone, ambulatory blood pressure monitoring, normotensive subjects, diastolic blood pressure
- MeSH terms
- Adrenal Glands, Adult, Aged, Aldosterone, Blood Pressure, Combined Modality Therapy, Cortisone, Female, Homeostasis, Humans, Hypothyroidism, Male, Middle Aged, Regression Analysis, Renin, Sympathetic Nervous System, Thyroid Hormones, Thyroid Neoplasms, Thyroidectomy
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
A language model drew the claims from the paper on 2026-10-28, under version 3 of the claim definition (model deepseek-v4.1-flash, prompt extract-v3).
A second model labelled each claim on 2026-10-28 (model jev-1.13-20260917, definition revision gold-guideline-v0.2).
Cited sources are checked with a language model’s help (gpt-6-sol).
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
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