Suppression of TSH in Congenital Hypothyroidism Is Significantly Related to Serum Levels and Dosage of Thyroxine

Brown, Justin; Datta, Vipan; Sutton, Alex J.; Swift, Peter

doi:10.1159/000068576

Cited by 6 publications

(8 citation statements)

References 33 publications

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“…Some authors draw blood every 4 to 5 days during the first few weeks of treatment, 30 whereas others sample much less frequently. 31 The schedule recommended by the American Academy of Pediatrics has been evaluated in one study of children treated with 6.6 to 10 lg/kg per day, which did not include IQ as the outcome. 32 We follow the recommendation of Fisher and Foley 9 and wait until at least 4 half-lives of thyroxine have elapsed before taking the first sample on treatment, and then follow the schedule outlined above.…”

Section: Discussionmentioning

confidence: 99%

Cognition and behavior at school entry in children with congenital hypothyroidism treated early with high-dose levothyroxine

Simoneau-Roy¹,

Marti²,

Deal³

et al. 2004

The Journal of Pediatrics

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Section: Discussionmentioning

confidence: 99%

Cognition and behavior at school entry in children with congenital hypothyroidism treated early with high-dose levothyroxine

Simoneau-Roy¹,

Marti²,

Deal³

et al. 2004

The Journal of Pediatrics

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“…A recent smaller study by Brown et al [11] found that delayed TSH suppression was significantly related to plasma T4 levels and dosage of L-T4, suggesting that it may be due to undertreatment. The authors recommended an initial starting dose of 50 µg/day of L-T4 for early TSH suppression.…”

Section: Discussionmentioning

confidence: 99%

“…Recent studies including a randomised trial have recommended a higher initial dose of L-T4 to achieve more rapid TSH suppression [11, 24]. However, some authors have reported persistently raised TSH in infants in whom adequate L-T4 was given and whose plasma T4 levels were in the upper range of normal [8, 25, 26].…”

Section: Discussionmentioning

confidence: 99%

“…The intra-assay coefficient of variation for plasma TSH was 1.3% at 17.6 mU/l and 4.6% at 0.045 mU/l. Adequate TSH suppression was defined as plasma TSH concentration <6 mU/l [11, 19]. The normal reference range from our laboratory for total T4 is 138–282 nmol/l from 2 to 10 days and 92–187 nmol/l from 11 to 45 days.…”

Section: Methodsmentioning

confidence: 99%

“…Possible explanations of persistently raised TSH include undertreatment or intermittent compliance [6, 8, 11]. Others propose that there may be a variation in the maturation of the pituitary threshold for regulation of TSH mediated through thyroid hormone levels [11,12,13].…”

Section: Introductionmentioning

confidence: 99%

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Multivariate Analysis on Factors Affecting Suppression of Thyroid-Stimulating Hormone in Treated Congenital Hypothyroidism

Ng¹,

Wong²,

Isherwood³

et al. 2004

Horm Res Paediatr

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Aims: To determine the factors which influence the suppression of thyroid-stimulating hormone (TSH) in infants with congenital hypothyroidism (CH) following treatment. Methods: We examined retrospectively the patterns of thyroid function tests from diagnosis to 3 years of age in 140 infants diagnosed with CH from screening. Patients were classified into 3 groups: athyreosis, ectopia and presumed dyshormonogenesis on the basis of thyroid scans. Adequate TSH suppression was defined as plasma TSH concentration <6 mU/l. The factors affecting the suppression of TSH at 6 months and 1 year of age which were evaluated were: initial confirmatory plasma TSH, initial plasma thyroxine (T4), mean age of starting treatment with L-T4, dose of L-T4 at diagnosis, 6 weeks, 3 months and 6 months, and aetiology of the congenital hypothyroidism. Variables were then entered in a stepwise logistic regression model for TSH suppression at 6 months and 1 year of age. Results: All infants had radionuclide scans prior to treatment: athyreosis (n = 39), ectopia (n = 78) and dyshormonogenesis (n = 23). 58% of patients had persistently raised TSH at 6 months of age while 31% of patients had a persistently raised TSH at 1 year of age. There was a significant delay in the normalisation of plasma TSH in athyreosis and ectopia groups compared with dyshormonogenesis. Multiple regression analysis for TSH suppression at 6 months of age found plasma T4 levels and aetiology of CH as independent factors affecting the timing of TSH suppression. Aetiology of CH was the only independent factor affecting TSH suppression at 1 year of age. Conclusion: At 6 months of age, plasma T4 levels at 6 weeks and 3 months, and aetiology of CH were independent factors affecting timing of TSH suppression. However, by 1 year of age, the aetiology of CH was the only independent factor affecting suppression of TSH.

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Mineralocorticoid Receptor-Associated Hypertension and Its Organ Damage: Clinical Relevance for Resistant Hypertension

Shibata

Itoh

2012

American Journal of Hypertension

109

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The role of aldosterone in the pathogenesis of hypertension and cardiovascular diseases has been clearly shown in congestive heart failure and endocrine hypertension due to primary aldosteronism. In resistant hypertension, defined as a failure of concomitant use of three or more different classes of antihypertensive agents to control blood pressure (BP), add-on therapy with mineralocorticoid receptor (MR) antagonists is frequently effective, which we designate as "MR-associated hypertension". The MR-associated hypertension is classified into two subtypes, that with elevated plasma aldosterone levels and that with normal plasma aldosterone levels. The former subtype includes primary aldosteronism (PA), aldosterone-associated hypertension which exhibited elevated aldosterone-to-renin ratio and plasma aldosterone levels, but no PA, aldosterone breakthrough phenomenon elicited when angiotensin-converting enzyme inhibitor (ACE-I) or angiotensin II receptor blocker (ARB) is continued to be given, and obstructive sleep apnea. In contrast, the latter subtype includes obesity, diabetes mellitus, chronic kidney disease (CKD), and polycystic ovary syndrome (PCOS). The pathogenesis of MR-associated hypertension with normal plasma aldosterone levels is considered to be mediated by MR activation by pathways other than high aldosterone levels, such as increased MR levels, increased MR sensitivity, and MR overstimulation by other factors such as Rac1. For resistant hypertension with high plasma aldosterone levels, MR antagonist should be given as a first-line therapy, whereas for resistant hypertension with normal aldosterone levels, ARB or ACE-I should be given as a first-line therapy and MR antagonist would be given as an add-on agent.

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Suppression of TSH in Congenital Hypothyroidism Is Significantly Related to Serum Levels and Dosage of Thyroxine

Cited by 6 publications

References 33 publications

Cognition and behavior at school entry in children with congenital hypothyroidism treated early with high-dose levothyroxine

Cognition and behavior at school entry in children with congenital hypothyroidism treated early with high-dose levothyroxine

Multivariate Analysis on Factors Affecting Suppression of Thyroid-Stimulating Hormone in Treated Congenital Hypothyroidism

Mineralocorticoid Receptor-Associated Hypertension and Its Organ Damage: Clinical Relevance for Resistant Hypertension

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