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PubMed1993

Free thyroxine measured in undiluted serum by dialysis and ultrafiltration: effects of non-thyroidal illness, and an acute load of salicylate or heparin.

In vitro dilution of serum during processing of a free T4 assay explains to some extent the divergent results obtained in non-thyroidal illness. If serum from such patients contains low affinity T4 protein binding inhibitors, as has been suggested, in vitro dilution will result in spuriously reduced serum free T4 measurements. If these inhibitors cross the dialysis membrane in an equilibrium dialysis assay, their inhibitory effect will be weakened, and in vitro free T4 levels will decrease, even in undiluted serum. In contrast, ultrafiltration methods on undiluted serum seem accurate. We have compared a new, commercially available dialysis technique with an in-house ultrafiltration method for free T4 measurements in undiluted serum. Control subjects (n = 41) had 14% higher free T4 (P < 0.02) by ultrafiltration. Non-thyroidally ill patients not receiving glucocorticoids or dopamine (n = 54) had unaltered free T4 levels, 28.4 +/- 10.3 pmol/l (dialysis) and 31.0 +/- 10.3 pmol/l (ultrafiltration). Dopamine infusion in somatic ill patients (n = 11) resulted in reduced free T4 in both assays but only significantly for dialysis, and subjects with familial dysalbuminemic hyperthyroxinemia (n = 8) had unaltered free T4 levels in both assays. Salicylate (1.5 g) given orally 09:00 h. (n = 5) resulted within 30 min, in increased (P < 0.01) free T4 as measured by both techniques, although more pronounced and sustained as measured by ultrafiltration. Serum TSH decreased concomitantly (P < 0.01). These findings were confirmed when salicylate was administered at 13:00 h. (n = 8). The dialysis procedure resulted in a decrease in serum salicylate of 14% (P < 0.001).(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1991

Somatostatin increases plasma T3 concentrations in Tilapia nilotica in the presence of increased plasma T4 levels.

An injection of ovine growth hormone, porcine follicle stimulating hormone, and bovine thyrotropin stimulating hormone increased in Tilapia nilotica plasma concentrations of thyroxine (T4) and reverse triiodothyronine (rT3) after 4 and 8 hr, whereas plasma concentrations of T3 were unaffected. An injection of somatostatin (SRIF) alone did not influence thyroid hormone levels. If, however, SRIF was injected together with these hormones, which raised plasma T4, or together with T4 itself, an increase in plasma concentrations of T3 could be observed, whereas the increase in rT3 was less pronounced. It is concluded that SRIF may change the normal 5-deiodinase (5-D) activity and increased rT3 during hyperthyroxinemia into a 5'-D activity and a rise in T3, respectively, in T. nilotica.

Animals↗
PubMed1990

Review: thyroid function in psychiatric illness.

The development of highly sensitive immunometric assays for thyroid-stimulating hormone (TSH) has provided increased understanding of thyroid hormone regulation but, paradoxically, has contributed to a kaleidoscopic complexity of thyroid function test variability in hospitalized patients with nonthyroidal illness (NTI). In primary hypothyroidism, an elevated TSH is the most sensitive chemical index available, although early cases may show a hyperresponse of TSH to thyrotropin-releasing hormone (TRH) stimulation when the TSH is still within the normal range. The ability of the new TSH assays to discriminate between normal and low levels now allows the diagnosis of thyrotoxicosis to be confirmed by a suppressed TSH in the presence of elevated serum thyroxine (T4) and/or triiodothyronine (T3). The TRH stimulation test is virtually obsolete for the diagnosis of thyrotoxicosis but remains of much interest in the investigation of psychiatric syndromes. Approximately 25% of patients with depression have a blunted TSH response (a rise of less than 5 microU/mL) that differs from thyrotoxicosis, wherein the TSH response is suppressed under 1 microU/mL. The cause of the blunted TSH is uncertain but is not due to hyperthyroidism. In contrast, close to 15% may have a TSH hyperresponse to TRH and/or elevated antithyroid antibodies. Thyroid hormone treatment may benefit the depression in some of these cases. In the sick thyroid state of nonthyroidal illness, a low T3 level is the initial manifestation. In more severe cases, the T4 also falls, the free T4 level in this situation is variable, both normal and low levels being reported from different laboratories. A diagnosis of hypothyroidism requiring treatment with thyroid hormone therapy is unlikely unless there is a concomitant lowfree T4 and elevated TSH in a patient who is not in the process of recovery. In acute psychiatric admissions, there is a high frequency of hyperthyroxinemia. The TSH in these cases is generally either normal or high, suggesting central activation of the hypothalamic-pituitary-thyroid axis. In most instances, the thyroid function tests normalize within 2 weeks, and treatment directed toward the thyroid gland is not indicated. Suppressed TSH levels, usually associated with a normal free T4, has also been described in such patients. Finally, various medications utilized in psychiatric practice have diverse effects on thyroid function and can cause diagnostic difficulty. These include lithium, phenytoin sodium, and carbamazepine, and their effects are reviewed.

Diagnosis, Differential↗
PubMed2005

Hyperthyroidism after parathyroid exploration.

BACKGROUND: We hypothesized that hyperthyroidism after parathyroid exploration may be an underreported phenomenon with a course more severe than recognized previously. METHODS: We examined pre- and postoperative thyroid function and outcomes in 199 consecutive patients who, since March 2000, had parathyroid exploration for primary sporadic hyperparathyroidism (HPTH). We excluded patients with prior thyroid or parathyroid surgery, preoperative thyroid medication, concurrent total thyroidectomy, or follow-up <5 months. RESULTS: Of 125 patients with normal preoperative serum thyroid-stimulating hormone levels, 39 (31.2%) were hyperthyroid postoperatively. Mean thyroid-stimulating hormone levels (mean +/- SD) dropped with operation from 2.0 +/- 1.1 microIU/mL to 1.2 +/- 1.4 microIU/mL (P < .0001). Nineteen patients (15%) reported symptoms 1 to 2 weeks after operation. The clinical course of hyperthyroidism typically was short, but 5 patients (4%) had symptomatic hyperthyroxinemia requiring medical therapy. Hyperthyroidism was independent of age, severity of HPTH, anatomic/pathologic features, operative time, and other measures of operative difficulty, but was associated with lithium therapy, bilateral exploration, and absence of concurrent thyroid lobectomy. CONCLUSIONS: Risk of hyperthyroidism may be underappreciated after routine parathyroid surgery for HPTH. Use of lithium and degree of dissection appear contributory. Patients undergoing parathyroid exploration need counseling and surveillance for hyperthyroidism, which may be reduced by minimizing the extent of parathyroid surgery.

Adolescent↗
PubMed1992

Acute thyroid dysfunction (thyroiditis) after therapy with interleukin-2.

Interleukin-2 (IL-2) is frequently incorporated in antineoplastic therapy: While the effect of interferon on the thyroid has been extensively studied the impact of other cytokines on thyroid function is less well understood. We monitored the thyroid function in six patients who received IL-2 in combination with tumor necrosis factor-alpha (TNF) or alpha-Interferon (alpha IFN). Hyperthyroxinemia with suppressed TSH developed within the first four weeks of IL-2 administration; during this phase, there was no technetium or iodine uptake by the thyroid gland. During the following few weeks, serum thyroxine decreased and serum TSH rose, consistent with the development of primary hypothyroidism; during this phase, thyroidal isotope incorporation was normal. All hypothyroid patients received thyroxine replacement therapy upon documentation of hypothyroidism; in several cases thyroxine was successfully discontinued after 2-3 months. None of the patients had detectable antithyroidal antibodies and none experienced thyroid-related pain, although two patients developed thyroid enlargement. We conclude that IL-2 administration is associated with the development of transient, subacute, painless thyroiditis. The frequency and severity of this complication requires further elucidation through systematic, prospective study.

Adult↗
PubMed1985

Prenatal exposure of the fetal rat to excessive L-thyroxine or 3,5-dimethyl-3'-isopropyl-thyronine produces persistent changes in the thyroid control system.

Studies were conducted to determine if brief exposure, in utero, to high levels of T4 or to the synthetic thyromimetic agent 3,5-dimethyl-3'-isopropyl-L-thyronine (DIMIT) can produce permanent disruption of the thyroid control system in a manner analogous to the changes in the "set point" reported to occur due to neonatal T4 exposure in the "neo-T4 syndrome". If such a change were to occur, it could explain the persistent thyroid disturbances seen in the progeny of hypothyroid mother rats. These latter progeny are exposed in utero to both low and high serum T4 levels. Maternal T4 treatment produced a 4-fold elevation in fetal serum T4 accompanied by a large decrease in serum TSH levels. The brief treatment in utero with high doses of T4 or of DIMIT resulted in higher neonatal mortality and the T4-treatment produce subsequent growth stunting. These treatments resulted in suppression of the fetal/neonatal thyroid which was very apparent at 5 days of age. At 30 days post-partum, the thyroid control system of the progeny of the T4 and DIMIT-treated animals was still abnormal with low serum T4 levels accompanied with normal serum TSH and T3 levels. At 60 days of age, serum T4 levels remained low in the progeny of the T4-treated animals and the TSH response to TRH was subnormal in both the progeny of the T4-treated and the DIMIT-treated animals. However, serum and pituitary TSH and serum T3 were normal. The thyroid control system of the rat is sensitive to prenatal exposure to hyperthyroxinemia as it is to postnatal exposure.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1990

Thyroid hormone elevations during acute psychiatric illness: relationship to severity and distinction from hyperthyroidism.

Acute psychiatric illness may be accompanied by transient hyperthyroxinemia. The mechanism of this phenomenon was examined by determining the role of thyrotropin (TSH) in the genesis of this state. Serial measurements of TSH, thyroxine (T4), free T4 index (FT4I), triiodothyronine (T3), and free T3 index (FT3I) were performed in 45 acutely hospitalized patients with major psychiatric disorders. Twenty-two (49%) patients exhibited significant elevations (greater than or equal to 2 SD above mean value of controls) of one or more thyroid hormone (or index) levels. Among depressed patients with elevated FT4I, TSH was higher (p less than .05) on the day of the peak FT4I than on the day of the FT4I nadir. There were significant positive correlations between psychiatric symptom severity and levels of FT4I among both depressed (p less than .01) and schizophrenic (p less than .025) patients. These data show that elevations of T4, FT4I, T3, and FT3I are common among psychiatric inpatients, especially early in their hospitalization, and that levels of thyroid hormones are correlated with severity of psychiatric symptomatology. TSH is higher early in the acute phase of illness and is not suppressed in the face of elevated thyroid hormone levels, a finding that distinguishes this phenomenon from ordinary hyperthyroidism. Elevations of peripheral thyroid hormone levels, particularly among depressed patients, may result from a centrally-mediated hypersecretion of TSH.

Adult↗
PubMed1994

T lymphocyte activation in Graves' disease.

We examined the proliferative response of T lymphocytes from thirty-eight patients with Graves' disease (17 untreated thyrotoxic and 30 euthyroid on antithyroid medication) to phytohemagglutinin, anti-CD3 MoAb and phorbol esters, as well as the capacities of these lymphocytes to produce interleukin 2 and the density of interleukin 2 receptors and major histocompatibility class II antigens. We found that the response of T lymphocytes to phytohemagglutinin, anti-CD3 monoclonal antibody and phorbol esters from untreated thyrotoxic Graves' disease was significantly enhanced as compared to treated patients and normal controls. Interleukin 2 production by mitogen-triggered T lymphocytes in both treated and untreated patients with Graves' disease was comparable to that of the control population. Interleukin 2 receptor density was found to be normal, whereas that of human leukocyte antigen-DR was increased in both untreated and treated patients. Following lymphocyte stimulation, there was an increase in human leukocyte antigen-DR and interleukin 2 receptor expression in patients with untreated Graves' disease. Significant correlations were found between thyroid hormone concentration and the proliferative responses to the polyclonal mitogen phytohemagglutinin, anti-CD3 monoclonal antibody and phorbol esters in untreated Graves' patients. Furthermore, during the follow-up of 9 patients, attainment of normal thyroid function after antithyroid treatment was associated with a decrease in and normalization of T-proliferative responses. Our data reveal that active Graves' disease is associated with T cell activation and this is probably related to immunological dysregulation as well as to hyperthyroxinemia.

Antibodies, Monoclonal↗
PubMed1991

Susceptibility to subacute thyroiditis is genetically influenced: familial occurrence in identical twins.

Subacute thyroiditis is thought to be virally induced in genetically predisposed individuals because a strong association has been suggested recently between HLA-B35 and patients in whom subacute thyroiditis has developed. Two identical twin brothers were seen at our clinic with the same symptoms and date of onset of hyperthyroidism and enlargement and tenderness of the thyroid, which gave us a unique opportunity to study the genetic predisposition and treatment of this thyroid disease. Diagnostic criteria for subacute thyroiditis were met in both twins, including hyperthyroxinemia, suppression of thyroidal 123I uptake, increased erythrocyte sedimentation rate, transient painful goiter, and absence of antimicrosomal antibodies. Twin B was treated with corticosteroids, and a nonsteroidal anti-inflammatory agent was prescribed for Twin A. The mode of treatment used did not make a difference in affecting the course of the disease. The erythrocyte sedimentation rate was normal after 2 months from onset of symptoms. Results of viral studies were inconclusive. The same HLA typing was found in each twin: A3, B18, B35, Cw4, DR2, DRw10, DQw1. Thus, each was heterozygous for HLA-B35. We reviewed the literature and found a strong association between HLA-B35 and subacute thyroiditis in various ethnic groups tested. Our experience with these identical twins provides additional evidence to suggest that HLA-35 and perhaps Cw4 confer genetic susceptibility in acquiring subacute painful thyroiditis in a possible dominant mode of inheritance.

Adult↗
PubMed1996

Increased urinary excretion of sulfated 3,3',5-triiodothyronine in patients with nodular goiters receiving suppressive thyroxine therapy.

Increased serum 3,3',5-triiodothyronine sulfate (T3S) levels have been detected in various pathophysiologic states. However, little is known about T3S concentrations in other biological fluids. By employing a highly sensitive, specific, and reproducible radioimmunoassay (RIA), we measured T3S in the serum and urine of 20 premenopausal women with benign nodular goiters before and after administration of thyroxine for 6 months (T4; 3.2 micrograms/kg/day). Serum T3 concentrations did not change significantly after treatment (2.0 vs. 1.7 nmol/L; p > 0.05). However, the mean serum T4 and free T4 concentrations were significantly higher after treatment (138 vs. 88 nmol/L and 28 vs. 17 pmol/L; p < 0.01, respectively). Serum thyroid stimulating hormone (TSH) levels were significantly reduced after T4 treatment (0.13 vs. 0.66 mU/L, p < 0.01) and the serum levels of T3S were significantly increased after treatment (82 vs. 45 pmol/L; p < 0.01). A good correlation was observed between increased serum T3S and T4 concentrations (r = 0.66; p < 0.001). The sulfoconjugate of T3 was significantly increased in creatinine-corrected urine after treatment (606 vs. 253 pmol/umol Cr.; p < 0.01). There was a significant correlation between increased creatinine-corrected urine T3S and increased serum free T4 (r = 0.65; p < 0.001). In summary, significant increases in serum and urine T3S levels were noted in T4-treated patients with subnormal serum TSH and borderline elevated T4. We thus conclude that the sulfation pathway may play a role in the homeostasis of thyroid hormone metabolism in T4-treated subjects with relative hyperthyroxinemia. In addition, the creatinine-corrected urine concentrations of T3S may serve as an index for the evaluation of T4-treated patients with elevated levels of T4.

Adult↗
PubMed1997

Radioiodine therapy for Graves' disease: case selection and restrictions recommended to patients in North America.

Each of the three major therapies for Graves' disease has its own advantages, disadvantages, indications, and contraindications. Today, radioactive iodine (RAI) therapy is the most commonly employed means of therapy for Graves' disease in the United States, with approximately 70% of patients so treated after initial presentation and an additional fraction of arguably 10-15% treated with RAI after failure of antithyroid drugs or surgery. RAI therapy is acknowledged to have the clear-cut advantage of being safe, with low morbidity and cost. The indications for RAI therapy are clear and noncontroversial for most patients with Graves' disease. Moreover, RAI treatment is employed by some thyroidologists for subclinical thyrotoxicosis (normal T4 or T3 but immeasurable TSH), particularly in patients > age 45 due to risks of atrial fibrillation. RAI therapy is not considered indicated or is contraindicated during breast feeding and in pregnancy, subacute thyroiditis, postpartum thyroiditis, struma ovarii, pituitary (TSH-driven) hyperthyroidism, euthyroid, hyperthyroxinemia, and thyroid hormone resistance. Opinions vary on the use of RAI therapy in children with Graves' disease; generally, a lower age cutoff of 17 years is acceptable in most clinics. Even more controversial is whether RAI therapy in the presence of Graves' ophthalmology constitutes a risk for worsening ophthalmopathy. Resolution of this latter issue awaits more definitive studies, but RAI therapy is likely to remain the first choice for most patients with Graves' disease.

Antithyroid Agents↗
PubMed1998

An abnormality of thyroid hormone receptor expression may explain abnormal thyrotropin production in thyrotropin-secreting pituitary tumors.

Thyrotropin (TSH)-secreting pituitary adenomas cause hyperthyroxinemia in the presence of "inappropriately" elevated concentrations of TSH. TSH production under these circumstances escapes the normal negative feedback effect of thyroid hormone. We propose that this defective negative feedback is mediated by an abnormality of thyroid hormone receptor (TR) expression. Two TSH-secreting pituitary adenomas were analyzed by immunocytochemistry for TR isoform protein expression and by semiquantitative reverse transcriptase polymerase chain reaction (RT-PCR) for TR isoform mRNA expression. The results obtained from these tumors were compared with the findings from six normal human pituitaries. Neither tumor examined expressed detectable levels of nuclear TRalpha or TRbeta proteins, in contrast to the normal pituitaries studied, which expressed all TR isoforms. Application of RT-PCR, however, revealed mRNAs encoding each TR isoform in all tumorous and normal tissues examined. Semiquantitative RT-PCR revealed similar levels of expression of TRalpha and TRbeta isoform mRNAs in tumors and normal tissue, in contrast to the observed difference in TR proteins. Absent TRalpha and TRbeta protein expression, in association with normal mRNA levels, implies a post-transcriptional defect in TR mRNA processing in TSH-secreting adenomas. Reduced TR expression in these tumors may explain defective negative feedback of thyroid hormone on TSH production, and may also contribute to uncontrolled tumor growth.

Adenoma↗
PubMed1999

Neonatal hypothyroidism: treatment and outcome.

Systematic neonatal screening for congenital hypothyroidism (CH), which was progressively implemented in industrialized countries over the past 15 to 25 years, has been extremely successful in eradicating severe mental deficiency resulting from CH. However, in the first generation of children diagnosed by screening, the concept that CH has a threshold effect on intelligence was confirmed. In spite of earlier diagnosis through screening, children with severe CH (i.e., those with a marked retardation of bone age and/or a low circulating thyroxine [T4] before treatment) still had clinically significant intellectual sequelae, amounting to a loss of 6 to 19 IQ points. Recent studies suggest that this developmental gap may be closed by treating more rapidly after birth (2 weeks instead of 4-5 weeks in the early years of the screening era) and by using a higher initial dose of levothyroxine (10-15 instead of 5-8 microg/kg per day). This regimen induces transient hyperthyroxinemia, but no clinical signs or symptoms of hyperthyroidism. Longer term follow-up of larger numbers of patients remains necessary to confirm the normalization of intellectual development and the absence of untowards effects of the treatment regimen in children with severe CH.

Congenital Hypothyroidism↗
PubMed2000

The thyroxine-binding proteins.

The slow clearance, prolonged half-life, and high serum concentration of thyroxine (T4) are largely due to strong binding by the principal plasma thyroid hormone-binding proteins, thyroxine-binding globulin (TBG), transthyretin (TTR), and albumin. These proteins, which shield the hydrophobic thyroid hormones from their aqueous environment, buffer a stable free T4 concentration for cell uptake. Free rather than bound T4 is subject to homeostatic control by the hypothalamic-pituitary thyroid axis. Although it is not a protease inhibitor, sequence analysis identifies TBG as a member of the serine protease inhibitor (serpin) family of proteins. Proteolytic cleavage of TBG appears to be a mechanism for site-specific release of T4 independently of homeostatic control. TBG probably facilitates the transport of maternal T4 and iodide to the fetus, although this remains to be proven. High-affinity cellular binding sites for TTR have been described; however, their function and that of choroid plexus synthesis of TTR and transport of T4 into the cerebrospinal fluid remain unclear. Albumin, with the lowest T4 affinity and fastest T4 release of the major T4-binding proteins may promote quick exchange of T4 with tissue sites. The affinity of albumin for T4 is increased by histidine substitution for arginine 218 in the most common form of dysalbuminemic hyperthyroxinemia. However, proline and alanine substitutions at the same site have a similar effect, suggesting that arginine 218 interferes with T4 binding.

Aging↗
PubMed1997

Hypothyroid Graves' disease.

BACKGROUND: Spontaneous conversion from hypothyroidism to hyperthyroidism has generally been considered uncommon. METHODS: Values obtained were serum thyroid-stimulating hormone (TSH), thyroxine, free thyroxine index, radioactive iodine uptake (RAIU), thyroid-stimulating immunoglobulins (TSI), and thyrotropin-binding inhibitory immunoglobulin (TBII). RESULTS: Five patients spontaneously had a minimum of two cycles in thyroid function with extremes of hypothyroxinemia to hyperthyroxinemia. One patient had four documented cyclic shifts in thyroid status. When measurements were obtained in the hyperthyroid phase, all patients had TSI, increased RAIU, and an undetectable TSH. When measurements were done in the hypothyroid phase, all patients had positive TBII but negative TSI. CONCLUSIONS: Spontaneous reversal of thyroid function may be more common than previously thought. Clinical features associated with lability of thyroid function were abrupt change in goiter size, exaggerated response to therapy, or the presence of TSH-receptor antibodies.

Adolescent↗
PubMed1992

Effect of arginine on the GHRH-stimulated GH secretion in patients with hyperthyroidism.

Patients with hyperthyroidism have reduced GH responses to pharmacological stimuli and reduced spontaneous nocturnal GH secretion. The stimulatory effect of arginine on GH secretion has been suggested to depend on a decrease in hypothalamic somatostatin tone. The aim of our study was to evaluate the effects of arginine on the GH-releasing hormone (GHRH)-stimulated GH secretion in patients with hyperthyroidism. Six hyperthyroid patients with recent diagnosis of Graves' disease [mean age +/- SEM, 39.2 +/- 1.4 years; body mass index (BMI) 22 +/- 0.4 kg/m2] and 6 healthy nonobese volunteers (4 males, 2 females; mean age +/- SEM, 35 +/- 3.5 years) underwent two experimental trials at no less than 7-day intervals: GHRH (100 micrograms, i.v.)-induced GH secretion was evaluated after 30 min i.v. infusion of saline (100 ml) or arginine (30 g) in 100 ml of saline. Hyperthyroid patients showed blunted GH peaks after GHRH (13.2 +/- 2.9 micrograms/l) as compared with normal subjects (23.8 +/- 3.9 micrograms/l, p < 0.05). GH peaks after GHRH were only slightly enhanced by arginine in hyperthyroid subjects (17.6 +/- 2.9 micrograms/l), whereas, in normal subjects, the enhancement was clear cut (36.6 +/- 4.4 micrograms/l; p < 0.05). GH values after arginine + GHRH were still lower in hyperthyroid patients with respect to normal subjects. Our data demonstrate that arginine enhances but does not normalize the GH response to GHRH in patients with hyperthyroidism when compared with normal subjects. We hypothesize that hyperthyroxinemia may decrease GH secretion, both increasing somatostatin tone and acting directly at the pituitary level.

Adult↗
PubMed1969

Acute release of thyrotropin in the newborn.

Measurements of serum thyrotropin (TSH) concentrations were conducted in maternal and fetal blood during labor and delivery and the early postnatal and neonatal periods. Mean TSH concentration was significantly higher in cord blood (9.5 muU/ml) than maternal blood (3.9 muU/ml), a finding suggesting a fetal-maternal TSH gradient at term. Serum TSH concentration in the newborn increased rapidly to mean levels of 60 muU/ml at 10 min and 86 muU/ml at 30 min of age. Between 30 min and 3-4 hr serum levels decreased rapidly, then fell more gradually to a mean concentration of 13 muU/ml at 48 hr. The half-time of the decrease in serum TSH concentration between 30 and 90 min was 77 min, a value slightly greater than the half-time of disappearance of radioiodinated TSH measured in adults. This indicates that the early high rate of TSH secretion in the newborn ceases by 30 min, and that the rapid rise and fall in serum TSH concentrations may represent release of stored pituitary TSH. A more chronic TSH hypersecretion persisted throughout the first 24-48 hr of extrauterine life. Measurements of serum PBI concentrations were conducted in a separate group of maternal and cord blood samples and in the newborn infants during the first 48 hr of extrauterine life to relate the TSH and serum hormonal iodine concentration changes. Serum protein-bound iodine (PBI) concentrations were similar in maternal and cord blood, increased significantly by 4 hr of age in the newborn, and peaked at about 24 hr, presumably in response to the TSH hypersecretion. The pattern of TSH hypersecretion was similar in infants delivered vaginally and by caesarean section. Maternal serum TSH concentrations were stable throughout the perinatal period. Warming the infants at 99-103 degrees F during the first 3 hr of life did not prevent the early, acute release of thyrotropin. Cooling of warm infants at room temperature (72-78 degrees F) between 3 and 4 hr resulted in a decrease in mean rectal temperature of 3.3 degrees F and produced a significant increment in serum TSH concentration. These data suggest that the mechanism of the early, acute release of thyrotropin in the newborn may involve a potent stimulus other than cooling. However, the increase in serum TSH stimulated by delayed (3-4 hr) cooling indicates that neonatal hyperthyroxinemia is, at least, augmented by extrauterine cooling. Thus, cold exposure is capable of increasing TSH secretion in humans.

Blood Proteins↗
PubMed1990

Thyroxine uptake by perfused rat liver. No evidence for facilitation by five different thyroxine-binding proteins.

Rates of hepatic uptake of thyroxine (T4) from dilute solutions of five different plasma T4-binding proteins were measured in the isolated perfused rat liver using an indicator dilution method. For each protein, this rate was compared with the rate of spontaneous dissociation of the T4-protein complex measured in vitro. Proteins studied were human T4-binding globulin (TBG), human T4-binding prealbumin (TBPA), human albumin, rat TBPA, and human albumin isolated from subjects with familial dysalbuminemic hyperthyroxinemia. For each of the five protein-hormone complexes studied, the rate of hepatic uptake of T4 (measured under conditions expected to result in dissociation-limited uptake) closely approximated the rate of spontaneous dissociation of the protein-hormone complex within the hepatic sinusoids. These findings indicate an absence of special cellular mechanisms that facilitate the hepatic uptake of T4 from its plasma binding proteins, and support the view that uptake occurs from the free T4 pool after spontaneous dissociation of T4 from its binding proteins.

Animals↗