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PubMed1987

Effect of thyrotropin-releasing hormone on the carbohydrate structure of secreted mouse thyrotropin. Analysis by lectin affinity chromatography.

Thyrotropin (TSH) is a glycoprotein hormone whose secretion from the anterior pituitary is regulated, in part, by the hypothalamic tripeptide thyrotropin-releasing hormone (TRH). We have used serial lectin affinity analysis to explore whether TRH, in addition to promoting TSH secretion, alters the carbohydrate structure of secreted TSH. Hypothyroid mouse hemipituitaries were incubated in medium containing [3H] mannose, [3H]glucosamine, or [3H]fucose either with or without 10(-7) M TRH. TSH was immunoprecipitated, proteolytically digested into glycopeptides, and chromatographed on serial lectin-Sepharose columns. Under basal conditions, 37% of secreted [3H]mannose-labeled TSH glycopeptides failed to bind to concanavalin A (ConA)-Sepharose, 55% bound and eluted with 10 mM alpha-methylglucoside, and 8% bound and eluted with 500 mM alpha-methylmannoside. Approximately 35% of glycopeptides not binding to ConA-Sepharose were bound by pea lectin-Sepharose, suggesting the presence of certain core fucosylated triantennary complex oligosaccharides. TRH caused a 2-fold increase in secretion of [3H]mannose-labeled TSH glycopeptides due almost exclusively to a specific increase in structures that bound to ConA-Sepharose and eluted with 10mM alpha-methylglucoside, corresponding to biantennary complex or unusual hybrid species. There was no change in the distribution of intrapituitary TSH glycopeptides with TRH. Acid hydrolysis of secreted proteins showed little metabolism of the tritiated sugar precursors, except for a 20% conversion of [3H]mannose to [3H]fucose. Moreover, ConA-Sepharose chromatography of secreted [3H]glucosamine- and [3H]fucose-labeled TSH glycopeptides showed similar increases in ConA-Sepharose binding with TRH as noted with [3H]mannose labeling. Subsequent lectin analysis of secreted [3H] mannose-labeled TSH glycopeptides on erythroagglutinating phytohemagglutinin-Sepharose and leukoagglutinating phytohemagglutinin-Sepharose disclosed no significant differences in TRH-treated versus control samples. These data suggest that secreted mouse TSH has greater carbohydrate heterogeneity than has been recognized previously. In addition, TRH in vitro promotes the secretion of specific TSH molecules apparently enriched in biantennary complex or unusual hybrid oligosaccharides.

Animals↗
PubMed1985

Serum concentrations of thyroxine, 3,5,3'-triiodothyronine, thyrotropin, and prolactin in dogs before and after thyrotropin-releasing hormone administration.

Serum concentrations of thyrotropin (TSH), prolactin, thyroxine, and 3,5,3'-triiodothyronine in 15 euthyroid dogs and 5 thyroidectomized and propylthiouracil-treated dogs after thyrotropin-releasing hormone (TRH) administration were measured. Although thyroidectomized and propylthiouracil-treated dogs had higher (P less than 0.01) base-line concentrations of TSH in serum than did euthyroid dogs, concentrations of TSH after TRH administration varied at 7.5, 15, and 30 minutes with 14 of 45 samples obtained from healthy dogs having lower TSH concentrations than before TRH challenge. Similarly, concentrations of 3,5,3'-triiodothyronine in the serum of euthyroid dogs 4 hours after TRH administration were similar (P less than 0.05) to concentrations before TRH challenge. Although the mean concentration of thyroxine in serum was elevated (P less than 0.05) 4 hours after administration of TRH to euthyroid animals, as compared with base-line levels, the individual response was variable with concentrations not changing or decreasing in 4 dogs. Therefore, the TRH challenge test as performed in the current investigation was of limited value in evaluating canine pituitary gland function. Although mean concentrations of TSH in serum were higher (P less than 0.05) in euthyroid dogs after TRH administration, the response was too variable among individual animals for accurate evaluation of pituitary gland function. Concentrations of prolactin in the sera of dogs after TRH administration, confirmed previous reports that exogenously administered TRH results in prolactin release from the canine pituitary and indicated that the TRH used was biologically potent.

Animals↗
PubMed1977

Effect of somatostatin on thyrotropin, prolactin, growth hormone and insulin responses to thyrotropin releasing hormone and arginine in healthy, hypothyroid and acromegalic subjects.

The effect of somatostatin on the thyrotropin (TSH), prolactin, growth hormone (GH) and insulin responses to the combined administration of thyrotropin releasing hormone (TRH) and arginine was studied in six healthy subjects, three hypothyroid patients and three acromegalic patients. Similar inhibition by somatostatin of the TSH and insulin responses was observed in the three groups. While the tetradecapeptide had no significant effect on the prolactin response in the healthy and acromegalic subjects, it caused an unexpected inhibition of the prolactin response in two of the hypothyroid subjects. Contrary to the findings in the healthy and hypothyroid subjects, somatostatin did not inhibit the GH response in the acromegalic patients. Normal inhibition by somatostatin of the insulin response, followed by a rebound in insulin secretion, was observed in all subjects. These preliminary data indicate increased sensitivity of the prolactin-secreting cells to somatostatin in hypothyroidism and suggest that decreased responsiveness of the somatotrophs to somatostatin could play a role in the pathogenesis of acromegaly.

Acromegaly↗
PubMed1978

Effect of oral thyrotropin releasing hormone on serum prolactin, thyrotropin and total thyroxine levels in postpartum women.

A study was designed to investigate the effects of oral administration of thyrotropin releasing hormone (TRH) on prolactin levels and on thyroid function during the early puerperium. Eight lactating mothers took a single dose of oral TRH (40 mg) while eight other volunteers had a placebo treatment. Serial serum samples taken before and after treatment were assayed for prolactin, thyrotropin (TSH) and total thyroxine (T4) by using specific radioimmunoassays. There was approximately twofold increase in prolactin level at 30--210 min, about sevenfold increase in the TSH level at 210 min, and a marked increasing trend in the T4 level during the study period only in the treatment group. Six mothers treated with TRH and two treated with placebo regarded milk secretion more abundant in post-test than pre-test feeding. However, before TRH could be extensively tested on mothers with deficient lactation a thorough study of the effects of oral TRH on thyroid function in the puerperium is mandatory.

Female↗
PubMed1983

Thyrotropin and prolactin response to thyrotropin-releasing hormone in healthy and asphyxiated full-term neonates.

To evaluate the effect of perinatal asphyxia on the pituitary response to thyrotropin-releasing hormone (TRH) in full-term newborn infants, serum thyrotropin (TSH) and prolactin (PRL) levels were measured before and 30 and 180 min after i.v. administration of 40 micrograms TRH. Birth weight, gestational and postnatal age were similar in the healthy (group NA) and in the asphyxiated (group A) babies. Hormone levels were determined by radioimmunoassay using commercial kits. It was demonstrated that the basal TSH level was slightly higher and the basal PRL level significantly (p less than 0.05) higher in group A than in group NA. In response to TRH administration in group A a marked increase in PRL occurred from 6781 +/- 887 to 11 072 +/- 1318 and 9636 +/- 1024 mU/l at 0, 30 and 180 min, respectively. A similar response was seen in group NA; the values, however, remained significantly lower during the TRH-test. The respective PRL values at 0, 30 and 180 min were 4672 +/- 411, 7945 +/- 343 (p less than 0.05) and 5963 +/- 372 mU/l (p less than 0.05). TRH administration also resulted in a significant elevation of the serum TSH level from 6.20 +/- 1.30 to 49.02 +/- 7.25 (p less than 0.01) and 18.72 +/- 6.35 mU/l (p less than 0.05) in group A, and from 3.90 +/- 0.57 to 24.01 +/- 3.81 (p less than 0.01) mU/l in group NA, but in group NA the 180 min TSH value of 6.07 +/- 1.25 mU/l did not differ statistically from the basal level (p greater than 0.1). It is concluded that the pituitary PRL and TSH reserves are maintained in full-term newborn infants recovering from perinatal asphyxia whose biochemical findings are indicative of subclinical hypothyroidism.

Asphyxia Neonatorum↗
PubMed1984

Normal reference interval for thyrotropin response to thyroliberin: dependence on age, sex, free thyroxin index, and basal concentrations of thyrotropin.

We measured the thyrotropin response (delta TSH) to 200 micrograms of thyroliberin in 131 subjects without thyroid dysfunction or other disease and with basal values for thyroid function that were within the normal reference intervals for our laboratory. By univariate and multivariate statistical methods we found delta TSH to be significantly influenced by the basal concentration of thyrotropin (TSH0) and the free thyroxin index (FT4I). When the effects of variations in TSH0 and FT4I were eliminated, delta TSH in men under 40 years of age did not differ from that in women. A decrease in delta TSH with increasing age was found in men but not in women. Thus a reference interval for delta TSH should consider TSH0, FT4I, and, in men, age. On the basis of multiple linear regression analysis, we constructed a formula for delta TSH reference intervals that takes into account individual values for TSH0 and FT4I. The formula should be applicable for women, regardless of age, up to 77 years and for men under 40 years. For older men a correction for the age-related decrease in delta TSH must be applied.

Adult↗
PubMed1984

Administration of thyrotropin-releasing hormone at weekly intervals results in a diminished thyrotropin response.

A diminished thyrotropin (TSH) response to the administration of thyrotropin-releasing hormone (TRH) has been widely reported in depressed patients. Repeated TRH administration at short intervals has been shown to produce a diminished TRH response in healthy subjects. In the present study, TRH (400 micrograms) was administered to ten healthy male subjects at weekly intervals for 4 weeks. The TSH response to TRH diminished steadily from 8.2 +/- 1.3 microU/ml on Trial 1 to 6.3 +/- 0.7 microU/ml on Trial 4 (p less than 0.05). No change in the prolactin response to TRH administration was observed over the four trials. Reduction in the TSH response to TRH was not correlated with basal concentrations of thyroxine, triiodothyronine, or cortisol.

Adult↗
PubMed1982

Hyperthyroidism due to a thyrotropin-secreting pituitary adenoma. Studies of thyrotropin and subunit secretion.

A 58-year-old man had symptoms of hyperthyroidism and congestive heart failure. While hyperthyroid, his serum thyrotropin (TSH) level was inappropriately elevated at 6.1 microunits/mL. The molar ratio of alpha subunit to TSH was 2.5, suggesting the presence of a TSH-secreting pituitary tumor. Further evaluation disclosed an enlarged sella turcica with posterior erosion, and an intrasellar mass was visualized on computed tomographic scan. Neither serum TSH nor alpha subunit levels became elevated after administration of thyrotropin-releasing hormone, nor were they suppressed by a dopamine infusion. Serum TSH but not alpha subunit levels rose during antithyroid drug therapy. Estrogens produced a partial reduction in serum alpha subunit concentration (presumably reflecting the nontumorous gonadotroph contribution to circulating alpha subunit). Dexamethasone completely suppressed serum TSH level but had no effect on the alpha subunit level, suggesting a differential feedback of glucocorticoids on TSH and alpha secretion. The patient was treated with pituitary irradiation rather than surgery because of his underlying heart disease.

Adenoma↗
PubMed1977

Serum thyrotropin response to thyrotropin-releasing hormone and free thyroid hormone indices in patients with familial thyroxine-binding globulin deficiency.

The response in serum thyrotropin (TSH) to synthetic thyrotropin-releasing hormone (TRH) as well as serum free thyroxine index (FT4I) and free triiodothyronine index (FT3I) was investigated in six patients with familial thyroxine-binding-globulin (TBG) deficiency. The total serum thyroxine (T4) and triiodothyronine (T3) concentrations were significantly decreased, compared with those of normal subjects (3.4 +/- 0.9 microgram/dl, mean +/- SD. vs. 9.0 +/- 1.5 microgram/dl, p less than 0.01 and 87 +/- 27 ng/dl vs. 153 +/- 37 ng/dl, p less than 0.01, respectively). FT4I was lower than the normal range in all but one (5.3 +/- 1.5 vs. 8.9 +/- 1.6, p less than 0.01), whereas FT3I was all in the normal range and of no significant difference from the normal control (132 +/- 22 vs. 148 +/- 25). Serum TSH concentrations in TBG deficiency were all in the normal range (1.0-4.2 muU/ml) and the maximum TSH increments following TRH 500 microgram iv were 8.9 +/- 2.0 muU/ml and of no significant difference from the normal control (10.2 +/- 4.5 muU/ml). These results indicate that the euthyroid state in familial TBG deficiency is more clearly defined by TRH-test and the normal response to TRH in familial TBG deficiency is presumably under the control of the serum free T3 level rather than the serum free T4 level.

Adult↗
PubMed1994

Suppression of the thyrotropin response to thyrotropin-releasing hormone and its association with severity of critical illness.

OBJECTIVE: To study whether the suppression of the thyrotropin (thyroid-stimulating hormone, TSH) response to thyrotropin-releasing hormone (TRH) correlates with severity of illness and death in patients with nonthyroidal critical illness. DESIGN: Prospective study. SETTING: Intensive care unit (ICU) of a university hospital. PATIENTS: Forty-one critically ill patients without thyroid disease with multiple organ failure who were admitted to the ICU. MEASUREMENTS AND MAIN RESULTS: The TSH response to TRH was tested within 24 hrs of ICU admission. Blood samples were obtained just before, and at 15, 30, 60, 90, and 120 mins after 500-micrograms injection of synthetic TRH. Triiodothyronine, free-triiodothyronine, thyroxine, free-thyroxine and TSH concentrations were measured in the samples obtained just before TRH injection. Acute Physiology and Chronic Health Evaluation (APACHE II) scores and Sepsis scores were calculated based on the data obtained within 24 hrs of ICU admission. Individual variables were compared between survivors and nonsurvivors. The APACHE II scores and Sepsis scores of nonsurvivors were significantly higher than those scores of survivors. The overall occurrence of suppressed TSH response to TRH was 88%. Peak TSH concentration of the TSH response was significantly lower in nonsurvivors than in survivors. Serial measurement of the TSH response showed that nonsurvivors experienced a decrease in peak TSH concentration from 1.55 +/- 0.78 to 0.55 +/- 0.30 microIU/mL; in survivors, it increased from 2.10 +/- 0.26 to 7.38 +/- 1.83 microIU/mL. Conversely, the basal TSH concentration did not change in either survivors or nonsurvivors. The "severity" of illness of nonsurvivors remained high; their mean APACHE II score varied from 20.0 +/- 1.9 to 22.1 +/- 1.3 and the mean Sepsis score varied from 20.0 +/- 4.3 to 25.4 +/- 4.0, while the same scores for survivors decreased significantly (p < .05): their APACHE II score decreased from 16.2 +/- 0.7 to 7.6 +/- 2.0 and the Sepsis score went from 14.0 +/- 1.9 to 6.0 +/- 1.6. CONCLUSIONS: In critically ill patients with multiple organ failure, suppression of the TSH response to TRH frequently occurs and correlates with severity of illness and outcome. Our data indicate that measurement of the TSH response is helpful in evaluating the severity of illness and prognosis for critically ill patients.

APACHE↗
PubMed1976

Serum thyrotropin response to thyrotropin-releasing hormone and free thyroid hormone indices in patients with familiar thyroxine-binding globulin deficiency.

The response in serum thyrotropin (TSH) to synthetic thyrotropin-releasing hormone (TRH) as well as serum free thyroxine index (FT4I) and free triiodothyronine index (FT3I) was investigated in six patients with familial thyroxine-binding-globulin (TBG) deficiency. The total serum thyroxine (T4) and triiodothyronine (T3) concentrations were significantly decreased, compared with those of normal subjects (3,4 +/- 0.9 microng/dl, mean +/- S.D. vs. 9.0 +/- 1.5 microng/dl, p less than 0.01 and 87 +/- ng/dl vs. 153 +/- 37 ng/dl, p less than 0.01, respectively). FT4I was lower than the normal range in all but one (5.3 +/- 1.5 vs. 8.9 +/- 1.6, p less than 0.01), whereas FT3I was all in the normal range and of no significant difference from the normal control (132 +/- 22 vs 148 +/- 25). Serum TSH concentrations in TBG deficiency were all in the normal range (1.0-4.2 micronM/ml) and the maximum TSH increments following TRH 500 microng iv were 8.9 +/- 2.0 micronU/ml and of no significant difference from the normal control (10.2 +/- 4.5 micronU/ml). These results indicate that the euthyroid state in familial TBG deficiency is more clearly defined by TRH-test and the normal response to TRH in familial TBG deficiency is presumably under the control of the serum free T3 level rather than the serum free T4 level.

Adult↗
PubMed1993

Effects of oral administration of anti-inflammatory doses of prednisone on thyroid hormone response to thyrotropin-releasing hormone and thyrotropin in clinically normal dogs.

Prednisone was given orally to 12 dogs daily for 35 days at an anti-inflammatory dosage (1.1 mg/kg of body weight in divided dose, q 12 h) to study its effect on thyroxine (T4) and triiodothyronine (T3) metabolism. Six of these dogs were surgically thyroidectomized (THX-Pred) and maintained in euthyroid status by daily SC injections of T4 to study peripheral metabolism while receiving prednisone; 6 dogs with intact thyroid gland (Pred) were given prednisone; and 6 additional dogs were given gelatin capsule vehicle as a control group (Ctrl). Baseline T4 concentration after 4 weeks of treatment was not significantly different in dogs of the THX-Pred or Pred group (mean +/- SEM, 2.58 +/- 0.28 or 3.38 +/- 0.58 micrograms/dl, respectively) vs dogs of the Ctrl group (2.12 +/- 0.30 micrograms/dl). A supranormal response of T4 to thyrotropin was observed in dogs of the Pred group, but the T4 response to thyrotropin-releasing hormone was normal. Baseline T3 concentration in dogs of both steroid-treated groups was significantly (P < 0.05) lower after 2 and 4 weeks of prednisone administration vs pretreatment values, but normalized 2 weeks after prednisone was stopped. Free T3 (FT3) and T4 (FT4) fractions and absolute FT3 and FT4 concentrations were not altered by prednisone administration. Reverse T3 (rT3) concentration in vehicle-treated Ctrl dogs (26.6 +/- 3.5 ng/dl) was not different from rT3 concentration in dogs of the THX-Pred (25.7 +/- 4.3 ng/dl) and Pred (28.9 +/- 3.8 ng/dl) groups after 4 weeks of medication.(ABSTRACT TRUNCATED AT 250 WORDS)

Administration, Oral↗
PubMed1998

Effect of endotoxin on hormonal responses to thyrotropin and thyrotropin-releasing hormone in dogs.

OBJECTIVE: To determine whether administration of endotoxin affects thyroid gland function in dogs. ANIMALS: 24 Beagles. PROCEDURE: Dogs were given thyrotropin (TSH) or thyrotropin-releasing hormone (TRH) on 2 occasions. Twenty-four hours before the second challenge with TSH or TRH, all dogs were given 5 micrograms of endotoxin/kg of body weight. Serum concentrations of thyroxine (T4), free T4 (fT4), 3,3',5-triiodothyronine (T3), reverse T3, autoantibodies to T3, and plasma concentrations of ACTH and cortisol were determined. RESULTS: Treatment with endotoxin was associated with reduced baseline concentration of serum T3 and increased baseline concentration of reverse T3 and free T4. Endotoxin treatment resulted in reduced peak serum concentration of T4 after TSH and TRH. However, peak serum concentration of fT4 after TSH and TRH were not affected by endotoxin. CONCLUSIONS: A single dose of endotoxin affects several aspects of thyroid gland function in dogs, including T4 binding, deiodinase activity, and the thyroidal response to TSH and TRH. CLINICAL RELEVANCE: Acute or chronic nonthyroidal illness may affect thyroid gland function in dogs. Determination of fT4 concentration may provide a means of differentiating the effects of nonthyroidal illness from those of thyroid dysfunction, because endotoxin treatment was associated with increased baseline serum free T4 concentration and unchanged peak serum fT4 concentration after administration of TSH or TRH.

Adrenocorticotropic Hormone↗
PubMed1997

Interaction between triiodothyronine and ovarian steroid hormones on the regulation of the release of thyrotropin and thyrotropin-releasing hormone in vitro.

In vivo and in vitro experiments were designed to examine [1] the effect of triiodothyronine (T3) and/or ovarian steroids on the spontaneous and thyrotropin-releasing hormone (TRH)-stimulated release of thyrotropin (TSH) by the anterior pituitary gland (AP) in vitro; and [2] the in vivo effects of T3 and ovarian steroids on TRH-release in vitro. In the experiment 1, ovariectomized-thyroidectomized (Ovx-Tx) rats were injected with triiodothyronine (T3, 2 micrograms/kg), estradiol benzoate (EB, 25 micrograms/kg), progesterone (P, 10 mg/kg), T3 plus EB, T3 plus P, EB plus P, or T3 plus EB and P for 6 days before decapitation. The AP was incubated with Locke's medium, challenged with TRH (30 nM), recovered and then with T3 (10 nM) only or with T3+TRH, 30 min for each interval. Mediobasal hypothalami (MBHs) were challenged with high potassium (60 mM) for 30 min. In the experiment 2, the APs of Ovx-Tx rats were enzymatically dispersed and the AP cells were pretreated with or without EB (0-6 nM) for 72 h, and further with T3 (10 nM) for 24 h, followed by an incubation for 30 min with TRH (0-100 nM). The spontaneous and TRH-induced release of TSH in vitro from rat APs, and pituitary TSH content were increased by T3, or T3 plus P as compared with the animals injected with vehicle, or P alone. EB inhibits the effect of T3 on TSH release in vitro. Application of T3 in vitro prevented the release of TSH in response to TRH. EB dose-dependently relieved the inhibitory effect of T3 on TRH-induced TSH release in vitro. TRH release from MBH was increased by EB and inhibited by T3 or P. EB prevented the inhibitory effect of T3 on TRH release. P plus T3 potentiated the stimulatory effects of EB on TRH release. These results suggest that [1] the reduction of the concentration of plasma TSH by T3 is at least in part due to the inhibitory effects of T3 on TRH release from mediobasal hypothalamus, and TSH release in response to TRH, [2] the increased content and release of TSH from rat AP tissue by T3 via an in vivo effect may be involved in a short feedback loop of TSH on TRH release, and [3] ovarian steroid hormones play an inhibitory role in regulating T3 effects on the release of TSH and TRH.

Animals↗
PubMedDate not supplied

Pilot investigation of thyrotropin-releasing hormone-induced thyrotropin and prolactin release in anxious patients treated with diazepam.

Benzodiazepines have been reported to inhibit thyrotropin (TSH) and prolactin (PRL) secretion in response to stressful and pharmacologic stimuli in experimental animals. The current study investigates basal and thyrotropin-releasing hormone (TRH)-stimulated TSH and PRL release in anxious patients treated with diazepam. Six hospitalized patients having generalized anxiety or adjustment disorder with anxious mood (DSM III-R criteria) were treated during 1 week with diazepam (mean daily dose 33.3 mg). TRH testing was performed comparatively before and after 7 days of diazepam administration (with 250 micrograms protirelin and blood sampling at 15-min intervals over 60 min). Steady-state plasma levels of diazepam and its metabolite nordazepam (desmethyldiazepam) were determined by high-performance liquid chromatography. After 7 days of diazepam treatment, basal plasma levels of TSH and PRL were not affected compared with pretreatment values. Similarly, the time-course of TRH-induced TSH release was not modified by the treatment. By contrast, there was a trend to decrease in the TRH-induced PRL release, and the decrease in the PRL response to TRH on day 7 was significantly correlated with plasma nordazepam concentrations (rs = 0.943, p = 0.02). These preliminary results suggest that benzodiazepines, at therapeutic doses for the treatment of anxiety, may alter TRH-induced PRL release in humans.

Adolescent↗
PubMed1989

Thyroglobulin, thyrotropin and thyrotropin binding inhibiting immunoglobulins assayed at the withdrawal of antithyroid drug therapy as predictors of relapse of Graves' disease within one year.

"Sensitive" thyrotropin (TSH), thyroglobulin (TG) and even thyrotropin binding inhibiting immunoglobulins (TBII) assays are now widely available. The objective of the present study was to determine the most accurate of these three parameters to predict the relapse of Graves' disease during the year following treatment discontinuation and to evaluate whether the assay of three markers is able to improve the prediction. TSH, TG and TBII were measured in the sera of 67 Graves' disease patients after at least 12 months of medical treatment. In 52 patients, TBII had also been determined before the beginning of the medical treatment. Under treatment, all the patients were clinically and biologically euthyroid, but in 9 goitrous patients it was impossible to lower the doses of carbimazole without an immediate relapse. The TSH levels of these 9 patients were still low in all cases but one; TG and TBII levels were abnormal in all. In the other 58 patients, the treatment was discontinued; 22 relapsed within one year, more frequently when a goiter was present. The most reliable parameter for the prediction of relapse was found to be TBII, as its specificity was high (94.5%), although its sensitivity was poor (45%); TG was more sensitive (64%) but far less specific (57%); TSH and "initial" TBII appeared to be of a little interest. When TBII was elevated prior to the withdrawal of treatment, the determination of TG was useful: abnormal values of both TBII and TG were always associated with a relapse. When TBII testing was negative, the relapse risk fell to 0.26, and to 0.08 when three criteria were matched: no goiter, negative TBII, normal TG.

Antibodies↗
PubMed1990

Serum thyrotropin in hospitalized psychiatric patients: evidence for hyperthyrotropinemia as measured by an ultrasensitive thyrotropin assay.

In order to gather further insight into the basis for high serum T4 and/or T3 of psychiatric illnesses, we studied thyroid function in 84 consecutive newly hospitalized psychiatric patients (HPP) in a 12-week period. Serum T4 and T3 were measured by immunoassay and thyrotropin (thyroid-stimulating hormone [TSH]) by an ultrasensitive immunoradiometric assay. Serum T4 was in the normal range in 64 (76%) and elevated in 20 (24%); free T4 index was elevated in 13 of 75 (16%), total T3 in 12 of 60 (20%), free T3 index in seven of 56 (13%), and TSH in 14 of 84 (17%) cases so studied. Serum TSH was subnormal in only one case (1%). Among the 14 patients with elevated serum TSH, serum free T4 index was normal in 12 and elevated in two. High serum T4 (or free T4 index) and high serum TSH were not correlated significantly by chi 2 analysis. None of the patients with elevated TSH demonstrated goiter or antithyroglobulin or antimicrosomal antibodies. On repeat testing 7 to 21 days after admission, serum TSH (and/or T4) normalized in the three of five patients studied. Serum TSH response to 500 micrograms intravenous (IV) thyrotropin-releasing hormone (TRH) was normal (serum TSH post-TRH, 8 to 28 microU/mL) in two patients with elevated TSH and T4, one patient with normal TSH and high T4, and one patient with normal TSH and T4. One patient with suppressed serum TSH (0.1 microU/mL) had elevated serum T4 (16.9 micrograms/dL, normal 4.8 to 11.5).(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1995

Effects of continuous and pulsatile administration of pituitary rat thyrotropin and recombinant human thyrotropin in a chronically cannulated rat.

Pulsatile secretion of thyrotropin (TSH) is a well characterized phenomenon in the human, yet only limited data are available from animal studies. We propose a combined model of chronic catheterization and suppression of endogenous TSH release in the rat allowing us to apply quantified pulses of different preparations of thyrotropin intravenously with minimal interference with endogenously produced hormone. Sprague-Dawley rats treated with drinking water containing 3,5,3'-triiodothyronine (T3) showed a significant 6-fold decrease of the rat TSH (rTSH) level after four days. Free thyroxine (FT4) levels were 9-fold below unsuppressed levels; FT4 response to exogenous TSH application above this suppressed baseline level was selected as an endpoint. Infusion studies compared pulsatile with continuous TSH administration. A low and a high dose of rTSH and recombinant human TSH (rec-hTSH) were administered. Levels of FT4 were compared after two and four days and responsiveness to a standard high bolus of rTSH 6 h after end of infusion was assessed. With regard to its potency for FT4 release, differences indicating a general trend as to superior efficiency of pulsatile TSH stimulation of the thyroid gland in comparison to continuous stimulation could be observed in all four experiments. More pronounced effects were seen after 2 and 4 days of high rTSH infusion and after 4 days of low rec-hTSH infusion. Comparison of FT4 responses to rTSH boli showed a 2- and 6-fold higher response in the pulsatile group compared to the continuous group after low and high rTSH infusion, respectively.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗