Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0432222 (SEM)
 47,337 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Thyrotropin-releasing hormone (TRH) has been shown to be present and have actions in the human gastrointestinal tract. We have studied urine TRH immunoreactivity (TRH-ir) levels in healthy subjects and patients with acute pancreatitis, gallstones, ulcerative colitis, or acute gastritis. The urine samples were prepurified by SP-Sephadex-C-25 cation exchange chromatography, subjected to reverse-phase high-pressure liquid chromatography, and assayed in our TRH radioimmunoassay. The mean urine TRH immunoreactivity values of healthy subjects were 4.42 +/- 1 ng/l (x +/- SEM); of patients with acute pancreatitis on the 1st day of hospitalization, 23 +/- 7 ng/l; on the 2nd day, 7 +/- 1 ng/l; and on the 3rd day 9 +/- 2 ng/l. Only the urine TRH levels of the pancreatitis patients on day 1 differed significantly (p less than 0.05) from the levels of the healthy subjects. Circulating TRH appears to be derived mostly from the pancreas, where the islets during acute pancreatitis are affected, and TRH is released into circulation and urine.
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PMID:Increased urinary levels of thyrotropin-releasing hormone immunoreactivity in acute pancreatitis. 241 Sep 74

Biological tests may help clarify the relationships of schizoaffective disorder to both major depressive disorder and schizophrenia. Thyrotropin-releasing hormone (TRH), 500 micrograms i.v., was administered to 14 schizodepressed, 23 schizophrenics, 41 unipolar major depressives (all by RDC) and 45 healthy controls, all males 20-67 years old with no significant differences in age, body height or weight. Results showed no differences in maximal delta TSH (dTSH max) amongst schizoaffective depressed, schizophrenia and healthy control groups (10.1 +/- 1.3, 9.2 +/- 1.1, 9.7 +/- 0.8 microU/ml, means +/- SEM respectively). Mean major depressives' dTSH max was lower than in each of the other three groups (6.2 +/- 0.4 microU/ml, P less than 0.01 for all). Utilizing a less than or equal to 5.0 microU/ml cut-off criterion for blunting, the schizodepressed had 36%, schizophrenics 44%, healthy controls 22% and major depressed 59% blunters (P less than 0.05 from other three groups). Schizodepressed patients appeared significantly different from major depressed but closer to schizophrenics (and healthy controls) on the TRH test.
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PMID:Thyrotropin response to thyrotropin-releasing hormone in RDC schizodepressed men. 297 Apr 96

Thyrotropin-releasing hormone (TRH) and insulin were measured by radioimmunoassay in acetic-acid extracts of 19 pancreatic islet cell tumors induced by streptozotocin and nicotinamide in rats. In addition, gel filtration properties of TRH-immunoreactivity and immunoreactive insulin (IRI) were examined in 5 and 14 tumors, respectively. TRH was demonstrated in 10 of 19 tumors, with a mean of 166 +/- 47 (SEM) pg/mg wet weight, whereas the concentration was less than 3 pg/mg wet weight in the other tumors. In contrast, all tumors contained IRI, with a mean of 11.0 +/- 1.6 micrograms/mg wet weight. Ten tumors in which TRH was demonstrated contained more IRI than those in which TRH was not detected (13.1 +/- 1.8 vs 6.5 +/- 1.7 micrograms/mg wet weight, P less than 0.02). After gel filtration, all TRH immunoreactivity was eluted at the same place as synthetic TRH in the 5 tumors. In addition, gel filtration elutes showed essentially the same pattern of IRI in the 14 tumors, with 3 peaks. The predominant IRI peak comigrated with marker insulin (95.7 +/- 0.8%), another prominent peak occurred coincident with proinsulin standard (3.3 +/- 0.5%), a third peak was present in the void volume (0.28 +/- 0.04%). These distributions of IRI were similar to those in extracts of normal pancreases. The present studies demonstrate TRH immunoreactivity in pancreatic islet cell tumors induced by streptozotocin and nicotinamide in rats. Chemically induced insulinomas can serve as a model for insulin storage which is analogous to islet B cells.
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PMID:Thyrotropin-releasing hormone and insulin in chemically induced pancreatic islet cell tumors in rats. 302 23

Thyroliberin (TRH) has been reported to be synthesized in anterior pituitary. Modulations of anterior pituitary concentrations of TRH and its precursor (proTRH) were investigated in rats rendered hypothyroid for 21 and 48 days. In hypothyroid rats, as expected, plasma TSH levels were increased and plasma free T4 concentrations were reduced, whereas anterior pituitary concentrations of TRH were markedly increased (mean +/- SEM fmol/mg protein, 106.9 +/- 21.1 at 21 days and 181.8 +/- 59.0 at 48 days vs 42.2 +/- 13.4 in controls). Significant increases of proTRH concentrations were found in hypothyroid rats (mean +/- SEM fmol/mg protein, 266.5 +/- 16.7 at 21 days and 320.4 +/- 51.1 at 48 days vs 214.1 +/- 18.3 in controls). Daily administration of L-T4 for the last week of PTU treatment (days 41 to 48) reversed hypothyroidism by lowering plasma TSH levels and by increasing plasma free T4 concentrations. Concomitantly, T4 administration significantly decreased anterior pituitary TRH contents (114.4 +/- 35.9) as well as proTRH contents (250.4 +/- 11.7). The fact that hypothyroidism regulates anterior pituitary TRH and proTRH contents strengthens the view that TRH might play a role in local regulatory mechanisms within the anterior pituitary on the thyrotropic function.
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PMID:Hypothyroidism increases TRH and TRH precursor levels in rat anterior pituitary. 802 68

A monoclonal antibody against gonadotropin releasing hormone (GnRH)-BSA was used in the development of a sensitive enzyme immunoassay of GnRH in the canine hypothalamus and in plasma. The method had a limit of detection of 4 pg per sample. The intra- and interassay coefficients of variation were < 7.3% and < 11.0%, respectively. Acid extracts of hypothalamus produced a dose response curve which was parallel to that obtained with the synthetic GnRH standard. Checking cross reactivity of various fragments of GnRH revealed that the antibody was formed predominantly against the C-terminal end of GnRH. Thyrotropin-releasing hormone and other hypothalamic hormones did not appear to influence the assay. In male dogs, hypothalamic GnRH levels increased with age up to 4 months, then fell to a plateau from 6 months to 2 years. The time required for a 50% reduction in plasma levels following intravenous administration of synthetic GnRH to five adult male dogs was 2.2 +/- 0.1 (SEM) min.
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PMID:Enzyme immunoassay of gonadotropin releasing hormone in the canine hypothalamus and plasma using monoclonal antibodies. 802 40

We have retrospectively studied 41 patients with hypothalamic-pituitary disease and central hypothyroidism associated with hypopituitarism. Sixteen patients had nonsecreting pituitary macroadenoma, whereas different sellar and suprasellar pathologies affected all other patients. Pretreatment thyrotropin (TSH) level (mean +/- standard error of the mean [SEM]) was 2.04 +/- 0.25 mU/L (normal, 0.4-4), and gradually decreased to 0.51 +/- 0.19 mU/L (range, 0.009-3.38) by treatment with levothyroxine in a mean dose of 86 +/- 6 microg/d. TSH was suppressed by thyroid replacement to less than 0.5 mU/L in 80% of patients. Mean baseline free thyroxine (FT4) was 7.55 +/- 0.51 pmol/L (normal, 11.8-24.6) and gradually increased with thyroid hormone to 15.19 +/- 1.0 pmol/L, whereas total thyroxine (TT4) increased from 57.4 +/- 2.6 to 104.4 +/- 5.0 nmol/L (normal, 77-154). Mean pretreatment total triiodothyronine (TT3) was 1.44 +/- 0.09 nmol/L (normal, 1.1-2.7), and was not altered by treatment. Thyrotropin-releasing hormone (TRH) test was performed in 20 patients before thyroid replacement, and mean baseline and peak TSH levels were 1.33 +/- 0.3 and 7.14 +/- 1.62 mU/L, respectively. In 5 subjects TSH was stimulated to 6 mU/L or more, whereas in 5 others TSH was not affected. Based on linear regression of logarithm (Ln) TSH against FT4, a leftward shift of the TSH/FT4 ratio was demonstrated in patients with central hypothyroidism compared to 17 patients with primary hypothyroidism. Plotting measurements of TSH against FT4 for 6 individuals with central hypothyroidism showed different regression slope for each patient. Suppression of TSH by thyroid replacement to levels below 0.1 mU/L predicted euthyroidism in 92% of cases, compared to 34% when TSH was above 1 mU/L (p < 0.0001). In conclusion, in central hypothyroidism baseline TSH is usually within normal values, and is further suppressed by exogenous thyroid hormone as in primary hypothyroidism, but to lower levels. Thus, insufficient replacement may be reflected by inappropriately elevated TSH levels, and may lead to dosage increment.
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PMID:Thyrotropin suppression by thyroid hormone replacement is correlated with thyroxine level normalization in central hypothyroidism. 1248 49

To evaluate the effect of long-term clomipramine administration on the hypothalamic-pituitary-thyroid axis in healthy dogs, 14 healthy adult dogs were enrolled in a prospective study. Clomipramine (3 mg/kg PO q12h) was administered to all dogs beginning on day 0, and continued for 112 days. Serum total thyroxine (T4), free thyroxine (fT4), 3,5,3'-triiodothyronine (T3), 3,3',5'-triiodothyronine (reverse T3; rT3), and thyroid-stimulating hormone (TSH) were measured on days 0, 7, 28, 42, 56, and 112. Thyrotropin-releasing hormone (TRH) response tests were performed concurrently. Significant decreases were noted in serum T4, f4, and rT3 concentrations beginning on day 28 through the end of the study period. The lowest mean (+/-SEM) concentrations of T4 (26 +/- 1.2 to 17 +/- 0.5 nmol/L) and rT3 (1.21 +/- 0.13 to 0.83 +/- 0.08 nmol/L) occurred at day 112, whereas the lowest mean fT4 (29 +/- 2.4 to 18 +/- 1.7 pmol/L) was found on day 56 of clomipramine treatment. The effect of treatment over time on serum T3 concentration also was significant, but the deviation in T3 from baseline was variable. No significant effect of clomipramine treatment was noted on either pre- or post-TRH TSH concentrations. The 35 and 38% decreases in serum T4 and fT4 concentrations, respectively, during clomipramine administration may lead to a misdiagnosis of hypothyroidism. Although no evidence of hypothyroidism was noted in this study population, subclinical hypothyroidism may have occurred. A longer duration of treatment might further suppress thyroid function, and concurrent illness or other drug administration might exacerbate clomipramine's effects.
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PMID:Evaluation of the effects of clomipramine on canine thyroid function tests. 1256 26