Thyrotropin Releasing Hormone

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Overview

What is Thyrotropin Releasing Hormone?

Chemically, TRH (protirelin) is identified as 5-oxo-L-prolyl-L-histidyl-L-proline amide. It is a synthetic tripeptide that is believed to be structurally identical to the naturally-occurring thyrotropin-releasing hormone produced by the hypothalamus. The CAS Registry Number is 24305-27-9. The structural formula is:

Figure 1

TRH is supplied as a solution of 1 mL in a 5 mL vial. Each vial contains 500 mcg protirelin, 1.8 mg Methylparaben, 0.2 mg Propylparaben, and 9.0 mg Sodium Chloride. TRH is intended for intravenous administration following dilution with 1 mL sterile water for injection

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TRH is indicated as an adjunctive agent in the diagnostic assessment of thyroid function. As an adjunct to other diagnostic procedures, testing with TRH (protirelin) may yield useful information in patients with pituitary or hypothalamic dysfunction.

TRH is indicated as an adjunct to evaluate the effectiveness of thyrotropin suppression with a particular dose of T4 in patients with nodular or diffuse goiter. A normal TSH baseline value and a minimal difference between the 30 minute and baseline response to TRH injection would indicate adequate suppression of the pituitary secretion of TSH.

TRH may be used, adjunctively, for adjustment of thyroid hormone dosage given to patients with primary hypothyroidism. A normal or slightly blunted TSH response, thirty minutes following TRH injection, would indicate adequate replacement therapy.

TRH is intended for intravenous administration with the patient in the supine position. The drug is administered as a bolus over a period of 15 to 30 seconds, with the patient remaining supine until all scheduled post injection blood samples have been taken. Blood pressure should be measured before TRH is administered and at frequent intervals during the first 15 minutes thereafter (see WARNINGS). Have the patient urinate before injecting TRH.

Adults: 500 μg. Doses between 200 and 500 μg have been used. 500 μg is considered the optimum dose to give the maximum response in the greatest number of patients. Doses greater than 500 μg are unlikely to elicit a greater TSH response.

Children age 6 to 16 years: 7 μg/kg body weight up to a dose of 500 μg.

Infants and children up to 6 years: Experience is limited in this age group; doses of 7μg/kg have been administered.

One blood sample for TSH assay should be drawn immediately prior to the injection of TRH, and a second sample should be obtained 30 minutes after injection.

The TSH response to TRH is reduced by repetitive administration of the drug. Accordingly, if the TRH test is repeated, an interval of seven days before testing is recommended.

Elevated serum lipids may interfere with the TSH assay. Thus, fasting (except in patients with hypopituitarism) or a low-fat meal is recommended prior to the test.

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Transient changes in blood pressure, either increases or decreases, frequently occur immediately following administration of TRH. Blood pressure should therefore be measured before TRH is administered and at frequent intervals during the first 15 minutes after its administration.

Increases in systolic pressure (usually less than 30 mm Hg) and/or increases in diastolic pressure (usually less than 20 mm Hg) have been observed more frequently than decreases in pressure. These changes have not ordinarily persisted for more than 15 minutes nor have they required therapy. More severe degrees of hypertension or hypotension with or without syncope have been reported in a few patients. To minimize the incidence and/or severity of hypotension, the patient should be supine before, during, and after TRH administration. If a clinically important change in blood pressure occurs, monitoring of blood pressure should be continued until it returns to base-line levels.

TRH should not be administered to patients in whom marked, rapid changes in blood pressure would be dangerous unless the potential benefit clearly outweighs the potential risk

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Clinical Information

Chemical Structure

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Clinical Pharmacology

Pharmacologically, TRH increases the release of the thyroid stimulating hormone (TSH) from the anterior pituitary. Prolactin release is also increased. It has recently been observed that approximately 65% of acromegalic patients tested respond with a rise in circulating growth hormone levels; the clinical significance is as yet not clear. Following intravenous administration, the mean plasma half-life of protirelin in normal subjects is approximately five minutes. TSH levels rise rapidly and reach a peak at 20 to 30 minutes. The decline in TSH levels takes place more slowly, approaching baseline levels after approximately three hours

Non-Clinical Toxicology

Transient changes in blood pressure, either increases or decreases, frequently occur immediately following administration of TRH. Blood pressure should therefore be measured before TRH is administered and at frequent intervals during the first 15 minutes after its administration.

Increases in systolic pressure (usually less than 30 mm Hg) and/or increases in diastolic pressure (usually less than 20 mm Hg) have been observed more frequently than decreases in pressure. These changes have not ordinarily persisted for more than 15 minutes nor have they required therapy. More severe degrees of hypertension or hypotension with or without syncope have been reported in a few patients. To minimize the incidence and/or severity of hypotension, the patient should be supine before, during, and after TRH administration. If a clinically important change in blood pressure occurs, monitoring of blood pressure should be continued until it returns to base-line levels.

TRH should not be administered to patients in whom marked, rapid changes in blood pressure would be dangerous unless the potential benefit clearly outweighs the potential risk

When probenecid is used to elevate plasma concentrations of penicillin or other betalactams, or when such drugs are given to patients taking probenecid therapeutically, high plasma concentrations of the other drug may increase the incidence of adverse reactions associated with that drug. In the case of penicillin or other beta-lactams, psychic disturbances have been reported.

The use of salicylates antagonizes the uricosuric action of probenecid (see ). The uricosuric action of probenecid is also antagonized by pyrazinamide.

Probenecid produces an insignificant increase in free sulfonamide plasma concentrations but a significant increase in total sulfonamide plasma levels. Since probenecid decreases the renal excretion of conjugated sulfonamides, plasma concentrations of the latter should be determined from time to time when a sulfonamide and probenecid are coadministered for prolonged periods. Probenecid may prolong or enhance the action of oral sulfonylureas and thereby increase the risk of hypoglycemia.

It has been reported that patients receiving probenecid require significantly less thiopental for induction of anesthesia. In addition, ketamine and thiopental anesthesia were significantly prolonged in rats receiving probenecid.

The concomitant administration of probenecid increases the mean plasma elimination half-life of a number of drugs which can lead to increased plasma concentrations. These include agents such as indomethacin, acetaminophen, naproxen, ketoprofen, meclofenamate, lorazepam, and rifampin. Although the clinical significance of this observation has not been established, a lower dosage of the drug may be required to produce a therapeutic effect, and increases in dosage of the drug in question should be made cautiously and in small increments when probenecid is being co-administered. Although specific instances of toxicity due to this potential interaction have not been observed to date, physicians should be alert to this possibility.

Probenecid given concomitantly with sulindac had only a slight effect on plasma sulfide levels, while plasma levels of sulindac and sulfone were increased. Sulindac was shown to produce a modest reduction in the uricosuric action of probenecid, which probably is not significant under most circumstances.

In animals and in humans, probenecid has been reported to increase plasma concentrations of methotrexate (see ).

Falsely high readings for theophylline have been reported in an study, using the Schack and Waxler technic, when therapeutic concentrations of theophylline and probenecid were added to human plasma.

General:

Thyroid hormones reduce the TSH response to TRH. Accordingly, patients in whom TRH is to be used diagnostically should be taken off liothyronine (T3) approximately seven days prior to testing and should be taken off thyroid medications containing levothyroxine (T4), e.g., desiccated thyroid, thyroglobulin, or liotrix, at least 14 days before testing. Hormone therapy is NOT to be discontinued when the test is used to evaluate the effectiveness of thyroid suppression with a particular dose of T4 in patients with nodular or diffuse goiter, or for adjustment of thyroid hormone dosage given to patients with primary hypothyroidism.

Chronic administration of levodopa has been reported to inhibit the TSH response to TRH.

It is not advisable to withdraw maintenance doses of adrenocortical drugs used in the therapy of known hypopituitarism. Several published reports have shown that prolonged treatment with glucocorticoids at physiologic doses has no significant effect on the TSH response to thyrotropin releasing hormone, but that the administration of pharmacologic doses of steroids reduces the TSH response. Therapeutic doses of acetylsalicylic acid (2 to 3.6 g/day) have been reported to inhibit the TSH response to protirelin. The ingestion of acetylsalicylic acid caused the peak level of TSH to decrease approximately 30% as compared to values obtained without acetylsalicylic acid administration. In both cases, the TSH peak occurred 30 minutes post-administration of protirelin.

Side effects have been reported in about 50% of the patients tested with TRH. Generally, the side effects are moor, have occurred promptly, and have persisted for only a few minutes following injection.

Cardiovascular reactions:

Marked changes in blood pressure, including both hypertension and hypotension with or without syncope, have been reported in a small number of patients.

Endocrine reaction:

Breast enlargement and leakage in lactating women for up to two or three days.

Other reactions:

Headaches, sometimes severe, and transient amaurosis in patients with pituitary tumors. Rarely, convulsions may occur in patients with predisposing conditions, e.g., epilepsy, brain damage. Nausea; urge to urinate; flushed sensation; light-headedness; bad taste in mouth; abdominal discomfort; and dry mouth.

Less frequently reported were:

Anxiety; sweating; tightness in the throat; pressure in the chest; tingling sensation; drowsiness; and allergic reactions.

Pituitary apoplexy requiring acute neurosurgical intervention has been reported infrequently for patients with pituitary macroadenomas following the acute administration of protirelin injection in the setting of combined anterior pituitary function testing in conjunction with LHRH and insulin.

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Reference

This information is obtained from the National Institute of Health's Standard Packaging Label drug database.
"https://dailymed.nlm.nih.gov/dailymed/"

While we update our database periodically, we cannot guarantee it is always updated to the latest version.

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Clonazepam Description Each single-scored tablet, for oral administration, contains 0.5 mg, 1 mg, or 2 mg Clonazepam, USP, a benzodiazepine. Each tablet also contains corn starch, lactose monohydrate, magnesium stearate, microcrystalline cellulose, and povidone. Clonazepam tablets USP 0.5 mg contain Yellow D&C No. 10 Aluminum Lake. Clonazepam tablets USP 1 mg contain Yellow D&C No. 10 Aluminum Lake, as well as FD&C Blue No. 1 Aluminum Lake. Chemically, Clonazepam, USP is 5-(o-chlorophenyl)-1,3-dihydro-7-nitro-2H-1,4-benzodiazepin-2-one. It is a light yellow crystalline powder. It has the following structural formula: C15H10ClN3O3 M.W. 315.72

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Interactions

A total of 440 drugs (1549 brand and generic names) are known to interact with Imbruvica (ibrutinib). 228 major drug interactions (854 brand and generic names) 210 moderate drug interactions (691 brand and generic names) 2 minor drug interactions (4 brand and generic names) Show all medications in the database that may interact with Imbruvica (ibrutinib).

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