Normal thyrotrophin response to intravenous thyrotrophin releasing hormone administration: the best index of optimal L-thyroxine therapy in primary hypothyroidism

Kabadi, Udaya M.

doi:10.1136/pgmj.61.718.685

Cited by 12 publications

(6 citation statements)

References 12 publications

(17 reference statements)

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“…Patients with the presence of any concomitant chronic disorder as well as those who were receiving chronic administration of other medications were excluded, since thyroid hormone metabolism is well documented to be disrupted resulting in altered circulatory thyroid hormone concentrations in presence of nonthyroidal illnesses (Chopra, Chopra, Smith, Reza and Solomon 1975;Chopra and Smith l975;Nomura, Pittman, Chambers, Buck and Shimizu 1975;Pittman, Suda, Chambers and Ray 1979;Fujii, Akai, Tanaka, Nakatani, Kinoshita, Seki and Wada 1981;Kabadi, Premachandra andMaayan 1982;Wartofsky and Burman 1982;Kabadi and Premachandra 1983;Kabadi and Premachandra 1984). All subjects were euthyroid as reflected by normal T4, T3 and basal TSH concentration as well as normal TSH response to IV TRH administration as described previously (Kabadi 1985;Kabadi and Rosman 1987). The healthy status of the subjects at the time of study was further confirmed by an absence of acute disorder, normal physical examination, normal blood chemistries and urinalyses.…”

Section: Methodsmentioning

confidence: 99%

“…We previously suggested that hyperglucagonemia may be one of the factors responsible for low serum T3 and high serum rT3 concentrations observed in 'euthyroid sick' states (Kabadi, Premachandra andMaayan 1982;Kabadi This study was supported by research grants from Veterans Administration and Narveen Medical Research Foundation, St. Louis, Missouri.…”

Section: Introductionmentioning

confidence: 96%

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Decline of T3 and Elevation in Reverse T3 Induced by Hyperglucagonemia: Changes in Thyroid Hormone Metabolism, Not Altered Release of Thyroid Hormone

Kabadi¹,

Premachandra²

1988

Horm Metab Res

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Recently we reported that hyperglucagonemia induced by glucagon infusion causes a decline in serum Triiodothyronine (T3) and a rise in reverse T3 (rT3) in euthyroid healthy volunteers. These changes in T3 and rT3 levels were attributed to altered T4 metabolism in peripheral tissues. However, the contribution of altered release of thyroid hormones by the thyroid gland could not be excluded. Since the release of thyroid hormones is suppressed by exogenous administration of L-thyroxine (L-T4) in appropriate dosage, we studied thyroid hormone levels for up to 6 hours after intravenous administration of glucagon in euthyroid healthy subjects after administration of L-T4 for 12 weeks. A control study was conducted using normal saline infusion. Plasma glucose rose promptly following glucagon administration demonstrating its physiologic effect. Serum T4, Free T4 and T3 resin uptake were not altered during both studies. Glucagon infusion induced a significant decline in serum T3 (P less than 0.01) and a marked rise in rT3 (P less than 0.01) whereas saline administration caused no alterations in T3 or rT3 levels. Thus the changes in T3 and rT3 were significantly different during glucagon study when compared to saline infusion. (P less than 0.01 for both comparisons). Therefore, this study demonstrates that changes in serum T3 and rT3 caused by hyperglucagonemia may be secondary to altered thyroid hormone metabolism in peripheral tissues and not due to altered release by the thyroid gland, since the release of thyroid hormones is suppressed by exogenous L-T4 administration.

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Section: Methodsmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 96%

Decline of T3 and Elevation in Reverse T3 Induced by Hyperglucagonemia: Changes in Thyroid Hormone Metabolism, Not Altered Release of Thyroid Hormone

Kabadi¹,

Premachandra²

1988

Horm Metab Res

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“…There has been much debate regarding the significance of undetectable TSH concentrations in patients taking thyroxine replacement who are considered clinically to be euthyroid. Although few studies have demonstrated over-exposure of tissues other than the pituitary to thyroxine, several reports have advocated maintaining pituitary responsiveness toTRH (Evered et al, 1973;Squire & Gimlette 1982;Wehman et al, 1983;Davis et al, 1984;Kabadi, 1985). It is now possible to measure basal TSH levels by sensitive assays which can predict the response to TRH in most of these patients (Spencer et al, 1986;Wheatley et al, 1987).…”

Section: Introductionmentioning

confidence: 99%

Restoration of Normal Thyrotrophin Secretion Reduces the Abnormally High Serum Glutathione S‐transferase Levels Found in Patients Receiving Thyroxine Replacement Therapy

Gow

Caldwell

Toft

et al. 1988

Clinical Endocrinology

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The peripheral tissue thyroid status of 12 patients receiving thyroxine replacement therapy was investigated both when pituitary secretion of TSH was suppressed and later, when on a lower dose of thyroxine that restored thyrotroph responsiveness. Heart rate and various analytes in serum known to be sensitive to thyroid status were measured in addition to TSH by immunoradiometric assay. Initially, the serum T4 concentration was raised in seven patients and free T4 raised in nine; all patients had normal T3 concentrations. Later, on the lower dose of thyroxine, most patients had concentrations of thyroid hormones within reference limits. Concentrations of the liver-specific form of glutathione S-transferase (GST) in serum decreased (P less than 0.01) after the reduction in thyroxine dose; abnormally high GST levels, found in eight patients when TSH was suppressed, returned to normal in six of these patients when normal basal and TRH-stimulated TSH concentrations had been restored. The response of the pituitary to excess thyroxine may be more representative of other tissues (e.g. the liver) than previously thought.

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“…Thyrotropin‐releasing hormone stimulation test was performed at this time in which serum TSH concentrations were determined before as well as 30 and 60 minutes after IV administration of TRH (500 μg). Thyroid‐stimulating hormone response (ΔTSH) was noted to be within normal range established in our laboratory (5 to 25 μ U/mL) 6 . The patient was readministered “disalcid” 3 g/day for six weeks and thyroid function tests as well as serum salicylate concentrations were evaluated by the same commercial laboratory as done initially.…”

Section: Case Reportmentioning

confidence: 81%

Misleading Thyroid Function Tests and Several Homeostatic Abnormalities Induced by “Disalcid” Therapy

Kabadi

Danielson

1987

J American Geriatrics Society

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S everal drugs are reported to inhibit thyroid hormone binding to serum proteins resulting in alteration in values of thyroid function tests in euthyroid subjects.'-" In this paper we report a patient who presented with thyroid function tests suggestive of secondary or tertiary hypothyroidism and several other metabolic abnormalities while on salsalate (disalcid) therapy. All metabolic abnormalities as well as thyroid function tests returned to normal on withdrawal of "disalcid," thus suggesting that the patient was euthyroid and the abnormalities of thyroid function tests were factitious. The patient's euthyroid state was further confirmed by the finding of normal thyroid-stimulating hormone (TSH) responses to IV thyrotropin-releasing hormone (TRH) administration prior to as well as during readministration of "disalcid" which again induced lowering of T4 and Free T4 concentrations. CASE REPORTAn 82-year-old white woman presented to family practice health clinic at Lutheran Medical Center, Des Moines, Iowa, with complaints of increasing fatigue, tiredness, lethargy, and generalized weakness of several days duration. On inquiry, she denied changes in body weight and anorexia. No muscle cramps were reported, however, she related a history of constipation and cold intolerance. Physical examination re-From the Induced vealed an alert and oriented elderly woman looking younger for her age, and in no distress. Pulse rate was 76/min with blood pressure 130/85 mmHg. Thyroid gland was not palpable and there was no pedal edema or lymphadenopathy. Skin appeared normal and there was no pallor or clubbing of fingers. Systemic examination showed normal heart size and sounds, devoid of murmur and normal breath sounds. Abdominal examination was essentially unremarkable with no organomegaly or ascites. Neurological examination revealed no focal signs. Muscles were normal with no wasting or fasciculations. Deep tendon reflexes were somewhat decreased in all extremities without apparent delayed relaxation phase observed in patients with hypothyroidism and cerebellar function was intact. Thyroid function tests were evaluated because of several symptoms suggestive of hypothyroidism which are often mistakenly attributed to old age and also because of a known increased incidence of hypothyroidism in elderly "assymptomic" p~pulation.~ These tests included Serum Tl, T3 resin uptake, Free T4/ and TSH concentration which were determined by a commercial laboratory. Complete blood count, serum electrolytes, and blood chemical profile as well as urinalysis were assessed simultaneously at the hospital laboratory to determine the cause of patient's symptoms.These tests showed a normal complete blood count, mild metabolic acidosis, hypouricemia, abnormal liver profile, as well as lowering of T4 and Free T4 levels with normal TSH concentration (Tables 1 and 2). At the next visit, the patient was questioned more thoroughly regarding use of any medications, because of abnormal laboratory findings. She revealed that she was taking 3 to 4 g of "disal...

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Normal thyrotrophin response to intravenous thyrotrophin releasing hormone administration: the best index of optimal L-thyroxine therapy in primary hypothyroidism

Cited by 12 publications

References 12 publications

Decline of T3 and Elevation in Reverse T3 Induced by Hyperglucagonemia: Changes in Thyroid Hormone Metabolism, Not Altered Release of Thyroid Hormone

Decline of T3 and Elevation in Reverse T3 Induced by Hyperglucagonemia: Changes in Thyroid Hormone Metabolism, Not Altered Release of Thyroid Hormone

Restoration of Normal Thyrotrophin Secretion Reduces the Abnormally High Serum Glutathione S‐transferase Levels Found in Patients Receiving Thyroxine Replacement Therapy

Misleading Thyroid Function Tests and Several Homeostatic Abnormalities Induced by “Disalcid” Therapy

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