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Biomedical subjects

L Wartofsky

Publications and source records attributed to L Wartofsky.

At least 163 records · Page 9Linked to original sources
PubMed1975

Hemiagenesis of the thyroid gland.

Three patients with hemiagenesis of the typhoid gland are described. One was clinically euthyroid, whereas the other two were more unusual in that one had coincident Graves' disease with thyrotoxicosis, and one had primary myxodema. In all three cases diagnosis of hemiagenesis was established by the administration of thyroid-stimulating hormone (TSH). The literature on hemiagenetic thyroid glands with and without associated thyroid disease is reviewed. Although the anomaly is uncommon, awareness and recogniton of its existence may clarify an otherwise puzzling clinical thyroid evaluation, and thus possible avert an unnecessary surgical procedure.

Adult↗
PubMed1975

Failure of oral water loading and intravenous hypotonic saline to suppress plasma prolactin in man.

To test the effect of acute changes in plasma osmolality on plasma prolactin concentrations, the hormone was measured before and during oral water loading, hypotonic saline infusion, and hypertonic saline infusion in normal subjects. In 10 normal men there was a small but statistically significant rise in mean prolactin, from 7.6 to 12.3 ng/ml, occurring within half an hour after the ingestion of a water load of 20 ml/kg. A small but statistically insignificant rise in mean plasma prolactin was observed in 11 normal women, although there was a significant negative correlation between plasma prolactin and plasma osmolality in these subjects. No effect of the intravenous infusion of either hypotonic saline (0.45%) or hypertonic saline (5%) on mean plasma prolactin was noted in 5 normal men. These studies do not confirm a previously reported suppression of prolactin concentrations by oral water loading of hypotonic saline infusions in normal subjects. While the data suggest a negative correlation between plasma osmolality and plasma prolactin, at least after water loading, they do not support a physiological role for prolactin in the short-term regulation of plasma osmolality in humans.

Administration, Oral↗
PubMed1975

Failure of propranolol to alter thyroid iodine release, thyroxine turnover, or the TSH and PRL responses to thyrotropin-releasing hormone in patients with thyrotoxicosis.

A dual isotope method allowing simultaneous analysis of both endogenous thyroidal release and peripheral thyroxine disposal was employed in four patients with thyrotoxicosis before and during propranolol therapy (160 mg/day) to determine whether beta adrenergic blockade with this agent affected the secretion or metabolism of thyroid hormone. Since catecholamines may be involved in the regulation of both thyrotropin (TSH) and prolactin (PRL) release from the pituitary, the effect of propranolol on the TSH and PRL responses to thyrotropin-releasing hormone (TRH) was also examined. In the dosage employed in these patients, propranolol had no demonstrable effect on either thyroid hormone secretion, the peripheral disposal of T4, or the TSH and prl responses to TRH.

Humans↗
PubMed1975

Effect of an oral water load on serum TSH in normal subjects, and on TSH and prolactin response to thyrotropin-releasing hormone (TRH) in patients with primary hypothyroidism.

Reports of suppression of plasma prolactin (PRL) in humans by water loading led us to examine the effect of a 20 cc/kg water load on serum TSH in 21 normal volunteers. In addition, the effects of a water load on basal and TRH-stimulated TSH and PRL levels were evaluated in seven patients with primary hypothyroidism. The water load had no effect on pasal serum TSH levels in either normal or hypothyroid subjects, and did not alter the TSH response to TRH in hypothyroid subjects. Basal or TRH-stimulated plasma PRL was also unaffected by water loading in the hypothyrpid subjects. These data suggest that a water load of 20 cc/kg does not significantly affect TSH release by the anterior pituitary, and also provide further evidence that water loading does not consistently suppress PRL secretion.

Administration, Oral↗
PubMed1975

Klinefelter's syndrome: examination of thyroid function, and the TSH and PRL responses to thyrotropin-releasing hormone prior to and after testosterone administration.

Thyroid function and prolactin (PRL) responsiveness to thyrotropin-releasing hormone (TRH) were examined in 6 patients with Klinefelter's syndrome prior to and after therapy with testosterone. The thyroid function tests, including serum triiodothyronine (T3), thyroxine (T4), thyroxine binding globulin (TBG), resin T3 uptake (RT3U), radioactive iodine uptake (RAIU), thyrotropin (TSH) stimulation and the TSH response to TRH were normal during both periods of study. Testosterone treatment had no significant effect on any of these parameters with the exception of the RT3U which increased. PRL response to TRH were significantly higher than those observed in normal men (P less than 0.05). Despite the fact that mean plasma PRL responses to TRH were decreased when the patients were restudied during testosterone therapy, they remained greater than those of normal men. Mean serum estradiol concentrations were normal and did not increase significantly during testosterone therapy. These studies suggest that: (1) thyroid function may be normal in patients with Klinefelter's syndrome more often than previously reported, and (2) patients with Klinefelter's syndrome may manifest PRL hyper-responsiveness to TRH that is decreased but not normalized during testosterone therapy. Because estradiol levels failed to increase despite a marked rise in testosterone, further studies are warranted to examine testosterone and estradiol clearance and conversion rates in patients with Klinefelter's syndrome.

Adolescent↗
PubMed1972

Alterations in thyroid iodine release and the peripheral metabolism of thyroxine during acute falciparum malaria in man.

Previous studies of thyroid function during various infections have yielded conflicting results, but most have suggested an acceleration of peripheral thyroxine (T(4)) turnover during the acute infectious illness. In the present studies, thyroid function was examined by a method allowing simultaneous analysis of both endogenous thyroidal release and peripheral T(4) disposal in normal volunteers after induction of acute falciparum malaria. Subjects received iodide-(125)I, followed in 5-7 days by (131)I-T(4) intravenously. 4 days later, infection was induced by the injection of parasitized red blood cells. Bidaily measurements of serum protein-bound (125)I and protein-bound (131)I, and urinary (125)I and (131)I, together with frequent estimates of serum (127)I-T(4) (Murphy-Pattee) and free T(4) (FT(4)), were made during a control period, during acute illness, and during convalescence. Alterations in the peripheral metabolism of (131)I-T(4) during infection included significant decreases in the fractional disappearance rate for T(4) [(k)], and in the clearance and daily disposal of T(4), all of which returned to control values during convalescence. Total serum (127)I-T(4) increased late in the infected period to become greater during convalescence than either before or during infection, while FT(4) did not increase significantly until convalescence. An analysis of serum (131)I-T(4)/(127)I-T(4) and (131)I-T(4)/PB(125)I ratios confirmed these observations. The slope with time of ratios for urinary (125)I/(131)I, a reflection of thyroidal iodine release, was decreased during infection, but rebounded to control values during the convalescent period. The observed increments in serum (127)I-T(4) concentration in the convalescent phase may reflect in part the slowing of (k), but together with the rising ratios of urine (125)I/(131)I suggests enhanced thyroidal T(4) secretion immediately after the acute illness. Thus, with malarial infection, there appears to be an initial depression followed by a rebound in rates of thyroidal iodine release. In contradistinction to other infections, fractional turnover and daily disposal of hormone is decreased in malaria, perhaps due to hepatic dysfunction and the consequent impairment in cellular deiodinative processes.

Antimalarials↗
PubMed1970

Inhibition by iodine of the release of thyroxine from the thyroid glands of patients with thyrotoxicosis.

A method has been devised which is free of many of the shortcomings of serial epithyroid counting techniques as an index of the rate of thyroid hormone secretion. By means of this method, the effect of treatment with Lugol's iodine on the rate of thyroidal secretion of thyroxine (T(4)) has been assessed in eight patients with thyrotoxicosis due to diffuse or multinodular goiter. The technique involves administration of a tracer dose of inorganic (125)I followed several days later by an intravenous tracer dose of (131)I-labeled T(4). Serial observations of serum protein-bound (PB) (125)I and (131)I are accompanied by frequent measurements of endogenous serum T(4) (T(4)-(127)I) concentration. Regardless of whether or not its administration was anteceded and accompanied by the administration of large doses of methimazole, iodine induced a rapid decrease in serum T(4)-(127)I concentration which could not be explained by an increase in the peripheral turnover of T(4), as judged from the metabolism of the (131)I-labeled hormone. Hence, the decreased serum T(4) concentration could only have resulted from decreased secretion of the hormone by the gland. Analyses of specific activity relationships between PB(125)I or T(4)-(127)I and PB(131)I made possible estimations of the extent to which iodine had decreased the rate of secretion of T(4). From such analysis, and in view of other considerations, it is concluded that the rapid decrease in T(4) secretion induced by iodine is not the result of an acute, sustained inhibition of T(4) synthesis, but rather results from an abrupt decrease in the fractional rate of thyroidal T(4) release.

Adult↗
PubMedDate not supplied

Iodine treatment of iodine-induced thyrotoxicosis.

A 62-year-old female who had received prolonged iodine therapy for asthma presented with severe thyrotoxicosis and severe asthma. Her history, elevated serum thyroxine and triiodothyronine, low 131I uptake, and elevated intrathyroidal iodine content by fluorescent scan were most consistent wiht a diagnosis of iodine-induced thyrotoxicosis (IITT). The clinical course of her thyrotoxicosis was protracted, and in spite of its etiologic role in the precipitaton of thyrotoxicosos, iodine was therapeutically efficacious, although combined treatment with methimazole was required to ultimately restore euthyroidism. Therapy with lithium was also employed but appeared to be only transiently effective and combined no additional decrement in serum T4 than that seen with iodine alone. The case exemplifies the heterogeneity of what is considered "iodine-induced" thyrotoxicosis, the complexities inherent in establishing a diagnosis of IITT, and the use of other rapid acting pharmacologic agents in IITT when beta blockade is contraindicated by asthma.

Asthma↗