TRH Stimulation Research Articles

Association of thyroid-stimulating immunoglobulins and thyrotropin-releasing hormone responsiveness in women with euthyroid goiter.

Thyroid-stimulating immunoglobulins (TSI) were measured, using a highly sensitive cytochemical bioassay, in plasma from 26 euthyroid women with idiopathic diffuse or multinodular goiter selected on the basis of their serum TSH responses to TRH stimulation. Thirteen were chosen because they were previously identified to have impairment in TRH responsiveness and were compared with 13 consecutive patients who had normal responses to TRH. TSI were present in a significantly greater number of those who had subnormal TRH responses (11:13) compared to those who had normal responses (3:13) P less than 0.005. Although serum T4, T3, and basal TSH values were all within the normal range, mean serum T4 and T3 values were significantly higher and basal TSH significantly lower in the 14 patients who had TSI than in the 12 in whom TSI was absent. The coexistence of impaired TRH responsiveness and TSI was associated with a family history of thyroid disease. The data suggest that TSI in patients with euthyroid goiter cause a modest increase in thyroid secretion sufficient to blunt the TSH response to TRH but not to cause clinical hyperthyroidism.

Influence of dopaminergic inhibition on serum levels of thyrotrophin and prolactin in patients with hypothyroidism before and after prolonged oral administration of TRH.

Forty mg TRH/day given orally for 3 weeks to 8 patients with mild primary hypothyroidism decreased serum TSH from a mean of 4.0 ng/ml +/- 1.2 (SE) to 2.0 ng/ml +/- 0.4 (49%), and their mean incremental TSH response to iv TRH was equally reduced from 8.6 ng/ml +/- 2.5 to 4.0 ng/ml +/- 1.9 (46%). In the same patients serum Prl was 8.2 ng/ml +/- 2.2 before oral TRH treatment and 6.6 ng/ml +/- 1.5 (81%) after treatment, and the mean incremental Prl response to iv TRH was reduced from 43.5 ng/ml +/- 5.0 to 35.9 ng/ml +/- 7.5 (83%). The oral administration of 10 mg of the dopamine antagonist metoclopramide increased mean serum TSH from 0.6 ng/ml +/- 0.1 (SE) to 0.7 ng/ml +/- 0.1 (120%) in euthyroid subjects and from 4.0 ng/ml +/- 1.2 to 5.7 ng/ml +/- 1.6 (145%) in patients with primary hypothyroidism, and mean serum Prl from 8.6 ng/ml +/- 0.8 to 109.5 ng/ml +/- 24.3 (1251%) and from 8.2 ng/ml +/- 2.2 to 119.6 ng/ml +/- 45.5 (1460%), respectively. The incremental TSH responses to iv TRH increased 2.3-fold in euthyroid subjects pre-treated with metoclopramide, while no change was observed in the TSH responsiveness in patients with primary hypothyroidism following metoclopramide pre-treatment. In the euthyroid subjects metoclopramide treatment had no effect on the Prl response to iv TRH.(ABSTRACT TRUNCATED AT 250 WORDS)

Calcium influx is not required for TRH to elevate free cytoplasmic calcium in GH3 cells.

TRH stimulation of prolactin secretion is thought to be mediated by an elevation of free cytoplasmic Ca2+. However, whether TRH-induced influx of extracellular Ca2+ is required to elevate cytoplasmic Ca2+ remains controversial. We measured cytoplasmic free Ca2+ concentration in GH3 cells with an intracellularly trapped fluorescent indicator, Quin 2. In unstimulated cells incubated in medium containing 1.5 mM Ca2+, cytoplasmic free Ca2+ concentration was 118 +/- 18 nM (mean +/- SD). TRH (1 microM) caused a rapid transient elevation of free cytoplasmic Ca2+ to a level estimated to be at least 500 nM. High extracellular K+, which induces extracellular Ca2+ influx, caused an elevation of free cytoplasmic Ca2+ which was greater and longer in duration that that caused by TRH. When cells were incubated in medium containing 3 mM EGTA, the K+ depolarization-induced increase in free cytoplasmic Ca2+ was abolished. By contrast, the TRH-induced increase was not affected by incubating cells in medium with 3 mM EGTA, or high K+, or both; incubation of cells in medium with EGTA and high K+ abolishes the electrochemical driving force for Ca2+ influx. These data demonstrate that Ca2+ influx is not required for TRH-induced elevation of free cytoplasmic Ca2+ in GH3 cells. We conclude that in GH3 cells TRH induces an elevation of free cytoplasmic Ca2+ leading to stimulated prolactin secretion by mobilizing cellular Ca2+.

Human pancreatic growth hormone-releasing factor-40 (hpGRF-40) allows stimulation of GH release by TRH.

The effects of synthetic hpGRF-40 on GH release from continuously perifused male rat anterior pituitary cells were studied. Pulses (2.5 min) of hpGRF-40 stimulated GH release in a log-linear dose response relationship: concentrations of 0.03, 0.1, 0.3, 1, 3, 10, 30 and 100 nM given in a random order elicited a GH response above baseline of 1.2 +/- 0.3, 2.4 +/- 0.4, 2.8 +/- 0.2, 4.3 +/- 0.2, 6.2 +/- 0.7, 7.0 +/- 1.0, 8.7 +/- 1.7, and 10.8 +/- 0.8 micrograms/10(7) cells (mean +/- SEM; n = 3; r = 0.93), respectively. During a 5-h hpGRF-40 infusion, GH stimulation peaked within 5 min and waned to near baseline by the end of the fifth h. The integrated GH responses to 0.03, 0.1 and 0.3 nM hpGRF-40 were 37.6 +/- 7.4, 52.9 +/- 8.5, and 66.15 +/- 8.2 micrograms/10(7) (mean +/- SEM; n = 3; r = 0.72), respectively. The interaction of TRH and hpGRF-40 in the control of GH secretion was studied to investigate the mechanism of the "paradoxical" TRH stimulation of GH release associated with GH excess states in humans. Dispersed cells were perifused with either 100 nM TRH for 0.5 h, 5 nM hpGRF-40 for 4 h, or 5 nM hpGRF-40 for 4 h, to which a 0.5 h pulse of TRH was added at 2 h. GH levels did not change significantly in the presence of TRH alone. When TRH was added to the ongoing hpGRF-40 perifusion, GH release increased from 1.4 +/- 0.06 to 4.0 +/- 1.0 micrograms/min.10(7) cells (n = 4; P = 0.03). Thus, dispersed pituitary cells are highly sensitive to very low concentrations of hpGRF-40 administered as both an acute pulse and as a tonic infusion. When the cells are exposed to a maximal concentration of hpGRF-40 (i.e. 5 nM), TRH becomes a secretagogue at the pituitary level, thus suggesting the site and mechanism of the "paradoxical" GH response to TRH observed in some acromegalics.

The interrelationships between prolactin and thyrotrophin secretion following dopaminergic blockage in patients with mild hyperprolactinaemia without any demonstrable pituitary tumour.

PRL, TSH and gonadotrophin responses to the dopaminergic antagonist, metoclopramide, were studied in mildly hyperprolactinaemic patients with normal sella radiology and CT scan. Eleven female patients with basal PRL levels ranging from 23 to 124 ng/ml were challenged with intravenous metoclopramide (10 mg) and on subsequent occasions with TRH (200 micrograms) and LHRH (100 micrograms). On the basis of the PRL secretory pattern following metoclopramide and TRH stimulation, the patients were divided into two groups. Group I comprised six subjects who were PRL non-responsive to TRH and metoclopramide. Group II (five subjects) demonstrated PRL responses to TRH and metoclopramide indistinguishable from female controls. Mean +/- SD basal PRL levels were 68.5 +/- 29.9 ng/ml in Group I and not different in Group II (40.6 +/- 12.0 ng/ml). Basal LH levels were increased in Group II, whereas FSH was increased in Group I. Basal TSH levels were lower in Group I than the controls. Following metoclopramide, Group I patients had an increase in TSH from a basal of 2.4 +/- 0.7 microU/ml to a peak of 5.9 +/- 2.7 microU/ml (P less than 0.005) which occurred at 30 min. TSH values were increased above basal at all time intervals following metoclopramide. In contrast, TSH levels did not change in Group II patients or the controls after metoclopramide administration. Both patient groups had TSH responses to TRH similar to the controls. Following LHRH, the LH increase was greater in Group II and the FSH in Group I. In neither group nor the controls did gonadotrophin levels change after metoclopramide. In Group II females, PRL responsiveness to metoclopramide was associated with TSH non-responsiveness. In Group I females, PRL levels failed to rise, whereas TSH increased. The PRL and TSH profile in Group I females is typical of a prolactinoma. It is concluded that PRL as well as TSH determinations following metoclopramide are useful indices in the assessment of hyperprolactinaemia and may be of value in differentiating the functional state from that of a pituitary tumour.

Ipodate restores the fasting-induced decrement in thyrotropin secretion.

Radiocontrast agents decrease T4 to T3 conversion and enhance the TSH response to TRH stimulation in the postabsorptive state. Since fasting is a condition in which T4 and T3 conversion is decreased and TSH responses are diminished, we designed the present study to determine if ipodate, a radiocontrast agent, could affect either iodothyronine levels or TSH responsiveness in this condition. It was anticipated that the use of ipodate during fasting would supply information relating to the mechanism of the fasting-induced decrement in TSH. Furthermore, the administration of physiological amounts of T3, either alone or in combination with ipodate, allowed us to examine the possibility in vivo that ipodate might block pituitary T3 uptake and subsequent biological action. Twenty-four euthyroid obese subjects were randomly allocated to one of four groups, although the general study design, consisting of 6 days of a weight-maintaining diet, followed by 9 days of fasting, was identical. TRH was administered on day...

Diminution of prolactin and increase of thyrotrophin response to thyrotrophin releasing hormone occurring independently of changes in basal level of these hormones during treatment of hypothyroidism.

In order to study the effect of rising thyroid hormone levels in hypothyroidism upon prolactin responses to TRH, in relation to changes in basal prolactin concentration and to changes in TSH responses, we followed 18 patients by performing TRH tests before and after 14, 28, 42 and 56 d on gradually increasing levothyroxine dosages, plus a final test when euthyroidism was achieved. Basal prolactin rose initially, at day 14, followed by a return on days 28, 42 and 56 to a level similar to the pretherapeutic value, while at euthyroidism prolactin had fallen below the original value. The area under the prolactin response curve on TRH stimulation was unchanged at 14 d, notwithstanding the rise of basal prolactin concentration. At 28, 42 and 56 d the responses declined progressively along with basal prolactin concentrations that remained equivalent to the pretreatment level. The TSH response to TRH rose at 14, 28, and 42 d along with a continuous downward course of basal TSH. Thus, substitution with L-thyroxine inhibited the responsivity of prolactin but enhanced that of TSH to TRH. The fact that these changes occurred in opposite directions, appears to rule out a negative feed-back effect of T4 on hypothalamic TRH secretion. The effects on responses were shown to occur independently of those on basal secretion of prolactin and TSH.

Visual field defects and pituitary enlargement in primary hypothyroidism.

In 14 patients with overt primary hypothyroidism, we examined visual fields by Goldmann's isopter perimetry. An unexpectedly high incidence (10 patients, 71.4%) of visual field defects was found. Two patients complained of visual failure, whereas 12 had no subjective symptoms. The extent of visual field change varied over a wide range, from early chiasmal compression to apparent bitemporal hemianopsia. The abnormality was characteristically restriction in the central visual field; peripheral vision was less often affected. The sella turcica was significantly enlarged in these patients as compared to controls. The volume of the sella turcica correlated significantly with both basal serum TSH and total pituitary reserve of TSH (r = 0.82, P less than 0.001). There was no correlation between the extent of visual field change and the volume of the sella turcica or pituitary TSH reserve. Of 10 patients with visual field defects, 8 improved during 1-4 months of T4 replacement. In 2 patients, however, the visual field defect deteriorated during replacement. The deterioration occurred when serum TSH levels had decreased to about 50% and 20% of pretreatment values, respectively. The peak serum TSH after TRH stimulation was higher at the time of deterioration than before treatment. Visual fields became normal during treatment with an increased dose of T4 (200 micrograms/day), when serum TSH was suppressed to an undetectable level. The paradoxical course of visual failure during T4 replacement may be due to an imbalance between TSH synthesis in the pituitary and TSH release which may induce an increase in pituitary size. The data suggest that visual field defects and their deterioration are due to pituitary hyperplasia and are reversible with T4 replacement. In order to rule out a pituitary tumor, hypothyroid patients with visual failure should be followed during T4 replacement therapy.

Effects of trifluoperazine on rat prolactin, growth hormone, thyroid stimulating hormone and adrenocorticotrophin secretion in vitro

We have studied the effects of trifluoperazine, a proposed inhibitor of calmodulin directed cellular function, on adrenocorticotrophic hormone (ACTH), thyroid stimulating hormone (TSH), prolactin (Prl) and growth hormone (GH) secretion from primary cultures of rat adenohypophyseal cells. 5 X 10(-6)M and 10(-5)M trifluoperazine caused a significant (P less than 0.005) reversible dose-related decrease in basal Prl secretion but was less effective on basal GH secretion, significant reversible inhibition (P less than 0.005) occurring only with 10(-5)M. Trifluoperazine did not consistently alter basal ACTH or TSH secretion but did inhibit 10(-2)M theophylline stimulation of ACTH, Prl and GH secretion and 1.5 X 10(-7)M TRH stimulation of TSH and Prl secretion. Paradoxically 10(-5)M trifluoperazine enhanced theophylline stimulation of TSH secretion. Our results show trifluoperazine to have differential effects on Prl, GH, ACTH and TSH secretion, which are consistent with the known calcium dependence of pituitary hormone secretion and may suggest a role for calmodulin in this process.

Excess of beta-subunit of thyrotropin (TSH) in patients with idiopathic central hypothyroidism due to the secretion of TSH with reduced biological activity.

alpha-Subunit and beta-subunit of TSH were measured in the sera of five patients with idiopathic central hypothyroidism due to the secretion of biologically inactive TSH, in seven normal controls matched for bone age and sex, and in five subjects with mild primary thyroid failure before and after TRH (200 micrograms, iv) stimulation. Basal serum alpha-subunit concentration in patients did not differ from that in normal controls (mean +/- SD, 0.40 +/- 0.20 vs. 0.38 +/- 0.28 ng/ml; P, NS), whereas TSH and TSH-beta were significantly higher in patients (TSH, 1.51 +/- 0.74 vs. 0.59 +/- 0.53 ng/ml, P less than 0.025; TSH-beta, 0.56 +/- 0.18 vs. 0.10 +/- 0.02 ng/ml, P less than 0.001). The concentration of TSH-beta was also significantly higher in patients with central hypothyroidism than in subjects with mild primary thyroid failure (0.56 +/- 0.18 vs. 0.24 +/- 0.08 ng/ml; P less than 0.01), although serum TSH levels did not differ in the two groups (1.51 +/- 0.74 vs. 2.16 +/- 0.52 ng/ml; P, NS). alpha-Subunit was significantly higher in primary hypothyroid subjects (1.50 +/- 0.87, P less than 0.05 compared with patients with central hypothyroidism). After TRH, alpha-subunit, TSH, and TSH-beta net increases (peak) were significantly higher in patients with central hypothyroidism than in normal controls (alpha-subunit: 0.95 +/- 0.5 vs. 0.47 +/- 0.19 ng/ml, P less than 0.05; TSH: 7.1 +/- 3.1 vs. 2.9 +/- 1.8 ng/ml, P less than 0.005; TSH-beta: 0.89 +/- 0.35 vs. 0.22 +/- 0.18 ng/ml, P less than 0.005), whereas they did not significantly differ from those recorded in hypothyroid controls. The beta/alpha ratio, which was 1.67 +/- 0.86 in patients and 0.35 +/- 0.18 in normal controls (P less than 0.005), slightly decreased after TRH to 1.24 +/- 0.78 in patients, but remained unchanged in normal controls (0.39 +/- 0.1). After TRH the alpha-subunit peak occurred at 20 min both in patients and in controls, whereas TSH and TSH-beta peaked at 60 min in patients and at 20 min in controls. One patient was given oral TRH (40 mg/day for 4 weeks). The beta/alpha ratio fell from 1.85 to 0.13. Interestingly, serum thyroid hormones, which did not increase after iv TRH and after the first doses of oral TRH, showed a definite increase. Sera from two patients were filtered on Sephadex G-100: in one of them TSH-beta eluted in the same position as labeled reference standard, whereas in the other one radioimmunoassayable TSH-beta eluted near the void volume. The above data indicate that in patients with idiopathic central hypothyroidism due to biologically inactive TSH there is an excess of circulating TSH-beta and suggest that TRH is implicated in the secretion of TSH of full biological potency.

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Down-Regulation of Prolactin Secretion in Men during Continuous Thyrotropin-Releasing Hormone Infusion: Evidence for Induction of Pituitary Desensitization by Continuous TRH Administration

TRH was administered as a 5-h constant rate iv infusion (5 micrograms/min) to seven healthy adult men. Serum samples were collected at regular intervals for measurement of PRL, TSH, and T3. Serum levels of PRL during TRH infusion increased sharply to maximum level by 40 min, and then, despite continued TRH stimulation, PRL levels declined gradually to a plateau value after 100 min. No further rise in serum PRL was observed when a bolus of 200 micrograms TRH was administered to three subjects after 240 min of infusion. Conversely, an iv bolus of sulpiride (25 mg), a dopaminergic antagonist, given to four subjects after 240 min, brought about a marked increase in serum PRL values above the plateau level. These results are consistent with the interpretation that down-regulation in PRL secretion which follows the initial peak of response most likely represents pituitary desensitization to TRH. During the infusion serum TSH increases in two phases. A first phase of secretion was observed by 40 min followed by a plateau, with a second phase of increase occurring between 80-180 min.

Calcium influx is not required for thyrotropin-releasing hormone stimulation of prolactin release from GH 3 cells

TRH stimulation of prolactin release from GH 3 cells is dependent on Ca 2+; however, whether TRH-induced influx of extracellular Ca 2+ is required for stimulated secretion remains controversial. We studied prolactin release from cells incubated in medium containing 110 mM K + and 2 mM EGTA which abolished the electrical and Ca 2+ concentration gradients that usually promote Ca 2+ influx. TRH caused prolactin release and 45Ca 2+ efflux from cells incubated under these conditions. In static incubations, TRH stimulated prolactin secretion from 11.4±1.2 to 19±1.8 ng/ml in control incubations and from 3.2±0.6 to 6.2±0.8 ng/ml from cells incubated in medium with 120 mM K + and 2 mM EGTA. We conclude that Ca 2+ influx is not required for TRH stimulation of prolactin release from GH 3 cells.

Relationship between cerebrospinal fluid amine metabolites, neuroendocrine findings and personality dimensions (Marke-Nyman scale factors) in psychiatric patients.

5-Hydroxyindoleacetic acid (5-HIAA) and homovanillic acid (HVA) were measured in the spinal fluid of 45 women hospitalized in a psychiatric department for major depression (14 cases), schizophrenia (18 cases) and alcohol dependence (13 cases). Dexamethasone suppression tests were performed following CSF examinations in all patients, and TRH stimulation tests were also made in six subjects. All biological examinations were carried out in a drug-free state. The Marke-Nyman Temperament scale was administered to all patients as soon as severe psychotic disturbances subsided and sufficient cooperation was achieved, but no later than 10 days following biological examinations. The MNT was repeated after recovery to check reliability of the test results during an episode of a psychiatric disorder. CSF amine metabolite concentrations did not differ significantly in the three patient groups; postdexamethasone average cortisol levels were above the critical level (5 micrograms/dl) in each group, the highest values being found in major depression. One of the three MNT factors was inhomogeneous among diagnostic groups (validity: low in depression and alcoholism), but the other two also differed from a healthy control population. Correlation structure between biological and psychological variables was homogeneous throughout the diagnoses and a significant inverse correlation was found only between CSF 5-HIAA and the validity factor of MNT. Maximal TSH response to TRH stimulation correlated with both solidity and stability in the MNT scale. Since MNT results proved to be stable even during an illness episode, a possible link is suggested between personality traits and central serotonin metabolism.

Hypothalamic-pituitary function in patients with prolonged coma.

In eight patients (six males and two females) hospitalized for prolonged coma (164-1320 days; five patients were in traumatic coma, two after cardiac arrest during surgery, and one after a venomous scorpion sting), diurnal variation of cortisol secretion, human (L) GH, PRL, TSH secretion as well as the release of the pituitary hormones after TRH and L-dopa stimulation were assessed. Serum T4 cortisol, hGH, hPRL, and hTSH levels were normal. The cortisol diurnal variation was preserved in six patients. In seven of eight patients, the hPRL and hTSH responses to TRH test were normal and in five patients, there was a rise of more than 150% in serum hGH concentrations. After L-dopa administration, five patients responded with a rise in hGH. In three patients, there was no response of hGH to TRH or L-dopa. Five patients responded with significant reduction in the serum hPRL concentration after L-dopa, and in three patients, no change was observed. It was concluded that patients with prolonged coma have variable hypothalamic pituitary function. They preserve the cortisol diurnal variation and the hypothalamic-pituitary-thyroid axis as well as PRL secretion; however, hGH secretion may respond abnormally to various stimuli.

Different prolactin, thyrotropin, and thyroxine responses after prolonged intermittent or continuous infusions of thyrotropin-releasing hormone in rhesus monkeys.

Serum PRL, TSH, and T4 secretion during prolonged continuous or intermittent iv infusions of TRH were studied in 14 adult ovariectomized rhesus monkeys (Macaca mulatta). For 9 days, TRH was administered intermittently at 0.33 or 3.3 micrograms/min for 6 of every 60 min and continuously at 0.33 micrograms/min. With both modes, the PRL levels and responsiveness to TRH simulation peaked on day 1 and then fell to levels that were still higher than the preinfusion values; levels for the intermittently treated group on days 3-9 were 2- to 4-fold above prestimulation levels and significantly (P less than 0.01) higher than levels for the continuously treated group. Elevated basal levels and PRL responses to TRH pulses were similar during the 0.33 and 3.3 micrograms/min pulses of the 9-day treatment period. For both TRH modes, TSH levels were elevated significantly (P less than 0.001) on day 1 [this increase was higher with continuous infusion (P less than 0.001)] and then fell to preinfusion levels by day 3. Serum T4 also increased during both continuous and intermittent TRH stimulations. However, serum T4 levels were significantly lower (P less than 0.01) after intermittent TRH (both 0.33 and 3.3 micrograms/min) than after continuous (0.33 micrograms) TRH (8 +/- 1.1 and 10 +/- 1.8 micrograms T4/dl vs. 18 +/- 3.1 micrograms, respectively). These PRL and T4 responses were replicated when the mode of administering 0.33 micrograms/min TRH was reversed after 9 days. An iv bolus of TRH (20 micrograms) after 9 days of continuous or intermittent TRH infusion caused significant release of PRL and TSH, an indication that neither mode of administration resulted in pituitary depletion of releasable hormone. We have concluded that intermittent TRH is more effective in elevating serum PRL, and continuous TRH is more effective in raising TSH and T4 levels. Thus, the manner of TRH secretion by the hypothalamus may determine its relative physiological importance in the stimulation of lactotropes and thyrotropes.

Comparison of plasma thyroxine levels following short exposure to cold and TRH administration in intact and pituitary autografted quail ( Coturnix coturnix japonica)

The thyrotropic functional abilities of ectopically transplanted anterior pituitaries were tested by subjecting quail bearing their adenohypophysis in juxtarenal position either to a short cold exposure or to an intravenous injection of TRH. Thyroxine was determined in plasma samples collected from 20 to 120 min after treatment. Intact birds exhibited increasing T 4 levels up to a peak at 40 min, then decreasing slowly within 2 hr after either cold or TRH stimulation. Autografted birds exhibited significant although lower and delayed increase of plasma thyroxine following both stimuli.

Thyroid function tests in thyroid and nonthyroid disease.

Modern day evaluation of thyroid disorders requires a combination of accurate clinical judgement and reliable, sensitive, and specific thyroid functions tests. Principle among the latter are thyroxine (T4) 3, 5, 3'-triiodothyronine (T3), and thyroid-stimulating hormone (TSH). Also playing an important role in special situations are free thyroxine, an assessment of bound and unbound thyroid-binding globulin, TRH stimulation, long-acting thyroid stimulator (LATS), antibodies to thyroid hormone and to thyroid receptors. Basic to interpretation of these tests in the clinical setting is a comprehension of the relationship of the hypothalamus, the pituitary, and the thyroid gland as well as a knowledge of the peripheral metabolism of thyroxine and triiodothyronine. The role of each of these laboratory tests in the evaluation of hyper- and hypometabolic states, their alteration in nonthyroid and other endocrine disorders, and the effects of environmental and physiological factors on these tests are reviewed.

Evaluation of Thyroid Function in Patients Treated with Continuous Ambulatory Peritoneal Dialysis (CAPD)

Abnormal thyroid function has been described in chronic renal insufficiency, and further changes occur with increasing time on hemodialysis. This study on two groups of patients was done to determine whether treatment with CAPD induces changes in thyroid function. Group A included 16 patients with an average duration of treatment of 2.1 ± 1.1 months; group B included 12 patients with 8.1 ± 2 months. We measured total T4 and T3, free T4, TBG, RT3U, FTI, T4/T3 and basal TSH, and TSH induced by TRH stimulation in plasma, and total and free T4 in dialysate. The results showed a significant decrease in total T4 and T3 in plasma, but no change in free T4 or TSH and no appreciable amounts of the hormones in the dialysate. We believe the decrease in total T4 and T3 is secondary to alterations in transport proteins while thyroid function is maintained by normal free T4 and TSH levels more dependable parameters for the interpretation of thyroid function in chronic diseases.

Effect of induced hyperprolactinemia on the plasma levels of C19 steroids in humans

In order to investigate the relationship between the increment of plasma prolactin (PRL) levels and the change of plasma levels of PRL, DHEA-S, cortisol, aldosterone and 17 alpha OH delta 5-P were quantified by respective RIA in patients treated with TRH parenterally or with sulpiride orally. The results were as follows: During the infusion of TRH, plasma levels of PRL reached the maximal values within 30 min and then declined gradually in spite of continued TRH stimulation. Sulpiride given orally for 12 consecutive days in the luteal phase of the menstrual cycle caused a significant increase in the plasma PRL level. This increase was higher than that obtained in the experiment during the follicular phase. No significant change in the plasma level of 17 alpha OH delta 5-P was observed TRH sulpiride administration. In 3 out of 9 cases, plasma DHEA-S levels were elevated significantly on day 13 to 14 of the experimental course. These results indicate that the responsiveness of plasma levels of adrenal androgens to the raised plasma PRL level requires a certain period of time in the hyperprolactinemic state in the human female.