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Biomedical subjects

E Endert

Publications and source records attributed to E Endert.

At least 91 records · Page 5Linked to original sources

Soluble receptors for tumor necrosis factor are markers for clinical course but not for major metabolic changes in human immunodeficiency virus infection.

Tumor necrosis factor alpha (TNF) is a potential mediator of the metabolic changes in human immunodeficiency virus type 1 (HIV) infection. Soluble TNF receptor types I and II (sTNFR-I and -II) presumably reflect TNF activity. To examine the relationship between s TNFRs and host metabolism, resting energy expenditure (REE), body composition, and transferrin, albumin, triglyceride, retinol-binding protein, and sTNFR concentrations were measured in 12 asymptomatic and 18 symptomatic HIV-infected male subjects and 15 male control subjects. sTNFRs were increased in parallel with disease severity. REE was elevated approximately 8% in HIV-infected subjects (P = .005). REE correlated positively with fat free mass (FFM) and the presence of HIV infection, but not with sTNFRs. Inverse correlations existed between sTNFR-I or -II and albumin concentration (r = -.48, P = .007, and r = -.49, P = .006, respectively), between sTNFR-II and transferrin concentration (r = -.53, P = .003), and between In(sTNFR-II) and percent body fat (r = -.37, P < .05), but not between sTNFRs and triglyceride or retinol-binding protein. Thus, sTNFRs are markers for clinical course but not for major metabolic changes in HIV infection.

Adult↗

Liquorice-induced hypertension--a new understanding of an old disease: case report and brief review.

The case is described of a 40-year-old female with severe hypertension and hypokalaemic metabolic alkalosis, due to prolonged liquorice ingestion. The pseudo-aldosterone-like effects of liquorice have always been attributed to glycyrrhizic acid, but its biochemical substrate has remained elusive. It is now known that glycyrrhetenic acid, the hydrolytic metabolite of glycerrhizic acid, is the active component of liquorice which causes inhibition of the peripheral metabolism of cortisol. Cortisol binds with the same affinity as aldosterone to the mineralocorticoid receptor resulting in a hypermineralocorticoid condition. Ingestion of liquorice may therefore result in retention of sodium and water, hypertension, hypokalaemia, alkalosis and suppression of the renin-aldosterone system. The literature on liquorice-induced hypertension is briefly reviewed with emphasis on the biochemical features of this mineralocorticoid excess syndrome.

Adult↗

Endocrinologic and metabolic effects of interleukin-6 in humans.

Interleukin-6 (IL-6) is one of the major circulating cytokines in catabolic states. To investigate its endocrinologic and metabolic actions in vivo, we studied eight patients with metastatic renal cell cancer two times, once during infusion of saline (control) and once during a 4-h infusion of 150 micrograms recombinant human IL-6 (rhIL-6). Rates of appearance (Ra) of glucose and free fatty acids (FFA) in plasma were measured by using the isotope dilution method. Energy expenditure and substrate oxidation were determined by indirect calorimetry. rhIL-6 induced increases in plasma norepinephrine (+261 +/- 97%, P < 0.001), cortisol (+210 +/- 48%, P < 0.001), and glucagon (+70 +/- 18%, P < 0.001), in resting energy expenditure (+25 +/- 2%, P < 0.001 vs. control), and in plasma FFA concentration (+60 +/- 30%, P < 0.001), FFA Ra (+105 +/- 18%, P < 0.001), and fat oxidation (+38 +/- 16%, P < 0.001). Glucose Ra increased by 20 +/- 5% (P < 0.01) during rhIL-6 infusion with a concomitant increase in the metabolic clearance rate of glucose. In conclusion, our data demonstrate that rhIL-6 induces many of the endocrinologic and metabolic changes found in catabolic states and thus may mediate some of the metabolic effects previously ascribed to other cytokines.

Blood↗

Truncal vagotomy does not affect postabsorptive glucose metabolism in humans.

To evaluate the effects of hepatic vagal denervation on the adaptation of glucose metabolism to short-term starvation (i.e., < 24 h), glucose metabolism was studied after 16 and again after 22 h of fasting in postsurgical patients with truncal vagotomy (n = 9; radical resection of esophageal carcinoma) and without truncal vagotomy (n = 5; partial resection of the large bowel for carcinoma). Glucose metabolism was studied 3-7.5 mo postoperatively by [3-3H]glucose turnover and by indirect calorimetry. Basal glucose production, plasma glucose concentration, glucose oxidation, serum free fatty acid concentration, and fat oxidation were not different between groups; neither were plasma concentrations of glucoregulatory hormones. The adaptation to prolongation of the fast by 6 h was not different for any of these parameters between both groups. In conclusion, truncal vagotomy does not affect the adaptation of glucose metabolism to the postabsorptive state (16-22 h of fasting).

Aged↗

Acute effects of interferon-alpha administration on thyroid hormone metabolism in healthy men.

Both hyper- and hypothyroidism have been reported during prolonged recombinant human interferon-alpha (rhIFN alpha) therapy. To assess the short term effects of IFN alpha therapy on thyroid hormone metabolism, we measured thyroid hormone concentrations in eight healthy volunteers for 24 h after sc administration of rhIFN alpha and, on another occasion, after sc administration of saline (control study). There were no effects of rhIFN alpha on plasma T4 and free T4 or on thyroid hormone binding index. However, rhIFN alpha induced a significant decrease in the plasma concentrations of TSH (P < 0.03) and T3 (P < 0.02) compared with those in the control study, associated with an increase in rT3 concentrations (P < 0.02). IFN alpha induced a moderate increase in interleukin-6 (IL-6) concentrations (P < 0.02 vs. control study), whereas IL-1 and tumor necrosis factor concentrations remained below the detection limit in all subjects. It is concluded that IFN alpha administration induces major changes in thyroid hormone metabolism, possibly mediated in part by IL-6. The acute effects of rhIFN alpha mimic the euthyroid sick syndrome and appear to be different from the effects of chronic rhIFN alpha treatment on thyroid hormone metabolism.

Adult↗

Interleukin-1 receptor blockade does not affect endotoxin-induced changes in plasma thyroid hormone and thyrotropin concentrations in man.

Interleukin-1 (IL-1) has been implicated as a mediator of the euthyroid sick syndrome. The effects of IL-1 can be blocked by the naturally occurring IL-1 receptor antagonist (IL-1ra). In the present study, iv administration of endotoxin was used as a human model of the euthyroid sick syndrome. To assess the role of endogenous IL-1 in endotoxin-induced changes in plasma thyroid hormone and TSH concentrations, 18 healthy postabsorptive humans were studied on a control study day, followed 3 days later by a study day on which they were randomly assigned to one of three treatments: a 6-h infusion of recombinant human IL-1ra alone (133 mg/h), endotoxin alone (lot EC-5; 20 U/kg), or both endotoxin and IL-1ra. Administration of IL-1ra alone did not affect the plasma concentrations of thyroid hormones or TSH compared with those on the control day. Endotoxin injection was associated with decreases in T4 (P = 0.06 vs. the control day), free T4 (P = 0.02), T3 (P < 0.001), and TSH (P < 0.0001) and a rise in rT3 (P < 0.001), reproducing the major features of the euthyroid sick syndrome. Coinfusion of IL-1ra did not influence these endotoxin-induced changes. Our results suggest that endogenous IL-1 does not play an important role in the alterations in plasma thyroid hormone and TSH concentrations induced by mild endotoxemia in healthy humans.

Adult↗

Increased basal glucose production in type 1 Gaucher's disease.

To evaluate the metabolic effects of Gaucher's disease, glucose metabolism and parameters of fat metabolism were studied by indirect calorimetry and primed continuous infusion of [3-3H]glucose in seven clinically stable untreated patients with type 1 Gaucher's disease and in seven healthy matched control subjects. Studies were performed in the postabsorptive state. In Gaucher patients, resting energy expenditure was increased by approximately 24% (29.4 +/- 0.7 vs. 23.7 +/- 0.8 kcal/kg.day; P < 0.01). Glucose production was increased by approximately 30% in patients compared to controls (14.00 +/- 0.51 vs. 10.77 +/- 0.26; P < 0.01), although plasma glucose concentrations and net glucose oxidation were not different. Although C peptide concentrations were not different, insulin concentrations were slightly increased in Gaucher patients (P < 0.05). The differences in basal glucose production were not related to differences in plasma concentrations of insulin or other glucoregulatory hormones. In conclusion, the increase in basal glucose production is a remarkable feature of type 1 Gaucher's disease, which cannot merely be explained by endocrine mechanisms. Because Gaucher's disease is manifested within the liver in macrophages, but not in hepatocytes, altered intrahepatic regulatory mechanisms might be involved in this increase in glucose production.

Adaptation, Physiological↗

Sex differences in the adaptation of glucose metabolism to short-term fasting: effects of oral contraceptives.

The adaptation to long-term starvation is different in men and women. To evaluate whether there are also sex differences during short-term fasting (< 24 hours), we studied glucose metabolism after 16 and again after 22 hours of starvation in healthy subjects: six men, six women in both the follicular and luteal phases of their menstrual cycle, and six women on oral contraceptives ([OCC] day 12 of cycle). Glucose oxidation was measured by indirect calorimetry, and hepatic glucose output by infusion of 3-3H-glucose. There were no differences in hepatic glucose output between men and women during short-term fasting. The basal (16 hours) plasma glucose concentration was lower in women on OCC than in men (P < .05). Prolongation of the postabsorptive state induced a similar decline in plasma glucose concentrations in all groups. Basal (16 hours) glucose oxidation was lower in women on OCC than in men (P < .05). Prolongation of the postabsorptive state by 6 hours caused a significant decrease in glucose oxidation only in men. After 22 hours of fasting, glucose oxidation was lower in women on OCC than in women with normal menstrual cycles. In conclusion, the metabolic adaptation to the postabsorptive state (< 24 hours of fasting) is regulated differently in women on OCC as compared with women with normal menstrual cycles and men. These differences preclude inclusion of women on OCC in studies of glucose metabolism in the postabsorptive state.

Adaptation, Physiological↗

Pulsatile thyrotropin secretion in patients with Cushing's syndrome.

Pulsatile and circadian thyrotropin (TSH) secretion were studied in 16 healthy controls and in three patients with Cushing's syndrome who were studied twice (before and after treatment). Blood was sampled every 10 minutes over 24 hours for TSH (immunoradiometric assay [IRMA]). Mean 24-hour TSH in Cushing's syndrome was lower than in controls (0.4 +/- 0.2 v 1.7 +/- 0.7 mU/L, P < .001), related to a lower mean 24-hour TSH pulse amplitude (Desade: 0.16 +/- 0.15 v 0.44 +/- 0.20 mU/L, P < .001; Cluster: 0.17 +/- 0.14 v 0.39 +/- 0.20 mU/L, P < .001; mean +/- SD). TSH pulse frequency was unchanged with approximately 10 pulses/24 h. The nocturnal TSH surge was diminished relative to controls (median-0, range- -0.03 to 0.2 mU/L v 0.9 and 0.3 to 2.5 mU/L, respectively), related to a loss of the usual nocturnal increase in TSH pulse amplitude, but not of TSH pulse frequency. In the eucorticoid state, there was an increase of mean 24-hour TSH to 1.3 +/- 0.8 mU/L (P < .001) under normalization of the mean 24-hour TSH pulse amplitude. The nocturnal TSH surge also increased (median, 0.21; range, 0.15 to 0.4 mU/L) under restoration of the usual nocturnal increase in TSH pulse amplitude. In conclusion, Cushing's syndrome is associated with a decrease of mean 24-hour plasma TSH, related to a decrease of TSH pulse amplitude (not of TSH pulse frequency). The nocturnal TSH surge is decreased in Cushing's syndrome associated with a loss of the usual nocturnal increase of TSH pulse amplitude.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

Thyroid function and thyroid size in normal pregnant women living in an iodine replete area.

OBJECTIVE: The interpretation of the changes in thyroid hormone concentrations during normal pregnancy is a matter of debate involving, in some geographical regions, enhanced thyroid activity in early pregnancy and a hypothyroid state in the third trimester. A clinically detectable increase in thyroid size has been found in areas of mild iodine deficiency ('goitre of pregnancy'), but not in iodine replete areas. DESIGN: A prospective study. We have studied thyroid size and function in normal pregnant women living in an iodine replete area. PATIENTS: Healthy women before and during a normal pregnancy resulting from artificial insemination (n = 10) and other women during the normal menstrual cycle (n = 11), in the iodine replete area of Amsterdam. MEASUREMENTS: Thyroid volume was measured by ultrasonography. Plasma T4, free T3, free reverse T3, TSH, thyroxine binding globulin, hCG, progesterone and thyroid autoantibodies were measured. RESULTS: Thyroid volume did not change during pregnancy (data given before pregnancy and during 1st, 2nd and 3rd trimesters, respectively: 10.3 +/- 5.1, 10.6 +/- 4.4, 9.6 +/- 3.8 and 9.4 +/- 3.0 ml, NS). Free T4 and free T3 levels declined during pregnancy (13.7 +/- 2.0, 13.5 +/- 4.1, 11.2 +/- 2.8, 10.2 +/- 1.6 pmol/l, P = 0.005; 4.55 +/- 0.63, 4.64 +/- 0.88, 3.72 +/- 0.67 and 4.01 +/- 0.75 pmol/l, P = 0.003), whereas free reverse T3 levels increased during pregnancy (0.16 +/- 0.04, 0.19 +/- 0.07, 0.14 +/- 0.03 and 0.20 +/- 0.07 pmol/l, P = 0.001). Thyroglobulin levels remained unchanged. Thyroid hormones and thyroid volume did not differ between follicular and luteal phases of the menstrual cycle. CONCLUSION: Thyroid volume does not increase during pregnancy in iodine-replete areas. The decrease in free T4 and free T3 and the increase in free reverse T3 concentrations during pregnancy resemble the changes in thyroid hormones seen in non-thyroidal illness. This could be a physiological adaptation enabling energy conservation during the high metabolic demands of pregnancy.

Environment↗

Increased cortisol levels in aging and Alzheimer's disease in postmortem cerebrospinal fluid.

The hypothalamo-pituitary-adrenal (HPA) axis is activated during aging and even more so in dementia. Increased levels of corticosteroids may be neurotoxic. Therefore we have investigated cortisol levels in cerebrospinal fluid (CSF) of Alzheimer patients and controls. Ventricular postmortem CSF was collected from clinically and neuropathologically well-defined Alzheimer patients (n = 26) and control subjects (n = 21). In the group of Alzheimer patients the mean CSF total cortisol level was 83% higher than that in the controls. In presenile Alzheimer patients (< 65 years of age; n = 13) the CSF-cortisol level was 5 times higher than that of presenile controls (n = 7). In contrast, senile Alzheimer patients (n = 13) and controls of over 65 years of age (n = 14) did not show a significant difference in CSF-cortisol levels. The presence or absence of a difference in the cortisol-CSF levels in, respectively, presenile or senile Alzheimer patients as compared to controls was due to the 3.5-fold rise of CSF-cortisol in control subjects over 65 years of age as compared with controls under 65 years of age. The CSF-cortisol levels in presenile and senile Alzheimer patients were similar. No significant correlation was observed in the Alzheimer patients between age of onset of the dementia and CSF cortisol levels or duration of Alzheimer's disease and CSF cortisol levels. The finding that in senile Alzheimer patients cortisol levels were similar to those of unaffected age-matched controls does not seem to support the cortisol neurotoxicity hypothesis.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

Noradrenaline inhibits lipopolysaccharide-induced tumor necrosis factor and interleukin 6 production in human whole blood.

Sepsis and lipopolysaccharide (LPS) trigger the systemic release of both cytokines and catecholamines. Cytokines are known to be capable of eliciting a stress hormone response in vivo. The present study sought insight into the effect of noradrenaline on LPS-induced release of tumor necrosis factor alpha (TNF) and interleukin 6 (IL-6) in human whole blood. Whole blood was incubated with LPS for 4 h at 37 degrees C in the presence and absence of noradrenaline and/or specific alpha and beta antagonists and agonists. Noradrenaline caused a dose-dependent inhibition of LPS-induced TNF and IL-6 production. This effect could be completely prevented by addition of the specific beta 1, antagonist metoprolol, while it was not affected by the alpha antagonist phentolamine. Specific beta-adrenergic stimulation by isoprenaline mimicked the inhibiting effect of noradrenaline on LPS-evoked cytokine production, whereas alpha-adrenergic stimulation by phenylephrine had no effect. Fluorescence-activated cell sorter analysis demonstrated that beta-adrenergic stimulation had no effect on LPS binding to and internalization into mononuclear cells or on the expression of CD14, the major receptor for LPS on mononuclear cells. In acute sepsis, enhanced release of noradrenaline may be part of a negative feedback mechanism meant to inhibit ongoing TNF and IL-6 production.

Adult↗

Pentoxifylline inhibits basal glucose production in humans.

Adenosine stimulates hepatic glucose production in vitro. To investigate whether pentoxifylline, a xanthine derivative that blocks the adenosine receptor, inhibits basal glucose production, we measured hepatic glucose production in eight healthy postabsorptive subjects on two occasions: during continuous infusion of pentoxifylline and, in a control study, during saline infusion. Glucose production was measured by primed continuous infusion of [3-3H]glucose. Pentoxifylline infusion resulted in an approximately 22 (volume of distribution for glucose 40 ml/kg) to approximately 46% (volume of distribution for glucose 165 ml/kg) decrease in basal glucose production within approximately 1 h (P < 0.05), whereas in the control experiment glucose production declined by only approximately 4% in this time interval (P < 0.03 pentoxifylline vs. control). There were no differences in concentrations of insulin, C peptide, glucagon, or catecholamines between the two experiments. Because pentoxifylline inhibited glucose production in the absence of any changes in concentrations of glucoregulatory hormones, we conclude that pentoxyifylline inhibits hepatic glucose production through other mechanisms, e.g., by blocking the adenosine receptor.

Adult↗

Effects of acute and chronic interleukin-6 administration on thyroid hormone metabolism in humans.

Cytokines, such as tumor necrosis factor-alpha and interleukin-1 beta (IL-1 beta), alter thyroid hormone metabolism, and may be involved in the pathogenesis of the euthyroid sick syndrome. Both cytokines also induce the production of IL-6. To assess whether IL-6 itself modulates thyroid hormone metabolism, we studied the acute and chronic effects of recombinant human IL-6 (rhIL-6) on thyroid hormone concentrations in patients with renal cell cancer. In the first study protocol, plasma thyroid hormone concentrations were measured during a 4-h infusion of rhIL-6 (150 micrograms) or, on another day, during infusion of saline (control; n = 8). There were no effects of rhIL-6 infusion on T4, free T4, or thyroid hormone-binding index. However, rhIL-6 induced a significant decrease in the plasma concentrations of TSH (P < 0.001) and T3 (P < 0.001) compared with those in the control study, associated with an increase in rT3 concentrations (P < 0.001). In the second study, a dose of 150 micrograms rhIL-6 was administered sc for 42 consecutive days (n = 8). Weekly assessment of thyroid hormone and TSH concentrations showed a decrease in the T3 concentration (P < 0.001) and a transient increase in rT3 (P < 0.01) and free T4 concentrations (P < 0.01). There were no changes in T4 concentrations during chronic administration of rhIL-6. It is concluded that IL-6 induces major changes in thyroid hormone metabolism and may be another pathogenetic factor in the euthyroid sick syndrome.

Carcinoma, Renal Cell↗

Pulsatile thyrotropin and prolactin secretion in a patient with a mixed thyrotropin- and prolactin-secreting pituitary adenoma.

The circadian and pulsatile thyrotropin (TSH) and prolactin (PRL) release was investigated in a patient with slight hyperthyroidism due to a mixed TSH- and PRL-secreting pituitary adenoma. Blood was withdrawn every 10 min for 24 h (before and after medical treatment); pulse characteristics were analyzed by Desade and Cluster programs (values as mean +/- SD). The inappropriately high mean 24-h TSH concentration of 3.55 +/- 0.31 mU/l was associated with a higher mean 24-h TSH pulse amplitude but unaltered mean 24-h TSH pulse frequency relative to healthy controls. The nocturnal TSH surge (absolute surge 0.5 mU/l, relative surge 16%) was low, related to a loss of the usual nocturnal increase of TSH pulse amplitude and TSH pulse frequency. Chronic treatment with octreotide resulted in a modest clinical and biochemical improvement of the hyperthyroid state; addition of bromocriptine at a later stage had no further beneficial effect. At the end of the follow-up period the mean 24-h TSH paradoxically had increased to 5.33 +/- 0.81 mU/l. The nocturnal TSH surge also increased (absolute surge 1.9 mU/l, relative surge 42%), but circadian changes in TSH pulsatility remained absent. In the untreated period the increased mean 24-h PRL concentration of 234 +/- 24 micrograms/l was associated with an increased mean 24-h PRL amplitude, whereas the 24-h PRL pulse frequency (N = 4) was lower relative to controls. No circadian PRL rhythm was present. After octreotide and bromocriptine treatment the mean 24-h PRL concentration and mean 24-h PRL pulse amplitude were unchanged, but a clear nocturnal increase of PRL now was observed.(ABSTRACT TRUNCATED AT 250 WORDS)

Adenoma↗

Lesions of the suprachiasmatic nucleus do not disturb sexual orientation of the adult male rat.

An enlarged suprachiasmatic nucleus (SCN) has been found earlier in a group of homosexual men, as compared to heterosexual controls. In order to assess a possible relationship between the SCN and sexual orientation, the present study was undertaken to investigate whether the rat SCN might play a role with respect to the expression of sexual orientation. Sexual orientation was measured in partner preference tests as the percentage of time spent in the vicinity of sexually active male and female incentives, that were separated from the experimental animal by a wire mesh. The results show that established patterns of sexual orientation towards female incentives by the adult male rat are not influenced by SCN-lesions. Disturbances in circadian rhythmicity of activity in SCN-lesioned animals did not affect this conclusion.

Analysis of Variance↗

Effects of tumor necrosis factor on the hypothalamic-pituitary-testicular axis in healthy men.

Tumor necrosis factor (TNF) has been implicated as a mediator of many diseases associated with alterations in hypothalamic-pituitary-testicular (HPT) function. To assess the effects of TNF on the HPT axis, we performed a saline-controlled cross-over study in six healthy men, sequentially measuring serum concentrations of gonadotropins, testosterone, and sex hormone-binding globulin (SHBG) after a bolus intravenous injection of recombinant human TNF (50 micrograms/m2). TNF induced an early and transient increase in serum luteinizing hormone (LH) levels from 6.0 +/- 1.0 to a maximum of 8.0 +/- 1.0 U/L after 30 minutes (P < .005), whereas the concentrations of follicle-stimulating hormone (FSH) remained unchanged. The increase in LH concentrations was followed by a transient decrease in serum testosterone levels from 18.2 +/- 0.3 to 9.1 +/- 1.2 nmol/L after 4 hours (P < .0001). Remarkably, LH levels had returned to control values when the testosterone level reached its nadir. SHBG levels were not affected by TNF. Our results suggest that TNF affects the HPT axis at multiple levels and may be involved either directly or indirectly in the decrease in circulating testosterone concentrations in systemic illnesses.

Adult↗

Hypothyroid-like regulation of the pituitary-thyroid axis in stable human immunodeficiency virus infection.

Thyroid function and regulation were studied in 14 consecutive male outpatients with asymptomatic human immunodeficiency virus (HIV) infection (CDC II/III, n = 8) or AIDS (CDC IV, n = 6) who were free of concomitant infections and hepatic dysfunction, and in eight healthy, age- and weight-matched male controls. Blood was sampled every 10 minutes over 24 hours for measurement of thyrotropin (TSH). Thereafter, thyroid hormones and TSH responsiveness to thyrotropin-releasing hormone (TRH) were measured. Triiodothyronine (T3) and thyroxine (T4) did not differ between HIV-infected patients and controls, but HIV patients had lower thyroid hormone-binding index ([THBI] HIV patients, 1.01 +/- 0.02; controls, 1.11 +/- 0.03; P < .02), free thyroxine (FT4) index (94 +/- 3 v 110 +/- 4, P < .01), FT4 (11.8 +/- 0.4 v 14.3 +/- 0.4 pmol/L, P < .01), and reverse triiodothyronine (rT3) values (0.18 +/- 0.01 v 0.26 +/- 0.02 nmol/L, P < .001) and higher thyroxine-binding globulin ([TBG] 20 +/- 1 v 16 +/- 1 mg/L, P < .02) values. Mean 24-hour TSH levels were increased in HIV patients (2.39 +/- 0.33 v 1.44 +/- 0.16 mU/L, P < .05), associated with increased mean TSH pulse amplitude and TSH responsiveness to TRH. No differences were observed between asymptomatic HIV-seropositive and AIDS patients. In conclusion, there is a hypothyroid-like regulation of the pituitary-thyroid axis in stable HIV infection, which differs distinctly from the euthyroid sick syndrome in non-HIV-nonthyroidal illnesses.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗