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Biomedical subjects

I Kostoglou-Athanassiou

Publications and source records attributed to I Kostoglou-Athanassiou.

17 recordsLinked to original sources
PubMed2004

Mixed medullary-follicular thyroid carcinoma. Report of a case and review of the literature.

OBJECTIVE: The aim was to describe the case of a female patient with a mixed medullary-follicular thyroid carcinoma. METHODS: The patient underwent thyroidectomy for the treatment of multinodular goiter. A tumor was found which exhibited the features of a mixed medullary-follicular thyroid carcinoma. Immunohistochemistry was performed. RESULTS: Immunohistochemistry was positive in the area of the carcinoma for calcitonin and thyroglobulin. She developed extensive metastatic deposits in the bones of the pelvis and in the calvarium causing hyperthyroidism. CONCLUSION: A patient with a mixed medullary-follicular thyroid carcinoma is described, who had elevated levels of both calcitonin and thyroglobulin and developed metastatic deposits, which could produce thyroid hormones.

Adenocarcinoma, Follicular↗
PubMed2003

Scintigraphy with [111In]octreotide and 201Tl in a Hürthle cell thyroid carcinoma without detectable radio-iodine uptake. Report of a case and review of the literature.

AIM: To describe the visualization of recurrent disease by [111In]octreotide and 201Tl scintigraphy in a patient with Hürthle cell thyroid carcinoma, increased thyroglobulin levels, and a negative radio-iodine total-body scan. METHODS: Scintigraphy with [111In]octreotide and 201Tl was performed, and a local recurrence in the thyroid bed was detected which was excised by surgery. RESULTS: On histology, the tumour proved to be a Hürthle cell carcinoma, and within the tumour somatostatin receptors were detected by RT-PCR. CONCLUSION: Scintigraphy with [111In]octreotide and 201Tl is an alternative imaging method for the detection of residual disease in patients with a differentiated thyroid carcinoma having increased thyroglobulin levels and a negative radio-iodine total-body scan.

Adenoma, Oxyphilic↗
PubMed2002

Malignant struma ovarii: report of a case and review of the literature.

Malignant struma ovarii is a very rare disease and therefore there is neither common agreement on treatment regimens nor sufficient follow-up experience. The case of a 38-year-old woman with malignant struma ovarii is described. The patient presented with a clinically silent ovarian neoplasm discovered incidentally during investigations for metrorrhagia. The ovarian mass was resected and the tumor was found to be a teratoma. Within the teratoma a papillary thyroid carcinoma of the follicular variant was found. Subsequently, in order to make follow-up of the patient possible by thyroglobulin measurement and radioiodine whole body scintigraphy, near-total thyroidectomy was performed and the thyroid was found to be normal on histology. Whole body radioiodine scintigraphy with (131)I and ablation of the thyroid remnant by the administration of 80 mCi (131)I was performed. The patient recovered uneventfully and is now well.

Adult↗
PubMed1998

Effect of 5-hydroxytryptamine and pineal metabolites on the secretion of neurohypophysial hormones.

It has been shown that 5-hydroxytryptamine and melatonin, an indoleamine for which 5-hydroxytryptamine is a precursor, influence the release of vasopressin and oxytocin from the rat hypothalamus both in vivo and in vitro. The oral administration of melatonin has been shown to decrease oxytocin release and modulate the nocturnal vasopressin release in humans. 5-hydroxytryptamine and its metabolites, 5-hydroxytryptophol, 5-methoxytryptamine and 5-methoxytryptophol, are detected within the pineal, and there is evidence that 5-methoxytryptamine and 5-methoxytryptophol may have some physiological role. The aim of this study was to evaluate the effects of 5-hydroxytryptamine, 5-hydroxytryptophol, 5-methoxytryptamine and 5-methoxytryptophol on neurohypophysial hormone release from the rat hypothalamus in vitro. It was found that 5-hydroxytryptamine and 5-hydroxytryptophol increased neurohypophysial hormone release, 5-methoxytryptamine decreased the release of vasopressin and oxytocin and 5-methoxytryptophol was found to have no effect, thus providing further evidence for a role of indole compounds in the control of neurohypophysial hormone secretion.

5-Methoxytryptamine↗
PubMed1998

Endotoxin stimulates an endogenous pathway regulating corticotropin-releasing hormone and vasopressin release involving the generation of nitric oxide and carbon monoxide.

Although the administration of endotoxin in vivo activates the neuroendocrine stress axis in the process of crosstalk between the immune and endocrine axes, the direct application of endotoxin to the hypothalamus in vitro does not stimulate the release of the hypothalamic peptides controlling the hypothalamo-pituitary-adrenal (HPA) axis, corticotropin-releasing hormone (CRH) and vasopressin. The hypothesis has therefore been tested that endotoxin may also activate inhibitory pathways, specifically those involving the generation of nitric oxide (NO) and carbon monoxide (CO). Studies were performed on the isolated rat hypothalamus using endotoxin in the presence or absence of inhibitors of heme oxygenase (which generates CO) and nitric oxide synthase, and ferrous hemoglobin. Endotoxin alone decreased both CRH and vasopressin secretion from the hypothalamus. However, when applied together with a nitric oxide synthase inhibitor, the inhibitory effect on CRH was lost. Conversely, co-administration with heme oxygenase inhibitors transformed the inhibition of vasopressin to stimulation, while having no effect on the inhibition of CRH. Ferrous hemoglobin reversed the inhibition of vasopressin, but did not lead to stimulation. It is therefore concluded that endotoxin may stimulate endogenous pathways that lead to the generation of NO, which in turn inhibits CRH. In addition, it generates CO, which modulates the release of vasopressin. These gases are thus potential counter-regulatory controls to the activation of the HPA.

Animals↗
PubMed1998

Acute and subacute effects of endotoxin on hypothalamic gaseous neuromodulators.

Although two-way communication between the hypothalamus and the immune system in now well established, particularly for the hypothalamo-pituitary-adrenal axis, the role of the gaseous neurotransmitters nitric oxide (NO) and carbon monoxide (CO) is much less well understood in terms of hypothalamic function. These agents are an important part of the peripheral inflammatory response; and their synthetic enzymes, NO synthase (NOS) and heme oxygenase (HO), respectively, have been localized to the hypothalamic PVN and SON. The induced generation of both NO and CO leads to the suppression of CRH and vasopressin, the major stimulators of the HPA. Thus, the addition of hemin to hypothalamic explants is maximally active at 1 microM in attenuating the release of CRH and vasopressin, and this dose is also most effective in generating biliverdin and associated CO. CO generation is also able to stimulate cyclooxygenase to produce prostaglandin E2, an established intermediary in the cytokine-stimulated activation of the HPA. Finally, inducible NOS mRNA is specifically induced in the hypothalalmus in response to endotoxin, in parallel to interleukin-1. These data provide increasing evidence in favor of NO and CO as counterregulatory agents in the HPA response to immune activation.

Animals↗
PubMed1998

Melatonin administration and pituitary hormone secretion.

OBJECTIVE: The relationship between the pineal gland and pituitary function remains controversial, while the role of melatonin in the adaptation of the organism to the light-dark cycle of the environment is becoming increasingly recognized. The aim of this study was to investigate the effect of a manipulation of the melatonin rhythm on pituitary hormone secretion in man. DESIGN: Double-blind controlled clinical study. SUBJECTS: Ten adult healthy male volunteers, aged 21-33 years, were studied on two occasions: once after the administration of melatonin 5 mg orally for 4 days at 1700 hours and once after the administration of placebo, at similar times. On the day of each study the subjects undertook their normal duties but refrained from taking heavy exercise, from smoking and drinking alcohol. MEASUREMENTS: Serum cortisol, growth hormone, prolactin and plasma vasopressin, oxytocin, melatonin, sodium, potassium, osmolality and packed cell volume were measured over the following 24 hours. RESULTS: The cortisol peak was advanced and prolactin release increased after melatonin administration, while growth hormone was not affected. Vasopressin and oxytocin levels were found to increase during the night in the control study, but the period of the nocturnal increase in vasopressin concentrations was reduced after the administration of melatonin and the nocturnal increase of oxytocin was absent. CONCLUSION: Altering the melatonin rhythm may affect neuroendocrine function, influencing the nocturnal pattern of neurohypophysial hormone secretion, augmenting prolactin release and advancing the peak of cortisol release.

Administration, Oral↗
PubMed1998

Bright light exposure and pituitary hormone secretion.

OBJECTIVE: Exposure to bright light inhibits melatonin secretion in man. As the relationship between melatonin and pituitary function remains controversial, we investigated the effect of altering the melatonin rhythm by bright light during the early hours of darkness on pituitary hormone secretion in man. DESIGN: The investigation took the form of a randomized controlled clinical trial. SUBJECTS: Ten adult healthy male volunteers, who were non-smokers and aged 21-33 years, were studied on two occasions: once during exposure to bright light from 2000 h to 0200 h and once during exposure to normal room lighting over the same period. On each day of the study, the subjects were allowed to sleep after lights were switched off at 0200 h. Observations were also performed when subjects were exposed to normal room lighting from 2000 h to 2400 h, thereafter being allowed to sleep. On each study day the subjects undertook their normal duties but refrained from taking heavy exercise and drinking alcohol. MEASUREMENTS: Serum cortisol, GH and PRL, plasma vasopressin, oxytocin, melatonin, sodium, potassium and osmolality and packed cell volume were measured over 24 hours. RESULTS: Bright light delayed the nocturnal melatonin peak by 2 hours and resulted in a decrease in cortisol concentrations. Growth hormone levels decreased but subsequently there was a significantly greater nocturnal increase. The PRL peak was delayed and nocturnal vasopressin concentrations were lower in both the studies where subjects were exposed to a modified sleep schedule. CONCLUSION: Exposure to bright light during the early hours of darkness delays the nocturnal melatonin peak and alters cortisol, GH, PRL and nocturnal vasopressin secretion, while modification of the sleep pattern decreases vasopressin concentrations and alters its nocturnal peak.

Adult↗
PubMed1998

Neurohypophysial hormone and melatonin secretion over the natural and suppressed menstrual cycle in premenopausal women.

OBJECTIVE: Vasopressin, oxytocin and melatonin have been reported to be influenced by ovarian steroids. The neurohypophysial hormones have also been shown to display a diurnal pattern of secretion in men. We therefore studied the diurnal pattern of neurohypophysial hormone and melatonin secretion in premenopausal women and in women on oral contraceptives. DESIGN: Healthy normally cycling premenopausal women were studied over 24 hours during the midfollicular and midluteal phases of the menstrual cycle. Healthy premenopausal women on oral contraceptives were studied over 24 hours at similar times. SUBJECTS: Eight healthy normally cycling women and 7 healthy premenopausal women on oral contraceptives. MEASUREMENTS: Plasma vasopressin, oxytocin and melatonin were measured by radioimmunoassay. RESULTS: Vasopressin concentrations and its nocturnal peak were highest in the follicular phase of the natural menstrual cycle and attenuated in the women on oral contraceptives. Oxytocin concentrations did not vary between the two phases of the menstrual cycle, but increased on oestrogen administration. Overall melatonin secretion was augmented in the women on oral contraceptives. CONCLUSIONS: Vasopressin release and its nocturnal peak were greatest in the follicular phase of the menstrual cycle, while melatonin secretion was augmented in the women on oral contraception.

Adult↗
PubMed1998

Thyroid function in postmenopausal women with breast cancer on tamoxifen.

In 42 postmenopausal women with breast cancer, aged 48-85 years (mean age 62.4 years) serum thyroid hormone concentrations were measured before and after 6 months of tamoxifen therapy (20 mg daily). In particular triiodothyronine (T3), thyroxine (T4), free triiodothyronine (FT3), free thyroxine (FT4), thyroxine-binding globulin (TBG) and thyroid-stimulating hormone (TSH) concentrations before and 30 minutes after thyrotrophin-releasing hormone (TRH) administration (200 microg i.v.) were measured before and 6 months after tamoxifen therapy. T3 and T4 concentrations increased significantly (p<0.001 and p<0.05, respectively) whereas FT3 and FT4 remained unchanged (p>0.05), TBG increased significantly (p<0.001) and basal TSH concentrations as well as TSH response to TRH injection increased significantly (p<0.05) after tamoxifen therapy. It is concluded that tamoxifen administration changes thyroid hormone concentrations. However free thyroid hormone levels remain unchanged and the patients remain euthyroid after long-term tamoxifen therapy.

Aged↗
PubMed1997

Activation of heme oxygenase and consequent carbon monoxide formation inhibits the release of arginine vasopressin from rat hypothalamic explants. Molecular linkage between heme catabolism and neuroendocrine function.

Heme oxygenase (HO)-catalyzed degradation of cellular heme moieties generates biliverdin and equimolar amounts of carbon monoxide (CO), which has been implicated as a possible modulator of neural function. Technical difficulties preclude direct measurements of CO within intact nervous tissues; hence, alternative procedures are needed to monitor the formation and possible biologic functions of this gas. In the present study rat hypothalamic explants were found to generate 114 +/- 5 or 127 +/- 11 pmol biliverdin/hypothalamus/1 h (n = 3) upon incubation with 1 or 10 microM hemin, respectively. Ten micromolar zinc-protoporphyrin IX (Zn-PP-IX), a known inhibitor of HO, significantly decreased the degradation of 10 microM hemin from 127 +/- 11 to 26 +/- 11 pmol biliverdin/hypothalamus/1 h (n = 3; P < 0.01). Biliverdin was the principal product of HO-dependent heme degradation, as its possible conversion into bilirubin was precluded by hemin-dependent inhibition of biliverdin reductase. Basal or hemin-supplemented hypothalamic incubations were also shown to generate sizable amounts of propentdyopents (PDPs), reflecting HO-independent degradation pathways which do not liberate CO and cannot be inhibited by Zn-PP-IX. Plotting the ratio of biliverdin to PDPs thus provided an index of the efficiency with which hemin was degraded through biochemical pathways involving CO. Under the experimental conditions of our study, the biliverdin/PDPs ratio varied from 0 to 32 or 15%, depending on the absence or presence of 1 or 10 microM hemin respectively: this suggested that the formation of CO was most efficient at 1 microM hemin. Under these defined conditions, 1 microM hemin was also found to inhibit the release of arginine vasopressin (AVP) evoked by depolarizing solutions of KCl. A series of experiments showed that the effect of hemin was counteracted by Zn-PP-IX, and also by tin-mesoporphyrin IX, which is even more selective in inhibiting HO; it was also attenuated in the presence of the gaseous scavenger ferrous hemoglobin. Furthermore, the inhibition of AVP release could be reproduced by omitting hemin and by incubating hypothalami under CO, whereas treatment with biliverdin had no effect. This suggested that the release of AVP was suppressed by HO degradation of hemin, yielding CO as a modulator of hypothalamic function. These observations may be relevant to diseases characterized by inappropriate secretion of AVP and enzymatic disturbances affecting the synthesis of heme and the formation of CO through the HO pathway (e.g., acute intermittent porphyria or lead intoxication).

Animals↗
PubMed1997

Sex hormones in postmenopausal women with breast cancer on tamoxifen.

In 42 postmenopausal women with breast cancer aged 48-85 (mean age 62.4) years, the blood sex hormone levels were measured before and after 6 months of tamoxifen administration (20 mg daily). Follicle-stimulating hormone and luteinizing hormone levels decreased after tamoxifen administration (p < 0.001), but remained in the postmenopausal range, oestradiol levels increased (p < 0.05), sex hormone binding globulin levels increased (p < 0.001), testosterone levels remained stable (p > 0.1), free testosterone levels decreased (p < 0.001), delta4-androstenedione, 17-hydroxyprogesterone, and dehydroepiandrosterone sulfate levels remained unchanged (p > 0.1), and basal prolactin levels and their response to thyrotrophin-releasing hormone injection decreased significantly (p < 0.001) after tamoxifen therapy. It is concluded that tamoxifen has many and diverse effects on sex hormone levels, and its adverse effects do not affect the biological status of the patient, except perhaps for oestradiol, that increases in some cases, whose possible effect must be studied.

Aged↗
PubMed1996

Oxytocin release is inhibited by the generation of carbon monoxide from the rat hypothalamus--further evidence for carbon monoxide as a neuromodulator.

Recent evidence suggests that the gas nitric oxide can modulate the secretion of a number of hypothalamic hormones, and may be co-localized particularly to oxytocin-containing neurons. Another gas, carbon monoxide (CO), has also been suggested to play a role in neural signaling in the brain, and the synthetic enzyme responsible for the generation of carbon monoxide has been reported to be present in the rat hypothalamus. In this study, we have therefore investigated whether CO has the ability to modify the release of oxytocin from acute rat hypothalamic explants. Hemin, a specific CO precursor through the enzyme heme oxygenase (the enzymatic pathway synthesizing endogenous CO, was found to inhibit KCl-stimulated oxytocin release, with a maximal effect at 10(-5) M, while showing no effect on basal oxytocin secretion. The stimulation of oxytocin by serotonin 10 ng/ml was also significantly antagonized by hemin 10(-7) M. An inhibitor of heme oxygenase, zinc-protoporphyrin-9, had no effect on basal or stimulated oxytocin release. When hemin and zinc-protoporphyrin-9 were given together, the hemin-induced inhibition of oxytocin was completely antagonized by the enzyme inhibitor. Ferrous hemoglobin A0, a substance known to bind CO with high affinity, had no effect on either basal or stimulated oxytocin release, but when hemin and ferrous hemoglobin A0 were given together the hemin-induced inhibition of oxytocin was completely blocked. These findings provide evidence that endogenous CO may play a role in the control of oxytocin release and that, by analogy with nitric oxide, CO may represent a major new neuroendocrine modulator.

Animals↗
PubMed1996

Release of vasopressin in response to altered plasma volume and sodium concentrations following pinealectomy in the rat.

Pinealectomy has been shown to alter daily rhythms of neurohypophysial hormone release, with plasma hormone concentrations being elevated in the morning, as compared to intact rats. To determine whether pineal removal also altered the response to known stimuli of hormone release, vasopressin concentrations were measured in control, sham-operated, and pinealectomized animals during extracellular fluid hypertonicity produced by an intraperitoneal (i.p.) injection of hypertonic saline or hypovolaemia produced by an i.p. injections of polyethylene glycol. In the combined sham-operated and unoperated groups, injection of hypertonic saline produced a marked increase in plasma vasopressin concentrations from 2.18 +/- 0.28 to 7.2 +/- 1.24 pmol/liter, but the response was attenuated in pinealectomized animals, concentrations increasing to only 3.4 +/- 1.2 pmol/liter. Similarly, following infusion of hypertonic saline, the increase in plasma vasopressin per unit increase in plasma sodium was lower in pinealectomized animals than the pineal intact controls. The response to hypovolaemia was also attenuated, plasma hormone concentrations following reduction in blood volume of approximately 10% increasing to only 3.6 +/- 0.6 pmol/liter as compared to 7.3 +/- 2.2 pmol/liter in the control groups. There were no significant differences in pituitary vasopressin content in any of the groups studied. Thus, the pineal may influence the vasopressin response to physiological stimuli.

Animals↗
PubMed1996

Paratesticular tumours in a patient with Nelson's syndrome.

An extremely rare case of a 39-year-old man with Nelson's syndrome and paratesticular tumours is presented. The patient had undergone bilateral adrenalectomy at the age 23 years for Cushing's syndrome. Later he developed skin and mucosal hyperpigmentation. Nelson's syndrome was diagnosed, and he underwent transfrontal hypophysectomy. At age 29, the presence of paratesticular tumours was noted which were excised together with the left testis. The preoperative levels of testosterone, produced by the paratesticular tumours, were extremely high; they fell after surgery.

Adrenal Hyperplasia, Congenital↗
PubMed1994

Endothelin-1 stimulates the in vitro release of neurohypophyseal hormones, but not corticotropin-releasing hormone, via ETA receptors.

The endothelins consist of a family of vasoconstrictor peptides originally isolated from endothelial tissue which are now known to be involved in neuroendocrine regulation. However, while there are data indicating the involvement of endothelins in the modulation of the hypothalamo-pituitary-adrenal (HPA) axis, the precise mechanisms involved have been unclear. We have therefore used a previously validated rat hypothalamic explant system in order to investigate the possible modulation of the neurohypophyseal hormones vasopressin and oxytocin, and corticotropin-releasing hormone (CRH), by endothelin-1 (ET-1) and endothelin-3 (ET-3). Following a period of stabilisation, the release of vasopressin, oxytocin and CRH remained approximately constant in successive 20-min incubations. Addition of ET-1 stimulated the release of vasopressin at a dose of 0.1 nmol/l (p < 0.05), and both vasopressin and oxytocin at 10 nmol/l (p < 0.01 and 0.05, respectively). The release of vasopressin and oxytocin induced by 10 nmol/l ET-1 were both totally blocked by co-incubation with either 1 or 10 mumol/l of the specific ETA receptor subtype antagonist cyclo (D-Trp-D-Asp-Pro-D-Val-Leu) (BQ-123). ET-1 had no effect on CRH release in the dose range of 0.1-1,000 nmol/l. In case any possible stimulation of CRH might be masked by simultaneous generation of nitric oxide (NO), an inhibitor of CRH secretion, addition of ET-1 was also carried out in the presence of the NO synthase inhibitor, L-NO-Arg: ET-1 was again without effect in this dose range.(ABSTRACT TRUNCATED AT 250 WORDS)

Amino Acid Oxidoreductases↗