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P D Papapetrou

Publications and source records attributed to P D Papapetrou.

18 recordsLinked to original sources
PubMed1996

Circulating levels of immunoreactive parathyroid hormone-related protein and intact parathyroid hormone in human fetuses and newborns.

Undetectable or extremely low levels of circulating immunoreactive parathyroid hormone (PTH) have been reported in human newborns while PTH bioactivity was high. This prompted the hypothesis that the fetal calcemic hormone might be PTH-related protein. The purpose of this study was to measure circulating immunoreactive PTH-related protein in human fetuses and newborns in order to investigate this hypothesis. Parathyroid hormone-related protein (PTHrP(1-86) and intact PTH were measured using two-site immunoradiometric assays in plasma obtained by cordocentesis from 23 fetuses (19-33 weeks of gestation), from 17 newborns at term (38-41 weeks), from their mothers and from 22 normal women of reproductive age. Plasma PTHrP was detectable in all but one of the fetuses and newborns and in all the mothers and the controls. The mean level was similar among fetuses (19-33 weeks) (0.43 +/- 0.18 pmol/l), newborns (0.48 +/- 0.12), mothers (0.48 +/- 0.14) and normal controls (0.46 +/- 0.09). Plasma PTH was found to be significantly higher in fetuses at midgestation (1.0 +/- 0.99 pmol/l) than in the newborns (0.22 +/- 0.21) (p < 0.0025); maternal PTH was significantly higher compared to fetal level at mid-gestation (2.1 +/- 1.0, p < 0.01) as well as at term (2.69 +/- 1.40, p < 0.001). In the control women PTH was 3.07 +/- 1.25 pmol/l. These results showed that plasma amino-terminal PTHrP-(1-86) is detectable during the second half of human fetal life and its level remains unchanged during this period of time, in contrast to changing levels of fetal plasma PTH. The relatively low PTHrP-(1-86) level that we found in the newborns is not responsible for the high PTH-like bioactivity found by some investigators in cord blood at term.

Adult↗
PubMed1986

The origin of a human chorionic gonadotropin beta-subunit-core fragment excreted in the urine of patients with cancer.

Immunoreactive human Chorionic Gonadotropin (hCG), its subunits and hCG beta-core fragment were analyzed, using Sephadex G-100 chromatography, in urine and tumour extracts from four patients with cancer. These patients were selected for investigation because they were excreting proportionally large amounts of the hCG beta-core fragment in their urine. Although 30-85% of the total immunoreactive urinary hCG was hCG beta fragment, traces of the fragment (2% of total hCG) were found in only two of the tumours and none in the other two. The predominant molecular form of hCG in the tumours was intact free beta-subunit of hCG. The conclusion is that the hCG beta-core fragment found in the urine of some patients with cancer is not a secretion product of the tumours. This fragment is very likely a peripheral degradation product of the free beta-subunit of hCG which is secreted by the tumours.

Adult↗
PubMed1985

A gonadotropin and alpha-subunit suppression test for the assessment of the ectopic production of human chorionic gonadotropin and its subunits after the menopause.

One contraceptive tablet [(CP) containing 0.05 mg ethinyl estradiol and 0.5 mg norgestrel] was administered daily for 7 days to 38 hypergonadotropic postmenopausal women who had benign illness and to 34 similar women with cancer, in order to suppress the gonadotropins (LH and FSH) and their alpha-subunit secreted by the pituitary. LH, FSH, alpha-subunit, and hCG were measured using RIA in serum and urine extracts obtained before and on the seventh day of treatment. In the control group serum alpha-subunit fell to 53%, serum LH to 51%, serum FSH to 36%, urine alpha to 42%, urine hCG to 54%, urine LH to 53%, and urine FSH to 44% of their mean pretreatment values. Serum hCG was undetectable after treatment in all except 11 women in whom serum LH was not adequately suppressed. This fact and the significant positive linear correlation found between basal serum hCG and LH imply that serum hCG measured in postmenopausal women, with a RIA using the SB6 antiserum, is mainly cross-reacting LH. The suppression proved to be useful in the assessment of ectopic production of hCG and its alpha-subunit in the cancer group. Before treatment, 3 patients (8.8%) had elevated serum alpha-subunit levels, whereas after treatment 9 patients (26.5%) had elevated levels. For urine alpha-subunit 3 patients (8.8%) had elevated levels before and 13 (38.2%) after treatment. Six patients (17.7%) had elevated serum hCG levels before and 7 (20.6%) after treatment; however, for urine hCG, 3 patients (9%) had elevated levels before and 8 (24.2%) after treatment. Sephadex G-100 chromatography of urine extracts from two control women showed that the predominant form of free alpha-subunit secreted by the pituitary and excreted in the urine had lower apparent molecular weight after treatment with the CP. Chromatography of urine extracts from two cancer patients demonstrated that a small amount of beta-subunit of hCG produced ectopically by the tumor and excreted into the urine along with a core-type fragment of the hCG-beta was masked in the basal urine by cross-reacting LH; these ectopic peptides were not suppressible and could be specifically measured only after elimination of the urine LH by treatment with the CP. We conclude that administration of contraceptive steroid to post-menopausal women with cancer, by suppressing pituitary gonadotropin secretion and thus minimizing their interference in the hCG RIAs, can be useful in the detection of ectopic production of the hCG and its subunits.

Aged↗
PubMed1980

Ectopic production of human chorionic gonadotropin (hCG) by neoplasms: the value of measurements of immunoreactive hCG in the urine as a screening procedure.

Immunoreactive human Chorionic Gonadotropin (hCG) was measured in serum and urine extracts from patients with malignant disease using a radioimmunoassay that detects efficiently hCG and its betasubunit. Of the 70 patients examined, 12 (17.1%) were positive for hCG in serum and 31 44.3%) in urine. Eleven patients who were positive in serum were also positive in urine; 20 patients (28.6%) were positive only in urine. Sephadex G-100 chromatography of urine from two serum-negative and urine-positive patients showed that the hCG immunoreactive material in the urine of these patients was mostly a molecular species smaller than hCG and hCG-beta. The nature of this molecule(s) is unknown and is called here metabolite(s) "X" of hCG-beta. The urine of 2 patients who where positive for hCG in both serum and urine contained considerable amount of metabolite(s) "X" as well as the native hCG-beta subunit, which was present also in the serum of these 2 patients. The metabolite(s) "X" was also shown by chromatography in the urine of a pregnant woman. It is concluded that the ectopic production of hCG is found more than twice as frequently in urine as compared to when serum alone is examined. The urine of serum-negative tumor patients can be positive for hCG because of the presence in it of the metabolite(s) "X" of hCG-beta or hCG which presumably circulates in the blood of these patients at non-detectable levels.

Chorionic Gonadotropin↗
PubMed1978

Hypothalamic hypothyroidism causing spastic paraplegia: recovery following thyroid medication.

A 63-year-old woman with longstanding spastic paraplegia and neurological evidence of long tract disturbance was found to have hypothyroidism, partial diabetes insipidus, hyperprolactinemia, and gonadotropin deficiency of hypothalamic origin. Replacement therapy with thyroxine and prednisone induced complete remission of the neurological abnormalities. The association of spastic paraplegia with hypothalamic insufficiency has not been reported previously. The possibility of hypothalamic disease should be considered in cases of spastic paraplegia of unknown cause.

Brain Diseases↗
PubMed1975

Cortisol secretion in Nelson syndrome: Persistence after "total" adrenalectomy for Cushing syndrome.

In two patients who were severely pigmented (Nelson syndrome) following bilateral adrenalectomy for Cushing syndrome, symptoms of hyper-cortisolism developed while they were receiving only physiologic steroid replacement. Cortical assays proved that endogenous cortisol production had not been obliterated. Even after total adrenalectomy, steroid measurement should be performed to guard against adrenocortical excess.

17-Hydroxycorticosteroids↗
PubMed1975

Thyrotoxicosis due to "silent" thyroiditis.

3 patients (2 male, 1 female) presented with symptoms of thyrotoxicosis associated with elevated blood-levels of thyroid hormone and a markedly depressed thyroidal uptake of 131-I. The male patients (aged 59 and 47) each had a cardiac arrhythmia, but did not have any thyroid pain or swelling. The female with a goitre had no discomfort in the neck. Thyrotoxicosis factitia was excluded by history. The subsequent course of their disease was typical of subacute thyroiditis. The elevated thyroid-hormone levels spontaneously fell to normal over a few weeks. In 1 patient, however, chemical hypothyroidism developed. These patients could have been diagnosed as having hyperthyroidism, rather than subacute thyroiditis, since thyroid pain--and swelling in 2 of the cases--was absent. The correct diagnosis was suspected only after finding a thyroidal uptake of 131-I near zero. The thyroidal uptake of 131-I is still important as a routine diagnostic aid in thyroid disease.

Adult↗
PubMed1975

Relation between thyroid iodine content and the accumulation and oxidation of [35-S] Methimazole in the rat.

The thyroid accumulation and oxidation of a single intraperitoneal dose of [35-S] methimazole has been studied in iodine-deficient, normal and iodine-treated rats. A highly significant positive linear correlation was found between the thyroid oxidation of methimazole to sulfate and intrathyroidal iodine content. A single dose of potassium iodide given intraperitoneally (ip) to rats 1 h before administration of [35-S] methimazole (1 mg/kg ip) increased the thyroid accumulation and oxidation of methimazole. Conversely, the thyroids of rats maintained on a low iodine diet for 21 days showed a markedly reduced capacity to accumulate and oxidize methimazole. The level of oxidation found in the iodine-deficient, normal and iodide-treated groups was 0.21, 4.15 and 12.6 nmol sulfate/g thyroid respectively. The animals maintained on the low iodine diet for 21 days showed significant increases in thyroid weight and thus the decrease in methimazole oxidation occurred in spite of increased stimulation by endogenous TSH. These results show that the intrathyroidal iodine content is a critical factor in the metabolism of methimazole in the thyroid.

Animals↗
PubMed1975

Binding of the 35-s of 35-s-propylthiouracil by follicular thyroglobulin in vivo and in vitro.

Radioactivity was found bound to follicular thyroglobulin after administration of 35-S-propylthiouracil (PTU) to rats. Denaturation of the thyroglobulin using various procedures could not separate the 35-S from the protein; it was concluded that the 35-S is bound to thyroglobulin covalently. Fractionation of saline-soluble thyroid proteins was performed by ultracentrifugation on sucrose gradients. The PTU-sulphur/thyroglobulin (S/Tg) molar ratio was calculated in all fractions. One hour after the injection of PTU the S/Tg molar ratio was the same for 19S thyroglobulin from rats on stock diet and 18S thyroglobulin from rats on low iodine diet. Injection of KI to the animals before administration of 35-S-PTU significantly reduced the ratio. The highest S/Tg ratio 1.10 was noted at 19S thyroglobulin, 17 h after a single injection of PTU. Daily injection of PTU for six days increased the S/Tg ratio to 3.3. Inverse relationship between dose of PTU and S/Tg ratio was noted at one hour. In animals injected with large dose of 35-S-PTU and sacrificed several hours later the S/Tg was higher at the 12S subunits than at the 19S protein. The amount of PTU bound to 3-8S subunits was minimal. Sulphite liberated 64 percent of the 35-S bound to thyroglobulin which appeared as four compounds on thin layer chromatography plates. The main 35-S compound liberated by sulphite was sulphate.

Animals↗
PubMed1973

Remission of thyrotoxicosis during treatment with propranolol.

Twenty-eight thyrotoxic patients were treated with propranolol. In seven patients the drug had to be discontinued after one or two months, but in the remaining 21 clinical improvement was observed. Serial clinical studies and tests of thyroid function performed at monthly intervals showed that in four patients thyrotoxicosis remitted and all indices of thyroid function returned to normal. A fifth patient shows distinct evidence of remission with the 20-minute (132)I uptake falling to normal, although the free-thyroxine index remains slightly raised. It is likely that these remissions reflect the natural tendency of the disease to remit since propranolol is not considered to have any direct in-vivo effect on thyroid function.However, because of failure to gain adequate control of symptoms in all patients treated, and the fact that circulating thyroid hormone levels were often not restored to normal, propranolol is considered an unsatisfactory alternative to conventional antithyroid drugs for routine treatment.

Female↗