Biomedical subjects

I Zofková

Publications and source records attributed to I Zofková.

At least 37 records · Page 2Linked to original sources

PubMed1997

The effect of 1,25(OH)2 vitamin D3 on CD4+/CD8+ subsets of T lymphocytes in postmenopausal women.

The effect of exogenous 1,25(OH)2 vitamin D3 (1,25(OH)2D3) on the CD3+, CD4+ and CD8+ subsets (counts/ul) of T lymphocytes was investigated in two randomized groups of postmenopausal women. Group one (16 subjects) received 1 ug/day of the secosteroid for 14 days, while group two (14 participants) was treated with 2 ug/day for the same period. The placebo group comprised another 10 postmenopausal women. Compliance of the treatment was controlled by serum intact parathyroid hormone (PTH) levels, which markedly declined at the end of the treatment (p<0.01 for both doses). The vitamin D status of the women before the treatment was defined by serum 25(OH) vitamin D (25(OH)D) levels. The lower dose of the secosteroid did not change any of the measured immune parameters. After a higher dose of 1,25(OH)2D3 the mean values of CD3+ and CD8+ increased (p<0.05 for the both parameters), but no changes in total lymphocytes and the CD4+ subset were observed. There were no correlations between the immune response (delta CD3+, delta CD4+ and delta CD8+) and basal circulating 25(OH)D. Briefly, then, 1,25(OH)2D3 slightly but significantly increases CD3+ and CD8+ subsets independently on the initial vitamin D status of the postmenopausal women.

CD3 Complex↗

PubMed1996

[Melatonin--the hormone of darkness].

Melatonin is a hormone produced mainly by the pineal gland during the dark phase of the circadian cycle with typical circadian rhythm with maximal secretion at night and depression during the day. The indoleamine has wide regulatory and integrative functions. Perhaps there is no organ and system which can escape the influence of epiphysis, incl. reproductive, cardiovascular gastrointestinal, respiratory as well as renal system and water and mineral metabolism. Melatonin regulates not only neuroendocrine functions but also has immunoenhancing and antitumor effects. That is why there are trials/attempts these properties to be utilized in the treatment of malignancies and AIDS patients. The hormone plays a certain role in temperature regulation in mammals as well as in the onset of puberty and senescence. Attention has been paid to its role as a scavenger of toxic free radicals and it is believed that melatonin is the most effective lipophilic antioxidant. However, the exact mechanism of action of this high active hormone remains to be elucidated. Further studies are also necessary for discovering the next its properties and functions.

Circadian Rhythm↗

PubMed1996

Effect of estrogen status on bone regulating hormones.

The effect of surgically induced menopause and a subsequent estrogen monotherapy on the secretion of calciotropic hormones and serum minerals was evaluated in 11 perimenopausal menstruating women. In seven of them, plasma insulin growth factor-I was also assessed. In the 12th-16th week after bilateral oophorectomy, a decline of serum PTH (p < 0.01) and an increase of calcemia (p < 0.05), phosphatemia (p < 0.05), and IGF-I (p < 0.01) were documented. A subsequent transdermal estrogen substitution (100 micrograms/day for 6 weeks) returned these values to the preoperative range. However, neither the operation nor the estrogen treatment altered calcitonin secretion (basal and calcium stimulated), serum 1,25(OH)2, vitamin D3, or magnesium. The effectiveness of oophorectomy as well as compliance of estrogen substitution was documented by serum estradiol, FSH, and LH response. The results demonstrate a stimulating effect of estrogen on PTH secretion, secondary to an estrogen-induced reduction in plasma calcium. They further demonstrate an inhibitory effect on phosphatemia and IGF-I production, but no effect on calcitonin secretion and vitamin D metabolism.

Acute Disease↗

PubMed1996

Effect of surgically induced hypoestrinism on immunoregulation in perimenopausal women.

The object of the present study was to investigate the effect of bilateral oophorectomy (OOX) on CD4+ and CD8+ subsets of T-lymphocytes in 8 immunologically healthy perimenopausal women with regular bleeding. Between the 12th and 16th week after OOX, CD8+ (%) increased in all of the investigated women (mean values compared to values before OOX: 37.8 +/- 3.4 vs 26 +/- 4.13, p < 0.05). CD4+ increased in five women, and decreased in another three (means: 36.4 +/- 3.6 vs 38 +/- 4.6). The immunoregulatory index (CD4+/CD8+ ratio) declined in seven women, while it was unchanged in one (means: 1.09 +/- 0.2 vs 1.71 +/- 0.22, p < 0.05). The compliance of the treatment was controlled by serum estrogen, LH and FSH. From these results it is apparent that surgically induced hypoestrinism inhibits immunoregulation in perimenopausal women.

Adult↗

PubMed1996

Adenohypophyseal-gonadal dysfunction in male haemodialyzed patients before and after subtotal parathyroidectomy.

The function of the adenohypophyseal-gonadal axis in haemodialyzed male patients is modified: the serum testosterone level is low, and the gonadotropin levels are increased. The pathogenetic role of secondary hyperparathyroidism in this disorder has not previously been defined. The area under the curve (AUC) and the secretion kinetics of testosterone, luteinizing hormone (LH), and follicle-stimulating hormone after administration of LH-releasing hormone were examined in 7 dialyzed men with secondary hyperparathyroidism (mean age 36.2, range 20-47 years) before and 3 and 6 months after parathyroidectomy (PTX). The operation was successful in all 7 patients, as intact parathyroid hormone declined markedly during both postoperative periods as compared with the values before PTX: 81 +/- (SEM) 34 and 138 +/- 57 ng/1 versus 965 +/- 116 ng/l (p < 0.01 and p < 0.0l). The testosterone AUC prior to PTX (63 +/- 115 nmol/l x min) and 3 months (-4 +/- 36 nmol/l x min) and 6 months after PTX (-62 +/- 69) did not differ significantly, as was the case with LH AUC (1,110 +/- 223 and 1,214 +/- 331 and 1,020 +/- 314 U/l x min, respectively) and follicle-stimulating hormone AUC (525 +/- 334 and 634 +/- 347 and 533 +/- 264 U/l x min, respectively). The secretion kinetics of all three hormones was atypical as compared with healthy men of similar age, but it did not change after PTX. There were no correlations between the sexual indicators and parathyroid hormone, 1,25(OH)2D3, calcium, or phosphate during the individual periods. These findings indicate that secondary hyperparathyroidism is probably not involved in the dysfunction of the adenohypophyseal-gonadal axis in dialyzed men.

Adult↗

PubMed1995

The effect of nifedipine on serum parathyroid hormone and calcitonin in postmenopausal women.

The effect of calcium channel blockers on calcium homeostasis in postmenopausal osteoporotic women with arterial hypertension has not to date been defined. In the submitted study, the influence of nifedipine on serum parathyroid hormone (PTH), calcitonin and osteocalcin is followed in 11 patients. After one month of treatment, serum PTH markedly declined in all women and osteocalcin decreased in 10 patients. In contrast, serum calcitonin increased in five patients, whilst in another five the effect was just the opposite. In one woman this indicator was not affected. There are no mutual correlations between the mentioned indices. In conclusion, the calcitonin secretory process is not sensitive to calcium channel blockade within the present study. In spite of the fact that nifedipine inhibits PTH secretion in postmenopausal osteoporotic women, the direct effect of the drug on osteoblasts (not mediated by PTH) cannot be excluded.

Calcitonin↗

PubMed1995

A decreasing CD4+/CD8+ ratio after one month of treatment with stanazolol in postmenopausal women.

Androgens influence some immunological processes, including the differentiation of T-cells in CD4+ (helpers) or CD8+ (suppressors/cytotoxic) phenotype. In nine postmenopausal osteoporotic women the effect of stanazolol on lymphocyte counts, CD3+ and the immunoregulatory index (CD4+/CD8+) were investigated. In the placebo group, ten postmenopausal osteoporotic women of similar age were included. The means of the investigated indices after stanazolol as compared with the values before treatment were as follows: lymphocyte counts (cells/microL +/- SEM) 2974 +/- 225 versus 2313 +/- 166, CD3+ (%) 54.3 +/- 5.5 versus 70.9 +/- 1.6 (P < 0.05); CD4+/CD8+ ratio 1.8 +/- 0.02 versus 2.5 +/- 0.28 (P < 0.05). The values after placebo as compared with the values before placebo were: 2558 +/- 201 versus 2370 +/- 256, 62.9 +/- 2.1 versus 64.8 +/- 1.7 and 1.6 +/- 0.2 versus 1.6 +/- 0.1 in sequence. The treatment was controlled by the serum stanazolol levels before and after steroid administration (unmeasurable versus 20.8 +/- 3.4 nmol/L, P < 0.01). The good compliance of the therapy was confirmed by a decline of serum LH (U/L; 30.1 +/- 3.1 versus 24.7 +/- 2.8, P = 0.014), FSH (U/L; 108.9 +/- 13.1 versus 93.3 +/- 12.8, P = 0.012) and serum sex hormone binding globulin (SHBG; nmol/L; 53.3 +/- 13.3 versus 11.2 +/- 1.9, P < 0.01). The decline of SHBG indicates a good tissue sensitivity to the androgen. There were no significant differences between hormonal parameters before and after placebo treatment. In conclusion, the immunosuppressive effect of the androgen, stanazolol, was confirmed in the investigated postmenopausal osteoporotic women.(ABSTRACT TRUNCATED AT 250 WORDS)

Anabolic Agents↗

PubMed1995

Effect of parathyroidectomy on thyrotropic and lactotropic function in patients with renal osteopathy.

To test the effect of parathyroidectomy on thyrotropic and lactotropic function, a thyrotropin-releasing hormone (TRH) test was performed before and between the 2nd and 3rd month after operation in 13 haemodialysed patients with secondary hyperparathyroidism. The thyrotropin response to TRH was higher in the postoperative period as compared with the values before the operation (p < 0.01). The prolactin response to TRH did not differ from the values before the operation. No correlations between thyrotropin response and serum parathyroid hormone (PTH), ionised calcium and haemoglobin or haematocrit were found. The lower sensitivity of the thyrotropic system to TRH in patients with renal osteopathy is not dependent on serum PTH or calcium.

Calcium↗

PubMed1995

The relationship between magnesium and calciotropic hormones.

There is an important functional link between magnesium and calciotropic hormones. PTH stimulates magnesium reabsorption in the renal tubule, absorption in the gut and release of the ion from bone. Magnesium on the other hand is essential for the normal function of the parathyroid glands, metabolism of vitamin D and adequate sensitivity of target tissues to PTH and active vitamin D metabolites. Magnesium deficit is usually associated with hypoparathyroidism, low production of active vitamin D metabolites, in particular 1,25(OH)2 vitamin D3 and resistance to PTH and vitamin D. On the contrary, magnesium excess, similar to calcium, inhibits PTH secretion. Bone metabolism is impaired under positive as well as under negative magnesium balance. Because of the great importance of magnesium in the regulation of calcium homoeostasis, appropriate attention should be paid to the early diagnosis and treatment of magnesium imbalance.

Animals↗

PubMed1994

[Evaluation of the results of clinical trials using a new non-statistical method].

The author presents information on the possibilities and some advantages associated with the application of a new nonstatistical (gnostic) method for evaluation of results in clinical trials. The mentioned method is among other properties very robust, i.e. suited for evaluation of small groups of highly scattered data, a situation very frequently encountered in clinical research.

Clinical Trials as Topic↗

PubMed1994

Stanazolol--an anabolic steroid that does not influence parathyroid hormone response to hypercalcemia in postmenopausal women.

Estrogen influences the calcium-induced suppressibility of parathyroid hormone (PTH) in postmenopausal women. We tested the hypothesis that parathyroid gland function is also sensitive to the anabolic steroid, stanazolol. The calcium-induced suppressibility of PTH was investigated in 11 osteoporotic postmenopausal women on two occasions, before and after 1 month's oral treatment with stanazolol. Compliance to treatment was checked by the determination of serum luteinizing hormone (LH) and testosterone. Serum intact PTH and ionized calcium were estimated before and 5, 60, and 120 minutes after I.V. calcium load. Calcium-induced PTH suppression was of a similar magnitude before and after stanazolol, although calcium increments were identical. The results imply that stanazolol--at biologically effective doses--does not affect PTH responsiveness to hypercalcemia in postmenopausal women.

Administration, Oral↗

PubMed1994

Lack of stimulatory effect of 1,25(OH)2 vitamin D3 on beta-endorphin and cortisol secretion.

The aim of the work was to investigate the effect of 1,25 (OH)2 vitamin D3 on beta-endorphin and cortisol secretion in vivo. beta-Endorphin, cortisol, calcium and phosphate in blood were measured in ten healthy unstressed volunteers before and after 4-day oral administration of 1,25 (OH)2 vitamin D3 in doses of 3 micrograms/d. The biological effectiveness of the treatment was proved by a significant increase of calcemia as compared with control values (2.71 +/- 0.03 vs 2.57 +/- 0.02 mmol/l, mean +/- SE, p < 0.01) and phosphatemia (1.18 +/- 0.06 vs 0.89 +/- 0.01 mmol/l, p < 0.01). beta-Endorphin after treatment was 39.1 +/- 9.2 (vs 42.7 +/- 7.6) ng/l and cortisol 369 +/- 35 (vs 377 +/- 31) nmol/l. In conclusion, in spite of the good compliance of the treatment, 1,25 (OH)2-vitamin D3 stimulates neither beta-endorphin nor cortisol secretion in healthy subjects.

Administration, Oral↗

PubMed1994

Does exogenous hypermagnesaemia inhibit insulin secretion in patients with impaired glucose tolerance or non-insulin-dependent diabetes mellitus?

Acute exogenous hypermagnesaemia in healthy subjects retards glucose assimilation (Kg) and inhibits B cell function. The glycoregulatory effect of hypermagnesaemia was investigated in the course of the intravenous glucose tolerance test (IVGTT) in 16 subjects, incl. eight with impaired glucose tolerance (IGT) and eight with non-insulin dependent diabetes mellitus (NIDDM). Hypermagnesaemia was induced by intravenous infusion of 6 g MgSO4. The secretory response of insulin (IRI) and C-peptide were expressed as the incremental area (IA of S-IRI and IA of S-C-peptide). The results were compared with control IVGTT following infusion of saline. Hypermagnesaemia did not affect glucose assimilation in subjects with IGT as compared with control values nor in subjects with NIDDM. Hypermagnesaemia did not change IA of S-IRI nor of S-C-peptide in IGT as compared with control values (IA of S-IRI were 4308 +/- 1126 vs 3309 +/- 610 microU/ml x min and IA of S-C-peptide 191 +/- 43 vs 177 +/- 46 ng/ml x min) (means +/- SEM). In NIDDM there was no significant difference between the response of C-peptide during hypermagnesaemia and the response during control IVGTT (IA were 72 +/- 20 ng/ml x min vs 73.5 +/- 22.4 ng/ml x min). As no significant insulin response to glucose was obtained after saline or magnesium in NIDDM, the effect of hypermagnesaemia was not possible to evaluate. In conclusion, no significant decline of glucose assimilation and B-cell function in IGT and NIDDM can be proved in the course of exogenous hypermagnesaemia.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

PubMed1993

Does estrogen replacement therapy influence parathyroid hormone responsiveness to exogenous hypercalcemia in postmenopausal women?

In postmenopausal women PTH suppression by exogenous calcium is reduced. To test whether this finding might be caused by estrogen deficiency 9 postmenopausal women were given transdermal estradiol (E2) treatment for 3 months at a dose of 100 micrograms/day. PTH reactivity to iv administration of CaCl2 was determined before and at the end of the E2-treatment period. Compliance to treatment was checked by determination of serum levels of E2 and FSH. The E2 level rose from 0.1 +/- 0.02 (mean +/- SE) to 0.46 +/- 0.10 mmol/l p < 0.01), whereas the corresponding FSH level declined from 77.5 +/- 7.4 to 33.9 +/- 5.7 U/l p < 0.01). This suggests good compliance. At the end of E2-treatment period calcium administration induced a higher PTH suppression as compared with control value (the PTH decremental area 2123 +/- 270 vs 1253 +/- 253 ng/l x min, p < 0.05), although a lower calcemic response was attained (the Ca incremental area 32.6 +/- 6.1 vs 47.4 +/- 4.5 mmol/ml x min, p < 0.05). These results imply that parathyroid glands are dependent on an adequate estrogen provision to respond normally to serum calcium changes.

Calcium Chloride↗

PubMed1993

Effect of hypermagnesemia on the adenohypophyseal-gonadal function, parathyroid hormone secretion and some other hormonal indicators.

Hormonal secretory mechanisms are influenced positively or negatively by magnesium, the effect depending on its concentration. The submitted study is concerned with the effect of acute hypermagnesemia induced by intravenous infusion of 6 g MgSO4 on quiescent and LHRH-induced secretion of FSH, LH, prolactin and testosterone; on the levels of intact parathyroid hormone; and on other hormonal and mineral indicators in 10 healthy male subjects. Gonadotropin secretion was not altered by hypermagnesemia. Quiescent testosterone levels decreased moderately (p < 0.01), and the secretory kinetics of the hormone slightly changed. Parathyroid hormone levels markedly dropped in the 60th minute of hypermagnesemia duration (p < 0.01), the drop depending on the initial values of the hormone prior to the administration of magnesium (r = 0.923, p < 0.01). Although in hypermagnesemia no correlations between the levels of parathyroid hormone and those of magnesium, calcium and phosphorus could be found, in normomagnesemia significant correlations were confirmed between the levels of parathyroid hormone and magnesemia (r = -0.8068, p < 0.05), and the levels of parathyroid hormone and calcemia (r = -0.9451, p < 0.01). In hypermagnesemia there were no alterations in the levels of the plasma prolactin, cortisol or catecholamines, nor was there any alteration in the rate at which catecholamines were excreted in urine. In conclusion, magnesium in supraphysiologic concentrations does not significantly change the function of the adenohypophyseal-gonadal axis or other hormonal indicators studied. The slight decline of quiescent testosterone levels does not seem to have any clinical significance, although this must be verified by further studies.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

PubMed1992

Lack of stimulating effect on thyrotropic and lactotropic secretion during prolonged calcitriol administration.

The stimulating effect of calcitriol, administered in the dose of 3 micrograms/day for four days, on the thyrotropic and lactotropic secretion has been proved in earlier studies in healthy humans. The present study was undertaken to confirm or eliminate the stimulatory action of the drug using increasing dosages of 0.75-1.50 micrograms/day for one month. In spite of the fact, that the biologically efficient levels of calcitriol were attained (confirmed indirectly by the rise of urinary calcium excretion, p less than 0.01), the stimulating effect of calcitriol on the basal and TRH induced thyrotropic and lactotropic secretion has not been manifested. In conclusion, the clinical importance of stimulating effect of calcitriol on the thyrotropic and lactotropic secretion is neglected, if only commonly accepted therapeutic dosages up to 1.50 micrograms/day are used.

Adult↗

PubMed1992

Glycoregulation is not altered by short-term administration of diltiazem in nondiabetic humans.

In this study changes in glucose assimilation during an intravenous glucose tolerance test (IVGTT) was investigated in 12 clinically healthy normotensive women with a body mass index (BMI) of 25 kg/m2 (range 22-31). This was assessed by coefficient Kg, the level of glycosylated proteins and insulin, C-peptide and contraregulating hormone secretion after seven days of oral administration of diltiazem, a calcium current blocker (180 mg per day). In spite of the fact that diltiazem protracted electrocardiographic QT interval from 0.16 +/- 0.008 to 0.18 +/- 0.009 s. (p < 0.01), QaT from 0.29 +/- 0.007 to 0.31 +/- 0.008 s. (p < 0.05), QeT from 0.35 +/- 0.009 to 0.37 +/- 0.009 s. (p < 0.01), it did not affect Kg in any significant way, nor did it affect the glycosylated protein levels, insulin and C-peptide secretion, nor the secretion of adrenaline, noradrenaline, dopamine, cortisol and growth hormone. Thus although diltiazem is a highly effective drug as far as the cardiovascular system is concerned, short-term administration of therapeutic doses of 180 mg/day is not associated with glycoregulatory risks.

Adult↗

PubMed1990

Effect of calcitriol and trifluoperazine on glucose stimulated B cell function in healthy humans.

The authors investigated the effects of pharmacological doses of calcitriol (1,25(OH)2-vitamin D3) and trifluoperazine on metabolic and hormonal indicators of glycoregulation in the course of the intravenous glucose tolerance test (IVGTT) in healthy subjects. Calcitriol administered by the oral route for four days, 3 micrograms/d, did not alter the blood sugar and plasma IRI levels at rest nor glucose stimulated values throughout the IVGTT. The slight increase of the glucose assimilation coefficient was not significant, as compared with values of the control test (Kg = (3.9 +/- 0.5) x 10(-2) [min-1] vs. Kg = (3.4 +/- 0.3) x 10(-2) [min-1], respectively). C-peptide plasma levels after calcitriol were slightly higher, significantly during the 14th minute following glucose administration (p less than 0.05), while the two-peak shape of the curve was preserved. Trifluoperazine administered by the oral route for seven days, 10 mg/d, did not significantly affect the blood sugar, IRI and C-peptide values at rest nor glucose induced values throughout the IVGTT nor values of glucose assimilation (Kg = (3.0 +/- 0.4) x 10(-2) [min-1] vs. Kg = (3.4 +/- 0.3) x 10(-2) [min-1] in the control test). In conclusion, neither calcitriol nor trifluoperazine treatment leads to clinically significant alteration of glycoregulation.

Adult↗