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Biomedical subjects

M Kárteszi

Publications and source records attributed to M Kárteszi.

At least 19 recordsLinked to original sources
PubMed1989

[Liver-protective action of silymarin therapy in chronic alcoholic liver diseases].

The effects of silymarin (Legalon) therapy on liver function tests, serum procollagen III peptide level and liver histology were studied in 36 patients with chronic alcoholic liver disease in a six month double blind clinical trial. During silymarin treatment serum bilirubin, aspartate aminotransferase and alanin-aminotransferase values have been normalized, while gamma-glutamyl transferase activity and procollagen III peptid level decreased. The changes were significant, and there was a significant difference between post-treatment values of the two groups, as well. In the placebo group only gamma-glutamyl transferase values decreased significantly but to a lesser extent than that in the silymarin group. The histological alterations showed an improvement in the silymarin group, while remained unchanged in the placebo group. These results indicate that silymarin exerts hepatoprotective activity and is able to improve liver functions in alcoholic patients.

Chronic Disease↗
PubMed1989

[Familial occurrence of carcinoid of the small intestine].

The case of a 41 year old woman has been reported, whose "flush" syndrome was caused by a carcinoid tumor originated from the jejunum. The patient's father had to be operated for intestinal carcinoid tumor several times. The occurrence of different forms of carcinoid tumors, especially in the gastrointestinal tract, has been discussed in connection with the diagnostic approaches and therapeutical possibilities. The authors considered the case interesting for publications, because carcinoid is a rather rare tumor, and one cannot find its familiar occurrence in the available literature.

Adult↗
PubMed1988

Dopaminergic-opioidergic interaction is reflected by changes in pituitary hormone secretion in patients with essential hypertension.

In a randomized, double-blind crossover study 13 untreated patients with mild essential hypertension were exposed to submaximal bicycle exercise. Sixty minutes before ergometry 10 mg metoclopramide or placebo, and 10 min before exercise 0.4 mg naloxone or placebo, were given intravenously. Plasma adrenocorticotrophic hormone, beta-endorphin and cortisol levels increased significantly after ergometry, whether performed after placebo, naloxone, metoclopramide or metoclopramide + naloxone treatment. However, only naloxone administration potentiated plasma adrenocorticotrophic hormone, beta-endorphin and cortisol responses to workload. Plasma levels of adrenocorticotrophic hormone, beta-endorphin and cortisol were 45 +/- 14 pg/ml, 6.2 +/- 1.2 pmol/l and 141 +/- ng/ml, respectively, after ergometry, when performed after placebo, but these values were increased to 61 +/- 10 pg/ml, 11.4 +/- 2.8 pmol/l and 207 +/- 22 ng/ml, respectively, after naloxone treatment. This naloxone-induced potentiation of hormonal release was blocked by metoclopramide pretreatment, suggesting a close interaction between dopaminergic and opioidergic mechanisms, regulating hormonal responses to physical exercise.

Dopamine↗
PubMed1988

Determination of the aminoterminal peptide of procollagen type III and laminin P1 in serum of patients with chronic liver disease.

Serum concentration of the aminoterminal peptide of procollagen type III (P III P) and that of the high-molecular-weight glycoprotein laminin P1 (LP1) were determined by a specific radioimmunoassay (RIA) in patients with different chronic liver diseases. Besides the routine laboratory tests, histological verification of the liver samples obtained by needle biopsy and a complex hepatitis B virus marker analysis by RIA (Biomedica-Sorin), or ELISA (Behringwerke, Marburg, FRG) kits were carried out in order to set up the correct clinical diagnosis. In normal controls, the P III P and LP1 concentrations were 7.8 +/- 1.1 ng/ml (n = 10) and 0.08 +/- 0.1 units/ml (n = 7), respectively. Patients with fatty liver (n = 25) showed a significant elevation in P III P concentration (18.6 +/- 2.7 ng/ml). Such an elevation was not unequivocally demonstrated before. In this group of patients LP1 level was also increased (1.4 +/- 0.2 units/ml, n = 10). In liver cirrhosis (n = 51) both P III P and LP1 concentrations were found to be consistently elevated.

Biomarkers↗
PubMed1988

Life expectancy in chronic liver disease.

Life-table analysis is a suitable method for evaluating the effectiveness of therapeutical approaches to and the progression of, chronic diseases. The authors performed 324 liver biopsies in patients with liver disease between 1976 and 1986. The cumulative life-table analysis of Cutler and Ederer was applied in this retrospective study. Survival rates of different groups of patients expressed as the 7-year life expectancy were as follows: toxic hepatitis 90%, steatosis hepatitis 87%, chronic persistent hepatitis 87%, nonspecific reactive hepatitis 76%, chronic active hepatitis 72%, acute alcoholic hepatitis 66%, liver cirrhosis 40%. There seems to be a correlation between the severity of histological alteration and live expectancy. A similar correlation between the inflammatory cell infiltration and life expectancy cannot be observed. The life expectancy of patients with chronic active hepatitis has significantly improved recently. Further improvement of survival of patients with liver cirrhosis can be expected only from a reduction of alcohol consumption. The results can be regarded as a reference data for life expectancy of patients with chronic liver disease in Hungary.

Biopsy↗
PubMed1988

Serum type-III-procollagen and laminin concentration after interferon therapy in chronic myeloproliferative disorders.

Serum procollagen-III-peptide (P-III-P) and laminin P 1 (LP1) concentrations were measured in 24 patients with various chronic myeloproliferative diseases, viz., essential thrombocythaemia (ET), chronic myelogenous leukaemia (CML) and myelofibrosis (MF). The highest P-III-P values were found in myelofibrosis. As compared to the controls, the serum laminin concentration was higher in all there groups of patients. No significant difference was found between the groups of patients. After three months of alpha-IFN therapy the P-III-P values became significantly higher, the laminin concentration slightly decreased in all investigated patients. Longitudinal follow-up myeloproliferative patients should be carried out in order to prove whether P-III-P and laminin determinations provide a useful test to monitor the progression of the disease and the effect of the therapy.

Adult↗
PubMed1987

A prospective multicenter study of insulin and glucagon infusion therapy in acute alcoholic hepatitis.

A randomized, single-blind controlled multicenter study of insulin and glucagon infusion was carried out in 66 patients with acute alcoholic hepatitis. Thirty-three patients were treated with insulin 10 U and glucagon 1 mg in 500 ml 5% glucose in water via a peripheral vein for 2-6 h three times every day for 3 weeks. Patients in the control group received 5% glucose in an identical fashion. Fourteen control patients and five treated patients died from liver failure during the study (P less than 0.02). Clinical features of liver disease on entry into the study were similar in the two groups, but the total serum bilirubin, aspartate aminotransferase, gamma-glutamyltranspeptidase activities and prothrombin time significantly improved in the treated patients (P less than 0.05). Insulin and glucagon infusion appears to be a promising treatment of acute alcoholic hepatitis.

Adult↗
PubMed1985

Rapid changes in growth hormone regulation and hypothalamic somatostatin after transection of anterolateral pathways to the medial-basal hypothalamus in the rat.

Plasma and pituitary GH content, in-vitro GH release and somatostatin-like immunoreactivity (SLI) in the stalk-median eminence were studied up to 7 days after making an anterolateral cut (ALC) around the medial-basal hypothalamus. Plasma GH concentration increased within 15 min to a very high level, then fell to a high level which was unchanged for several hours. The GH concentration then steadily decreased between days 2 and 7. The SLI content in the stalk-median eminence decreased to 3.5% of the control value within 3 days. The GH content of the anterior pituitary gland was 58.8% of the control value by 1 week after the operation but the in-vitro sensitivity to somatostatin of the GH cells failed to change. Pentobarbitone injection stimulated GH release in the sham-operated controls but decreased it in the rats with an ALC. These findings suggest that transection of somatostatin-containing fibres is followed by a rapid rise and a lasting high concentration of plasma GH which slowly returns towards lower levels in parallel with a marked depletion of pituitary GH content. In rats with transected somatostatin innervation of the median eminence, sodium pentobarbitone probably decreases GH secretion by depressing the secretion of GH-releasing hormone.

Animals↗
PubMed1984

Inhibition of growth hormone and prolactin secretion by a serine proteinase inhibitor.

The action of the tripeptide aldehyde t-butyloxycarbonyl-DPhe-Pro-Arg-H (boc-fPR-H), belonging to a family of serine proteinase inhibitors, on the release of immunoreactive prolactin (iPRL) and growth hormone (iGH) has been studied. In rat anterior pituitary cell cultures and pituitary quarters 1 mM boc-fPR-H inhibited basal iPRL and iGH release. Thyroliberin-induced iPRL release by cultured cells was also markedly inhibited with a concomitant accumulation of intra-cellular iPRL. During the short- and long-term exposure of cells to boc-fPR-H there no changes in total cell protein contents and in activities of some lysosomal marker enzymes. A wide scale of unchanged parameters characteristic for cellular metabolism indicated that the tripeptide aldehyde has no cytotoxic effect. The marked inhibition of basal as well as stimulated hormone release in the presence of the enzyme inhibitor might suggest that at least a portion of the hormones is released via a proteolytic enzyme-dependent process.

Animals↗
PubMed1983

Responsiveness of adenohypophysial corticotrophs to hypothalamic (SME) extract remains unchanged in rats with hypothalamic lesions inhibiting CRF release.

The corticotrophin-releasing activity of stalk-median eminence (SME) extract was studied using incubated quarters of anterior pituitary glands obtained from rats with long-term anterolateral deafferentiation or complete surgical lesion of the medial basal hypothalamus, as well as with the lesion of the paraventricular nuclei. These hypothalamic interventions are known to cause a complete or partial but significant deficiency in hypothalamic corticotrophin-releasing factor (CRF) release, however, such lesions failed to alter the sensitivity of the ACTH response from incubated pituitary segments towards the SME extract. These results suggest that the specific responsiveness of adenohypophysial corticotrophs is maintained when hypothalamic CRF supply is decreased for a long period of time.

Adrenocorticotropic Hormone↗
PubMed1983

Effects of arginine-8-vasopressin and 1-deamino-8-D-arginine-vasopressin on ACTH secretion in rats.

The corticotropin-releasing effect of arginine-8-vasopressin (AVP) has been compared to that of 1-deamino-8-D-arginine-vasopressin (dDAVP) in male rats of R-Amsterdam strain. AVP increased the level of ACTH and corticosterone in the peripheral blood in a dose-dependent manner. In contrast to AVP, a very potent antidiuretic agent dDAVP which is devoid of pressor activity had no effect on ACTH release and did not stimulate the secretion of corticosterone. It is concluded that CRF activity of vasopressin in vivo is related to its pressor activity. These data are in agreement with the previous findings of these authors demonstrating that dDAVP shows a very low affinity for vasopressin receptors of the cell membranes in the adenohypophysis.

Adrenocorticotropic Hormone↗
PubMed1982

Lack of episodic growth hormone secretion in rats with anterolateral deafferentation of the medial-basal hypothalamus.

Growth hormone secretory dynamics were studied in rats sampled through chronic indwelling right atrial cannulae at time-intervals ranging from 2 days to 2 months after placing an anterolateral cut (ALC) around the medial-basal hypothalamus (MBH). The episodic secretion normally occurring in the control animals could not be seen in the rats with an ALC. Instead of the usual high bursts and low trough levels occurring between 09.00 and 13.00 h in the controls, the operated animals had fairly constant plasma GH levels with only minor fluctuations at all postoperative time-points studied. These results suggest that (1) the isolated MBH is incapable of maintaining the episodic secretion of GH and (2) the pulsatile hormone release is dependent on neural pathways entering the MBH from an anterolateral direction.

Afferent Pathways↗
PubMed1981

Effects of paraventricular lesions on stimulated ACTH release and CRF in stalk-median eminence of the rat.

The effects of destroying the paraventricular nucleus (PVN) of the rat hypothalamus on pituitary-adrenal function were studied. Four days after PVN lesions were placed with a rotating knife, the basal plasma corticosterone level was normal, but the corticosterone response to electrical stimulation of the medial basal hypothalamus, surgical trauma, and ether-venesection stress was significantly inhibited. Four and 8 days after PVN lesioning and adrenalectomy, the basal plasma ACTH level was lower, and the rise of plasma ACTH level elicited by a 3-min ether inhalation was significantly smaller than in the adrenalectomized controls. Corticotropin-releasing factor (CRF) activity in the stalk-median eminence extracts from PVN-lesioned rats was significantly less than in the control extracts. The weight of the adrenals was decreased by both 2 and 4 wk after PVN destruction, and 2 wk after hemiadrenalectomy, the compensatory adrenal hypertrophy was inhibited. The plasma corticosterone response to ether-venesection stress was inhibited only temporarily because it returned to normal by the end of the 4th postoperative week. The results are consistent with the hypothesis that a substantial portion of CRF-containing fibers in the stalk-median eminence region either originate from or run though the PVN or its immediate vicinity.

Adrenal Glands↗
PubMed1981

Corticoliberin activity of rat neurohypophysis is distinct from vasopressin.

Electrical stimulation of the neural lobe of the pituitary resulted in an increase of corticosterone secretion in both normal and Brattleboro rats. Bioassaying the corticoliberin (CRF) activity of stalk-median eminence and neural lobe extracts obtained from normal and Brattleboro rats revealed that the endogenous vasopressin was not a prerequisite of ACTH-releasing potency. Arginine-8-vasopressin failed to potentiate the CRF activity of the different extracts. These data suggest that a nonvasopressin substance(s) with CRF activity can be released from the neurohypophysis of the rat, and it may contribute to activating the pituitary-adrenal axis under certain experimental conditions.

Adrenocorticotropic Hormone↗
PubMed1981

Effects of treatment with adrenocorticotrophin on the hypothalamo-pituitary-adrenal system.

Long-term treatment with adrenocorticotrophin (ACTH) inhibited the stress-induced response of the hypophysial-adrenocortical system 24 h after the final ACTH injection. The mechanism of this phenomenon was studied in both normal and adrenalectomized rats, the latter receiving corticosterone at various doses. The effect of electrical stimulation of the medial basal hypothalamus on the concentration of corticosterone in plasma (an indicator of ACTH secretion), the corticotrophin releasing factor (CRF) content of the stalk median eminence (SME), the ACTH content of the pituitary gland and the in-vitro release of ACTH by the pituitary gland incubated with or without addition of SME extract were investigated. Electrical stimulation of the medial basal hypothalamus failed to induce a rise in concentrations of corticosterone in plasma of normal rats treated with ACTH; moreover the levels of hypothalamic CRF and hypophysial ACTH were significantly decreased. Hemipituitary glands of ACTH-treated rats released markedly less ACTH in vitro in response to SME extract than did the control glands. This indicated that long-term hormone administration caused a serious impairment of the responsiveness of the corticotrophic cells toward CRF. Pituitary ACTH content and in-vitro responsiveness of pituitary glands obtained from ACTH-treated, adrenalectomized rats receiving corticosterone replacement seemed to be dependent on the amount of exogenous corticosteroid, but not on that of exogenous ACTH. Our previous and present findings suggest that long-term treatment with ACTH elicits repeatedly increased secretion of endogenous corticosterone, impairing the stress-induced CRF-ACTH release at both the hypothalamic and hypophysial levels. Our data challenge the view that ACTH itself is able to inhibit its own secretion.

Adrenalectomy↗
PubMed1980

Effect of electrical stimulation of the neurohypophysis on ACTH release in rats with hypothalamic lesions.

Electrical stimulation of the neural lobe (NL) of the pituitary induces a rise in plasma corticosterone indicating the release of adrenocorticotropin (ACTH) in rats pretreated with dexamethasone, morphine and pentobarbitone. 7-8 days after placing an anterolateral cut around the medial basal hypothalamus (MBH), the rats failed to respond with ACTH release to electrical stimulation of the NL; the number of nerve fibers and terminals in the NL decreased to less than 5% of the normal; and ACTH releasing activity of acid extracts of the NL was undetectable using both in vivo and in vitro tests, which are insensitive to vasopressin. After lesions of the paraventricular nuclei the stimulation of the NL elecited a rise of plasma corticosterone that was significantly less than that in the controls. These results suggest that the NL of the pituitary contains electrically excitable fibers capable of releasing corticotropin-releasing factor (CRF; distinct from vasopressin) and that these fibers probably originate from outside the MBH, with a portion of them coming from or through the paraventricular nuclei or their immediate vincinity.

Adrenocorticotropic Hormone↗