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Miklós Góth

Publications and source records attributed to Miklós Góth.

8 recordsLinked to original sources
PubMed2005

[Ghrelin--a hormone with multiple functions].

The growth hormone secretagogue ghrelin is in the centre of interest since its discovery in 1999. It stimulates growth hormone, corticotropic hormone and prolactin secretion, but also plays an important role in the regulation of appetite, carbohydrate- and lipid metabolism and possibly on gastric acid secretion, gastric motility, heart function and as well as immune functions and cell proliferation. Ghrelin was originally identified from the stomach but it is also present in all tissue among others in: hypothalamus, pituitary, pancreas, lung, immune cells, placenta, ovary, testis, kidney and in different tumours including pituitary adenoma, neuroendocrine tumours, thyroid carcinomas, endocrine tumours of the pancreas and lung. The gene structure and its receptor are similar to motilin, they are both synthesized in the upper gastrointestinal tract and both have prokinetic activity on gut motility. The ghrelin receptor (growth hormone secretagogue receptor) is a member of G protein-coupled seven transmembrane domain receptor. The receptor is localised in the central nervous system, kidney, thyroid, pancreas, myocardium and spleen. Starvation and low body mass index decrease, while food intake, hyperglycaemia, elevated insulin levels and high body mass index increase the endogenous ghrelin levels. Although we know much about the ghrelin, number of questions remain unanswered, such as the effects of the locally-produced ghrelin or its role in the cell metabolism.

Animals↗
PubMed2005

[Correlations between the hypothalamo-pituitary-adrenal axis and the metabolic syndrome].

The metabolic syndrome has several similarities with Cushing's syndrome (impaired glucose tolerance, hypertension, dyslipidemia, central obesity) suggesting that abnormalities in the regulation of the hypothalamic-pituitary-adrenal axis may have a link with the metabolic syndrome. Several studies suggested an association between the clinical signs of the metabolic syndrome and the increased hypothalamic-pituitary-adrenal axis activity based on increased cortisol concentration at 09.00 a.m. and increased cortisol response to corticotropin. According to the Barker hypothesis the fetal malnutrition could determine adult cardiovascular diseases (coronary heart disease, hypertension), some endocrine and metabolic disorders (obesity, type 2 diabetes and hyperlipidemia). The suggested mechanism of the phenomenon is that the suboptimal fetal nutrition results in glucocorticoid overproduction. The 11beta-hydroxysteroid dehydrogenase (converts biological inactive cortisone to cortisol and vice versa) is an important enzyme in cortisol metabolism. The increased expression of 11beta-hydroxysteroid dehydrogenase type 1 in fat tissue could lead to central obesity and impaired glucose tolerance. The hypothesis that increased corticotropin-releasing hormone production drives the overactive hypothalamo-pituitary-adrenal axis was not proven. Further investigations are needed to identify additional pathogenetic factors and to find new therapeutic possibilities.

11-beta-Hydroxysteroid Dehydrogenase Type 1↗
PubMed2003

[Macroprolactinemia in the differential diagnosis of hyperprolactinemia].

INTRODUCTION: Biologically active prolactin and the inactive fraction of macroprolactin can be present in hyperprolactinaemic sera. The reaction of routinely used prolactin assays with macroprolactin is variable. AIMS: The present study was undertaken to analyse the leading clinical signs of hyperprolactinemia in macroprolactinemia and true hyperprolactinemia and to assess the prevalence of macroprolactinemia in hyperprolactinemic females. METHODS: 1571 consecutive female patients were investigated for hyperprolactinemia. Prolactin was measured before and after precipitation of macroprolactin by polyethylene glycol in 285 hyperprolactinemic (> 520 mlU/l) patients. Since not a single case of macroprolactinemia (recovery < 40%) was found in the range of 520-700 mlU/l, only in women with prolactin > 700 mlU/l (N = 254) entered the study. RESULTS: In 59 patients (23%) macroprolactinemia was found. In women, the occurrence of macroprolactinemia increased with advancing age (p < 0.05). "A priori" clinical signs indicating hyperprolactinemia occurred less frequently in patients with macroprolactinemia than in those with true hyperprolactinemia. Pituitary microadenoma was found in 9.8% of macroprolactinemia vs. 31.6% in true hyperprolactinemia (p < 0.01); galactorrhea: 4% in macroprolactinemia vs. 19% in true hyperprolactinemia, (p < 0.05); infertility: 17% in macroprolactinemia vs. 44% in true hyperprolactinemia (p < 0.05). In 8 out of 59 women with macroprolactinemia, true hyperprolactinemia appeared simultaneously (15.3%). Occurrence of polycystic ovaries syndrome was more frequent in the true hyperprolactinemia (12%) that in macroprolactinemia (4.5%). CONCLUSIONS: It has been shown that macroprolactin does not occur in mild hyperprolactinemia. In women, the occurrence of macroprolactinemia increases with age. "A priori" clinical signs indicating hyperprolactinemia and pituitary abnormality are less frequent in macroprolactinemia than in true hyperprolactinemia. The diagnosis of macroprolactinemia should be used only, when the PRL levels fall to the normal range after precipitation. To avoid diagnostic and therapeutic pitfalls the screening for macroprolactin of all patients with prolactin > 700 mlU/L is recommended.

Adenoma↗
PubMed2002

[Novel pharmacologic therapies in acromegaly].

The primary aim of therapy should be to remove symptoms, reduce tumor bulk, prevent relapse, and improve long-term outcome. Surgery, radiotherapy and medical therapies are used to achieve these aims. Post-treatment mean "safe" serum growth hormone values of < 2.5 ng/ml should be the therapeutic goal. Transsphenoidal surgery remains the first line treatment for acromegaly. Patients with microadenoma can expect 85%, while those with macroadenoma 50% chance to achieve safe serum growth hormone levels. Less than 20% of acromegalics respond to treatment with bromocriptine, while quinagolide and cabergoline may show better clinical response; the success rate is higher for tumors secreting both growth hormone and prolactin. Dopamine agonists may be considered either in combination with somatostatin-analogues or as monotherapy in selected patients, and in those with co-secretion of prolactin. Octreotide (Sandostatin, Novartis) is a synthetic somatostatin-analogue, which is administered subcutaneously in doses between 100 and 250 micrograms 3 times daily. Long-acting octreotide (Sandostatin LAR, Novartis) contains octreotide incorporated into microspheres of biodegradable polymer. To effectively lower serum growth hormone levels, monthly injections of 10-30 mg of long-acting octreotide are needed, serum growth hormone falls to 2.5 ng/ml in 70% of cases, and serum insulin-like growth factor I normalizes in 67%. Slow release lanreotide (Somatuline SR, Ipsen) is an alternative depot long-acting somatostatin-analogue, which is administered in a dose of 30 mg intramuscularly every 14, 10 or 7 days. Both compounds are equally, if not more, effective than subcutaneous octreotide, and significantly improve patient compliance. Pegvisomant (Sensus Drug Development Corporation) is a genetically engineered growth hormone receptor antagonist, which inhibits growth hormone action. When given subcutaneously in a dose of 20 mg/day, serum insulin-like growth factor I levels return to normal in 90% of patients. Theoretical concerns of tumor expansion have not been a problem to date, but long term studies are needed. Primary medical--somatostatin-analogue--therapy is recommended if surgery fails, if the patient refuses or unsuited for surgery and it may be also considered in patients with macroadenoma with extra--but not suprasellar extension, since the surgical "cure" rates of these tumors are low.

Acromegaly↗
PubMed2002

[Thyrotropin-secreting pituitary adenomas--diagnosis and treatment in five case].

The authors report five cases of thyrotropin secreting pituitary adenomas (4 males and 1 female) in whom the diagnosis was established by a combined occurrence of elevated serum free thyroid hormone levels and measurable serum thyrotropin concentration, as well as by visualisation of the pituitary adenomas using magnetic resonance imaging (pituitary microadenoma in two and macroadenoma in three cases). Other tests were less diagnostic: only two out of 4 patients proved to be non-responders during testing with thyrotropin releasing hormone, and serum alpha subunit was elevated in only 2 out of 3 cases. There was a significant decrease of serum thyrotropin concentration in all of the four patients tested by 100 micrograms octreotide (Sandostatin, Novartis). Somatostatin-analogue treatment (slow release preparation in two cases) restored euthyroidism in all three cases treated prior to surgery. In one case the hyperthyroidism persisted after surgery of the macroadenoma, but irradiation of the pituitary area and subsequent somatostatin-analogue treatment resulted finally in a complete cure (euthyroidism and no tumor remnant). In the three other operated patients surgery resulted in euthyroidism. These cases demonstrate the variety of diagnostic and therapeutical modalities in the management of thyrotropin secreting pituitary adenomas.

Adenoma↗
PubMed2002

[Serum tumor marker levels during a 12-months growth hormone replacement therapy in patients with adult growth hormone deficiency].

INTRODUCTION: High growth hormone/insulin-like growth factor-1 level may have oncogenic potential in animal experiments, and in patients with acromegaly. There are also some data suggesting the development of different neoplasms in animals after growth hormone administration and in humans upon growth hormone replacement therapy. AIMS: The general opinion is however, that growth hormone replacement therapy has no oncogenic effect, but the tumor marker levels have not been studied so far. PATIENTS/METHODS: Nine patients participated in the study: 3 women, 6 men, aged between 21-52 years. 6 of them had multiple pituitary hormone deficiency and were on replacement therapy (thyroxine: 2, cortisone: 1, sexual steroids: 6 and desmopressin: 2 patients). The cause of growth hormone deficiency was the removal of pituitary tumor (6 patients) or craniopharyngioma (2 patients), and in 1 case the deficiency was idiopathic. The mean dose of growth hormone was 0.53 in female and 0.51 mg/day in male patients. Insulin-like growth factor-1, carcinoembryonal antigen, human choriogonadotropin hormone, alpha-fetoprotein, prostate specific antigen, tissue polypeptide antigen-M, ferritin, gastrointestinal carcinoma antigen, ovarian antigen, breast specific antigen, carcinoma antigen 50 were measured at baseline and after 3, 6 and 12 months of GH replacement. RESULTS: Insulin-like growth factor-1 standard deviation score increased: baseline: -4.1 +/- 0.5; 3 months: -0.3 +/- 0.3; 6 months: 0.7 +/- 0.2; 12 months: -0.2 +/- 0.6, P < 0.001 vs. baseline. The mean value of all tumor markers remained within the normal range and there was no significant increase within the normal range either. CONCLUSION: The lack of increase of tumor marker levels does not indicate possible oncogenic effect of one-year GH treatment in hypopituitary adults. The authors can not draw any far-reaching conclusions because of the low patient number and the short follow-up, but the measurement of tumor marker levels may provide useful means to follow up long-term therapy and for the early diagnosis of possible occult malignancy.

Adult↗
PubMedDate not supplied

Efficacy of conservative voice treatment in male-to-female transsexuals.

A voice assessment was performed before and after conservative voice treatment in 3 male-to-female transsexuals and in 2 nontreated transsexuals serving as control persons. The characteristics studied were voice quality, habitual speaking pitch, vocal pitch range, vocal intensity range, maximum phonation time and 'communicative impairment', a subjective self-estimation by the patient. Based on these parameters the Friedrich dysphonia index (DI) was calculated. The habitual speaking pitch of the 3 transsexuals who had received voice treatment became female, in contrast to that of the nontreated transsexuals, which remained in the so-called 'indifferent pitch range'. The DI of the treated patients was close to the normal value, in contrast to the DI of controls, which continued to be pathological. Even based on this small population, study results reflected the effectiveness of voice therapy in transsexuals.

Adult↗