Browsing by Author "Nesovic, M. (7004028634)"

[No abstract available]

Corticosteroid hormones administered into the organism for therapeutic purposes have a certain effect on different organs and systems, especially on the endocrine system. It was interesting to find out the effect of corticosteroid therapy of different duration on the sympathetic adrenal system i.e. on urinary elimination of norepinephrine. The examination concerned 28 patients with systemic diseases and 8 healthy individuals who never were given corticosteroids. The patients were divided into 3 groups: 1). group on a short therapy; 2). group on a long therapy and 3). group on a prolonged therapy. The amount of norepinephrine in urine was determined by spectrophotofluorometric method. A multiphasic urinary elimination of norepinephrine was registered. After a short therapy corticosteroids provoked a decreased norepinephrine elimination i.e. a decreased activity of the sympathetic nervous system. After a several-month-therapy the elimination of norepinephrine returned to normal. However, after a prolonged corticosteroid therapy a definite decrease of sympathetic activity was observed. The result showed a positive correlation between norepinephrine excretion and administered dose of Pronison. The greatest fall of sympathetic activity was observed during small, suppressive doses of Pronison (5 mg daily). A prolonged administration of 80 mg doses increased urinary elimination of norepinephrine. This is possibly due to a central stimulating activity of corticosteroids on the sympathicus. It is concluded that a prolonged corticosteroid therapy provoked a fluctuation of sympathetic activity. Therefore the therapy should be intermittent. It is known that a prolonged corticosteroid treatment, especially a synthetic corticosteroid therapy, can provoke hypertension which is the consequence not only of water and salt retention, but also of increased sympathetic activity.

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[No abstract available]

OBJECTIVE: The goal of our study was to determine the rate of neoplasms in patients with other pituitary adenomas (non-functioning and prolactinomas) in comparison with acromegaly which is known to favour the development of neoplasia. DESIGN AND PATIENTS: We reviewed clinical records for 220 patients with acromegaly, 151 patients with non-functioning pituitary adenoma (NF) and 98 patients with prolactinomas. Incidence rates of cancer for patients with pituitary tumours were calculated per person-years of follow-up study. These rates were then compared with sex and age adjusted incidence rates reported by National Tumour Registry. An internal control group of 163 subjects with a nonneoplastic condition, i.e. Graves' disease followed chronically in the same clinic was also studied. The ratios observed to expected were expressed as standardized incidence rates (SIR). The only significant difference between the acromegalic and other pituitary tumours patients was in hypopituitarism, present in 18.2% (acromegaly) 47% (NF) and 18.6% (prolactinomas). RESULTS: Twenty-three malignant tumours were registered in 19 acromegalics (1 Hodgkin disease, 1 myelogenous leukaemia, 1 lymphocytic leukaemia, 3 papillary thyroid carcinomas, 1 ovarian carcinoma, 2 colorectal carcinoma, 1 renal cell carcinoma, 4 cervical carcinoma, 2 skin cancers, 2 pancreatic carcinoma, 4 breast carcinoma, 1 bladder carcinoma). Three acromegalics harboured two malignancies. Patients with acromegaly had a 3.39- fold increased rate of malignant tumours compared with the general population and a 3.21-fold increased rate compared with our internal control group. Eleven malignant tumours were found in patients with NF-pituitary adenomas and 2 in prolactinoma patients (1 lymphoma, 1 multiple myeloma, 1 colonic cancer, 1 renal cell cancer, 1 stomach cancer, 2 lung cancers, 1 cervix carcinoma, 1 breast cancer, 1 testicular carcinoma and 3 melanoma). Patients with NF pituitary adenomas had a 3.91-fold increased rate of malignant tumours compared with the general population and 4.07-fold increase compared with the internal control group. Patients harbouring prolactinomas did not have an increased incidence rate of malignancy compared with the general population or our internal controls. Female patients with acromegaly and male patients with NF-pituitary adenoma had higher incidences of neoplasia. CONCLUSION: We have demonstrated that the overall incidence of malignant tumours in patients with non-functioning pituitary adenomas and acromegaly is significantly higher than expected for general population and for our internal control group.

OBJECTIVE: The goal of our study was to determine the rate of neoplasms in patients with other pituitary adenomas (non-functioning and prolactinomas) in comparison with acromegaly which is known to favour the development of neoplasia. DESIGN AND PATIENTS: We reviewed clinical records for 220 patients with acromegaly, 151 patients with non-functioning pituitary adenoma (NF) and 98 patients with prolactinomas. Incidence rates of cancer for patients with pituitary tumours were calculated per person-years of follow-up study. These rates were then compared with sex and age adjusted incidence rates reported by National Tumour Registry. An internal control group of 163 subjects with a nonneoplastic condition, i.e. Graves' disease followed chronically in the same clinic was also studied. The ratios observed to expected were expressed as standardized incidence rates (SIR). The only significant difference between the acromegalic and other pituitary tumours patients was in hypopituitarism, present in 18.2% (acromegaly) 47% (NF) and 18.6% (prolactinomas). RESULTS: Twenty-three malignant tumours were registered in 19 acromegalics (1 Hodgkin disease, 1 myelogenous leukaemia, 1 lymphocytic leukaemia, 3 papillary thyroid carcinomas, 1 ovarian carcinoma, 2 colorectal carcinoma, 1 renal cell carcinoma, 4 cervical carcinoma, 2 skin cancers, 2 pancreatic carcinoma, 4 breast carcinoma, 1 bladder carcinoma). Three acromegalics harboured two malignancies. Patients with acromegaly had a 3.39- fold increased rate of malignant tumours compared with the general population and a 3.21-fold increased rate compared with our internal control group. Eleven malignant tumours were found in patients with NF-pituitary adenomas and 2 in prolactinoma patients (1 lymphoma, 1 multiple myeloma, 1 colonic cancer, 1 renal cell cancer, 1 stomach cancer, 2 lung cancers, 1 cervix carcinoma, 1 breast cancer, 1 testicular carcinoma and 3 melanoma). Patients with NF pituitary adenomas had a 3.91-fold increased rate of malignant tumours compared with the general population and 4.07-fold increase compared with the internal control group. Patients harbouring prolactinomas did not have an increased incidence rate of malignancy compared with the general population or our internal controls. Female patients with acromegaly and male patients with NF-pituitary adenoma had higher incidences of neoplasia. CONCLUSION: We have demonstrated that the overall incidence of malignant tumours in patients with non-functioning pituitary adenomas and acromegaly is significantly higher than expected for general population and for our internal control group.

This study has shown that there were not any significant increments (during ITT) or decrements (during OGTT) of plasma gastrin values in patients with acromegaly. Neither did gastrin response to ITT or OGTT differ in patients who had hyperprolactinaemia also. There is experimental evidence for increased concentration of gastrin in blood following insulin injection and for reduced concentration in the presence of hyperglycaemia. The release of gastrin depends both on the degree of hypoglycaemia achieved and the adrenergic response provoked as shown by Frier, Cirall, Adrian and Bloom (1982). There is no clear evidence however that these agents are involved in the physiological control of gastrin release (Blair, Grund, Kay, Lund, Reed, Sanders, Thompson and Venables 1978). The fact that gastrin circulates in a number of different molecular forms with different biological potencies further complicates the interpretation.

This study has shown that there were not any significant increments (during ITT) or decrements (during OGTT) of plasma gastrin values in patients with acromegaly. Neither did gastrin response to ITT or OGTT differ in patients who had hyperprolactinaemia also. There is experimental evidence for increased concentration of gastrin in blood following insulin injection and for reduced concentration in the presence of hyperglycaemia. The release of gastrin depends both on the degree of hypoglycaemia achieved and the adrenergic response provoked as shown by Frier, Cirall, Adrian and Bloom (1982). There is no clear evidence however that these agents are involved in the physiological control of gastrin release (Blair, Grund, Kay, Lund, Reed, Sanders, Thompson and Venables 1978). The fact that gastrin circulates in a number of different molecular forms with different biological potencies further complicates the interpretation.

[No abstract available]