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Biomedical subjects

D Manojlović

Publications and source records attributed to D Manojlović.

At least 19 recordsLinked to original sources
PubMed1992

Androgen-producing bilateral large cortical adrenal adenomas associated with polycystic ovaries in a young female.

An association of bilateral large adrenocortical androgen-producing adenomas with polycystic ovaries in a young female is presented. She developed mild hirsutism and secondary amenorrhoea at the age of 17, and was treated for 3 years with an anti-androgen (cyproterone acetate) and ethinyloestradiol. Routine follow-up at the age of 21 showed bilateral large adrenal tumours and polycystic ovaries, together with high serum testosterone and dehydroepiandrosterone sulphate values. Bilateral adrenalectomy was performed, which resulted in lowering of the elevated androgens, and large bilateral adrenocortical adenomas were confirmed histologically. Contrary to expectations, the polycystic appearance of the ovaries persisted after adrenalectomy. This case supports the possible role of adrenal androgens in the pathogenesis of polycystic ovaries as well as the possibility of the persistence of polycystic ovaries without adrenal androgens once they have developed.

Adenoma↗
PubMed1991

Follicle stimulating hormone-secreting pituitary adenoma: inappropriate secretion and effect of pulsatile luteinizing hormone releasing hormone analogue (buserelin) administration.

A patient with an FSH secreting pituitary adenoma is reported. Elevated FSH and serum free alpha-subunit (SU) with low levels of LH and testosterone (T) were found. Immunostaining showed the presence of alpha-SU, FSH-beta and LH-beta subunits. LHRH analogue (buserelin) was administered in a pulsatile manner, by portable computerized infusion pump sc for ten days. During the first 24 h of treatment FSH, LH (p less than 0.001) and T (p less than 0.01) rose significantly. Ten days later, the expected desensitization phenomenon did not occur, but further increases of T (8.4 +/- 2.6, mean +/- SD, vs 17.4 +/- 4.1 nmol/l, p less than 0.001) and FSH (58.9 +/- 9.6 vs 70.7 +/- 3.8 mlU/ml, p less than 0.001) were registered. LH decreased (12.5 +/- 2.4 vs 7.1 +/- 0.6 mlU/ml, p less than 0.001) at day 10, but remained higher than basal level (5.0 +/- 0.6, p less than 0.001). Free alpha-SU also rose (2.8 +/- 0.4 vs 4.4 +/- 1.7 mlU/ml, p less than 0.001) after ten days of treatment. The chronic stimulatory effect of analogue on LH with a lack of desensitization suggests tumorous secretion despite a partially preserved negative feedback of testosterone. Low basal LH levels, in some patients with FSH secreting tumors may not be due to tumor mass effect, but rather may be the consequence of altered LH production and/or secretion by the tumor. Although buserelin may not have a therapeutic effect, it is of use in differential diagnosis of hypergonadotropinemia.

Adenoma, Chromophobe↗
PubMed1990

How reliable is the euglycaemic hyperinsulinemic clamp test for the confirmation of autonomous endogenous hyperinsulinemia?

Inhibition of C-Peptide secretion by exogenous insulin was studied during euglycemic clamp in 13 patients with histologically verified causes of organic hyperinsulinaemia (10 with beta cell adenoma; 2 with beta cell carcinoma and 1 with beta cell hyperplasia) and in 10 healthy controls. Euglycemic clamps were performed using artificial endocrine pancreas (Clamp Mode 9:1) while insulin infusion (Humulin Normal-Lilly) rate was 0.1 U/kg BW/h. Blood samples for serum insulin (RIA INEP) and C-Peptide (RIA-Biodata) were taken at 0; 30; 60; 90 and 120 min. Statistical analysis was done using SPSS on IBM-PC with Wilcoxon sum rank test and one way ANOVA. All the patients were studied before the operation and in four of them clamp studies were repeated after the operation. Statistically significant suppression of C-Peptide values in 120 min was established in the control group (p less than 0.05) while there was no significant suppression in insulinoma group (p greater than 0.05), except in one patient with beta cell hyperplasia. Various types of responses (suppression, no change, paradoxical increase) were observed after the operation in the insulinoma group. Possible mechanisms and the meanings of the absence of insulin induced C-Peptide suppression in insulinoma group are discussed. It is concluded that euglycemic hyperinsulinemic clamp study could be useful and a complementary test to other established tests for the confirmation of the diagnosis of insulinoma. Further work on beta cell response after the operation in patients with insulinoma is necessary.

Adenoma↗
PubMed1990

A comparison among the effectiveness of growth hormone suppression in active acromegaly of bromocriptine and long acting somatostatin analogue (SMS 201-995).

The aim of our study was to compare the effectiveness of bromocriptine vs. long acting somatostatin analogue (SMS 201-995) on growth hormone suppression in active acromegaly. A twenty year old female, student of law, was previously treated with Parlodel LA 50 mg i.m. injection and then with bromocriptine 30 mg orally for 2.5 years because of active acromegaly and very large intrasellar and suprasellar pituitary adenoma. She was partial bromocriptine responder with mean growth hormone levels prior the treatment 30 mU/L and after bromocriptine 13.7 mU/L and with gross tumor shrinkage. Since she failed to restore menstrual cycles, had clinical signs of the disease, she was taken off bromocriptine and treated with somatostatin analogue (SMS 201-995) 300 mcg s.c. daily and 400 mcg s.c. daily with mean growth hormone levels 10 mU/L. She was also treated with combined treatment (400 mcg s.c. SMS 201-995 plus 30 mg bromocriptine orally) and mean growth hormone levels were 11 mU/L. SMS 201-995 had a long lasting inhibitory effect on growth hormone secretion in acromegaly (p less than 0.01) but in comparison to daily growth hormone levels during bromocriptine treatment no difference was found (p greater than 0.01). Combined treatment with SMS 201-995 and bromocriptine did not achieve greater suppression of daily growth hormone levels than those achieved with SMS 201-995 alone (p greater than 0.1) or with bromocriptine alone (p greater than 0.05). No significant tumor shrinkage during chronic SMS treatment was seen. Severe clinical and biochemical signs of hypoglycaemia were registered on one occasion only during the first month of treatment with SMS 201-995.(ABSTRACT TRUNCATED AT 250 WORDS)

Acromegaly↗
PubMed1990

Discordance between growth hormone responses after growth hormone-releasing hormone (GHRH) and insulin hypoglycemia in ectopic GHRH syndrome.

Dynamic studies of growth hormone (GH) secretion were performed in two patients with ectopic GHRH syndrome. Patient 1 (female, 33 years old) had a growth hormone releasing hormone (GHRH) producing carcinoid of the lung with clinical features of acromegaly while patient 2 (50 years old male) had small cell carcinoma of the lung without acromegaly. Insulin hypoglycemia stimulated GH secretion in both patients (i.e. from a basal level of 10 mU/l to 48 mU/l in patient 1, while the respective values in patient 2 were 5 mU/l and 61 mU/l), TRH acutely stimulated GH in both patients. Synthetic GHRH 1-29 (KABI) i.v. bolus 100 micrograms did not stimulate GH release in either patient (i.e. basal GH 14 mU/l and peak 18 mU/l (patient 1); basal GH 4.6 mU/l and peak 8.8 mU/l (patient 2). It is concluded that: 1. prolonged pituitary exposure to GHRH is associated with chronic GH hypersecretion with or without clinical acromegaly; 2. GH response to TRH may be mediated at the pituitary level and results from prolonged exposure to GHRH; 3. the discordant response of GH after GHRH and insulin induced hypoglycemia might suggest the involvement (at least partially) of somatostatin in the mechanism of GH release after hypoglycemia and after GHRH.

Adult↗
PubMed1990

Naloxone interaction with pituitary response to TRH and LHRH test in patients with polycystic ovary syndrome.

The response of TSH, PRL, LH and FSH to combined test with LHRH (Relefact LH-RH, HOECHST; 0.1 mg) and TRH (Relefact TRH, HOECHST; 0.2 mg) was examined before (day I) and after naloxone (Narcanti, DUPONT) bolus of 0.8 mg (day III) in 8 patients with polycystic ovary syndrome (POC) diagnosed by established criteria (hirsutism, oligoamenorrhoea, ultrasound appearance of polycystic ovary and serum LH/FSH greater than 2.0). TSH (RIA-INEP), PRL (MAIA-SERONO), LH (MAIA-SERONO) and FSH (MAIA-SERONO) were determined at -15, 0, 10, 20, 30, 45, 60, 90 and 120 min. The hormone responses were calculated as the areas under hormone curves and tested with Wilcoxon sum rank test. No significant difference was found in the hormone responses before and after naloxone injection. In terms of absolute values lower TSH level was found at 30 min after naloxone administration (14.7 +/- 12.0 vs. 9.73 +/- 7.61; P less than 0.05). In conclusion, our data based on short term naloxone application argue against the significant alteration of the opioid activity in patients with POC.

Adult↗
PubMed1989

Nutritional status and plasma lipids in diabetic subjects.

The aim of the present work was to determine and analyse the nutritional status and plasma lipid levels in diabetic and control subjects dependent on the type of lipidemia. The investigations involved four groups: controls with normal lipidemia, diabetic (NIDDM) subjects with normal lipidemia, persons with hyperlipidemia type IV, and without diabetes mellitus, and diabetic subjects with hyperlipidemia type IV. The values for the concentrations of plasma triacylglycerol, cholesterol, phospholipids and HDL-phospholipids were significantly higher in both diabetic groups than in controls. The values for the relative amount and concentration of HDL-cholesterol were significantly lower in diabetics than in the control groups.

Body Weight↗
PubMed1988

Hypersensitivity reaction with intravenous GnRH after pulsatile subcutaneous GnRH treatment in male hypogonadotrophic hypogonadism.

Chronic pulsatile subcutaneous administration of low doses of gonadotrophin releasing hormone (GnRH) is an effective therapy for men with hypogonadotrophic hypogonadism. Hypersensitivity reactions to GnRH are rare. We wish to report hypersensitivity reactions with intravenous GnRH after low dose subcutaneous pulsatile GnRH treatment in two men with hypogonadotrophic hypogonadism due to suprasellar disease.

Adolescent↗
PubMed1987

The prolactin response to TRH and domperidone does not differentiate male hypothalamic hypogonadism and constitutional delay of puberty.

In order to test whether prolactin response to challenge with TRH and domperidone, dopamine receptor antagonist, is diagnostic for idiopathic hypothalamic hypogonadism (IHH) we studied 8 normal controls, 9 subjects with delayed sexual development and 6 patients with IHH. TRH test (200 micrograms i.v. bolus) and domperidone (10 mg i.v. bolus) were given on two different days. Prolactin (RIA-Biodata) was determined in blood samples during the test. The basal value of prolactin in subjects with delayed puberty and healthy controls did not differ from basal values of prolactin in patients with IHH. The peak elevation of prolactin after TRH in subjects with delayed puberty and healthy controls did not differ from that in patients with IHH. After successful treatment of one patient with IHH (Kallmann's syndrome) with pulsatile s.c. LHRH we did not find any change in the response of prolactin to TRH challenge after 1, 3 and 6 months of treatment, while prolactin response to domperidone increased. Prolactin responses to TRH and domperidone are not differential for the early diagnosis of IHH. Successful treatment of a patient with IHH did not change the response of prolactin to TRH, but increased prolactin response to domperidone possibly due to altered steroid milieu.

Adolescent↗