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Biomedical subjects

G M Prelevic

Publications and source records attributed to G M Prelevic.

At least 19 recordsLinked to original sources
PubMed1998

The effect of hormone replacement therapy on diastolic left ventricular function in hypertensive and normotensive postmenopausal women.

OBJECTIVES: To evaluate the effect of hormone replacement therapy (HRT) on left ventricular diastolic function in a group of hypertensive and normotensive postmenopausal women. METHODS: Left ventricular diastolic function at rest was evaluated by M-mode, two-dimensional and Doppler echocardiography in 19 postmenopausal women with normal blood pressure and 11 postmenopausal women with mild hypertension, before treatment and during 12 months of HRT. Transdermal estradiol was used in women with a surgical menopause and a sequential regimen of transdermal estradiol and peroral medroxyprogesterone acetate in women with a spontaneous menopause. The parameters assessed were: body mass index, heart rate, ejection fraction of the left ventricle (EF), septal (SW) and posterior wall (PW) dimensions, left ventricular end-systolic (LVsd) and end-diastolic (LVdd) dimensions and volumes (ESV, EDV), total diastolic time (DT), duration of the early (Ei) and of the late (Ai) filling phase, peak velocity of the early (E) and late mitral flow (A), A/E velocity ratio and systolic and diastolic blood pressure. Quantitative data were analyzed using unpaired t-test, MANOVA and multiple regression analysis where appropriate. RESULTS: Hypertensive postmenopausal women had significantly higher SW (P < 0.05), PW (P < 0.05), A/E (P < 0.05) and A (P < 0.001) than normotensive postmenopausal women, before therapy. After 12 months of HRT a significant decrease in SW, PW, LVsd, ESV and increase in EF, DT, Ei and E was observed in both hypertensive and normotensive postmenopausal women. Heart rate slowed and systolic pressure decreased significantly only in normotensive postmenopausal women on HRT. CONCLUSION: HRT of 12 months' duration does not deteriorate left ventricular diastolic function of both hypertensive and normotensive postmenopausal women. Improvement in some parameters of diastolic function could be partially explained by the decrease in heart rate and systolic pressure, induced by therapy.

Administration, Cutaneous↗
PubMed1998

Metabolic effects of tibolone in postmenopausal women with non-insulin dependent diabetes mellitus.

OBJECTIVE: Postmenopausal women with non-insulin dependent diabetes (NIDDM) are frequently obese, hypertensive and hyperlipidaemic and hence at particular risk of coronary heart disease (CHD). They might therefore benefit from menopausal therapy. In view of the improvement in insulin sensitivity and the reduction in triglyceride levels induced by tibolone in healthy postmenopausal women we evaluated the effects of 12 months of tibolone on glycaemic control, serum insulin and lipid levels in postmenopausal women with NIDDM. DESIGN: A prospective 12 months before/after intervention study. PATIENTS: Fourteen postmenopausal women (mean age 58.14 +/- 1.25 years; mean duration of menopause 121.21 +/- 13.42 months; mean BMI: 26.55 +/- 0.97) with NIDDM (mean duration of diabetes 113.79 +/- 13.89 months). MEASUREMENTS: Fasting and postprandial blood glucose levels were assessed monthly, serum fructosamine, fasting and postprandial insulin every 3 months and serum lipids (total cholesterol, triglyceride, HDL-cholesterol and LDL-cholesterol) every 6 months. RESULTS: Changes in blood glucose, both fasting and postprandial, were not statistically significant during the treatment period. Serum fructosamine concentration increased significantly after 9 months. A significant decrease in fasting and postprandial insulin concentrations was observed after 9 months. A non-significant decrease was observed in total cholesterol, LDL cholesterol and triglyceride but no change in HDL cholesterol. Body weight did not change during the period of observation. CONCLUSION: A slight deterioration in glycaemic control, a fall in insulin concentration and no change in serum lipids were observed in women with NIDDM during 12 months treatment with tibolone.

Anabolic Agents↗
PubMed1997

The effect of tibolone on cardiac flow in postmenopausal women with non-insulin dependent diabetes mellitus.

OBJECTIVE: Postmenopausal women with non-insulin dependent diabetes (NIDDM) are frequently obese, hypertensive and hyperlipidaemic and hence at particular risk of coronary heart disease (CHD). They might therefore benefit from menopausal therapy. In view of the fact that oestrogen replacement increases cardiac flow but not limb flow whilst tibolone dilates forearm flow in healthy postmenopausal women, a study was undertaken to evaluate the effects of tibolone on cardiac flow in postmenopausal women with NIDDM. DESIGN: A prospective 12 months before/after intervention study. PATIENTS: 15 postmenopausal women (mean age 58.36 +/- 1.25 years; mean duration of menopause 115.20 +/- 13.97 months; mean BMI: 26.22 +/- 1.02) with NIDDM (mean duration of diabetes 106.07 +/- 15.66 months). MEASUREMENTS: Cardiac flow was measured every 6 months for 1 year by pulsed Doppler echocardiography. The parameters assessed were: stroke volume (SV), cardiac output (CO), ejection fraction (EF), pre-ejection time (PEP), ejection time (ET), peak systolic flow velocity (PFV), acceleration time (AT), flow velocity integral (FVI), mean acceleration (MA), early diastolic filling time (Ei), atrial filling time interval (Ai), peak velocity of the early diastolic filling (E) and peak velocity of the early atrial filling (A). Blood pressure was also recorded during Doppler echocardiography. RESULTS: Stroke volume, cardiac output and ejection fraction increased significantly after 6 months. There was also a significant increase in peak flow velocity (PFV), flow velocity integral (FVI) and mean acceleration (MA) together with a significant increase in early diastolic filling time (Ei) and peak velocity of the early diastolic filling (E). Blood pressure was unchanged throughout the 12-month study period. CONCLUSION: The significant increase in stroke volume, cardiac output and flow velocity over the aortic valve parallel the effects of oestrogens in healthy postmenopausal women. The fact that tibolone improved left ventricular relaxation suggests the drug might help prevent or at least defer the development of cardiac dysfunction in diabetic women.

Anabolic Agents↗
PubMed1997

Menopause and post-menopause.

From the endocrine point of view, menopause is considered a deficiency state and oestrogen therapy regarded as restoring the pre-menopausal endocrine milieu. Oestrogen therapy alleviates acute climacteric symptoms and also reduces the risk of cardiovascular disease, osteoporosis and Alzheimer's disease. Cardiovascular protection seems to be the major benefit of oestrogen replacement: it reduces morbidity and mortality from coronary heart disease by approximately 50%. The mechanisms are complex and not fully under-stood. In this review we discuss currently available data on the effects of hormone replacement therapy on serum lipids and lipoproteins, the vessel wall (endothelium dependent and endothelium independent), blood flow, cardiac function, blood pressure, haemostasis, insulin sensitivity and direct anti-atherosclerotic effect as possible mechanisms of cardioprotection. Oestrogen therapy reduces the rate of post-menopausal bone loss, increases bone mineral density (BMD) and decreases fracture rate. Recent evidence suggests that initiation of oestrogen therapy in older women produces larger increases in BMD which might provide a significant protective effect at the time when fracture is common. The incidence of Alzheimer's disease is reduced by 50% in post-menopausal women taking oestrogen replacement. Limited clinical trials of oestrogen treatment in women with this disease have documented beneficial effects on cognitive function. The results of epidemiological studies of the effects of oestrogens on breast cancer risk are conflicting but recent evidence suggests that the risk is increased in current users after 5 years of use and among older women. In contrast, increase in the risk of venous thromboembolism is most significant within the first 12 months of therapy, strongly suggesting the importance of individual susceptibility.

Adult↗
PubMed1997

Insulin resistance in polycystic ovary syndrome.

Hyperinsulinaemia is found in 30% of slim and 75% of obese women with polycystic ovary syndrome. Despite resistance to insulin action in terms of glucose transport, increased insulin levels may cause hyperandrogenaemia by enhancement of androgen production in the ovaries where insulin acts as co-gonadotrophin. Recent interest in insulin resistance results from the recognition that it predisposes to various metabolic abnormalities, and could be involved in the pathogenesis of atherosclerosis. Women with polycystic ovary syndrome frequently have metabolic disturbances associated with insulin resistance, and recent long-term follow-up studies have indicated that they also have a higher incidence of diabetes and hypertension later in life compared with control populations. This review describes the association of hyperinsulinaemia with hyperandrogenism, metabolic and circulatory changes in women with polycystic ovary syndrome. Special emphasis is placed on recent studies of molecular mechanisms of insulin resistance in polycystic ovary syndrome and clinical implications of hyperinsulinaemia in these women.

Androgens↗
PubMed1997

New developments in postmenopausal hormone replacement therapy.

In this review we summarize background data that have steadily accumulated to help explain the beneficial actions of oestrogen replacement treatment on cardiovascular disease. The range of beneficial actions on the cardiovascular system is extraordinary, and goes far beyond the widely acknowledged effects on lipoprotein action. We also review recent reports on the beneficial actions of oestrogen treatment on Alzheimer's disease and colorectal cancer. The emphasis throughout is on understanding the mechanisms of benefit.

Alzheimer Disease↗
PubMed1996

Cause of vaginal bleeding in postmenopausal women taking tibolone.

OBJECTIVE: To determine the cause of vaginal bleeding in postmenopausal women treated with tibolone. SUBJECTS: Forty seven consecutive unselected women who bled in the course of treatment with tibolone between 1986 and 1995. STUDY METHODS: Clinical evaluation and pelvic ultrasound scanning in all women and additional Doppler flow assessment in 12. Hysteroscopy was performed in 20 women and D and C in nine. RESULTS: An endometrial polyp was found responsible for the bleeding in 11 women and uterine fibroids in seven. Thickened endometrium was seen on ultrasound in six women; there was no histological abnormality in three of these women, two had benign simple hyperplasia and the remaining woman had an early carcinoma in situ. Carcinoma in situ was also found in another woman as an incidental finding in the endometrial curettings taken at hysteroscopy in the course of polypectomy. In over half, however, (24 women), no intrauterine cause could be found to account for vaginal bleeding. The occurrence of vaginal bleeding after tibolone clustered in two groups; 30 women who bled within 4 months of starting tibolone (of whom 17 had recently taken oestrogens) and 17 who bled after at least a years' therapy. CONCLUSION: Bleeding after tibolone requires investigation. A morphological abnormality may be present even in women who have recently taken oestrogens and experienced cyclical bleeding. Despite full investigation, no cause for bleeding was however found in over half the group. The majority (37 women) of those who reported bleeding nevertheless continued on tibolone after completion of investigations with no recurrence of bleeding.

Aged↗
PubMed1996

Comparative effects on bone mineral density of tibolone, transdermal estrogen and oral estrogen/progestogen therapy in postmenopausal women.

The aim of the study was to assess the comparative effects on bone mineral density (BMD) in routine clinical practice of tibolone and estrogen (given either unopposed or combined with cyclical progestogen) in postmenopausal women who had not previously received estrogen or other menopausal therapy. BMD was measured in the spine and hip by dual energy X-ray absorptiometry (DEXA) at 12-month intervals over 3 years in 82 consecutive postmenopausal women referred for climacteric therapy. Of these, 35 women received tibolone, 24 transdermal estradiol alone and 12 conjugated equine estrogens together with cyclical progestogen; 11 received no therapy other than calcium. BMD increased significantly in the spine in those taking tibolone over 3 years (p < 0.0001 at 1 year; p < 0.0001 at 2 years; and p = 0.03 at 3 years). In those treated with conjugated equine estrogens and cyclical progestogen, BMD in the spine also increased significantly over the first 2 years (p = 0.03 at 1 year; p = 0.004 at 2 years), but not at 3 years. However, although BMD in the spine also rose over 3 years in the women treated with transdermal estradiol alone, the increase was not statistically significant. No significant change in the BMD of either the spine or the hip was observed in the control group. A significant difference in the increase of BMD in the spine between the different treatment groups was observed at 2 years (p = 0.004) in favor of those taking tibolone or conjugated equine estrogens, compared to women who received transdermal estradiol. The highest proportion of individual responders to therapy after 2 years' treatment was observed in those receiving tibolone or conjugated equine estrogens. There was no significant change in the BMD of the hip over 3 years, irrespective of the therapy taken, although there was a tendency towards a progressive increase in the women on tibolone. Neither the age of the women, their body mass index or pretreatment BMD had a significant effect on changes in bone density. Since tibolone effected a greater increase in spine BMD than did either conjugated equine estrogen with progestogen or transdermal estradiol alone, it is particularly suitable for older women who often have more advanced osteoporosis and who would not accept a return of cyclical bleeding.

Administration, Cutaneous↗
PubMed1995

Effect of recombinant human growth hormone treatment on insulin-like growth factor (IGF-I) levels in insulin-dependent diabetic patients.

Basal and recombinant human growth hormone (rhGH)-stimulated insulin-like growth factor (IGF-I) levels were studied in 19 insulin-dependent diabetic patients and 4 healthy subjects. Diabetic patients were divided according to glucagon test result into CpN (10 patients without residual beta cell activity) and CpP (9 patients with preserved beta-cell activity) and CpP (9 patients with preserved beta-cell activity) groups, and according to age into three groups (A = 21-30 years; B = 31-40 years; C = 41-50 years). All control subjects belonged to group B. Blood glucose and growth hormone were measured at hourly intervals and IGF-I every 6 h during 24 h before and after 7 days treatment with 4 IU of rhGH given subcutaneously at 8 p.m. The age-related decrease in basal IGF-I levels was evident in both CpN and CpP groups of diabetic patients. IGF-I net increase with rhGH treatment was variable and insignificant in comparison with basal value without age-related differences in CpN diabetics. Progressively larger, age-related increases in IGF-I concentrations were observed in CpP diabetic patients. This study indicates impairment of hepatic IGF-I generation capacity in diabetic patients without residual beta-cell activity and the importance of simultaneous actions of portal insulin and GH on hepatic IGF-I production.

Adult↗
PubMed1995

The effects of the somatostatin analogue octreotide on ovulatory performance in women with polycystic ovaries.

The elevated luteinizing hormone (LH) and androgen concentrations characteristic of women with polycystic ovaries (PCO) are considered crucial factors in their infertility. The somatostatin analogue octreotide lowers LH and androgen concentrations in women with PCO. The effects of octreotide given concurrently with human menopausal gonadotrophin (HMG) were therefore compared with that of HMG alone in 28 infertile women with PCO resistant to clomiphene. In 56 cycles of combined HMG and octreotide therapy there was more orderly follicular growth compared with the multiple follicular development observed in 29 cycles in which HMG was given alone (mean number of follicles > 15 mm diameter on the day of human chorionic gonadotrophin (HCG) administration: 2.5 +/- 0.2 and 3.6 +/- 0.4 respectively; P = 0.026). There was a significantly reduced number of cycles abandoned (> 4 follicles > 15 mm diameter on day of HCG) in patients treated with octreotide+HMG, so that HCG had to be withheld in only 5.4% of cycles compared to 24.1% with HMG alone (P < 0.05). The incidence of hyperstimulation was also lower on combined treatment. Octreotide therapy resulted in a more 'appropriate' hormonal milieu at the time of HCG injection, with lower LH, oestradiol, androstenedione and insulin concentrations. Although growth hormone concentration was similar on both regimens, significantly higher insulin growth factor-I concentrations were observed on the day of HCG in women on combined therapy than on HMG alone.

Adult↗
PubMed1995

Osteopenia as a feature of the androgen insensitivity syndrome.

OBJECTIVE: The syndrome of androgen insensitivity, a paradigm of a hormone resistance syndrome, manifests as failure of masculinization despite normal or high concentrations of serum testosterone. The defect in these 46 XY patients resides in the androgen receptor gene, with consequent defective androgen action and abnormal sexual differentiation. We sought to evaluate whether the adverse sequelae of androgen resistance may extend to skeletal tissue by measuring bone mineral density in six patients with androgen insensitivity. DESIGN: A cross-sectional retrospective study. MEASUREMENTS: Bone mineral density was measured by means of a Dexa (Hologic QDR 1000 scanner). The diagnosis of androgen insensitivity was confirmed in each patient by karyotype and assay of sex hormones. RESULTS: The five adult patients with androgen insensitivity had been exposed to both defective androgen action and variable periods of oestrogen deficiency. The latter resulted from the low circulating oestrogen concentrations (for premenopausal females) before gonadectomy and inadequate oestrogen replacement after gonadectomy. All five adults with androgen insensitivity had osteopenia in both the lumbar spine (T-score -1.52 to -3.85) and femoral neck (T-score -1.34 to -4.91). CONCLUSIONS: Osteopenia in patients with androgen insensitivity may relate to defective androgen action, oestrogen deficiency or a combination of the two. These observations have implications for the management of patients with androgen insensitivity and may provide insight into the effects of androgens on the female as well as the male skeleton.

Adolescent↗
PubMed1995

Cardiac flow velocity in women with the polycystic ovary syndrome.

OBJECTIVE: Women with the polycystic ovary syndrome (PCOS) often have several of the known risk factors for cardiovascular disease, including hyperinsulinaemia. We have therefore investigated variables of cardiac flow in young women with PCOS and related them to blood levels of reproductive hormones (LH, FSH, oestradiol and testosterone) and also of insulin. DESIGN: A prospective study. PATIENTS: Twenty-six young women with PCOS (mean age 22.8 +/- 0.9 years; mean BMI 23.0 +/- 0.8) and 11 healthy age matched women with regular ovulatory cycles (mean age 26.3 +/- 1.7 years; mean BMI 22.9 +/- 0.9). MEASUREMENTS: Cardiac flow was measured by pulsed wave Doppler echocardiography in the follicular phase of the cycle in controls and oligomenorrhoeic women; there was no special timing for amenorrhoeic women. The indicators assessed were: ejection fraction (EF), pre-ejection time (PEP), ejection time (ET), peak systolic flow velocity (PFV), acceleration time (AT), flow velocity integral (FVI), mean acceleration (MA), diastolic time (DT), early diastolic filling time (Ei), atrial filling time interval (Ai), peak velocity of the early diastolic filling (PE) and peak velocity of the atrial filling (PA). Serum LH, FSH, oestradiol, testosterone, SHBG and insulin concentrations were analysed by standard RIA. RESULTS: Significantly lower PFV (1.055 +/- 0.025 vs 1.242 +/- 0.054, P = 0.0006) and MA (17.06 +/- 0.57 vs 23.00 +/- 1.49, P = 0.0001) and longer AT (0.063 +/- 0.001 vs 0.056 +/- 0.004, P = 0.026) were found in women with PCOS as compared to age matched controls. Significant negative correlation between serum fasting insulin concentration and EF (r = -0.725, P = 0.002), PFV (r = -0.719, P = 0.0025), FVI (r = -0.654, P = 0.008) and MA (r = -0.757, P = 0.001) was observed in the 15 women with PCOS in whom insulin was measured. CONCLUSION: An inverse relation between serum fasting insulin level and left ventricular systolic outflow parameters suggests that insulin is associated with the decreased systolic flow velocity observed in women with PCOS.

Adult↗
PubMed1994

The effect of oestrogen and progestogen replacement therapy on systolic flow velocity in healthy postmenopausal women.

The effects on left ventricular systolic outflow velocity of 3 months' treatment with either continuous transdermal oestradiol or cyclical transdermal oestradiol with medroxyprogesterone acetate were assessed in 34 healthy postmenopausal women. Cardiac flow was measured by pulsed wave Doppler echocardiography in 14 of these women and by continuous wave Doppler echocardiography in 20. Control studies were made in ten premenopausal women using pulse wave Doppler and in ten with continuous wave Doppler. The indicators assessed were: ejection fraction (EF), preejection time (PEP), ejection time (ET), peak systolic flow velocity over the aortic valve (PFV), acceleration time (AT), flow velocity integral (FVI) and mean acceleration (MA). Postmenopausal women had significantly lower EF, PFV, FVI, MA but longer AT and ET compared to premenopausal women. After 3 months' transdermal oestradiol significant increases in EF, PFV, FVI and MA were observed whilst AT decreased. The response in all cardiac flow indicators was similar with added progestogen. Blood pressure, however, increased after the addition of progestogen. Nevertheless the addition of progestogen does not attenuate the effect of oestrogen therapy on left ventricular systolic flow velocity.

Administration, Cutaneous↗
PubMed1993

Growth hormone levels in patients with type 1 diabetes are age related.

Possible effects of age on the growth hormone (GH) levels in Type 1 diabetes were examined. The study was performed in 71 patients with Type 1 diabetes (40 C-peptide negative (CpN), without residual beta cell activity; 31 C-peptide positive (CpP), with preserved beta cell activity) and 11 healthy subjects. The patients and controls were divided into three age groups (A = 21-30; B = 31-40; C = 41-50 years). Blood glucose and growth hormone (GH) were measured at hourly intervals during 24 h in all subjects in hospital conditions. GH levels decreased significantly with age in patients with Type 1 diabetes (mean 24-h GH group A: 7.3 +/- 1.0, group B:5.3 +/- 0.6, group C: 3.7 +/- 0.4 mU 1(-1); A vs C: p = 0.0007; B vs C: p = 0.03). In all age groups GH levels were significantly higher in CpN than either in CpP diabetic patients or controls (group A CpN: 8.3 +/- 1.2, CpP: 4.7 +/- 1.0, controls: 2.2 +/- 0.3 mU 1(-1); p < 0.001; group B CpN: 7.3 +/- 0.8, CpP: 3.2 +/- 0.5, controls: 1.6 +/- 1.0 mU 1(-1); p < 0.0002; group C CpN: 5.2 +/- 0.5, CpP: 2.5 +/- 0.4, controls: 1.4 +/- 0.4 mU 1(-1); p < 0.001). Mean GH levels were significantly higher in C-peptide positive patients than in controls in all age groups (p < 0.001).(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1993

The effect of recombinant human growth hormone on regulation of growth hormone secretion and blood glucose in insulin-dependent diabetes.

GH hypersecretion in insulin-dependent diabetes (IDDM) is well documented. Although it has recently been shown that residual insulin secretion determines the magnitude of this GH hypersecretion, the underlying mechanisms of the disorder have not yet been clarified. The 24-h GH and blood glucose profiles, insulin-like growth factor I (IGF-I) concentrations and GH responses to GRF were analyzed in 21 insulin-dependent diabetics and 4 healthy subjects before and after 7 days treatment with recombinant human GH (rhGH) (4 IU given sc at 0800 h). According to C-peptide response to glucagon IDDM patients were subdivided into C-peptide negative (CpN, n = 12) patients without endogenous pancreatic beta-cell activity and C-peptide positive (CpP, (n = 9) patients with endogenous insulin secretion. No significant difference could be observed between the mean 24-h blood glucose profile before and after rhGH treatment in any treated group. Before and on rhGH treatment the highest 24-h GH values were observed in CpN patients when compared to CpP and controls. The rhGH treatment induced a similar increase in the mean 24-h GH concentrations in all groups studied which was statistically significant only in CpP diabetics. Mean pretreatment serum IGF-I concentrations were not significantly different between CpN, CpP patients and controls. The net increase in IGF-I concentrations after rhGH treatment was however, significantly lower in CpN patients than in CpP and control subjects. GRF-induced GH response before and after rhGH treatment was significantly greater in diabetics than in controls. The response of GH to GRF in CpN diabetics was however, almost unchanged after treatment whereas it became lower in CpP diabetics and controls. The dose of 4 IU of rhGH increased significantly GH levels in diabetics with preserved beta-cell function with consequent increase in IGF-I levels and attenuation of GRF induced GH response. In contrast, the same dose of rhGH failed to induce significant increase in GH levels in diabetics without residual beta-cell activity, most probably due to already high pretreatment levels. In addition, neither increase in IGF-I levels nor suppression of GH response to GRF on rhGH treatment was observed in CpN diabetics. The results are in keeping with an important role of portal insulin in GH-induced hepatic IGF-I secretion.

Adult↗
PubMed1992

The effect of the somatostatin analogue octreotide on growth hormone secretion in insulin-dependent diabetics without residual insulin secretion.

Growth hormone (GH) hypersecretion is well documented in insulin-dependent diabetes mellitus (IDDM). Somatostatin inhibits GH in acromegalics and healthy subjects although data on its inhibitory effects on high GH levels in IDDM patients are controversial. The effect of treatment with the somatostatin analogue octreotide ("Sandostatin") on GH secretion, IGF1 levels and metabolic control was investigated in insulin-dependent diabetics. Growth hormone and blood glucose were measured at hourly intervals whilst IGF-I was measured every 6 hours during the 24-h period before and after 7 days' treatment with octreotide (200 micrograms subcutaneously three times daily) in 10 C-peptide negative diabetics. Octreotide significantly reduced mean 24 h GH profile (7.2 +/- 0.7 mU/L before; 5.2 +/- 0.5 mU/L on octreotide, p less than 0.01), IGF-I levels (0.62 +/- 0.06 before; 0.47 +/- 0.05 on octreotide, p less than 0.005) mean 24 h blood glucose (14.4 +/- 0.5 mmol/L before; 12.6 +/- 0.4 mmol/L on octreotide, p less than 0.001) and daily insulin requirements (44.8 +/- 3.0 IU before; 37.2 +/- 3.0 IU on octreotide, p less than 0.02). The shape of 24 h GH profile curve changed significantly on octreotide treatment (p less than 0.05) when it consisted of three nadirs and three peaks closely linked with the time of octreotide administration. Moderate (abdominal discomfort) to severe hypoglycaemia) transient side effects have been observed in all treated patients. The results of this study showed that short-term treatment with octreotide given s. c. every eight hours modulates the pattern of GH secretion in C-peptide negative insulin-dependent patients.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗