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Biomedical subjects

C Naidoo

Publications and source records attributed to C Naidoo.

At least 19 recordsLinked to original sources

A new predictor of cephalopelvic disproportion?

Cephalopelvic disproportion (CPD) is a recognised obstetric problem with potential risk to both mother and infant. Identification of those mothers at risk of CPD is difficult and has concentrated in the past on such measurements as maternal shoe size and height. Our objective in this study was to examine new anthropomorphic parameters as indicators of CPD. This was a case controlled study of sixty consecutive women, and their partners, who had caesarean section performed for CPD and 60 case matched controls. Measurements included maternal and paternal head circumference, height, shoe-size, body mass index (BMI), infant weight and head circumference. Parity, gestation at delivery, and mode of onset of labour were recorded. Data were analysed using Stata Release 6. Prognostic factors were tested for association with CPD using conditional logic regression. The most important anthropomorphic risk factors for CPD were maternal head circumference in relation of height (P < 0.001), and paternal head to height ratio (P = 0.017). Head to height ratio is taken as the head circumference in centimeters divided by the height in metres. Body mass index was higher in CPD cases (maternal case mean = 27.1, control mean = 25.5; paternal case mean = 27.2, control mean = 26.2). Infant head circumference was not a predictor. Primiparity was an important independent predictor (P<0.001), regardless of the mode of onset of labour. Maternal or paternal shoe-size, induction of labour and gestation at delivery were not predictors. The risk profile for CPD which emerges is one of a tall father where both mother and father have large head-to-height ratios.

Adult↗

Cyclotron production of 67Ga(III) with a tandem natGe-natZn target.

Production of 67Ga(III) at the National Accelerator Centre is by proton bombardment of a natZn target, and uses 15-20 h of cyclotron beam time per production. A study was undertaken to use a tandem natGe-natZn target to produce the same amount of 67Ga, but using less beam time (7-8 h). 67Ga(III) was separated from the tandem target material by a method based on acid dissolution of the target and chromatography on an organic polymer resin (Amberchrom CG-71cd) containing no ion exchange groups. The separated 67Ga(III) has high radionuclidic purity and complies with the British and US Pharmacopoeia requirements for chemical purity.

Calibration↗

Maternal serum fructosamine values after delivery of macrosomic babies and unexplained stillbirths.

Measurement of serum fructosamine and haemoglobin A1 levels and glucose tolerance tests were performed in 75 women in the immediate postpartum period. None had predisposing factors to gestational diabetes. They were divided into three groups: group I consisted of 15 women who delivered an unexplained stillbirth; group II of 30 women who gave birth to babies weighing between 2,500 g and 3,900 g at term; and group III of 30 women who delivered babies weighing greater than or equal to 4,000 g. There was a significant difference in the mean level of serum fructosamine between the unexplained stillbirth and control groups (P less than 0.001). Although the HbA1 values varied in the three groups, there was a significant difference between the unexplained stillbirth group and the macrosomic infant group (P less than 0.05). All patients had normal glucose tolerance tests.

Adult↗

Metabolic profiles and lipoprotein lipid concentrations in non-obese and obese patients with polycystic ovarian disease.

Clinical parameters, androgen status and lipoprotein lipid profiles were assessed in 10 non-obese and 10 obese patients with polycystic ovarian disease (PCOD) and reference subjects matched for age, height and weight. Both obese and non-obese women with PCOD had significantly higher androgen levels when compared to the reference groups. When comparison of lipoprotein lipid profiles were made between groups, non-obese women with PCOD had significantly higher total cholesterol, triglycerides and LDL-cholesterol levels than non-obese reference subjects. Obese PCOD women manifested significantly higher total cholesterol, LDL-cholesterol, cholesterol/HDL, and LDL/HDL values than did obese reference subjects. Correlations between serum androgens and lipoprotein lipid concentrations in PCOD and normal women were unhelpful. Both non-obese and obese patients with PCOD had significantly higher systolic and diastolic blood pressures (BPs) than the reference groups. Thus, both non-obese and obese women with PCOD manifest hyperandrogenaemia which may result in a male pattern of lipoprotein lipid concentrations.

Adolescent↗

125I-insulin binding to circulating erythrocytes, monocytes and cultured fibroblasts in non-obese patients with polycystic ovarian disease.

The insulin receptor status of circulating erythrocytes, monocytes and cultured fibroblasts were studied in non-obese Indian women with polycystic ovarian disease (PCOD) with no clinical evidence of acanthosis nigricans and age, height and weight matched reference subjects. The women with polycystic ovaries had decreased mean maximum specific binding to erythrocytes (PCOD 7.4 +/- 0.6%, normal women 11.5 +/- 0.3%; p less than 0.0001) and monocytes (PCOD 2.4 +/- 0.3%, normal women 4.1 +/- 0.4%; p less than 0.003) when compared to the normal women. This decreased binding was attributed to a change in both receptor number and affinity. 125I-insulin binding to cultured fibroblasts revealed similar mean maximum specific binding and affinity values in both groups studied. Although further work is necessary to exclude genetic or post-receptor defects, it is likely that an environmental factor is implicated in the decreased 125I-insulin binding to erythrocytes and monocytes.

Adult↗

Glucose, insulin and C-peptide secretion in obese and non obese women with polycystic ovarian disease.

Plasma glucose, immunoreactive insulin (IRI) and C-peptide responses during oral glucose tolerance testing (OGTT) were evaluated in 10 non obese women with polycystic ovarian disease (NOB-PCOD) and 10 obese women with polycystic ovarian disease (OB-PCOD). Mean plasma glucose response at 120 minutes in OB-PCOD showed impaired glucose tolerance. Also in this group, 1 patient had frank diabetes mellitus, whilst 3 other patients had impaired glucose tolerance 1 NOB-PCOD patient had impaired glucose tolerance. Mean plasma glucose levels and mean incremental glucose areas were higher in the OB-PCOD at all time intervals and reached statistical significance at 60 and 90 minutes. Mean plasma IRI levels were also higher in OB-PCOD at all time intervals, and reached statistically significant higher levels at 0, 60 and 90 minutes. Mean serum C-peptide valves were also higher at all time intervals in OB-PCOD. The relationship between acanthosis nigricans, obesity and PCOD was also analysed. It is evident from this study that obesity has a significant negative impact on the overall carbohydrate status in women with PCOD.

Blood Glucose↗

Insulin and C-peptide secretion in non-obese patients with polycystic ovarian disease.

Plasma glucose, immunoreactive insulin (IRI) and C-peptide responses during an oral glucose tolerance test (oGTT) were assessed in 11 non-obese patients with polycystic ovarian disease (PCOD) and 11 reference subjects matched for age, height and weight. Also, 6 patients with PCOD and 6 normal women were subjected to intravenous glucose tolerance testing (ivGTT) On oGTT, all subjects exhibited normal glucose tolerance; however, PCOD patients had significantly higher mean plasma glucose levels at 30, 60, 90 and 120 min and higher mean incremental glucose areas. In addition the patients with polycystic ovaries showed higher mean basal IRI and C-peptide levels, higher mean glucose stimulated IRI and C-peptide levels and higher mean incremental IRI and C-peptide values. The molar ratios of C-peptide/IRI were significantly lower in the PCOD group at all time intervals after glucose stimulation when compared to the normal women. During ivGTT, there were significantly higher mean glucose levels at 5, 40, 50 and 60 min in the PCOD group when compared to the reference group. The IRI response to intravenous glucose in the PCOD women was similar to the reference group. The findings on oGTT suggest that non-obese patients with PCOD have increased pancreatic IRI secretion as well as impaired hepatic extraction of the hormone.

Administration, Oral↗

Evidence for increased absorption of glucose and decreased hepatic extraction of insulin in South African Indians.

It has been previously demonstrated that Indians have an exaggerated insulin response to oral glucose when compared to Africans. In an attempt to determine the reasons for this phenomenon matched groups of Indian and African volunteers were subjected to oral and intravenous glucose tolerance testing. It was concluded that the increased absorption of glucose and reduced hepatic extraction of insulin contributed to the hyperinsulinism in Indians.

Adult↗

Evaluation of the integrated 3-hour plasma cortisol concentration as a test for Cushing's syndrome.

Twenty-four hour urinary free cortisol and mean and integrated 13h00-16h00 plasma cortisol levels were measured in 9 patients with proven Cushing's syndrome (5 with Cushing's disease, 2 with ectopic adrenocorticotrophic hormone production due to bronchial carcinoma and 2 with adrenal adenomas) and in 21 patients without Cushing's syndrome. The 24-hour urinary free cortisol levels and mean and integrated 13h00-16h00 plasma cortisol estimations clearly distinguished patients with Cushing's syndrome from those without. However, adequate suppression on dexamethasone suppression tests (false negatives) were obtained in 3 of the 9 patients with Cushing's syndrome. Since the integrated 13h00-16h00 plasma cortisol estimation is cheaper and simpler than the mean 13h00-16h00 plasma cortisol estimation, we recommend it as an adjunct in the diagnosis of Cushing's syndrome.

Cushing Syndrome↗

Insulin binding to circulating monocytes and erythrocytes in patients with non-insulin-dependent diabetes in the young.

125I-insulin binding to circulating monocytes and erythrocytes was carried out in 9 patients with non-insulin-dependent diabetes in the young (NIDDY), who belonged to families in which non-insulin-dependent diabetes was transmitted through 3 generations. The diabetics had a decreased mean maximum specific binding to monocytes 2.1 (1.1-4.1%) compared to 4.0 (2.6-6.2%) in their age, sex and weight matched reference subjects. This decreased binding was primarily due to a decrease in receptor number as all diabetics had normal affinity values (2-10 ng/ml). We have attributed the decreased binding in NIDDY to the down regulatory effect of the basal hyperinsulinemia (23.6 +/- 3.2 vs 11.7 +/- 0.5 microU/ml). By contrast the maximum specific binding to erythrocyte was similar in both groups (9.7 +/- 0.5; 8.9 +/- 0.5%; p greater than 0.5).

Adolescent↗

125 I-insulin binding to cultured fibroblasts in non-insulin-dependent diabetes in the young.

125 I-insulin binding to circulating monocytes was found to be decreased in Indian patients with non-insulin-dependent diabetes in the young, when compared to controls. To determine whether this was due to an inherent defect in the insulin receptor, fibroblasts from diabetics and controls were grown in an environment free from the diabetic milieu. Under these conditions 125 I-insulin binding to fibroblasts in patients with non-insulin-dependent diabetes in the young was similar to that obtained in controls. (1.5 +/- 0.4% and 1.3 +/- 0.3% per 10(6) cells, p greater than 0.5). It thus appears that the receptor defect manifest on circulating monocytes is unlikely to be a primary defect.

Adult↗

Endocrine studies in patients with isolated gonadotrophin-releasing hormone deficiency.

Twelve black women with isolated gonadotrophin deficiency were studied. After administration of intravenous gonadotrophin-releasing hormone (GnRH), all patients had subnormal gonadotrophin responses. However, after priming with subcutaneous GnRH (in 9 patients) follicle-stimulating hormone responses improved in 4 patients and luteinizing hormone responses in 7 patients. Prolactin responses to intravenous thyrotrophin-releasing hormone were significantly decreased at 20 and 60 minutes, when compared with reference subjects (P less than 0.01). In response to insulin-induced hypoglycaemia, prolactin responses were heterogeneous in 11 patients, while those of growth hormone were suboptimal in 8 of the 11 patients tested.

Black or African American↗

Clinical studies in black women with isolated gonadotrophin-releasing hormone deficiency.

Twelve black patients with primary amenorrhoea as a result of hypogonadotrophic hypogonadism were studied to establish the diagnosis of isolated gonadotrophin-releasing hormone (GnRH) deficiency. All were eunuchoid with poor development of breasts and pubic hair. Chromosomal complement was female and none had midline facial defects or anosmia. Follicle-stimulating hormone (FSH) and luteinizing hormone (LH) levels were low or undetectable, while the levels of other pituitary hormones were normal. Patients did not respond to clomiphene citrate administration, but did bleed in response to an oestrogen/progestagen combination and responded to human menopausal gonadotrophin. This study clearly establishes that isolated GnRH deficiency occurs in black women and suggests that the male:female ratio is different from that in white populations.

Adult↗

The insulin and glucose response to an oral glucose load in non-insulin-dependent diabetes in the young. A study of 4 families.

Four Indian families with three-generation transmission of non-insulin-dependent diabetes were studied. Only 30% of the siblings were diabetic. The mean age of onset of diabetes was 20,1 years; 25% of the diabetics were obese, while all non-diabetic family members were of normal weight. All consenting living family members (12 diabetics and 16 non-diabetics) were subjected to an oral glucose tolerance test. After glucose administration, the 12 diabetics displayed a delayed and attenuated insulinaemic response. The area under the insulin curve and the insulin-glucose ratio were lower in the diabetics.

Adolescent↗

Prolactin secretion in Sheehan's syndrome. Responses to thyrotropin-releasing hormone and metoclopramide.

The prolactin response to thyrotropin-releasing hormone (TRH) and metoclopramide was studied in 16 patients with Sheehan's syndrome and 16 matched controls in the follicular phase. Metoclopramide resulted in a greater prolactin response than TRH did in the controls. However, both stimuli failed to evoke any appreciable prolactin response in the patients with Sheehan's syndrome. Since metoclopramide is generally free of side effects and far cheaper than TRH, we recommend the prolactin response to metoclopramide as the preferred screening test in the diagnosis of Sheehan's syndrome.

Adult↗

Insulin secretion during intravenous glucose tolerance tests in non-insulin-dependent diabetes in the young.

The phasic response of insulin to intravenous glucose was studied in 9 patients with non-insulin-dependent diabetes in the young (NIDDY), with 3-generation transmission of the disease; and 9 age-, weight- and sex-matched reference subjects. Furthermore, 10 non-diabetic siblings of these diabetic patients were submitted to the same test procedure in an attempt to identify a prodrome of impaired glucose tolerance. In comparison to the controls and non-diabetic family members, the diabetics had no first phase insulin release. In addition, the non-diabetic siblings had insulin and glucose responses similar to those of the reference subjects. Therefore, it would appear that there is no prodromal phase in this discrete syndrome of NIDDY.

Adult↗

Arginine-stimulated acute phase of insulin secretion in non-insulin-dependent diabetes in the young.

The acute insulin response to a 5 g pulse of arginine monohydrochloride was studied in 10 patients with non-insulin-dependent diabetes in the young (NIDDY) and 10 age-, weight- and sex-matched control subjects. All diabetics belonged to families in which non-insulin-dependent diabetes was transmitted through 3 generations. Mean peak insulin responses were similar in both groups (84.1 +/- 10.6; 68.2 +/- 8 microU/ml, p greater than 0.5). However, it is well known that hyperglycaemia accentuates the insulin response to non-glucose stimuli. To test this hypothesis, 5 of the diabetics were subjected to an intravenous insulin tolerance test, prior to the administration of the arginine pulse. At this lowered glucose level, the beta-cell secretory response was significantly decreased in the diabetics (C-peptide peak responses 2.5 +/- 0.3 vs 4.4 +/- 0.7 ng/ml, p less than 0.02). Thus it can be concluded that hyperglycaemia enhances the insulin secretory response to non-glucose stimuli and that following correction of the hyperglycaemia patients with NIDDY have an attenuated insulinaemic response.

Adult↗

The spectrum of non-insulin-dependent diabetes in the young in a migrant Indian population.

The familial aggregation and degree of adiposity of 108 Indian patients with non-insulin-dependent diabetes in the young was studied. All patients had onset of diabetes under 30 yr and the female to male ratio was 5:1. Obesity as defined was present in 52 patients (48.2%). A positive family history of diabetes was present in 90 patients (83.3%). Two distinct subtypes emerged in the patients with a positive family history; the offspring of conjugal diabetic parents (29%) and maturity onset diabetes of the young (MODY) with 3-generation transmission (13%). In conclusion, the syndrome of NIDDY in Indians comprises at least 3 subtypes: offspring of conjugal diabetic parents, MODY and patients without a family history (sporadic type).

Adolescent↗