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A O Olukoga

Publications and source records attributed to A O Olukoga.

At least 19 recordsLinked to original sources
PubMed1999

Macroprolactinaemia: validation and application of the polyethylene glycol precipitation test and clinical characterization of the condition.

OBJECTIVE: The clinical characteristics and natural history of macroprolactinaemia are yet to be fully established and there is currently no widely accepted simple in vitro test for routine identification of the condition. This study was designed to further validate the polyethylene glycol (PEG) precipitation test with assessment of percentage prolactin recovery (%R), for the detection of macroprolactinaemia and clinically characterize cases identified using the test. DESIGN: Analytical validation and application of the PEG precipitation test for diagnosis of macroprolactinaemia and a retrospective case-notes review of some of the patients identified with the condition. PATIENTS: Sera from 188 patients with elevated serum prolactin (PRL) concentrations were screened for macroprolactinaemia. Seventeen of the patients who were under follow-up at the local teaching hospital and were identified to have macroprolactinaemia were systematically characterized clinically. MEASUREMENTS: Prolactin was measured in sera, fractions from gel filtration chromatography and supernatant obtained after PEG precipitation, by the DELFIA fluoroimmunoassay. CLINICAL ENDPOINTS: Initial serum PRL and symptoms and their response to dopamine agonist therapy; imaging of the pituitary gland; serum PRL and symptoms after cessation of dopamine agonist therapy; course of serum PRL and symptoms without dopamine agonist therapy. RESULTS: The within-batch coefficient of variation (CV) of the PEG precipitation test ranged between 2.8 and 7.3% while the between-batch CV ranged between 3.4 and 9.7%. Intra-individual variability up to five months was 9.9%. A prolactin recovery </= 40% was indicative of macroprolactinaemia, while the condition was unlikely to be present at values > 50%. The prevalence of macroprolactinaemia was 15% without sex difference. Clinical characterization of 17 patients showed modest initial serum PRL concentrations and there was imaging evidence of a coexisting pituitary adenoma in three of them. Dopamine agonist therapy resulted in substantial falls in serum PRL and this was associated with improvement or resolution of symptoms in some patients. Stoppage of dopamine agonist resulted in rebound hyperprolactinaemia in all cases. Spontaneous improvement in symptoms occurred in three patients but hyperprolactinaemia persisted in all those who were not on treatment. CONCLUSIONS: The PEG precipitation test with assessment of 'free' prolactin has been shown to be reproducible and sensitive for the detection of macroprolactinaemia. Many of the patients who had macroprolactinaemia presented with at least one symptom of the hyperprolactinaemic syndrome. Dopaminergic therapy may influence the course of both serum PRL and symptoms in some of these patients.

Adolescent↗
PubMed1999

Three cases of macroprolactinaemia.

A woman with hirsutism but otherwise symptom-free was found to have a raised serum prolactin and a pituitary microadenoma. The hyperprolactinaemia persisted despite bromocriptine therapy and subsequent pituitary surgery, which yielded a non-functioning adenoma. After a further 15 years with persistent hyperprolactinaemia but no symptoms, macroprolactinaemia was diagnosed. Such cases might account for part of the failure rate of pituitary microsurgery for prolactinoma. Testing for macroprolactinaemia is advisable in a woman with hyperprolactinaemia, especially if her ovulatory cycle is normal. Two other cases are reported in which macroprolactinaemia was associated with menstrual disturbances and other hormonal effects: in these, treatment with dopamine agonists suppressed the hyperprolactinaemia and restored normal menstrual cycles.

Adult↗
PubMed1998

Serum sex-hormone-binding globulin is related to hepatic and peripheral insulin sensitivity but not to beta-cell function in men and women with Type 2 diabetes mellitus.

This study examined the relationship of hepatic and peripheral insulin sensitivity and beta-cell secretory function with serum sex hormone-binding globulin (SHBG) in men and women with Type 2 diabetes mellitus (DM). Fasting insulin, glucose and SHBG were measured in 58 Type 2 diabetic patients of both sexes (36 men) who were on diet treatment only and terms for insulin sensitivity and beta-cell secretion obtained by modelling. There was no significant difference in SHBG between men and women despite similar degree of obesity. SHBG was positively correlated (r = 0.41, p < 0.01) to hepatic insulin sensitivity derived from mathematical modelling of fasting glucose and insulin data using the homeostasis assessment model (HOMA). This relationship was independent of gender (men, r = 0.48, p < 0.01; women, r = 0.45, p < 0.05). Fasting insulin correlated negatively with SHBG in men (r = -0.34, p < 0.05). There were also significant negative correlations between SHBG and either plasma glucose (r = -0.29, p < 0.05) or body mass index (r = -0.34, p < 0.05). SHBG did not correlate with HOMA-modelled beta-cell function. In a multiple regression analysis, SHBG was independently correlated only with insulin sensitivity (p < 0.05). Further studies in 15 of the diabetic patients (11 men), showed a significant positive correlation (r = 0.52, p < 0.05) between SHBG and peripheral insulin sensitivity derived by continuous infusion of glucose with model assessment (CIGMA) but not between SHBG and CIGMA-modelled beta-cell function. These results indicate that both hepatic and peripheral insulin sensitivity are similarly related to serum SHBG in Type 2 diabetes of both sexes. The sex-difference in SHBG was abolished in the patients.

Diabetes Mellitus, Type 2↗
PubMed1996

Differences in serum luteinizing hormone measurements by immunoradiometric assay induced by kinetic manipulation of assay conditions are dependent on the endocrine milieu of serum.

Divergent estimates for luteinizing hormone (LH) in individual serum samples may be given by different immunoassays. In order to investigate this phenomenom further, we have studied the effect of differences in assay kinetics within the same immunoradiometric assay (IRMA) configuration on LH measurement in sera from different endocrine states. Three pairs of monoclonal/polyclonal two-site IRMA systems for LH were developed from three LH monoclonal antibodies and a common polyclonal anti-human chorionic gonadotrophin. For IRMA systems a short and long assay, which were different only with respect to the incubation time (1/2 h and overnight respectively), of the labelled monoclonal first antibody were performed. The IRMAs were all standardized against the LH international reference preparation 68/40. LH concentrations were measured by all the IRMAs in sera obtained from normal men (n = 11) and from women with polycystic ovarian syndrome (PCO; n = 13). In normal men, there were no differences in LH estimates between the short and the long assays of the three IRMA systems, and the ratios of long to short assays were similar for all the systems. However, in PCO there were significant differences between short and long assays and the ratios of long to short assays were different for the IRMA systems. These results indicate that kinetic differences between IRMAs of the same antibody configuration can be associated with differences in measured LH concentrations, depending on the endocrine status of the sera studied. As LH glycoform patterns are known to differ between normal men and PCO, the observed changes in LH estimates may be due to the different glycoform composition.

Adult↗
PubMed1994

Impaired glucose tolerance and insulin insensitivity in primary hyperparathyroidism.

OBJECTIVE: A high prevalence of diabetes mellitus has been shown in patients with primary hyperparathyroidism (PHPT). However, it is unclear whether this is related to the metabolic abnormalities in PHPT or to the presence of other risk factors for glucose intolerance in these patients. The aim of our study was to determine whether glucose intolerance and insulin insensitivity occur in subjects with PHPT who do not have other risk factors for diabetes mellitus. DESIGN: Cross-sectional study of glucose metabolism in PHPT patients without other risk factors for diabetes mellitus, compared to age and body mass index (BMI) matched healthy subjects. SUBJECTS: Nineteen non-obese, non-diabetic, normotensive patients with PHPT and 11 age and BMI matched healthy subjects. MEASUREMENTS: The continuous infusion of glucose test was used to assess glucose tolerance. Plasma glucose and insulin were measured during a 1-hour continuous infusion of glucose (5 mg/kg ideal body weight/min); insulin sensitivity and beta-cell function were derived from the glucose and insulin data by mathematical modelling. Fasting serum concentrations of parathyroid hormone, ionized calcium and 1,25-dihydroxyvitamin D (1,25(OH)2D) were measured in all subjects. RESULTS: PHPT patients attained higher plasma glucose levels at the end of the glucose infusion (median 9.0 (interquartile range 8.1-9.8) mmol/l) than did controls (7.9 (7.1-8.9) mmol/l, P < 0.05), and 8 (42%) PHPT patients had impaired glucose tolerance. Insulin sensitivity was lower in PHPT (60.3% (49.8-85.4)) than in controls (113.7% (89.3-149.2), P < 0.001); beta-cell function was not different in PHPT subjects. PHPT subjects with impaired glucose tolerance had reduced beta-cell function compared to PHPT subjects with normal glucose tolerance (89.9% (70.5-106.4) vs 120% (98.8-156.6) respectively, P < 0.05). No significant correlations were found between insulin sensitivity and PTH (rs = -0.21), 1,25(OH)2D (rs = -0.14), ionized calcium (rs = -0.11) and inorganic phosphate (rs = 0.34). Beta-cell function did not correlate with PTH (rs = 0.15), 1,25(OH)2D (rs = 0.04), ionized calcium (rs = 0.23) or inorganic phosphate (rs = -0.35). CONCLUSION: Insulin insensitivity is present in PHPT even in the absence of hypertension and obesity, and may be the cause of glucose intolerance and diabetes. PHPT subjects with reduced beta-cell function are more likely to develop glucose intolerance.

Adult↗
PubMed1994

Improvement in glucose tolerance and beta-cell function in a patient with vitamin D deficiency during treatment with vitamin D.

Glucose metabolism was studied in a patient with vitamin D deficiency during its treatment with small doses of vitamin D. A continuous infusion of glucose test was performed to assess glucose tolerance and insulin sensitivity and beta-cell function were derived by mathematical modelling. Fasting glucose was 5.6 mmol/l and achieved glucose after the infusion was 10.4 mmol/l confirming diabetes. The test was repeated 0.5, 1, 3 and 5 months after starting treatment. Serum calcium increased glucose intolerance from 1.76 to 2.0, 2.08, 1.96 and 2.0 mmol/l, respectively; vitamin D reached supraphysiological levels initially and returned to normal levels, and parathyroid hormone levels were normalized. Her weight did not change during treatment. Glucose tolerance improved during treatment and achieved glucose was 9.4, 8.6, 9.2 and 9.0 mmol/l at 0.5, 1, 3 and 5 months, respectively; insulin sensitivity did not change. Beta-cell function improved from 101% at diagnosis to 126%, 147%, 173% and 198% at 0.5, 1, 3 and 5 months, respectively. Improvement in beta-cell function and consequently in glucose tolerance is likely to have been due to correction of hypocalcaemia, vitamin D deficiency and secondary hyperparathyroidism.

Aged↗
PubMed1993

Relationship between serum butyrylcholinesterase activity, hypertriglyceridaemia and insulin sensitivity in diabetes mellitus.

1. The activity of serum butyrylcholinesterase ('pseudocholinesterase', EC3.1.1.8) was investigated in 56 patients with type 1 diabetes mellitus, 51 patients with type 2 diabetes mellitus and 101 healthy control subjects. 2. Butyrylcholinesterase activity was significantly elevated in both type 1 (8.10 +/- 3.35 units/ml) and type 2 (7.22 +/- 1.95 units/ml) diabetes compared with the control subjects (4.23 +/- 1.89 units/ml) (P < 0.001). 3. In the patients with type 1 and type 2 diabetes, serum butyrylcholinesterase activity was correlated with log serum fasting triacylglycerol concentration (r = 0.41 and r = 0.43, respectively, P < 0.001). In the type 2 population serum butyrylcholinesterase activity was also correlated with insulin sensitivity (r = -0.51, P < 0.001). 4. Serum butyrylcholinesterase activity was unrelated to age, gender, serum gamma-glutamyltranspeptidase activity, body mass index, or treatment for diabetes in both the diabetic populations. 5. In 37 non-diabetic patients with butyrylcholinesterase deficiency serum triacylglycerol levels were in the normal range. 6. These results are consistent with the view that butyrylcholinesterase may have a role in the altered lipoprotein metabolism in hypertriglyceridaemia associated with insulin insensitivity or insulin deficiency in diabetes mellitus.

Butyrylcholinesterase↗
PubMed1993

Effect of diabetes mellitus on the cardiovascular responses to induction of anaesthesia and tracheal intubation.

We have compared cardiovascular responses to induction of anaesthesia and to tracheal intubation after propofol 2.5 mg kg-1 and pancuronium 0.1 mg kg-1 in 10 diabetic and 10 matched, non-diabetic (control) ASA I patients. Anaesthesia was maintained with 0.8% enflurane and 50% nitrous oxide in oxygen, with assisted ventilation. The trachea was intubated 3 min after induction of anaesthesia. All 10 diabetic patients (but no controls) had abnormal autonomic function when tested on the day before surgery. There was no difference between the two groups in the pre-induction cardiovascular state. Mean arterial pressure and vascular resistance decreased after induction in each group (P < 0.05). Heart rate increased (P < 0.01) and cardiac index was sustained in the control group, but in the diabetic group heart rate did not change and cardiac index decreased (P < 0.01). There was an earlier decrease in stroke index in the diabetic group (2 min) compared with the controls (5 min). After tracheal intubation, heart rate and cardiac index in the control group and cardiac index in the diabetic group remained unchanged. However, there was a greater increase in heart rate, mean arterial pressure and vascular resistance in the diabetic group compared with the controls after tracheal intubation (P < 0.05). The exaggerated pressor response to tracheal intubation, in the diabetic patients, may reflect autonomic dysfunction.

Adult↗
PubMed1993

Urinary magnesium excretion in steady-state sickle cell anaemia.

Previous reports indicate that individuals with sickle cell anaemia may be magnesium deficient. The role of renal excretion of magnesium in the pathogenesis of this low magnesium status was investigated in 25 patients with sickle cell anaemia (sicklers) in the steady state and in 25 age- and sex-matched controls with haemoglobin genotype AA. The clearance, excretion fraction and excretion rates of magnesium were enhanced in the sicklers. These patients also had significantly lower erythrocyte and plasma magnesium concentrations than the controls. However expressed, urinary magnesium showed a significant positive correlation with plasma magnesium and a weak negative correlation with erythrocyte magnesium. Furthermore, a significant negative correlation was observed between erythrocyte and plasma magnesium in the sicklers. These results suggest that urinary disposal of magnesium in rates and amounts inappropriate to the body stores of the cation may be one of the mechanisms accounting for hypomagnesaemia and low erythrocyte magnesium content in patients with sickle cell anaemia.

Adolescent↗