bluuebunny/crossref_metadata_2025_split huggingface dataset:
Diabetes mellitus in the family: perceptions of offspring’s risk
Authors: Pierce M. , Hayworth J. , Warburton F. , Keen H. , Bradley C. 
Published: March 2003

Summary Aims The study aimed to explore the beliefs and concerns of people with Type 2 diabetes mellitus (DM) about their children’s risk of developing the disease and the possibilities for prevention. Methods Questionnaires were posted to all patients with Type 2 DM in four randomly selected general practices in South London. Two hundred and thirteen (73%) responded. The main outcome measures were: estimated risk of Type 2 DM in their offspring; worry about diabetes in their offspring; knowledge about the possibilities for prevention of Type 2 DM and its complications. Results Of the 159 respondents with children, at least 35% and perhaps as many as 64% underestimated the risk of their offspring developing Type 2 DM; 44% thought it possible to reduce the risk of Type 2 DM and its complications; 28% thought altering diet and 6% taking exercise might be useful preventive strategies; 49% worried about their children developing diabetes. Conclusions Although risk of Type 2 DM was underestimated for their children and little was known about prevention, about half of the respondents worried about their children developing diabetes. Education and counselling about risk and prevention are needed. This is important in view of growing interest in and opportunities for both the primary and secondary prevention of Type 2 DM.Diabet. Med. 16, 431–436 (1999)
Effect of metformin on patients with impaired glucose tolerance
Authors: Li C. L. , Pan C. Y. , Lu J. M. , Zhu Y. , Wang J. H. , Deng X. X. , Xia F. C. , Wang H. Z. , Wang H. Y. 
Published: March 2003

Summary Aims To evaluate the effect of metformin on glucose metabolism, insulin sensitivity and rate of conversion diabetes in people with impaired glucose tolerance (IGT). Methods Seventy subjects with IGT were randomized under double‐blind conditions to receive either placebo (n = 37) or metformin (n = 33) at a dosage of 250 mg three times daily for a duration of 12 months. Glycaemic control, plasma insulin and other biochemical indexes were assessed before and after 3, 6 and 12 months. Results At 12 months the conversion rate to diabetes was 16.2% in the placebo group compared to 3.0% for the metformin group (P = 0.011). Of subjects treated with metformin for 12 months, 84.9% became normoglycaemic compared to 51.4% of those receiving the placebo. Significant improvements in fasting glucose, glucose tolerance and insulin sensitivity were found at 12 months and at intermediate clinic assessments. Conclusions Metformin can improve glucose metabolism in IGT patients and may be a treatment option in their management of IGT subjects.
Amniotic fluid insulin levels identify the fetus at risk of neonatal hypoglycaemia
Authors: Fraser R. B. , Bruce C. 
Published: March 2003

Summary Aims To investigate the use of amniotic fluid insulin (AFI) as a predictor of neonatal morbidity in the macrosomic newborn of the diabetic mother, in view of the fact that raised AFI levels are a marker for fetal hyperinsulinaemia. Methods AFI was measured by radioimmunoassay in a group of pregnant diabetic women (n = 63) with normal (n = 41) or accelerated fetal growth (n = 22). Results Using log transformed data, liquor insulin was found to be significantly higher in pregnant women with Type 1 and Type 2 diabetes mellitus (17.6 mU/l; 95% confidence interval (CI) 11.7–26.4) compared with women with gestational diabetes mellitus (GDM) (8.2 mU/l; 95% CI 4.8–13.8, P = 0.02) or impaired glucose tolerance (IGT) (6.2 mU/l; 95% CI 4.9–8.0, P = 0.0001). In the group with macrosomic fetuses (birth weight > 90th centile for gestational age), there was a significantly higher incidence of elective Caesarean section (CS) and emergency CS (12/22) compared to those with appropriate for gestational age (AGA) fetal weights (birth weight > 10th and < 90th centiles for gestational age) (9/41, P = 0.009). There was no significant correlation between raised AFI and macrosomia except in the Type 1 diabetic women, in whom the AGA group mean was 13.2 mU/l (95% CI 7.4–23.3), and 34.6 mU/l (95% CI 17.5–68.4 P = 0.022) in macrosomia. In the latter group, hypoglycaemia requiring treatment was significantly more common in the macrosomic hyperinsulinaemic neonates (8/13), compared to normoinsulinaemic neonates in the same group (0/9, P = 0.005). Conclusions Identification of the hyperinsulinaemic fetus before delivery might allow the intensification of maternal insulin therapy leading to a reduction in incidence and severity of diabetic fetopathy. Pregnancy with a normoinsulinaemic fetus could be allowed to continue to the onset of spontaneous labour, which might result in a lower CS rate.
A paper which changed clinical practice (slowly). Jacob Holler on potassium deficiency in diabetic acidosis (1946)
Authors: Tattersall R. B. 
Published: March 2003

SummaryIt is often said that the introduction of insulin into clinical medicine made a ‘dramatic’ difference to the mortality resulting from diabetic coma. This is true in the sense that before 1922 it was almost uniformly fatal, but until the 1950s the mortality in many large hospitals was as high as 30–50%. Often autopsy did not establish a cause of death. Many may have been a result of hypokalaemia, a complication which was not recognized until 1946; in that year in the Journal of the American Medical Association, Jacob Holler described a patient who developed respiratory paralysis 12 h into treatment that, after several hours in an iron lung, was cured by potassium infusion. In the 5 years after Holler’s paper there were many reports of deaths resulting from hypokalaemia, as well as several ‘near misses’, but clinicians were extremely cautious about early replacement probably, as an editorialist in The Lancet suggested, because ‘the frightening effects of intravenous injections of potassium made clinicians reluctant to believe in a lack of potassium as a cause of trouble, except in very rare conditions such as familial periodic paralysis’.It had been known since 1923 that insulin lowered serum potassium, but this was not of great interest because the symptoms of hypokalaemia were not known. Also, potassium was not an electrolyte with which clinicians were familiar. Until the introduction of flame photometry in 1950, it was only measured in research studies as chemical methods took several hours to complete.
Comparison of vasodilator effects of substance P in human forearm vessels of normoalbuminuric Type 1 diabetic and non‐diabetic subjects
Authors: Meeking D. R. , Allard S. , Munday J. , Chowienczyk P. J. , Shaw K. M. , Cummings M. H. 
Published: March 2003

Summary Aims To compare the vasodilatory responses to substance P in human forearm vessels in Type 1 normoalbuminuric diabetic and non‐diabetic subjects. Methods Forearm blood flow (FBF) was measured using a plethysmography technique in 12 normoalbuminuric Type 1 diabetic subjects (six males, six females) (HbA1C 8.2 ± 0.3% (mean ± sem)) and 12 non‐diabetic healthy control subjects in response to the infusion of the vasodilators substance P (SP), acetylcholine (ACh) and nitroprusside. Results There was no significant difference in baseline FBF between the two groups (2.80 ± 0.29 ml/min per 100 ml forearm tissue (diabetic group) vs. 2.85 ± 0.37 ml/min per 100 ml (non‐diabetic group), P = 0.45). Infusion of SP was associated with an incremental increase in FBF in the diabetic (0.6, 2 and 6 ng/min – 6.08 ± 1.07, 7.82 ± 1.08 and 9.48 ± 1.14 ml/min per 100 ml, respectively) and the non‐diabetic group (0.6, 2 and 6 ng/min – 5.41 ± 0.80, 6.93 ± 0.96 and 9.25 ± 1.11 ml/min per 100 ml, respectively). Similarly, an incremental rise in FBF was observed during infusion of ACh (diabetic group: 7.5, 15 and 30 μg/min – 7.14 ± 1.22, 8.91 ± 1.40 and 11.67 ± 1.93 ml/min per 100 ml, respectively; non‐diabetic group: 7.5, 15 and 30 μg/min – 5.87 ± 0.81, 7.49 ± 0.96 and 10.74 ± 1.29 ml/min per 100 ml, respectively). When FBF was expressed as percentage change from baseline, there was no significant difference in vasodilatory responses between the two groups for SP (0.6 ng/min, P = 0.21; 2 ng/min, P = 0.19; 6 ng/min, P = 0.19) or ACh (7.5 μg/min, P = 0.20; 15 μg/min, P = 0.20; 30 μg/min, P = 0.35). Conclusions This study suggests that endothelium‐dependent vasodilatory responses to SP (and ACh) are not impaired in Type 1 diabetic subjects with normal urinary albumin excretion.
Rosiglitazone taken once daily provides effective glycaemic control in patients with Type 2 diabetes mellitus
Authors: Nolan J. J. , Jones N. P. , Patwardhan R. , Deacon L. F. 
Published: March 2003

Abstract Aims To evaluate the clinical efficacy and safety of rosiglitazone as a once daily treatment for Type 2 diabetes mellitus (DM). Methods Three hundred and sixty‐nine patients with Type 2 DM (mean age 63 years; mean body mass index (BMI) 29.4 kg/m2) were enrolled in a double‐blind, parallel group, placebo‐controlled, dose‐ranging study. Patients were randomly assigned to receive placebo or rosiglitazone at doses of 4, 8, or 12 mg daily for 8 weeks. Results At 8 weeks, fasting plasma glucose (FPG) decreased significantly in the rosiglitazone 4 mg, 8 mg, and 12 mg groups (−0.9, −2.0 and −1.7 mmol/l; P = 0.0003, < 0.0001, and < 0.0001, respectively) compared with placebo (+0.4 mmol/l). The improvements in FPG were dose ordered for 4 and 8 mg/day. The 12 mg/day dose produced no additional improvement. There were small decreases in haemoglobin and haematocrit in the rosiglitazone treatment groups. The overall incidence of adverse experiences was similar in all treatment groups, including placebo with no evidence of hypoglycaemia or hepatotoxicity. Conclusions Rosiglitazone improves glycaemic control when given once daily to treat Type 2 diabetes mellitus and is well tolerated at doses up to and including 12 mg.
Sensitivity to sulphonylureas in patients with hepatocyte nuclear factor‐1α gene mutations: evidence for pharmacogenetics in diabetes
Authors: Pearson E. R. , Liddell W. G. , Shepherd M. , Corrall R. J. , Hattersley A. T. 
Published: March 2003

SUMMARY Introduction  Maturity‐onset diabetes of the young (MODY) is characterized by autosomal dominantly inherited, early‐onset, non‐insulin‐dependent diabetes. Mutations in the hepatocyte nuclear factor (HNF)‐1α gene are the commonest cause of MODY. Individual patients with HNF‐1α mutations have been reported as being unusually sensitive to the hypoglycaemic effects of sulphonylurea therapy. We report three patients, attending a single clinic, with HNF‐1α mutations that show marked hypersensitivity to sulphonylureas.Case reports  In cases 1 and 2 there were marked changes in HbA1c on cessation (4.4% and 5.8%, respectively) and reintroduction (5.0% and 2.6%) of sulphonylureas. Case 3 had severe hypoglycaemic symptoms on the introduction of sulphonylureas despite poor glycaemic control and was shown with a test dose of 2.5 mg glibenclamide to have symptomatic hypoglycaemia (blood glucose 2 mmol/l) after 4 h despite eating.Conclusions  HNF‐1α MODY diabetic subjects are more sensitive to sulphonylureas than Type 2 diabetic subjects and this is seen in different families, with different mutations and may continue up to 13 years from diagnosis. This is an example of pharmacogenetics, with the underlying aetiological genetic defect altering the pharmacological response to treatment. The present cases suggest that in HNF‐1α MODY patients: (i) sulphonylureas can dramatically improve glycaemic control and should be considered as initial treatment for patients with poor glycaemic control on an appropriate diet; (ii) hypoglycaemia may complicate the introduction of sulphonylureas and therefore very low doses of short acting sulphonylureas should be used initially; and (iii) cessation of sulphonylureas should be undertaken cautiously as there may be marked deterioration in glycaemic control.Keywords  genetics, HNF‐1α, MODY, pharmacogenetics, sulphonylurea sensitivity
Different effects of glucose on extracellular and intracellular respiratory burst response in normal human neutrophils activated with the soluble agonist fMet‐Leu‐Phe
Authors: Oldenborg P. ‐A. , Sundqvist I. ‐M. , Sehlin J. 
Published: March 2003

SUMMARY Aims  The study evaluated the effects of glucose concentration on the extracellular and intracellular activation of the respiratory burst in fMet‐Leu‐Phe‐stimulated normal human neutrophils.Methods  Specific extracellular respiratory burst activity was measured as superoxide dismutase (SOD)‐inhibitable cytochrome c reduction. Intracellular respiratory burst activity was studied using luminol‐enhanced chemiluminescence in the presence of SOD and catalase, to quench extracellular chemiluminescence activity. Myeloperoxidase (MPO) release from activated neutrophils was studied by using the guaiacol technique.Results  The extracellular respiratory burst following activation with 1 μM fMet‐Leu‐Phe was significantly reduced at 15 and 25 mM d‐glucose (9.5 ± 1.0 and 8.5 ± 0.8 nmol/106 cells and 10 min; P < 0.01 and P < 0.001, respectively) as compared with that at 5 mM glucose (10.3 ± 1.0 nmol/106 cells and 10 min). When specifically studying the intracellular respiratory burst, no difference was found between the responses at 5, 15 or 25 mM glucose. Increasing glucose concentrations also reduced the secretion of MPO from fMet‐Leu‐Phe‐activated neutrophils.Conclusions  Elevated glucose concentrations inhibit the generation of extracellularly released reactive oxygen metabolites but have no effects on the intracellular respiratory burst in fMet‐Leu‐Phe‐stimulated normal human neutrophils.
A case of hand ulceration in the diabetic foot clinic – a reminder of hand neuropathy in ‘at risk’ patients
Authors: Coppini D. V. , Best C. 
Published: March 2003

SUMMARY Background  A case of hand ulceration in a diabetic patient with known lower extremity complications is presented. Although often asymptomatic, quantitative testing in patients indicates reduced hand sensation in patients with lower extremity neuropathy. Hand neuropathy may occasionally lead to anaesthetic injuries, particularly in certain ‘manual’ occupations, as seen in our patient.Conclusions   Education on hand care is virtually inexistent in most clinic settings, and our case highlights the need for more awareness on this potentially troublesome complication.
Does dietary protein intake correlate with markers suggestive of early diabetic nephropathy in children and adolescents with Type 1 diabetes mellitus?
Authors: O'hayon B. E. , Cummings E. A. , Daneman D. , Ossip M. G. , Lawson M. L. , Sochett E. B. 
Published: March 2003

SUMMARY Aims  To examine the relationship between dietary protein intake and possible early markers of diabetic nephropathy (creatinine clearance (CrCl), kidney volume and albumin excretion rate (AER)).Methods  One hundred and forty‐five subjects with diabetes for 5–10 years, divided into three pubertal groups, participated. Kidney volume was measured by ultrasound, and serum creatinine and HbA1c were assayed. Two or three 24‐h urine collections were obtained for albumin, creatinine and urea excretion rates. Dietary protein intake was estimated from urinary urea nitrogen excretion rate. Glomerular filtration rate was estimated by creatinine clearance.Results  Mean protein intake was 1.22 ± 0.48 g.kg−1.day−1 Protein intake was significantly higher in males than females (P < 0.0001) and highest in pre‐pubertal compared to mid‐pubertal and post‐pubertal subjects (P < 0.001). In multiple regression analysis, protein intake was positively associated with CrCl (P < 0.0001), and male sex (P < 0.0001) and negatively associated with body surface area (P = 0.0013) and age (P = 0.01). Kidney volume and AER were not related to dietary protein intake.Conclusions  This cross‐sectional study failed to show a significant relationship between dietary protein intake and markers of early nephropathy, other than CrCl. However, a longitudinal, prospective study is required to definitively assess the role of protein intake in the evolution of diabetic nephropathy.
Autonomic neuropathy – a complication less pronounced in patients with Type 1 diabetes mellitus who have lower blood glucose levels
Authors: Reichard P. , Jensen‐Urstad K. , Ericsson M. , Jensen‐Urstad M. , Lindblad L. E. 
Published: March 2003

SUMMARY Aims  Autonomic neuropathy is a serious diabetic complication, probably contributing to the death of many young people with Type 1 diabetes mellitus. It is often not diagnosed.Methods  Patients with Type 1 diabetes from the Stockholm Diabetes Intervention Study were investigated with power spectral analysis (n = 88), heart rate and blood pressure reactions to tilting (n = 66), and heart rate variability during deep breathing (n = 70) a mean of 11.4 years after randomization to intensified conventional treatment (ICT) or standard treatment (ST), the treatment groups similar with regard to age, duration of diabetes and metabolic control at baseline (HbA1c 9.4 (1.3)%, mean (sd)). Blood glucose levels (mean of 29 HbA1c values) during the 10 years were lower in the patients from the ICT group (7.2 (0.6) vs. 8.3 (1.0)%, P = 0.001).Results  Heart rate variability (HRV) in the high frequency range (P = 0.034), the expiration–inspiration ratio (P = 0.020), and the brake index during tilt (P = 0.044) were lower in the ST group, indicating more pronounced parasympathetic insufficiency. Systolic blood pressure fell by 10 (16) mmHg in the ST group, and by 2.5 (15) mmHg in the ICT group 8 min after rising from the supine to a 70° upright position (P = 0.034). A decreased autonomic function was associated with age and higher HbA1c.Conclusion  Better autonomic nerve function is associated with lower HbA1c and lower age which were both the same in the intensively and the conventionally treatment groups at baseline. After a mean of 11.4 years autonomic function was better in the intensively treated group.
Circulating plasma vascular endothelial growth factor and microvascular complications of Type 1 diabetes mellitus: the influence of ACE inhibition
Authors: Chaturvedi N. , Fuller J. H. , Pokras F. , Rottiers R. , Papazoglou N. , Aiello L. P. ,   the Euclid Study Group
Published: March 2003

SUMMARY Aims  To determine whether circulating plasma vascular endothelial growth factor (VEGF) is elevated in the presence of diabetic microvascular complications, and whether the impact of angiotensin‐converting enzyme (ACE) inhibitors on these complications can be accounted for by changes in circulating VEGF.Methods  Samples (299/354 of those with retinal photographs) from the EUCLID placebo‐controlled clinical trial of the ACE inhibitor lisinopril in mainly normoalbuminuric non‐hypertensive Type 1 diabetic patients were used. Albumin excretion rate (AER) was measured 6 monthly. Geometric mean VEGF levels by baseline retinopathy status, change in retinopathy over 2 years, and by treatment with lisinopril were calculated.Results  No significant correlation was observed between VEGF at baseline and age, diabetes duration, glycaemic control, blood pressure, smoking, fibrinogen and von Willebrand factor. Mean VEGF concentration at baseline was 11.5 (95% confidence interval 6.0–27.9) pg/ml in those without retinopathy, 12.9 (6.0–38.9) pg/ml in those with non‐proliferative retinopathy, and 16.1 (8.1–33.5) pg/ml in those with proliferative retinopathy (P = 0.06 for trend). Baseline VEGF was 15.2 pg/ml in those who progressed by at least one level of retinopathy by 2 years compared to 11.8 pg/ml in those who did not (P = 0.3). VEGF levels were not altered by lisinopril treatment. Results were similar for AER.Conclusions  Circulating plasma VEGF concentration is not strongly correlated with risk factor status or microvascular disease in Type 1 diabetes, nor is it affected by ACE inhibition. Changes in circulating VEGF cannot account for the beneficial effect of ACE inhibition on retinopathy.
Child and parental mental ability and glycaemic control in children with Type 1 diabetes
Authors: Ross L. A. , Frier B. M. , Kelnar C. J. H. , Deary I. J. 
Published: March 2003

SUMMARY Aims  Many psycho‐social factors can affect the glycaemic control of children with Type 1 diabetes, but the influence of the intelligence of the child and their parents has not been reported.Methods  Seventy‐eight children and adolescents with Type 1 diabetes and their mothers performed standardized tests to assess psychometric intelligence. The children were aged (median (range)) 12.0 (5–17) years with duration of diabetes 5.0 (1.0–13.0) years and required an insulin dose of (mean ± sd) 1.0 ± 0.3 U/kg per day. The children completed the Wide Range Achievement Test 3 reading test (WRAT3) and Raven's Standard Progressive Matrices (RSPM). A mean annual HbA1c was calculated for each subject (8.6 ± 1.4%). The mothers performed the National Adult Reading Test (NART) and provided details of the occupation of the main wage‐earner in the family from which social class (SC) was derived.Results  The HbA1c of the child correlated with their age (r = 0.26, P = 0.02), SC (Kendall's rank correlation, τ = 0.17, P = 0.03) and with the NART error score of their mother (r = 0.28, P = 0.01), but no correlation was observed with the child's WRAT3 or RSPM score. Stepwise regression revealed that age and NART error score were the strongest independent determinants of glycaemic control (total adjusted r2 = 0.117).Conclusions  Parental intelligence appears to have a significant influence on the glycaemic control of a child with Type 1 diabetes, accounting for 7.6% of the reliable variance in HbA1c.
Reversible amnesia in a Type 1 diabetic patient and bilateral hippocampal lesions on magnetic resonance imaging (MRI)
Authors: Holemans X. , Dupuis M. , Misson N. , Vanderijst J.‐F. 
Published: March 2003

AbstractAims  Intensive insulin therapy of Type 1 diabetes limits its chronic complications, but is associated with an increased risk of severe hypoglycaemia and its neuroglycopenic consequences.Methods  Case report.Results  A 24‐year‐old male with 15 years' history of Type 1 diabetes, who was missing for 48 h, was found at home in ketoacidosis coma. Intensive care permitted a rapid improvement revealing an unexpected severe anterograde amnesia, confirmed by neuropsychological testing. MRI performed 4 days after admission showed abnormal bilateral hyperintensity signals on T2‐weighted images in the hippocampus. Three months later, the patient had nearly completely recovered and resumed work. MR images and neuropsychological testing returned to normal.Conclusions  The most likely course of events favours an initial prolonged hypoglycaemic coma following insulin overdose. The hippocampal injury may be a result of hypoglycaemia. Neuropsychological testing and MRI abnormalities were completely reversible. This case underlines the potential risks of intensive insulin therapy.Diabet. Med. 18, 761–763 (2001)