Are diabetic pre-pregnancy clinics worth while?
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Ambulatory Care Facilities↗
Biomedical subjects
R B Tattersall
Publications and source records attributed to R B Tattersall.
A community survey of diabetes in the elderly.
All 98 elderly patients who were known to have diabetes on the lists of two inner-city general practices were interviewed and examined in their own homes. They were characterized in terms of their prevalence of vascular complications, metabolic control, perceived health (measured by the Nottingham Health Profile), frequency of hospital and general practice contacts and use of domiciliary 'support services' and compared to 98 control subjects with an identical age/gender distribution. Mean haemoglobin A1 in the diabetic patients was 9.9 +/- 2.5%, few of them had suffered severe hyperglycaemia (10%) or hypoglycaemia (5%) and they were little more obese than controls (mean body mass index 26.2 +/- 4.2 vs 24.6 +/- 4.1 kg m-2; 95% confidence interval for the difference 0.4-2.8; p < 0.01). All complications were more prevalent in diabetic patients and the difference was statistically significant for visual impairment, strokes, impaired mental test scores, absent vibration sense, and absent leg pulses. Cataract was more common than retinopathy as a cause of visual disability. Diabetic patients perceived their health to be much worse than controls and were more often depressed. No measure of perceived health correlated with haemoglobin A1. We conclude that care of the diabetic elderly should not be too narrowly focused on 'metabolic' goals.
Aged↗
Dressler's syndrome presenting as acute pneumonitis.
An elderly man developed acute pneumonitis three weeks after a myocardial infarction treated with streptokinase. The differential diagnoses are discussed and a short review of lung disease in the post-myocardial infarction syndrome is presented.
Acute Disease↗
Diabetic pregnancy 1977-1990: have we reached a plateau?
We have compared 81 pregnancies in women with type 1 (insulin dependent) diabetes in 1984-1990 with 58 in 1977-1983. In 1984-1990, women booked earlier (8 weeks [median] vs 12 weeks), mean haemoglobin A1 was lower in each trimester, and fewer days were spent in hospital before delivery (5.3 days [mean] vs 15). The latter was due to more experience in managing diabetic control as outpatients and fewer admissions for fetal monitoring. Most admissions are now for pre-eclampsia and intercurrent illnesses. The proportion of deliveries by caesarean section has not changed significantly (53% in 1984-1990 vs 66% in 1977-1983), but most are now done as emergencies. The incidence of macrosomia is constant (26% in 1984-1990 vs 21% in 1977-1983). There was one stillbirth, one intra-uterine death (complicating maternal ketoacidosis) and one perinatal death in 1984-1990, compared with no losses in 1977-1983. Two babies had major congenital abnormalities in 1984-1990, compared with one in 1977-1983. These results compare favourably with those from other centres in the United Kingdom. We conclude we have reached a nearly irreducible minimum for hospital days before delivery and congenital abnormalities, but that there is scope for a small reduction in the caesarean section rate.
Adult↗
Referral letters and case-notes.
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Correspondence as Topic↗
Unexplained deaths of type 1 diabetic patients.
The suggestion of an increase in the number of sudden deaths of young people with Type 1 diabetes in the UK has been investigated. It was suggested that such deaths were due to hypoglycaemia and related to the increasing use of human insulin. In total we were notified of 50 deaths of people with Type 1 diabetes under age 50 years in the UK in 1989 which our informants (relatives, physicians, and pathologists) considered sudden and unexpected. An autopsy had been done in all cases and we supplemented this with detailed clinical information from relatives and case records. Of the 50 cases we excluded five with a definite cause of death, 11 suicides or self-poisonings, six cases of ketoacidosis, and four in which there was insufficient information about the circumstances of death to drawn any conclusions. Of the other 24 cases, two patients had been found with irreversible hypoglycaemic brain damage and died after a period of artificial ventilation. The most puzzling group were 22, aged 12-43 years, most of whom had gone to bed in apparently good health and been found dead in the morning. Nineteen of the 22 were sleeping alone at the time of death and 20 were found lying in an undisturbed bed. Most had uncomplicated diabetes and in none were anatomical lesions found at autopsy. There are major difficulties in diagnosing hypoglycaemia post-mortem, but the timing of death and other circumstantial evidence suggests that hypoglycaemia or a hypoglycaemia-associated event was responsible. All patients were taking human insulin at the time of death but most had been changed from animal insulin between 6 months and 2 years earlier and there was nothing to implicate the species of insulin as a factor in these deaths.
Adolescent↗
Does knowledge of islet cell antibody status help in managing diabetes presenting in middle and old age?
It has been suggested that screening all patients with diabetes diagnosed in later life for islet cell antibodies (ICA) would help predict insulin dependence. We have surveyed the case notes of 55 patients (22 male; ages 37-88 years) who were found to be ICA positive over a 9-year screening period to assess what contribution knowledge of ICA status made to their management. Forty-two patients had been put on insulin (half within 6 months of diagnosis and the rest after up to 6 years). Of the 13 patients not on insulin, six were on diet alone and seven on oral hypoglycaemic agents after a median follow-up of 3 years. In 37 of the 42 patients, insulin treatment was started for clinical rather than immunological reasons (diabetic ketoacidosis, ketonuria, weight loss and/or severe symptoms). Five patients were started on insulin because of ICA status when there was no compelling reason on clinical grounds. Knowledge that seven non-insulin-treated patients were ICA positive made doctors reluctant to discharge them from clinic. The data suggest that routine ICA estimation in this age group is unnecessary, as the decision to treat with insulin is best made on clinical grounds, and ICA estimation can lead to unwarranted insulin treatment, or anxiety in patients and doctors who are aware of a positive result.
Adult↗
Maturity onset-type diabetes of the young (MODY): one condition or many?
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Adult↗
Megaduodenum due to hollow visceral myopathy successfully managed by duodenoplasty and feeding jejunostomy.
A 29 year old man with a history of childhood polymyositis developed insulin dependent diabetes and was found coincidentally to have chronic intestinal pseudo-obstruction due to visceral myopathy. Multiple full thickness biopsy specimens showed severe disease in the duodenum and the proximal jejunum only, with less involvement distally. Total parenteral nutrition has been avoided for more than a year by enteral feeding through a fine bore jejunostomy catheter positioned with its tip in the distal jejunum.
Adult↗
Double-blind evaluation of efficacy and tolerability of metformin in NIDDM.
OBJECTIVE: To test the efficacy and tolerability of metformin. RESEARCH DESIGN AND METHODS: An 8-mo double-blind placebo-controlled parallel-group trial was performed at University hospital diabetic clinics on 60 patients with non-insulin-dependent diabetes mellitus (NIDDM) treated by diet alone. Metformin was administered and built up to a maximum dosage of 1 g three times daily. RESULTS: Mean HbA1 fell from 11.7 +/- 0.4 to 10.3 +/- 0.4% (means +/- SE) on metformin but rose from 11.8 +/- 0.4 to 13.3 +/- 0.4% on placebo (P less than 0.001). Final mean fasting blood glucose was 5.1 mM lower with metformin than placebo (P less than 0.001). No other biochemical variable differed significantly, and weight did not change. A favorable glycemic response was not restricted to the obese. The mean final dosage of metformin was 1.7 +/- 0.1 g and was well tolerated. CONCLUSIONS: Metformin achieved a 23% lower mean HbA1 than placebo without weight gain or significant unwanted effects.
Body Weight↗
Alcohol causes hypoglycaemic unawareness in healthy volunteers and patients with type 1 (insulin-dependent) diabetes.
Both hypoglycaemia and alcohol consumption affect cognitive function but it is unclear whether moderate drinking alters awareness of hypoglycaemia. We have examined this in a single blind randomised hyperinsulinaemic clamp study in eight non-diabetic subjects and seven Type 1 (insulin-dependent) diabetic patients. After 30 min of euglycaemia (blood glucose 4.5 mmol/l) subjects drank either 0.75 g/kg ethanol or a placebo drink after which blood glucose was lowered to 2.5 mmol/l for 40 min. Awareness of hypoglycaemia, reaction time and physiological responses were measured before and after ethanol. At a blood glucose concentration of 4.5 mmol/l, ethanol (producing peak blood levels of 20-25 mmol/l) caused a transient increase in systolic blood pressure (p less than 0.05), a sustained increase in heart rate (p less than 0.01) and a slowing of reaction time in both normal subjects and diabetic patients. During hypoglycaemia in both groups, the slowing of reaction time and increase in sweating were more marked after ethanol than placebo (both p less than 0.05), while the increase in finger tremor (p less than 0.05) was blunted after ethanol, in both groups. Counter regulatory hormone secretion was not affected by ethanol. Despite increases in symptoms during hypoglycaemia, only 2 of 15 individuals "felt hypoglycaemic" after ethanol compared to 11 out of 15 after placebo. We conclude that after moderate drinking non-diabetic subjects and Type 1 diabetic patients are less aware of hypoglycaemia despite exaggerated physiological changes.
Adult↗
Beta-adrenoceptor blockade and hypoglycaemia. A randomised, double-blind, placebo controlled comparison of metoprolol CR, atenolol and propranolol LA in normal subjects.
1. The effect of 1 week of treatment with propranolol LA (160 mg), atenolol (100 mg) and metoprolol CR (100 mg) on awareness of and the physiological responses to moderate hypoglycaemia were compared with placebo using a randomised, cross-over design in 12 healthy volunteers. 2. All three beta-adrenoceptor antagonists reduced resting heart rate, systolic blood pressure and heart rate responses to submaximal exercise compared with placebo. 3. Under hyperinsulinaemic (60 mu m-2 min-1) clamp conditions, at a blood glucose of 2.5 mmol l-1, atenolol prevented the rise in systolic and atenolol and metoprolol CR prevented the fall in diastolic blood pressure usually associated with hypoglycaemia. At this level of hypoglycaemia, the expected increase in heart rate was inhibited by atenolol but not metoprolol CR. Pre-treatment with propranolol LA resulted in a significant pressor response and a bradycardia during hypoglycaemia. In addition the normal increase in finger tremor was abolished by propranolol LA. 4. During hypoglycaemia all three beta-adrenoceptor blockers augmented sweating compared with placebo but hypoglycaemic symptoms, awareness and slowing of reaction time were the same with drugs and placebo. 5. The rise in plasma adrenaline and other counter-regulatory hormones during hypoglycaemia was enhanced by beta-adrenoceptor blockade. 6. We conclude that beta-adrenoceptor antagonists modify the physiological and hormonal responses to, but do not adversely affect awareness of, moderate hypoglycaemia in healthy volunteers.
Adrenergic beta-Antagonists↗
Adaptation to mild hypoglycaemia in normal subjects despite sustained increases in counter-regulatory hormones.
In diabetes, loss of awareness of and a defective hormonal response to hypoglycaemia have been associated with long disease duration, improved glycaemic control and possibly a change in insulin species. In contrast it is assumed that normal subjects always have symptoms when their blood glucose is low. We have tested this in 7 normal subjects at 3 levels of blood glucose (4.5, 3.5 and 3.0 mmol/l) using a hyperinsulinaemic glucose clamp with a euglycaemic (4.5 mmol/l) clamp as a control. After 60 min at a blood glucose of 3.5 mmol/l adrenaline and glucagon increased slightly but significantly, whereas cortisol, growth hormone and pancreatic polypeptide were unchanged. As soon as glucose was lowered to 3.0 mmol/l adrenaline increased to 1.10 nmol/l and rose further to 1.43 nmol/l after 60 min. Glucagon secretion increased similarly but other counter-regulatory hormones were significantly raised only after 60 min at 3.0 mmol/l. Awareness of hypoglycaemia (symptom score) increased after 40 min at a blood glucose of 3.0 mmol/l but after 60 min decreased to baseline levels with loss of awareness in 5 subjects. Reaction time improved in parallel with the change in symptom score. Thus, despite high levels of adrenaline, normal subjects lose awareness during sustained mild hypoglycaemia. Improved reaction time may reflect cerebral adaptation.
Acclimatization↗
Influence of duration of hypoglycemia on the hormonal counterregulatory response in normal subjects.
Glucagon and epinephrine are the most important short term glucose counterregulatory hormones. The epinephrine response in patients with insulin-dependent diabetes mellitus is related to the level of glycemic control, but little is known about the factors influencing counterregulation in normal subjects. We, therefore, conducted hyperinsulinemic glucose clamp studies to examine the counterregulatory response to recurrent and prolonged mild hypoglycemia in normal women. Blood glucose was clamped for 20 min at 3.5 mmol/L. Thereafter, the subjects had their blood glucose maintained at 2.8 mmol/L for 90 min and on another occasion lowered to 2.8 mmol/L and raised to 3.5 mmol/L twice during the 90-min period. Continuous hypoglycemia produced augmented plasma glucagon, cortisol, and pancreatic polypeptide responses (all P less than 0.05) compared to these responses to recurrent hypoglycemia. Plasma GH increased, but the magnitude of the response was not altered by the duration of hypoglycemia. During the recurrent hypoglycemia study plasma epinephrine levels rose and fell in parallel with the fluctuations in blood glucose. The mean peak increase was similar [1.37 +/- 0.25 (+/- SE) nmol/L] to that during the continuous study (1.76 +/- 0.23 nmol/L). There was no change in plasma glucagon levels in response to hypoglycemia of less than 15-min duration. We conclude that 1) the duration of hypoglycemia influences the counterregulatory response, and 2) epinephrine release is under precise control and responds rapidly to fluctuations in blood glucose.
Adult↗
Comparison of high fibre diets, basal insulin supplements, and flexible insulin treatment for non-insulin dependent (type II) diabetics poorly controlled with sulphonylureas.
OBJECTIVE: To compare high fibre diet, basal insulin supplements and a regimen of insulin four times daily in non-insulin dependent (type II) diabetic patients who were poorly controlled with sulphonylureas. DESIGN: Run in period lasting 2-3 months during which self monitoring of glucose concentration was taught, followed by six months on a high fibre diet, followed by six months' treatment with insulin in those patients who did not respond to the high fibre diet. SETTING: Teaching hospital diabetic clinics. PATIENTS: 33 patients who had had diabetes for at least two years and had haemoglobin A1 concentrations over 10% despite receiving nearly maximum doses of oral hypoglycaemic agents. No absolute indications for treatment with insulin. INTERVENTIONS: During the high fibre diet daily fibre intake was increased by a mean of 16 g (95% confidence interval 12 to 20 g.) Twenty five patients were then started on once daily insulin. After three months 14 patients were started on four injections of insulin daily. ENDPOINT: Control of diabetes (haemoglobin A1 concentration less than or equal to 10% and fasting plasma glucose concentration less than or equal to 6 mmol/l) or completion of six months on insulin treatment. MEASUREMENTS AND MAIN RESULTS: No change in weight, diet, or concentrations of fasting glucose or haemoglobin A1 occurred during run in period. During high fibre diet there were no changes in haemoglobin A1 concentrations, but mean fasting glucose concentrations rose by 1.7 mmol/l (95% confidence interval 0.9 to 2.5, p less than 0.01). With once daily insulin mean concentrations of fasting plasma glucose fell from 12.6 to 7.6 mmol/l (p less than 0.001) and haemoglobin A1 from 14.6% to 11.2% (p less than 0.001). With insulin four times daily concentrations of haemoglobin A1 fell from 11.5% to 9.6% (p less than 0.02). Lipid concentrations were unchanged by high fibre diet. In patients receiving insulin the mean cholesterol concentrations fell from 7.1 to 6.4 mmol/l (p less than 0.0001), high density lipoprotein concentrations rose from 1.1 to 1.29 mmol/l (p less than 0.01), and triglyceride concentrations fell from 2.67 to 1.86 mmol/l (p less than 0.05). Patients taking insulin gained weight and those taking it four times daily gained an average of 4.2 kg. CONCLUSIONS: High fibre diets worsen control of diabetes in patients who are poorly controlled with oral hypoglycaemic agents. Maximum improvements in control of diabetes were achieved by taking insulin four times daily.
Blood Glucose↗
Alpha glucosidase inhibition in the treatment of non-insulin-dependent diabetes mellitus.
Two studies of the new alpha-glucosidase inhibitor, miglitol, in patients with non-insulin-dependent diabetes mellitus (NIDDM) are reported. In the first, 13 patients, poorly controlled on sulphonylureas, received miglitol 50mg three times daily for 4 weeks. Post-prandial blood glucose was reduced after breakfast, lunch, and tea compared with placebo (p less than 0.05-0.01) but there was no improvement in fasting blood glucose, serum fructosamine or haemoglobin A1. In a dose-response study the effect of a single dose of miglitol (0,50,100,150 or 200mg) on post-prandial glycaemia after a test breakfast was assessed in 20 patients with mean +/- SEM fasting blood glucose 9.9 +/- 0.4 mmol/l. With 50mg miglitol, there was a significant reduction in blood glucose from 30 to 120 min post-prandially compared with placebo. Increasing doses of miglitol further depressed the post-prandial rise in blood glucose and with 200mg there was no significant change from fasting levels. Side-effects were limited to flatus and loose stools particularly with the higher doses but were not severe. Miglitol effectively reduces post-prandial blood glucose rise in NIDDM with as little as 50mg but there is considerable individual variation. Larger doses may be necessary in patients already poorly controlled on sulphonylureas.
1-Deoxynojirimycin↗