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Biomedical subjects

R B Tattersall

Publications and source records attributed to R B Tattersall.

At least 37 records · Page 2Linked to original sources
PubMed1994

Peripheral neuropathy as a presenting feature of type 2 diabetes: a case-controlled study.

The characteristics and outcome of 68 newly diagnosed Type 2 diabetic patients who presented with clinically evident peripheral neuropathy were compared with matched controls who had no neuropathy at diagnosis. All subjects (34 male) whose median age was 68 (range 47-89) yr were identified from a computerized diabetes register and presented in 1982-1990. The groups were compared at diagnosis for haemoglobin A1, body mass index, blood pressure, smoking, and alcohol consumption, and for co-existent coronary and peripheral vascular disease. Mortality and morbidity were recorded to March 1991. Significantly more patients with neuropathy had co-existent peripheral vascular disease: 24(35%) compared to 6(9%) controls (p = 0.0021). Twenty (30%) of those with neuropathy and no controls had retinopathy at diagnosis, which was sight-threatening in 10. Seven (10%) with neuropathy but no controls presented with foot ulcers, one requiring limited amputation. Two more patients with neuropathy and one control subsequently developed foot ulcers resulting in one or more amputation in each group. Twenty-one (31%) of those with neuropathy and 14 (21%) controls died (p = 0.2109). In conclusion more diabetic patients with clinically evident peripheral neuropathy at diagnosis have peripheral vascular disease than matched patients without neuropathy. It is likely that macrovascular disease either exacerbates or causes the neuropathy in this group of patients. They are at high risk of developing foot ulceration and high priority should be given to foot care in planning their management.

Aged↗
PubMed1994

Charles-Edouard Brown-Séquard: double-hyphenated neurologist and forgotten father of endocrinology.

This year is the Centenary of the death of Brown-Séquard who, although remembered today only for his eponymous syndrome, was as well known in the Victorian medical world as Robert Maxwell was to newspaper readers in the past decade. His position in the history of endocrinology is paradoxical; a good case can be made for saying that he invented the doctrine of internal secretion. Yet, the excesses of the organotherapy movement he founded at the end of his life discredited endocrinology and probably delayed the discovery of insulin.

Diabetes Mellitus↗
PubMed1993

Bovine and human NPH insulins as T cell immunogens.

The aim of this study was to assess the immunocompetence of T cells from patients with poorly controlled diabetes with respect to Candida albicans antigen and to compare the relative immunogenicity of human insulin, bovine insulin and protamine at the T-cell level during 6 months treatment with human or bovine NPH insulins. T-cell proliferation was measured in vitro in response to C. albicans, bovine and human insulin, bovine and human NPH and protamine in 17 patients with newly-diagnosed type 1 (insulin-dependent) and 12 with poorly-controlled type 2 (non-insulin-dependent diabetes) before and after 0.5, 1, 3 and 6 months of treatment with either bovine or human NPH insulin. The following results were found: Baseline responses to C. albicans (as a recall antigen) were similar for patients and controls despite marked hyperglycaemia in the patients. No patient had a response greater than mean + 2 S.D. of controls to human or bovine insulin before starting treatment, or had insulin autoantibodies. Treatment with human NPH insulin did not induce T-cell responses to human or bovine insulin, but 3/13 (23%) patients treated with bovine NPH responded to bovine and human insulin after 6 months, of whom one responded exclusively to human. In contrast, 6 (46%) bovine and 3 (19%) human NPH-treated patients responded to protamine. It was concluded that there is no evidence of T-cell immunosuppression in poorly-controlled diabetes or of T-cell autoimmunity to insulin in newly-diagnosed type 1 diabetes. Treatment with bovine NPH insulin immunizes T cells to insulin, but human NPH does not.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗
PubMed1993

Effect of acute mild hypoglycaemia on counterregulatory responses to moderate hypoglycaemia induced immediately afterwards in healthy men.

1. This study was designed to determine whether a 1 h period of mild hypoglycaemia (3.3 or 3.7 mmol/l) affected the response to an episode of moderate hypoglycaemia (2.5 mmol/l) immediately afterwards. 2. Eleven non-obese healthy men (age 26 +/- 1 years, mean +/- SEM) underwent three separate 3 h hyper-insulinaemic glucose clamps in single-blind, random order. On all three occasions, blood glucose was 4.5 mmol/l for the first hour, and on a control visit was maintained at this level for the second hour. In the other two visits, blood glucose was lowered to 3.7 or 3.3 mmol/l during the second hour. In the third hour, blood glucose was lowered to 2.5 mmol/l on all three visits. 3. In the second hour, adrenaline rose significantly (P < 0.05, analysis of variance) with a blood glucose of 3.3 and 3.7 mmol/l, as did cortisol and heart rate at 3.3 mmol/l, but glucagon, prolactin, sweating rate, symptom score and blood pressure were the same during the second hour on all three visits. 4. In the final hour at 2.5 mmol/l, there were no differences in adrenaline, noradrenaline, glucagon, prolactin, cortisol, symptom score, heart rate, blood pressure or sweating rate. 5. Thus, the overall magnitude of hormonal responses to moderate hypoglycaemia (2.5 mmol/l) are not modified by exposure to mild hypoglycaemia (3.3 or 3.7 mmol/l) for 1 h immediately beforehand.

Adult↗
PubMed1993

Antecedent insulin level and pattern of induction of acute hypoglycaemia do not affect subsequent counterregulatory responses in healthy subjects.

1. This study was designed to determine whether the duration and pattern of prior insulin exposure modulate the symptomatic and counterregulatory responses to hypoglycaemia. 2. Ten healthy non-obese subjects (five males/five females age 25 +/- 1 years, mean +/- SEM) were made hypoglycaemic in three ways: (i) a hyperinsulinaemic (60 m-units min-1 m-2; plasma insulin concentration 95 m-units/I) clamp, with 1 h of euglycaemia, blood glucose level 4.5 mmol/l, followed by 30 min of hypoglycaemia, at a stable glucose nadir of 2.0 mmol/l (i.e. euglycaemic then hypoglycaemic clamp: E + HC); (ii) an identical hypoglycaemic clamp without preceding hyperinsulinaemic euglycaemia (i.e. a hypoglycaemic clamp: HC); (iii) insulin infusion only, discontinued at a blood glucose level of 3.0 mmol/l (II). Blood glucose level reached the same nadir as on E + HC and HC, and did not fall further. At the glucose nadir, and 15 and 30 min after, the plasma insulin concentration was 23, 7 and 4 m-units/l, respectively, on the II visit. 3. At the glucose nadir, plasma glucagon level, plasma adrenaline level, sweating rate, heart rate, blood pressure, and overall and individual symptom scores (using visual analogue scales) were the same on E + HC, HC and II. 4. There were no significant differences in neurohormonal response between E+HC and HC, but more subjects felt hypoglycaemic on E + HC on arrival at the glucose nadir (P < 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1993

The effects of 3-hydroxybutyrate and glucose on human T cell responses to Candida albicans.

Diabetic patients are particularly susceptible to mucocutaneous candidosis. T lymphocytes are central to the induction of antigen-specific immune responses and may be sensitive to the biochemical abnormalities associated with poorly controlled diabetes; namely, hyperglycaemia and/or ketonemia. To examine this we have studied the effect of varying concentrations of glucose and 3-hydroxybutyrate (3-HB) in cultures of human T cells stimulated with Candida albicans antigen. Proliferation of T cells from six type 1 diabetic and six non-diabetic control subjects was significantly inhibited (both P < 0.05) in glucose-free medium, and at a glucose concentration of 80 mmol l-1 as compared with cultures containing glucose at physiological concentration (5 mmol l-1). 16 and 32 mmol l-1 3-HB also inhibited T cell proliferation in the presence of 5 mmol l-1 glucose (P < 0.05). The effect of glucose and 3-HB were not additive and the inhibition was not due to cell death. 32 mmol l-1 3-HB had less effect when present solely during antigen pulsing than during subsequent lymphocyte stimulation, and was effective even when added after 72 h of a six day culture. This suggests that ketosis affects T cell proliferation more than antigen processing and presentation. We conclude that human antigen-specific T cell proliferation is inhibited in vitro only by concentrations of 3-HB encountered in moderately severe diabetic ketoacidosis, and by glucose concentrations found in severe hyperosmolar non-ketotic coma. The impairment of T cell function under such extreme conditions could be implicated in the close association of diabetic ketoacidosis with deep fungal infections, particularly invasive mucormycosis.

3-Hydroxybutyric Acid↗
PubMed1992

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↗
PubMed1992

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↗
PubMed1992

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↗
PubMed1991

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↗
PubMed1991

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↗
PubMed1991

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↗
PubMed1991

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↗
PubMed1990

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↗