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R Tattersall

Publications and source records attributed to R Tattersall.

At least 19 recordsLinked to original sources
PubMed1998

Maturity-onset diabetes of the young: a clinical history.

A mild form of diabetes in young people was recognized in the pre-insulin era but was forgotten, probably because of Joslin's dictum that all young people with diabetes should have insulin as a safeguard against complications. After the introduction of sulphonylureas in the 1950s it was found, most notably by Fajans and Conn at the University of Michigan, that tolbutamide could improve or normalize carbohydrate tolerance in some young non-obese mildly diabetic patients. These experiments were not primarily of genetic interest because diabetes was regarded as homogeneous with young and old patients forming part of the same continuum. The question was whether treatment could prevent young subjects with mild diabetes progressing to a total loss of insulin reserve. By 1973, Fajans had shown that the carbohydrate intolerance of 45 patients diagnosed under age 25 had not progressed after up to 16 years on sulphonylureas. Nearly all (43 out of 45) these subjects had a first degree relative with diabetes. In 1974, under the title 'Mild familial diabetes with dominant inheritance' Tattersall described three families in which diabetes, although diagnosed in adolescence, could be treated with sulphonylureas over 40 years later and was dominantly inherited. Collaboration between Fajans and Tattersall established that 'chemical' diabetes in Michigan was also predominantly inherited and distinct from classical 'juvenile-onset' diabetes. In Paris in 1973 Lestradet also described a non-insulin-dependent form of childhood diabetes and later established that it was dominantly inherited. In 1974, Tattersall and Fajans coined the acronym MODY which was defined as 'fasting hyperglycaemia diagnosed under age 25 which could be treated without insulin for more than two years'.

Adolescent↗
PubMed1996

A history of growth hormone.

After the debacle of Brown-Séquard testicular extracts, hormone replacement therapy proper began in 1891 with the use of sheep thyroid extract to treat myxoedema. The second success in the field was "bovine' insulin to treat human diabetes in 1992. In contrast, the first successful use of growth hormone in a human pituitary dwarf did not come until 1958. Growth hormone preparations of reasonable purity had been made in the 1920s and were shown to be effective in rats and dogs, but the need for primate growth hormone in primates was not recognised until the late 1940s.

Animals↗
PubMed1995

Targets of therapy for NIDDM.

Non-insulin-dependent diabetes (NIDDM) is a common multimetabolic disorder with potential (and potentially severe) long-term complications affecting large and small blood vessels. Where microvascular complications (retinopathy, nephropathy and neuropathy) are concerned, the Diabetes Control and Complications Trial (DCCT), as well as much circumstantial evidence, suggests that hyperglycaemia is the main aetiological factor and this is likely to apply in NIDDM as well as IDDM. Unfortunately, achieving normoglycaemia in NIDDM is not easy and it is unclear whether insulin has advantages over oral hypoglycaemic agents or vice versa. Turning to macrovascular disease, it is unclear which of the many potentially atherogenic abnormalities-hypertension, hyperinsulinaemia, hyperlipidaemia, etc-are most important. A further problem is that macrovascular disease is already well developed in many patients when NIDDM is diagnosed and we do not know whether secondary prevention is effective. Nevertheless, it is sensible to try to reverse the atherogenic milieu and this should be done in the first instance by lifestyle modification rather than drugs. Even if we cannot manipulate the biochemistry to prevent small or large vessel complications, much can still be done; proactive foot care can prevent ulceration, timely laser treatment can prevent visual loss and thrombolytic therapy is relatively more effective in diabetic patients with myocardial infarction than in their non-diabetic peers. Finally, patients with NIDDM need intensive education and each needs an individualised treatment plan and goals.

Adult↗
PubMed1995

Patient Education 2000: take-home messages from this congress.

A personal review is presented about the conclusions and highlights during the Congress on Patient Education 2000 (14 June 1994, Geneva, Switzerland). Attention is paid to differences between diseases concerning patient education. Further, a summary is presented of the discussion of quality of life, over-optimism, medical information supply, purpose of patient education, the need for discipline and the psychological problems due to wrong patient education.

Adaptation, Psychological↗
PubMed1995

Traditional pharmacological management of non-insulin-dependent diabetes.

Most traditional hypoglycemic treatments for non-insulin-dependent diabetes mellitus (NIDDM) are of considerable antiquity. What we would now call a low-carbohydrate diet was first used in 1796; insulin was introduced in 1922; the (toxic) biguanide synthalin was used sparingly from 1926 until the Second World War; and tolbutamide and chlorpropamide were marketed in the late 1950s. Amphetamine was available as an anorectic agent in the 1950s. Hence, representatives of all our present treatments for NIDDM have been available for over 30 y, but there is still great uncertainty about how to use them best. This uncertainty is reflected in major variations in prescription rates from country to country. In spite of this formidable pharmacological armamentarium, we have to face the fact that glycemic control is unsatisfactory in the majority of patients with NIDDM; irrespective of the mode of treatment, less than a quarter have a normal glycated hemoglobin. We clearly need new approaches to control glycemia in NIDDM. Furthermore, in addition to high blood glucose, many patients with NIDDM also have hypertension, hyperlipidemia, and other atherogenic abnormalities that need to be tackled if mortality (predominantly from atherosclerotic vascular disease) is to be reduced. It seems improbable that a single drug will be found to cure the many metabolic abnormalities. Polypharmacy thus seems inevitable for many patients.

Diabetes Mellitus, Type 2↗
PubMed1992

Bovine insulin.

Explore the source record for details and available documents.

Aged↗
PubMed1992

Rapid large-scale preparation of recombinant Erwinia chrysanthemi L-asparaginase.

L-asparaginase from Erwinia provides an alternative to the enzyme from E. coli for the effective treatment of acute lymphoblastic leukaemia. A procedure was required for the large-scale partial purification of the recombinant Erwinia enzyme cloned and expressed in Erwinia. Enzyme was extracted from Erwinia at high pH and extraneous protein precipitated at low pH. S-Sepharose FF was selected as the medium of choice for the chromatography step since it was adequate for the high flow rates required (linear flow rate 315 cm h-1) and the methylsulphonate functional groups exploited the high pI of the enzyme by allowing binding of L-asparaginase at pH 4.8 while most of the other proteins passed through the column. The useful capacity of the matrix was up to 34 mg enzyme/ml matrix at a linear flow rate of 95 cm h-1 and 15.4 mg enzyme/ml matrix at a linear flow rate of 315 cm h-1. Weakly bound protein was removed by a wash at pH 6.0. The L-asparaginase was eluted by a wash at pH 6.8 (linear flow rate 95 cm h-1) and was substantially pure, only requiring polishing steps to be suitable for use as a parenteral agent. The purity of the protein was complemented by a 92% recovery of active enzyme from this cation-exchange matrix.

Asparaginase↗
PubMed1991

Course of brittle diabetes: 12 year follow up.

OBJECTIVE: To determine the course of brittle diabetes. DESIGN: 12 year follow up of patients identified in 1977-9 as having brittle diabetes; retrospective review of the case notes. SETTING: Nottingham health district. SUBJECTS: 25 brittle diabetic patients were identified in 1979-9; 11 (five men) had three or more admissions with ketoacidosis between June 1977 and 1979 and 14 (eight men) had three or more attendances at the accident and emergency department with hypoglycaemia in 1978. Two controls from our diabetic register were matched to each patient for age, sex, and duration of diabetes. MAIN OUTCOME MEASURES: Frequency of ketoacidosis and severe hypoglycaemia in the 12 years after ascertainment; diabetic control and complications in 1988-90; retrospective attribution of the cause of brittleness. RESULTS: Patients with recurrent ketoacidosis had had a median (range) of 28 (8-67) episodes. One man died of a cerebral tumour but five of the surviving nine patients had not been admitted in the past two years, although diabetic control remained poor (median haemoglobin A1 concentration 14%). Seven patients had pure hypoglycaemic brittleness, and five had also had eight or more admissions with ketoacidosis (mixed brittleness). Two died of uraemia within a year after ascertainment and two others in hypoglycaemic coma seven and 12 years later. Brittle diabetes was in most cases related to a specific situation, usually unhappiness at home or school. CONCLUSIONS: Brittle diabetes is often episodic and almost always related to stressful life circumstances. Once the underlying cause is removed it tends to improve. Recurrent hypoglycaemic brittleness of psychological origin has a poor prognosis.

Adolescent↗