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Biomedical subjects

A Grenfell

Publications and source records attributed to A Grenfell.

At least 19 recordsLinked to original sources
PubMed1999

Implications of new diagnostic criteria for abnormal glucose homeostasis in women with previous gestational diabetes.

OBJECTIVE: To determine the consequences of applying revised American Diabetes Association (ADA) (1997) and World Health Organization (WHO) (1998) recommendations for the classification of glucose intolerance in women with previous gestational diabetes mellitus (GDM). RESEARCH DESIGN AND METHODS: There were 192 women with previous GDM who took an oral glucose tolerance test (OGTT) 1-86 months after delivery and were classified by WHO (1985), ADA (1997, fasting glucose), and revised WHO (1998) guidelines. RESULTS: Among the 165 women without a preexisting diagnosis of diabetes, WHO-1985 and ADA-1997 provided similar estimates of diabetes prevalence (13.3% vs. 11.5%) but widely differing estimates of impaired glucose homeostasis (31.5% impaired glucose tolerance [IGT] by WHO-1985 vs. 10.9% impaired fasting glucose by ADA-1997 criteria). Overall, 56 women (34%) showed a classification discrepancy between WHO-1985 and ADA-1997 criteria, including 44 with normal fasting glucose by ADA-1997 criteria, but abnormal 2-h glucose by WHO-1985 criteria (40 IGT, 4 diabetes). The cardiovascular risk profile of these women was more favorable than that of 18 women with impaired fasting glucose. WHO-1998 recommendations reproduced ADA-1997 findings when used as a fasting screen, but behaved similarly to WHO-1985 criteria when 2-h glucose values were also analyzed. CONCLUSIONS: All criteria produced similar estimates of diabetes prevalence. However, analyses based on a single fasting glucose screen (and a threshold of 6.1 mmol/l) failed to identify 60% of women with abnormal 2-h glucose levels. Screening women with previous GDM (and by analogy, other groups at high risk of diabetes) with a single fasting glucose has low sensitivity for the detection of abnormal glucose tolerance. Recent guidelines recommending this approach require reevaluation.

Adult↗
PubMed1996

A hot ankle.

Explore the source record for details and available documents.

Adult↗
PubMed1995

Reduction of gangrene and amputations in diabetic renal transplant patients: the role of a special foot clinic.

This 4-year prospective study investigated the reasons for high levels of gangrene and major amputation in diabetic renal transplant patients and whether regular multidisciplinary foot care could reduce morbidity. All foot lesions were documented and investigated in 50 diabetic patients, mean age 49.2 +/- 11.0 (SD) years, duration of diabetes 25.3 +/- 9.0 years, time since renal transplantation 60.2 +/- 35.1 months, who attended a special foot clinic monthly for education, vascular and neurological assessment, podiatry and footwear. Foot lesions included: neuropathic ulcers, ischaemic ulcers, traumatic lesions, Charcot's arthropathy, pathological fracture. Treatment included antibiotics, podiatry, footwear, and angioplasty or distal bypass where appropriate. Only 13 patients were deemed ischaemic but peripheral neuropathy was a very common finding (mean VPT 24.8 +/- 12.9 V). Gangrene and major amputations showed a decrease on previous years and healing times for lesions were similar to those previously reported in diabetic patients without renal transplants. The majority of foot lesions, both in soft tissue and bone, were related to neuropathy and trauma and responded well to optimal foot care within the renal unit. Gangrene and major amputations were usually preventable.

Ambulatory Care Facilities↗
PubMed1994

Effect of sulphonylurea therapy on plasma insulin, intact and 32/33 split proinsulin in subjects with type 2 diabetes mellitus.

This study was undertaken to clarify the effect of sulphonylurea therapy on beta cell function in 27 subjects with newly diagnosed Type 2 diabetes mellitus. Plasma glucose, insulin, intact and 32/33 split proinsulin were measured at diagnostic OGTT. After 8-12 weeks on a conventional diet, subjects with a fasting glucose > 9 mmol l-1 (n = 12) were commenced on sulphonylurea therapy. At diagnosis, the sulphonylurea requiring group were more hyperglycaemic (p < 0.0001), less obese (p < 0.05) and more insulin deficient with a lower 30 min insulin (p < 0.0002) than the diet group. Following dietary intervention in the sulphonylurea group, weight remained unchanged but there was a reduction in fasting glucose (p < 0.009). Fasting insulin, intact proinsulin, and 32/33 split proinsulin remained unchanged. After 12 weeks of sulphonylurea therapy there was a weight gain of 1.5 kg (p < 0.01), but a reduction in fasting glucose (p < 0.0001). Fasting insulin and intact proinsulin increased (p < 0.004) but 32/33 split proinsulin remained unchanged. There was a significant increase in both the fasting insulin to glucose ratio (p < 0.005), and intact to 32/33 split proinsulin ratio (p < 0.02). Final fasting glucose following sulphonylurea therapy was positively correlated with the initial intact and 32/33 split proinsulin and the fasting glucose following dietary treatment. It is clear from this work that sulphonylureas have a complex effect on beta cell physiology and as well as stimulating release of insulin they increase the release of intact proinsulin but not that of 32/33 split proinsulin, hence they increase the intact to 32/33 split proinsulin ratio.

Aged↗
PubMed1994

Loss of the first phase insulin response to intravenous glucose in subjects with persistent impaired glucose tolerance.

Loss of the first phase insulin response to intravenous glucose is one of the earliest detectable defects of beta cell dysfunction in Type 2 diabetes mellitus. Impaired glucose tolerance (IGT) is considered a prediabetic condition, therefore loss of first phase insulin secretion in subjects with IGT would suggest beta cell dysfunction as an early lesion in the development of Type 2 diabetes. Three groups of subjects were studied, 7 subjects with persistent IGT (classified as having IGT at two 75 g oral glucose tolerance tests (OGTT) done 6 months apart), 6 subjects with transient IGT (IGT at the first OGTT, but normal glucose tolerance at a repeat OGTT 6 months later), and 7 normal controls. First phase insulin secretion was studied using an intravenous glucose tolerance test with arterialized blood sampling. Fasting, 3, 4 and 5 min samples were assayed for glucose and insulin (specific two-site immunoradiometric assay). The fasting insulin was similar in all three groups, however the 3 min insulin response was significantly lower in those with persistent impaired glucose tolerance (p < 0.02). Thus subjects with persistent impaired glucose tolerance demonstrated loss of the first phase insulin response as an early indicator of beta cell dysfunction while subjects with transient IGT had a normal insulin response to intravenous glucose. During the OGTT, the 30 min glucose was not significantly different (p = 0.1) but the 30 min insulin to glucose ratio was significantly lower in subjects with persistent IGT (p < 0.03).(ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗
PubMed1988

Non-insulin-dependent diabetes and renal replacement therapy.

Reports of renal replacement therapy in diabetes usually refer to patients with insulin-dependent diabetes mellitus (IDDM) only, and little is known about renal failure in non-insulin-dependent diabetics (NIDDM). A high proportion, 46/141 (32%), of the diabetics treated at our unit since 1974 had NIDDM. They were older at treatment (56 +/- 9 years, mean +/- SD) compared to the IDDM patients (39 +/- 10 years, p less than 0.001), and had a shorter duration of diabetes (13 +/- 8 years versus 23 +/- 8 years, p less than 0.001). Asians and Afro-Caribbeans accounted for 48% of the NIDDM patients (22/46) compared to only 7% of those having IDDM (6/95, p less than 0.0001). Non-diabetic renal disease accounted for the renal failure in 32% (15/46) of the NIDDM patients but only in 10.5% (10/95) of the IDDMs (p less than 0.001). Despite these differences the prevalence of other diabetic complications (retinopathy, neuropathy, and cardiovascular disease) was similar. Patient survival after transplantation was poorer in NIDDM than IDDM (23% and 57%, respectively, at 2 years). Survival on dialysis was equally poor in NIDDM and IDDM. Thus, NIDDM patients treated for renal failure are more commonly non-European and more often have non-diabetic renal disease. Yet other diabetic complications occur to the same extent in both IDDM and NIDDM patients with diabetic nephropathy.

Adult↗
PubMed1988

Cardiac hypertrophy in diabetic nephropathy: an echocardiographic study.

Echocardiography was used to study the prevalence and severity of left ventricular hypertrophy in patients with established diabetic nephropathy (persistent proteinuria for at least 2 y plus severe retinopathy). Fifteen patients had mild renal impairment (serum creatinine less than 150 mumol l-1), 14 patients had moderate renal impairment (serum creatinine 150-400 mumol l-1), and 20 patients had severe renal impairment (serum creatinine greater than 400 mumol l-1). Thirty-six of the 49 (73%) were on anti-hypertensive treatment, despite which mean blood pressure was 161 +/- 25/89 +/- 9 (+/- SD) mmHg. Left ventricular hypertrophy was demonstrated in 42 of the 49 patients (85%), and increased in severity with increasing renal impairment. Interventricular septal + left ventricular posterior wall thickness was 25 +/- 3 mm in those with mild renal impairment, 28 +/- 6 mm in those with moderate renal impairment and 30 +/- 4 mm in those with severe renal impairment. The most severe left ventricular hypertrophy was seen in the Afro-Caribbean patients. Left ventricular hypertrophy was present even in those with marginally raised blood pressure and was related to age and serum creatinine but not to present blood pressure or duration of proteinuria.

Adult↗
PubMed1986

Clinical diabetic nephropathy: natural history and complications.

Diabetic nephropathy develops in about 45% of insulin dependent diabetics of whom two-thirds will develop renal failure, the rest dying from cardiovascular disease. Most of the excess mortality of insulin dependent diabetics occurs in those with proteinuria. Among non-insulin dependent diabetics nephropathy is also an important cause of increased mortality but this is mainly from cardiovascular disease. Once diabetic nephropathy is established it progresses relentlessly to end-stage renal failure over about seven years, but ranging from five to 20 years. The explanation for the different rates of progression in individual patients is not understood. Hypertension accompanies diabetic nephropathy and its treatment may retard the progression of renal failure. Other forms of intervention include glycaemic control which has not been shown to have any effect, and protein restriction for which no conclusions can be drawn at present. The diagnosis of diabetic nephropathy is straightforward in the presence of a typical history and clinical features. Non-diabetic renal disease is sometimes the cause of renal failure and may require specific treatment; prognosis for renal failure treatment may be better than for nephropathy patients with other diabetic complications. Other diabetic complications develop as diabetic nephropathy progresses, most notably cardiac and peripheral vascular disease. Proliferative retinopathy and neuropathy are considerable problems and their management needs attention both before and after renal failure treatment.

Acute Kidney Injury↗
PubMed1986

Diabetic pregnancy following renal transplantation.

Renal transplantation for diabetic nephropathy prolongs survival and the return of fertility makes pregnancy possible. We describe a successful pregnancy in a 38-year-old diabetic renal transplant recipient despite blindness, gangrenous toes, cardiac impairment, and both sensory and autonomic neuropathy. Renal function remained stable throughout the pregnancy which was complicated by supine hypertension, postural hypotension and increasing proteinuria. Fetal distress and increasing proteinuria precipitated delivery by Caesarean section at 29 weeks of a female infant weighting 1.1 kg. Following delivery, hypertension improved, gangrene resolved, proteinuria decreased, and renal function remained stable. Pregnancy in long-standing diabetic patients with renal transplants, although hazardous, may be successful yet the maternal morbidity and mortality makes them inadvisable.

Adult↗
PubMed1986

Pregnancy in diabetic women who have proteinuria.

Pregnancy in diabetic women known to have proteinuria is thought to have a poor outcome. We report 22 pregnancies in 20 women with proteinuria in or before the first trimester culled from 396 diabetic pregnancies between 1974 to 1984. Despite a poor obstetric history all the present pregnancies were successful. Half were delivered before 37 weeks compared with 20 per cent of pregnancies in diabetic women without proteinuria. Hypertension precipitated two-thirds of the premature deliveries. The babies were small for dates with 65 per cent below the 50th centile, compared with 36 per cent in those without proteinuria. Serum creatinine levels were raised (greater than 150 mumol/l) in four of 19 patients in the third trimester. Since delivery one patient has died from renal failure, three have serum creatinine levels of 150 to 440 mumol/l, 11 have normal creatinine levels, and five have been lost to the study. The poor long-term maternal prognosis is an important reason for discouraging such pregnancies despite the good short-term results.

Adult↗
PubMedDate not supplied

Vascular calcification, autonomic neuropathy, and peripheral blood flow in patients with diabetic nephropathy.

The possibility that digital gangrene in patients with diabetic nephropathy might be due to abnormalities of peripheral blood flow secondary to vascular calcification has been investigated. Twenty patients with renal failure due to diabetic nephropathy were studied. Peripheral blood flow was measured using venous occlusion plethysmography, together with an assessment of medial arterial calcification on plain radiographs of the hands and feet, and transcutaneous oxygen tension (TcPO2). Hallux blood flow was markedly raised (median 22.5, range 11.5-56.5, ml min-1 100-ml-1) compared with non-diabetic control subjects (4.7, 1.1-10.5, ml min-1 100-ml-1; p less than 0.01) and similar to that in diabetic patients with autonomic neuropathy (29.5, 16.7-49.6, ml min-1 100-ml-1). Although vascular calcification was common and extensive in the patients with diabetic nephropathy, TcPO2 measurements in the supine foot were normal and did not indicate tissue ischaemia. We conclude that despite extensive vascular calcification high peripheral blood flow occurs in the feet of these patients at rest together with normal transcutaneous oxygen tension.

Adult↗
PubMedDate not supplied

Improved beta cell function, with reduction in secretion of intact and 32/33 split proinsulin, after dietary intervention in subjects with type 2 diabetes mellitus.

Diet in Type 2 diabetes often reduces both hyperglycaemia and weight and both these factors may contribute to improvement in beta cell function. Sixty-nine subjects with newly diagnosed Type 2 diabetes had their glucose, insulin, intact and 32/33 split proinsulin measured at diagnosis, and after 16 (12-20) weeks of conventional diet. In the whole group following diet there was reduction in weight (p < 0.0001), Haemoglobin A1 (p < 0.0001), and fasting glucose (p < 0.0001). There was a fall in fasting intact proinsulin (p < 0.03), 32/33 split proinsulin (p < 0.0001), and the percentage of fasting proinsulin to total insulin-like molecules (p < 0.0001). Subjects were separated according to weight loss (group 1 < 0.5 kg, group 2 0.5-4 kg, group 3 > 4 kg). Only subjects in group 3 (mean weight loss 6.2 kg) had a fall in fasting insulin (p < 0.04). The fasting glucose achieved following diet was positively correlated with the initial fasting glucose (r = 0.7) and negatively correlated with the degree of insulin deficiency at diagnosis (with the initial 30 min insulin r = -0.62). The effect of diet on the final concentration of insulin, 32/33 split proinsulin and intact proinsulin was examined using multiple regression. The final insulin concentration was determined by the initial BMI and absolute weight loss, 32/33 split proinsulin concentration by the initial fasting glucose and absolute glucose fall, and intact proinsulin concentration by a combination of both weight loss and glucose reduction.(ABSTRACT TRUNCATED AT 250 WORDS)

Blood Glucose↗