Ian W Campbell

Immediate heart-rate response to standing: simple test for autonomic neuropathy in diabetes.

The immediate heart-rate response to standing was measured in 22 normal controls and 25 patients with diabetes, 15 of whom had autonomic neuropathy. The response in the controls and patients without autonomic neuropathy was characteristic and consistent, with tachycardia maximal at around the 15th beat and relative bradycardia maximal at around the 30th beat. The diabetics with autonomic neuropathy, however, showed a flat response. In three controls the response was abolished with intravenous atropine but not with propranolol, showing that it is mediated through the vagus. A simplified test using routine ECGs and measuring the R-R interval at beats 15 and 30 with a ruler is easily performed as an outpatient procedure and may be used as a measure of autonomic function in diabetes.

Severe Amnesia After Hypoglycemia: Clinical, Psychometric, and Magnetic Resonance Imaging Correlations

Objective To determine the correlation between clinical, psychometric, and magnetic resonance imaging (MRI) findings after an episode of hypoglycemic coma resulting in amnesia. Research Design and Methods Detailed psychometric assessment, especially memory testing, performed with MRI in a man with severe amnesia after hypoglycemic coma. Results Psychometric testing confirmed impaired immediate recall. MRI findings were consistent with a lesion in the left temporal lobe. Conclusions This is the first description of MRI in determining the neurological damage in hypoglycemic coma.

Therapeutic experience with fludrocortisone in diabetic postural hypotension.

Fourteen patients with diabetic postural hypotension were treated with fludrocortisone for a mean 12 months (range 6-30 months). The mean daily dose of fludrocortisone was 0.2 mg (range 0.1 mg-0.4 mg). Standing systolic and diastolic blood pressures increased significantly (P less than 0.001) after treatment with fludrocortisone and the postural hypotension decreased significantly (P less than 0.001). Thirteen patients noted considerable symptomatic improvement. Fludrocortisone should be used cautiously in patients with congestive cardiac failure or the nephrotic syndrome.

Effect of Alcohol Intake on Symptomatic Peripheral in Diabetic Men

In a group of 541 white diabetic men aged 20–59 yr attending one clinic it was found that 91 (15%) drank heavily, while a further 39 (7%) had frank alcoholism. The prevalence of symptomatic peripheral neuropathy was much higher in the 120 men who drank excessively. It is considered important, therefore, when treating diabetic patients with peripheral neuropathy not to assume that the diabetes itself is the cause in all cases. The alcoholic intake of the patient should be ascertained and, if excessive, it should be pointed out to the patient that this may well be the predominant factor causing symptoms.

Sex difference in the relationship of calcium and magnesium excretion to glycaemic control in type 1 diabetes mellitus

In order to assess the variability and possible causes of calcium and magnesium losses in diabetes mellitus, urinary calcium and magnesium excretion were monitored six monthly over a 3-year period in 108 stable, type 1 diabetic patients who were having assessment of their clinical status and glycaemic control over the same period. In the patients studied the ranges of excretion of both calcium and magnesium were considerably wider than our non-diabetic reference ranges but the within subject variation in excretion was high. However, using mean values obtained over the study period, a direct relationship was observed between the excretion of both calcium and magnesium and HbA1 in female patients (P < 0.01) but not in males who had similar HbA1 values. The urinary excretion of calcium and magnesium did not relate to any of the other clinical or biochemical indices measured, including body mass index, daily insulin dose, retinal status or albumin excretion. It is suggested that, in poorly controlled patients, females may have a greater risk than males of developing the complications associated with chronic calcium and magnesium loss.

Review: Non-alcoholic fatty liver disease: natural history, pathogenesis and treatment

Non-alcoholic fatty liver disease (NAFLD) is the term used to describe the alcohol-like liver injury that occurs in the absence of alcohol abuse. It embraces a range of histological abnormalities including simple steatosis or fatty liver, non-alcoholic steatohepatitis (NASH) and NAFLD induced cirrhosis. The predominant risk factor for NAFLD appears to be insulin resistance. Simple steatosis and NASH are generally asymptomatic and it is only the development of cirrhosis that has clinical consequence. At present, therapy in NAFLD concentrates on managing risk factors but in the future clinical trials may provide robust evidence for the use of insulin sensitising agents and other potential therapies.

Is the current therapeutic armamentarium in diabetes enough to control the epidemic and its consequences? What are the current shortcomings?

The prevalence of diabetes is expected to rise together with an increase in morbidity and a reduction in life expectancy. A leading cause of death is cardiovascular disease, and hypertension and diabetes are additive risk factors for this complication. Selected treatment options should neither increase cardiovascular risk in patients with diabetes, nor increase risk of hyperglycaemia in patients with hypertension. The efficacy of present antihyperglycaemic agents is limited and new therapies, such as incretin-targeted agents, are under development. Even though most patients do not achieve glycated haemoglobin targets, trial data show that such interventions reduce the incidence of macrovascular events; however, intensive lowering may be detrimental in patients with existing cardiovascular disease. Currently available oral drugs do not address the key driver of type 2 diabetes—loss of functional beta-cell mass. In the future, new oral treatments must improve this, whilst providing durable blood glucose control and long-term tolerability.

Pioglitazone — an oral antidiabetic agent and metabolic syndrome modulator. Can theory translate into practice?

The metabolic syndrome, associated with insulin resistance, is a cluster of cardiovascular risk factors which results in premature morbidity and mortality from atherosclerotic vascular disease. Pioglitazone, a peroxisome-proliferator-activated receptor gamma (PPARγ) agonist, is an insulin sensitiser with the ability to address key features of the metabolic syndrome: glucose intolerance including type 2 diabetes, hypertension, dyslipidaemia, the pro-coagulant state, endothelial dysfunction, inflammation and atherosclerosis. The greatest potential benefit of pioglitazone is to influence atherogenesis itself through its pleiotrophic effects on vascular risk factors. This has been tested by the PROactive study, results of which are published in September 2005.

Type 2 diabetes mellitus: ‘the silent killer’

Type 2 diabetes mellitus (DM) is best regarded as a cluster of cardiovascular risk factors contributing to accelerating atherosclerotic (macrovascular) disease, often present for many years before the onset of clinical diabetes. It is better referred to as the metabolic syndrome or insulin resistance syndrome, leading to premature cardiovascular death, unless aggressive risk factor reduction targeting blood glucose, blood pressure, dyslipidaemia and the pro-coagulant state is implemented. As type 2 DM is expected to double world-wide over the next 25 years, the burden of type 2 DM presents a major challenge to health authorities to improve the prognosis of those subjects with type 2 DM. It is not a ‘mild disease’ but rather a ‘silent killer’. Copyright

Painful myocardial infarction in severe diabetic autonomic neuropathy.

SummaryTwo cases are reported of painful myocardial infarction in diabetics with severe autonomic neuropathy confirmed by abnormal autonomic function tests. Painless myocardial infarction in diabetics has traditionally been attributed to damage of cardiac pain fibres by autonomic neuropathy but other factors such as microangiopathy in the myocardium may be responsible. It may simply be that diabetics come into hospital more often for other reasons and a silent myocardial infarction diagnosed incidentally.