Hyperlipidaemia screening among patients with both diabetes mellitus and hypertension-experience at a public health centre

OBJECTIVE: To assess the frequency of screening for hyperlipidaemia among patients with both diabetes mellitus and hypertension who attended a public health centre in Jamaica between June 1997 and December 2000. METHODS: This study was conducted among all patients with both diabetes mellitus and hypertension who attended the Hermitage August Town Health centre between June 1997 and December 2000. Subjects were identified from the clinic daily register using the International Classification of Disease (ICD-9) codes for hypertension (ICD-401) and diabetes mellitus (ICD-250). Patients' dockets were reviewed to identify those who had any test for hyperlipidaemia during this period. Results of these tests were noted. Abnormal blood lipid results (in mmol/l) were assessed as: total cholestorol> 6.50; low density lipoprotein> 3.60; triglycerides> 2.37; high density lipoprotein< 1.17. RESULTS: For the period of the study, 127 persons with both diabetes mellitus and hypertension were seen at the clinic (78 percent females and 22 percent males) ranging in age from 37 to 91 years with a median age of 61 years. Only 17 (13.4 percent) patients had a screening test for cholesterol over the study period. Six patients were screened only for cholesterol and 11 screened for both cholesterol and triglycerides. Screening frequency was slightly among persons older than 60 years compared to those less than 60 years (14.2 percent vs 12 percemnt; p> 0.05). Men were more likely to be screened than women (17 percent vs 12 percent; p> 0.05). Of the 17 patients screened, 46 percent had hypercholesterolaemia (total cholesterol> 6.5 mmol/l). CONCLUSIONS: Screening frequency for abnormal lipid profiles was extremely low in this sample of patients. The results of this study, though not generizable to all health centres, highlight what may be a major public health deficit in the control of atherosclerotic-related chronic non-communicable disease in Jamaica. (AU)

Diabetes in the peri-menopausal period - position statement

Interrelationship of one with the other includes the high prevalence of diabetes in peri-menopausal and menopausal women, and the adverse impact of the menopause on diabetes. MENOPAUSE AND DIABETES RISK: The risk increases for women predisposed to type 2 diabetes because of the loss of oestrogen, increased adipose tissue and increased insulin resistance. MENOPAUSE AND PRE-EXISTING DIABETES: There is a change in glycaemic control with an increase in marcovascular risk due to comorbidities such as hypertension and dyslipidaemia. DIABETES AND HORMONE REPLACEMENT THERAPY: This results in worsening of hyperlipidaemia with an increased risk of cardiovascular events and deterioration in glycaemic control. The management regime includes assessment and management of dyslipidaemia, renal problems, ophthalmic complications and neuropathy. The objectives are to achieve normal weight and blood pressure whilst maintaining tight glycaemic control as monitored by HbA measurement.(AU)

Prevalence of glucose intolerance and dyslipidaemias in Bermuda - Poster Presentation

Diabetes and dyslipidaemias are major problems in Bermuda. To assess the magnitude of this problem, we determined the prevalence of glucose intolerance

Hyperlipidaemia and insulin resistance

There is reason to believe that increased plasma fatty acid (FFA) levels may be a cause for the strong association between fat ingestion and obesity. It has been recently shown in offspring of parents with non-insulin dependent diabetes mellitus (NIDDM), known to be at high risk to develop the disease, that elevated FFA levels were associated with insulin resistance. Moreover, 80-85 percent of patients with NIDDM are obese, are insulin-resistant, and many have elevated FFA levels which correlate with glucose tolerance. In support of the notion that plasma FFA are responsible for the insulin resistance observed in obesity, it was demonstrated more than 30 years ago that increased availability of FFA decreased CHO oxidation and glucose uptake in perfused rat heart and to a lesser extent in rat diaphragm. Based on these findings, the researchers proposeda glucose-fatty acid cycle presumed to be of fundamental importance for the control of blood glucose and insulin sensitivity both in normal and in diabetic subjects. This intriguing concept has remained controversial mainly because many investigators were unable to reproduce the fatty acid-mediated inhibition of glucose uptake in striated muscle that had been observed in perfused rat hearts. We have recently reinvestigated that onset and duration of the inhibitory effect of intravascular lipolysis, produced by intravenous infusion of triglycerides and heparin, on total body CHO oxidation and glucose disappearance in normal men during euglycaemic-hyperinsulinaemia. These studies demonstrated that the fatty acid-mediated inhibition of insulin-stimulated CHO oxidation occurred early, i.e., within the first 20 minutes while the inhibition of glucose uptake developed after only 3-4 hours of fat infusion. Thus, insufficient time of fat infusion (2 hours in most studies) was the most likely reason why the inhibitory effect of FFA on glucose uptake was not found in many studies. In subsequent studies, we have examined the dose dependency of the fatty acid effect on insulin-stimulated glucose uptake. The results showed that FFA inhibited glucose uptake in a dose-dependent fashion throughout the physiological range of plasma FFA concentration (AU)

The diagnosis and treatment of lipid disorders in NIDDM - abstract

Dyslipidaemia in NIDDM is multifactorial due in part to diabetes mellitus and in part to the effects of aging, inactivity, obesity, late expression of genetic disorders and the use of drugs which may adversely influence lipid levels. The dyslipidaemia of NIDDM is characterized by hypertriglyceridaemia, low HDL-C and small dense LDL particles. Post-prandial lipaemia is also exaggerated in NIDDM due to impaired clearance of atherogenic particles (chylomicron remnants, small VLDL). Hypercholesterolaemia is not a typical feature of NIDDM except when the total cholesterol is increased due to increased VLDL-C. When LDL-C is increased, it is usually not due to NIDDM but to disorders or factors that commonly increase LDL-C in the adult non-diabetic population. Glycosylation of apoproteins and increased susceptibility of lipoproteins to oxidation probably also contribute to the increased risk of macrovascular disease. Treatment involves diet, exercise, weight loss, improved glycaemic control, elimination of secondary causes of dyslipidaemia and, when necessary, pharmocological lipid-lowering drugs. The response to diet may be variable. In some patients, the plasma triglyceride level may paradoxically increase in response to the NCEP diets which contain 55 - 60 per cent of calories from CHO and 45 per cent of calories from fat (saturated and polyunsaturated fat should each represent 10 per cent of calories and mono-unsaturated fat should represent 25 per cent of calories). Gemfibrozil and reductase inhibitors are the only drugs which can be consistently and safely utilized in NIDDM. Bile acid-binding resins may aggravate hypertriglyceridaemia and cause a paradoxical increase in serum total cholesterol level. Niacin is relatively contraindicated in NIDDM because it produces insulin resistance, intensifies hyperglycaemia and increases the requirement for oral sulfonylurea agents and/or insulin. Use of increased doses of an oral sulfonylurea agent may predispose to niacin-induced hepatotoxicity. Whether hyperinsulinaemia and the use of larger doses to control hyperglycaemia contribute to the risk of macrovascular disease is unresolved at this time (AU)

Diabetic nephropathy is not preventable - abstract

Renal failure in diabeties mellitus is becoming the commonest cause of end-stage renal disease (ERSD) in developed and developing countries. While ERSD occurs in about 35 percent of patients with insulin-dependent diabetes mellitus (IDDM), it occurs generally in about 15-60 percent with non-insulin-dependent diabetes mellitus (NIDDM), depending on ethnicity. Since most of the diabetes are NIDDM, it follows that most of these patients developing renal failure and requiring dialysis are NIDDM. When significant proteinuria begins, usually after about 15-20 years of NIDDM or IDDM, renal function will fall steadily and the patient will require dialysis in 3-5 years or sooner. The proteinuric patients also have a 20-40-fold increase in cardiovascular mortality. About one-quarter of the patients who have negative routine urinary protein dipstick tests will have sub-clinical amounts of urinary albumin (30-300 mg/24 hr), so-called microalbuminuria (MA). This has recently been correlated with a very high incidence of microvascular disease. This MA predicts about a 20-fold chance of the patient developing clinical proteinuria and a high chance of ERSD. The accumulated evidence suggests that a common pathogenic mechanism may exist for microalbuminuria, diabetic nephropathy, atherosclerosis and obesity. Obesity seems to be related to all of these factors in that it has been associated with insulin resistance, hypertension and so dium retention, atherosclerosis and hyperlipidaemia (HL). NIDDM patients are almost always obese and they always have insulin resistance, which improves with weight loss. There is growing clinical evidence of hereditary influence in NIDDM, HL, and hypertension with the clustering of diabetic nephropathy in these high-risk families. These data show that genetic factors may well play a major role, and it is therefore understandable that we may have difficulty in altering the already genetically charted course of proteinuria, hypertension, HL, and NIDDM (AU)

Aetiology, treatment and prevention of diabetic nephropathy: an overview - abstract

In the studies of the aetiology, treatment and prevention of diabetic nephropathy, several end-points can be used, including death due to renal failure, uraemia, azotaemia, proteinuria, microalbuminuria and changes in glomerular and tubular functions. The two parameters commonly used, though not ideal, are glomerular filtration rate and protein excretion. Several factors contribute to the development and progression of diabetic nephropathy. These include hereditary factors, severity of hyperglycaemia, hypertension and hyperlipidaemia. Siblings of probands free of diabetic nephropathy have less evidence of renal disease than do siblings of probands with diabetic nephropathy. Several studies have also shown that individuals with high glycosylated haemoglobin concentrations (poor glycaemic control) are more likely to develop diabetic nephropathy. It is not clear, however, if this is a direct relationship (e.g. via glycosylation) or indirect (e.g. increased flux through the aldose reductase pathway, or alteration in vascular permeability). It is also unclear whether there is a direct relationship between glucose level and the development of diabetic nephropathy. The route of administration of insulin, e.g. into systemic circulation or into the portal system, may be important in the development of diabetic nephropathy. Specific inhibitors in the metabolic pathways (e.g. aldose reductase inhibitors, glycosylation inhibitors) may slow or prevent the development of diabetic nephropathy. Several studies have shown that increase in albumin excretion rate and decrease in glomerular filtration rate precede the development of hypertension and, once present, contribute to the rate of progression of diabetic nephropathy. Some, on the other hand, feel that hypertension reduces protein excretion, and a few studies have shown that it also preserves renal function and/or prevents azotaemia. It is also not clear at what level blood pressure should be treated, as urinary albumin excretion decreases when normotensive individuals are treated with angiotensin-converting enzyme inhibitors. Reduction of protein consumption in humans (to approximately 0.6 gm protein/kg body weight per day) can slow the rate of decline in glomerular filtration. Also influencing the rate of development of hyperlipidaemia, if necessary, with hypolipidaemic drugs is potentially beneficial in hypertensive diabetic patients. In summary, although definite data are lacking, an attempt should be made to optimize glycaemic control and hypertension should be treated early and vigorously. Hyperlipidaemia which persists in the presence of normoglycaemia should be treated with diet and hypolipidaemic drugs (AU)