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Biomedical subjects

M A Crook

Publications and source records attributed to M A Crook.

At least 37 records · Page 2Linked to original sources
PubMed2000

No difference in serum sialic acid in type 2 diabetic patients from the United Arab Emirates with and without diabetic retinopathy.

Serum total sialic acid (TSA) has recently been shown to be related to diabetic retinopathy. However, there is some controversy as this may be true in European Type 2 diabetic patients but not South Asians. There are few data looking at serum TSA expression in Arab Type 2 diabetic patients from the United Arab Emirates (UAE) and we wished to test the hypothesis that there may be different serum TSA expression in Arab Type 2 diabetic patients as regard to retinopathy. Sixty-five Type 2 diabetic patients from the UAE were studied (19 male and 46 female, age 57.5+/-9.8 (45-74) years, duration of diabetes 9.4+/-5.7 (0-22) years. The serum TSA in 13 patients with diabetic retinopathy was 757+/-130 mg/l and 782+/-163 mg/l in those without retinopathy (NS). There was no significant correlation between serum TSA and patient age, serum fructosamine, diabetes duration, or blood pressure. As in South Asians serum TSA does not appear to be elevated in Type 2 diabetic patients from the United Arab Emirates with diabetic retinopathy.

Aged↗
PubMed2000

Lipid clearance and total parenteral nutrition: the importance of monitoring plasma lipids.

Lipid provides two major advantages for total parenteral nutrition (TPN). First, it provides essential fatty acids, thus avoiding essential fatty acid deficiency, and secondly, it is a useful energy source, providing 9 kcal/g. However, we describe a patient who had TPN containing Intralipid, where problems of lipid clearance developed. We also review the literature of lipid clearance problems in TPN patients and suggest ways by which such problems can be managed. We suggest that patients taking TPN should have their plasma lipids (triacylglycerols) measured before and during TPN initiation. This is particularly important in patients who are at high risk of impaired fat clearance, such as those who are hyperlipidemic, diabetic, septic, or with impaired renal or hepatic function, or those who are critically ill.

Aged↗
PubMed2000

Circulating concentrations of C-reactive protein and total sialic acid in tobacco smokers remain unchanged following one year of validated smoking cessation.

BACKGROUND: Elevated plasma concentrations of C-reactive protein (CRP) and total sialic acid (TSA) have been associated with increased cardiovascular risk. Additionally, levels of both CRP and TSA have been reported to be significantly elevated in smokers. However, it is not clear if the raised TSA and CRP levels noted in smokers are directly attributable to the smoking experience, or if they may be elevated due to a secondary mechanism(s), such as smoking-induced tissue inflammation. SUBJECTS AND METHODS: We measured the plasma concentration of CRP and TSA in a group of smokers at baseline and following one year of validated smoking cessation (n = 30) and in a control group of tobacco users who continued to smoke over the year (n = 30). RESULTS: The baseline concentration of TSA and CRP was 67.2 mg dL(-1) and 1.91 mg L(-1), respectively (n = 60). No significant dose-dependent relationship was noted between baseline CRP or TSA concentration and either plasma cotinine, expired-air CO or daily cigarette consumption. There was no difference in the mean change in CRP level in the quitters over one year (- 0.2 mg L(-1)) compared to the continuing smokers (+ 0.5 mg L(-1)), P = 0.80, or in the change in concentration of TSA in the quitters (- 2.7 mg dL(-1)) compared to the continuing smokers (+ 0.4 mg dL(-1)), P = 0.26. CONCLUSIONS: As the circulating concentrations of both CRP and TSA remain unchanged following one year of smoking cessation, these results would suggest that the elevated levels noted in smokers are not directly attributable to tobacco use and are more likely to be elevated due to a secondary process that is yet to be established.

Adult↗
PubMed2000

A paradoxical severe decrease in serum HDL-cholesterol after treatment with a fibrate.

There have been a handful of reports in the literature of a paradoxical decrease in serum high density lipoprotein (HDL)-cholesterol in patients on fibrate drugs. The reason for this decline in cardioprotective HDL-cholesterol is not known and may have potential deleterious effects on the patient. This report describes a decrease in serum HDL-cholesterol in a patient on both simvastatin and bezafibrate. This patient also developed abnormal renal function, probably interstitial nephritis. In addition, the literature of fibrate induced serum HDL-cholesterol decline is reviewed and possible mechanisms for this phenomenon discussed.

Bezafibrate↗
PubMed2000

Skin tags and the atherogenic lipid profile.

This report details four patients who had skin tags, mainly on their torso, neck, and axillae, and who also displayed an abnormal lipid profile. All showed an increased serum triglyceride (fasting > 1.70 mmol/litre) and a decreased high density lipoprotein (HDL) cholesterol (< 1.1 mmol/litre in women and 1.0 mmol/litre for men) concentration. The displayed lipid profile is also known as the atherogenic profile and is associated with insulin resistance, type 2 diabetes mellitus, and an increased risk of cardiovascular disease. Two of the patients had impaired glucose tolerance and one had type 2 diabetes mellitus. Three of the individuals had coronary artery disease. Skin tags might be a useful clinical sign that could alert clinicians to screen such individuals for abnormal lipids, type 2 diabetes mellitus, and cardiovascular disease.

Adult↗
PubMed2000

Renin-angiotensin system polymorphisms and coronary events in familial hypercholesterolemia.

The role of renin-angiotensin system polymorphisms as risk factors for coronary heart disease (CHD) is controversial. This study investigated their role in patients with heterozygous familial hypercholesterolemia (FH). Polymorphism frequencies for angiotensin-I-converting enzyme insertion/deletion (ACE I/D), angiotensinogen M235T, and angiotensin-II type I receptor (AG2R) A1166C were determined in 112 patients with FH and 72 patients with polygenic hypercholesterolemia, of whom 26.7% and 41.6%, respectively, had established CHD. None of the polymorphisms were associated with risk of CHD in patients with polygenic hypercholesterolemia in this study. Logistic regression analysis of risk factors for CHD in patients with FH identified male sex (odds ratio [OR]=3.03; 95% CI, 3.07 to 3.72; P=0.05), smoking (OR=2.91; 95% CI, 2.16 to 4.24; P=0.05), diastolic blood pressure (OR=3.70; 95% CI, 3.43 to 3.97; P=0.02), plasma glucose (OR=3.31; 95% CI, 3. 10 to 3.52; P=0.04), and the AG2R A1166C polymorphism as risk factors. The OR for the AG2R A1166C polymorphism was 2.26 (95% CI, 1.26 to 3.72; P=0.06) and increased to 3.10 (95% CI, 1.20 to 7.52; P=0.04) after adjustment for other risk factors. The AG2R A1166C polymorphism may interact with severe hypercholesterolemia and other risk factors to increase risk of CHD in FH patients.

Adult↗
PubMed2000

A comparison of algorithms for initiation of lipid lowering therapy in primary prevention of coronary heart disease.

OBJECTIVE: To compare nine different algorithms for determining the necessity for drug treatment of hyperlipidaemia in patients without cardiovascular disease. DESIGN: Risk-factor data on 400 patients were obtained. Algorithms assessed included the Framingham model, National Cholesterol Education Program, European, British, New Zealand, British Regional Heart Study, Sheffield, Munster Heart Study and Dundee guidelines and a local general rule for treatment of atheroma (General Rule to Enable Atheroma Treatment). SETTING: Three hospital lipid clinics. RESULTS: Patients were 56% male, aged 53.8 +/- 12.3 years, 38% smoked, 55% had a family history of disease (37% familial hypercholesterolaemia, 33% hypertension and 5.2% left ventricular hypertrophy); 31% were moderately obese and 15% were diabetic. The average cholesterol level was 7.9 +/- 2.6 mmol/l. Median Framingham risk was 1.66%/year and this risk was > 2%/year for 37% and > 3%/year for 17.5%. Treatment was required for 86% by National Cholesterol Education Program, 70% by General Rule to Enable Atheroma Treatment and European, 61% by New Zealand, 58% by British, 42% by Dundee, 40% by Munster Heart Study, 25% by British Regional Heart Study and 16% by Sheffield guidelines. Algorithms varied regarding recommendations for treatment of men, women, patients with familial hypercholesterolaemia and diabetes. Confounders included risk levels, definitions and weightings for additional risk factors. CONCLUSIONS: Different algorithms vary widely in their predictions of need for drug treatment of this high-risk population with hyperlipidaemia. Authors of guidelines for cardiovascular disease need to unify risk thresholds and definitions and audit the effects of additional weighting factors so that patients can be treated consistently.

Adult↗
PubMed2000

Differing relationships of methylene tetrahydrofolate reductase genotypes with cardiovascular risk in familial and polygenic hypercholesterolaemia.

BACKGROUND: Plasma homocysteine and the methylene tetrahydrofolate reductase C677T polymorphism have been suggested as being risk factors for cardiovascular disease. OBJECTIVE: To determine whether plasma homocysteine and the methylene tetrahydrofolate reductase C677T polymorphism are risk factors for coronary heart disease in patients with heterozygous familial hypercholesterolaemia as compared with those with polygenic hyperlipidaemia. METHODS: Plasma homocysteine and the methylene tetrahydrofolate reductase polymorphism were assessed with other risk factors in 112 patients with familial hypercholesterolaemia and 72 patients with polygenic hyperlipidaemia, of whom 29 (25.8%) and 30 (41%) respectively had established cardiovascular disease and in 100 healthy normal subjects. RESULTS: Plasma homocysteine was not significantly elevated in patients with and without coronary heart disease with familial hypercholesterolaemia or polygenic hyperlipidaemia compared with controls. The allele frequencies for C677T were significantly different in patients with coronary heart disease and with polygenic hyperlipidaemia (0.35 versus 0.29) (P = 0.02) as opposed to those with coronary heart disease and familial hypercholesterolaemia (0.25 versus 0.30) (P = 0.63). Methylene tetrahydrofolate reductase genotype but not homocysteine had a weak association with coronary heart disease in logistic regression analysis in patients with polygenic hyperlipidaemia (P = 0.05) but neither methylene tetrahydrofolate reductase genotype or plasma homocysteine was a risk factor in patients with familial hypercholesterolaemia. CONCLUSION: Whilst methylene tetrahydrofolate reductase genotype may be a weak risk factor for coronary heart disease in polygenic hyperlipidaemia as opposed to familial hypercholesterolaemia, homocysteine does not seem to be an important risk factor for coronary heart disease in patients in southern UK.

Adult↗
PubMed1999

Plasma sialic acid and coronary artery atheromatous load in patients with stable chest pain.

Serum or plasma sialic acid and C-reactive protein have recently been shown to be cardiovascular risk factors. Our aim was to determine whether plasma sialic acid or C-reactive protein concentration correlate with atheromatous load on coronary angiography. Plasma sialic acid concentration and plasma C-reactive protein concentration were determined in 128 consecutive patients attending day case coronary angiography. Patients were excluded for previous coronary angioplasty, coronary artery bypass grafting, recent myocardial infarction, acute or chronic inflammatory disease and proximal occlusions precluding analysis of distal coronary anatomy. Total cholesterol, triglyceride, HDL cholesterol and glucose concentrations were assayed on fasting samples of venous blood. Angiograms were graded according to a semisubjective scoring system. There was no significant correlation between plasma sialic acid (r = 0.19, P = 0.07), or C-reactive protein concentration (r = 0.17, P = 0.13) and atheromatous load. There was no significant correlation between sialic acid (P = 0.13), or C-reactive protein concentration (P = 0.32) and the number of diseased coronary vessels. The difference in plasma sialic acid concentration between those with normal coronary angiograms and those with coronary artery disease did not reach significance (P = 0.08). Plasma sialic acid concentration correlated with C-reactive protein (r = 0.58, P = 0.0001), serum triglyceride (r = 0.32, P = 0.002), and blood cholesterol concentration (r = 0.22, P = 0.04). Plasma sialic acid concentration does not correlate with atheromatous load on coronary angiography in patients with stable angina.

Adult↗
PubMed1999

Growth hormone (GH) replacement therapy reduces serum sialic acid concentrations in adults with GH-deficiency: a double-blind placebo-controlled study.

OBJECTIVES: Patients with adult GH-deficiency are thought to have an increased risk of cardiovascular disease. Sialic acid (SA) concentrations have been proposed as a marker of atherosclerotic disease probably related to an inflammatory response of the arterial wall. SA as a marker of cardiovascular disease in adult GH-deficiency and its relation to changes in fasting lipid profile and hormone concentrations have not yet been investigated. PATIENTS: We performed a randomised, double-blind placebo-controlled study in 18 patients with adult GH-deficiency before and after 3 months GH replacement therapy (0.036 U/kg/d; GH-treated group: 6 females, 3 males; age: 47.3 +/- 5.4 years., mean +/- SEM; placebo-group: 5 females, 4 males; mean age 50.2 +/- 4.7). In addition, SA concentrations were measured in 18 sex and age matched healthy control subjects. METHODS: Blood samples were obtained after an overnight fast. Serum SA, triglycerides and cholesterol were measured using enzymatic methods. Lipoprotein classes were separated by ultracentrifugation. Insulin and IGF-I were determined by radioimmunoassay, HbA1C was measured by anion exchange liquid chromatography. RESULTS: SA concentrations of the patients with adult GH-deficiency were not significantly different compared to the control group (GH-deficient group: 2.29 +/- 0.02 mmol/l, mean +/- SEM vs. control group: 2.09 +/- 0.13 mmol/l, P = 0.25). Before GH replacement therapy SA concentrations correlated positively with the patients age (r = 0.45; P < 0.04) and fasting insulin concentrations (r = 0.5; P < 0.03) but not with fasting lipid profile. GH replacement therapy significantly increased IGF-I (GH: + 27 +/- 2.6 vs. placebo: + 1.0 +/- 0.8 nmol/l, P < 0.001) and fasting insulin concentrations (GH: + 71.9 +/- 8.0 vs. placebo: + 19.6 +/- 22.6 pmol/l, P < 0.04) compared to placebo therapy. SA concentrations (GH: - 0.41 +/- 0.15 vs. placebo: - 0.01 +/- 0.12 mmol/l, P < 0.05), total cholesterol (GH: - 0.71 +/- 0.16 vs. placebo: 0.23 +/- 0.21 mmol/l, P < 0.003) and LDL-cholesterol (- 0.71 +/- 0.14 vs. placebo: - 0.12 +/- 0.21 mmol/l P < 0.04) significantly decreased after GH replacement therapy compared to placebo therapy. No significant correlation between changes in SA concentrations and changes in lipid profile were observed following GH replacement therapy. CONCLUSION: These results suggest that, firstly, GH replacement therapy may have a beneficial effect on the pathogenesis of atherosclerosis despite the increase in insulin concentrations, a surrogate marker of insulin resistance, secondly, the proposed beneficial effect of GH on the atherosclerotic process is likely to be multifactorial and cannot only be explained by changes in lipid profile and finally, SA might be a useful marker for the process of atherosclerotic disease in interventional studies.

Adult↗
PubMed1999

Atorvastatin compared with simvastatin-based therapies in the management of severe familial hyperlipidaemias.

We compared atorvastatin with simvastatin-based therapies in a prospective observational study of 201 patients with severe hyperlipidaemia. Atorvastatin 10 mg therapy was substituted for simvastatin 20 mg, 20 mg for 40 mg, 40 mg for simvastatin 40 mg plus resin, and 80 mg for simvastatin-fibrate-resin therapy. Lipid and safety profiles were assessed. Atorvastatin reduced total cholesterol by 31 +/- 11-40 +/- 14% vs. 25 +/- 12-31 +/- 11%; LDL by 38 +/- 16-45 +/- 18% vs. 31 +/- 18-39 +/- 18% and geometric mean triglycerides by 29.3-37.3% vs. 16.6-24.8%, but reduced HDL 11% +/- 47% at 80 mg compared with a 16% +/- 34% increase with simvastatin-based therapy. Target LDL < 3.5 mmol/l was achieved more often with atorvastatin (63% vs. 50%; p < 0.001). Atorvastatin increased geometric mean fibrinogen by 12-20% vs. a 0-6% fall with simvastatin (p << 0.001). Side effects were noted in 10-36% of patients, including one case of rhabdomyolysis, and 36% discontinued therapy. These data suggest that atorvastatin is more effective than current simvastatin-based therapies in achieving treatment targets in patients with familial hypercholesterolaemia but at the expense of a possible increase in side-effects. This issue needs further study in randomized controlled trials.

Anticholesteremic Agents↗
PubMed1999

Serum apolipoprotein H and its relationship to lipids and other apolipoproteins in normal human men and women.

Apolipoprotein H (apo H), also known as beta-2-glycoprotein I, has recently become of considerable interest in the field of haemostasis. Because of the possible involvement of apo H in lipid pathways, we wished to test the hypothesis that the serum concentration of apo H was related to serum lipids and other apolipoproteins in normal individuals. One hundred and twenty-three healthy young subjects (67 women and 56 men) aged 22.7 +/- 0.70 years (mean +/- SD) were recruited. Serum level of apo H was higher in male subjects that in age-matched female subjects (167.6 +/- 47.5 mg/l versus 148.8 +/- 30.5 mg/l; P < 0.04). Serum levels of apo H were significantly correlated with serum concentration of cholesterol, but only in female subjects (r = 0.28, P < 0.02). No significant correlations were found between serum levels of apo H and triglycerides, high-density lipoprotein cholesterol, apo A1, apo B or lipoprotein (a) in either of the sexes.

Adult↗