Search PubMed⌕ Search

Biomedical subjects

M A Crook

Publications and source records attributed to M A Crook.

At least 55 records · Page 3Linked to original sources
PubMed1999

Review of investigation and management of severe hyponatraemia in a hospital population.

The purpose of this study was to assess retrospectively the prevalence of severe hyponatraemia in a hospital population and its laboratory investigation, treatment and clinical outcome. Over a 6-month period 47 patients (27 women and 20 men) were found to have a plasma sodium concentration of < or = 120 mmol/L (this number made up less than 0.17% of all plasma sodium requests over that time period). The mean patient age was 75 +/- 16 years and the average hospital stay was 37 +/- 45 days (1-179 days). Patient mortality was 51% (women 57% and men 43%). The mean initial plasma sodium concentration was 116 +/- 4.5 mmol/L, rising after therapeutic intervention to a mean of 130 +/- 4.2 mmol/L. The mean plasma sodium correction rate was 4.7 +/- 4.3 mmol/L/24 h (0.9-17.5 range). Twelve per cent of the patients had their plasma sodium raised at a rate of greater than 10 mmol/L/24 h after their initial presentation. Two patients may have had symptoms and signs suggestive of cerebral oedema/cortical dysfunction: in one patient the sodium concentration was raised at a rate of 9.5 mmol/L/24 h and in the other at 12.0 mmol/L/24 h. Sixty-one per cent of the patients had a chest infection, 44% were on diuretics, 28% had congestive cardiac failure, 28% were post-operative (9% orthopaedic procedures), 19% had carcinoma and 9% were on a selective serotonin re-uptake inhibitor. Regarding laboratory investigations, 56% had liver function tests, 41% had thyroid function tests, 36% had plasma osmolality determination, 36% had urinary electrolytes including urinary osmolality and < 2% had tests to exclude hypoadrenalism.

Adolescent↗
PubMed1999

Hypocholesterolaemia in a hospital population.

The purpose of this study was to observe the prevalence of hypocholesterolaemia in a hospital population and also the causes and clinical outcome of this condition. Fifty-seven patients were found with a plasma cholesterol of < or = 3.0 mmol/L, which was less than 0.50% of all plasma cholesterol requests; there were 39 men and 18 women (P < 0.05, Chi-squared test). The mean age was 53.8 [21.3] (range 3-83 years). The mean plasma cholesterol concentration was 2.28 [0.56] mmol/L (1.16-3.0) and the mean triglyceride concentration was 1.58 [1.09] mmol/L (0.49-7.35). There was a significant correlation between plasma cholesterol concentration and plasma albumin (Rs = 0.48, P < 0.01) and between plasma total protein concentration (Rs = 0.49, P < 0.01). However, there was no relationship between the concentrations of plasma cholesterol and triglyceride (Rs = 0.10, P > 0.05). Eighteen per cent of patients with hypocholesterolaemia died during their hospitalization. Thirty-nine per cent of those who had a plasma cholesterol of < or = 2.0 mmol/L died whereas 71% of those who had a plasma cholesterol concentration of < 1.5 mmol/L died. Hypocholesterolaemia was more commonly seen in the intensive care unit and in post-operative patients, those with malignancy, sepsis, acute myocardial infarction, those who had inflammatory bowel disease and diabetics on insulin. Hypocholesterolaemia may be a useful predictor of mortality in hospital patients.

Adolescent↗
PubMed1999

Abnormal lipids and the acquired immunodeficiency syndrome: is there a problem and what should we do about it?

Recent research has shown abnormal lipids in acquired immunodeficiency syndrome (AIDS). In human immunodeficiency virus (HIV) infection hypocholesterolaemia, hypertriglyceridaemia and also low high density lipoprotein (HDL)-cholesterol have all been described. In addition, increased dense low density lipoprotein (LDL) particles and also lipoprotein (a) have been observed in some patients. The use of the protease inhibitors has been associated with diabetes mellitus and also features of insulin resistance. This article looks at these lipid abnormalities in detail and discusses possible therapeutic options that may be available, in order to address them.

Acquired Immunodeficiency Syndrome↗
PubMed1999

Comparison of therapy with simvastatin 80 mg and atorvastatin 80 mg in patients with familial hypercholesterolaemia.

This study compared the efficacy of simvastatin 80 mg and atorvastatin 80 mg in the treatment of 26 patients with familial hypercholesterolaemia over 12 weeks using an open crossover trial format. Both, similarly, reduced LDL by 47 +/- 13% and 43 +/- 16% and median triglycerides by 22% and 27% respectively. However, atorvastatin reduced HDL by 2 +/- 24% compared with 8 +/- 30% increase with simvastatin (p = 0.05) affecting the LDL:HDL ratio achieved (4.478 +/- 1.56 vs 3.74 +/- 0.93, p = 0.001). Atorvastatin raised median fibrinogen by 15% compared with a non-significant 5% increase with simvastatin (p = 0.05). Simvastatin reduced lipoprotein (a) by a median 20% compared with baseline (p = 0.05) compared with 5% for atorvastatin. Side-effects, mostly gastrointestinal, were seen in four patients (16%) with atorvastatin compared with one case of myalgia with simvastatin (4%). We conclude both drugs are equally effective in LDL reduction but that simvastatin is superior in raising HDL and causes fewer side-effects. These results require confirmation in larger studies.

Adult↗
PubMed1998

Is type II diabetes mellitus a disease of the innate immune system?

Type II (non-insulin-dependent) diabetes mellitus is associated with increased blood concentrations of markers of the acute-phase response, including sialic acid, alpha-1 acid glycoprotein, serum amyloid A, C-reactive protein and cortisol, and the main cytokine mediator of the response, interleukin-6. The dyslipidaemia common in Type II diabetes (hypertriglyceridaemia and low serum levels of HDL cholesterol) is also a feature of natural and experimental acute-phase reactions. We review evidence that a long-term cytokine-mediated acute-phase reaction occurs in Type II diabetes and is part of a wide-ranging innate immune response. Through the action of cytokines on the brain, liver, endothelium, adipose tissue and elsewhere, this process could be a major contributor to the biochemical and clinical features of metabolic syndrome X (glucose intolerance, dyslipidaemia, insulin resistance, hypertension, central obesity, accelerated atherosclerosis) but also provides a mechanism for many other abnormalities seen in Type II diabetes, including those in blood clotting, the reproductive system, metal ion metabolism, psychological behaviour and capillary permeability. In the short-term, the innate immune system restores homeostasis after environmental threats; we suggest that in Type II diabetes and impaired glucose tolerance long-term lifestyle and environmental stimulants, probably in those with an innately hypersensitive acute-phase response, produce disease instead of repair.

Acute-Phase Reaction↗
PubMed1998

High-dose atorvastatin therapy in severe heterozygous familial hypercholesterolaemia.

Lipid targets can be difficult to attain in familial hypercholesterolaemia. To compare atorvastatin with simvastatin-fenofibrate and simvastatin-cholestyramine therapy, we studied 54 patients with familial hypercholesterolaemia over periods of 2-6 months on each therapeutic regimen. The atorvastatin regimen reduced total cholesterol by 41.2 +/- 11.2%, LDL by 45.6 +/- 15.5%, triglycerides by 33.8 +/- 24.8%, and increased HDL by 2.3 +/- 37.0%. Simvastatin-fenofibrate therapy achieved reductions of 33.9 +/- 8.5% in cholesterol, 42.0 +/- 12.2% in LDL, 34.7 +/- 38.3% for triglycerides, and a 25.4 +/- 55.1% increase in HDL. Simvastatin-cholestyramine gave a reduction of 31.3 +/- 11.8% in cholesterol, 36.0 +/- 14.4% in LDL, 13.7 +/- 36.3% in triglycerides, and a 1.1 +/- 30.3% rise in HDL. The atorvastatin regimen was marginally but not significantly better than simvastatin-fenofibrate in improving the LDL:HDL ratio, LDL:apoB and and apolipoprotein B:A1 ratios. Eleven patients (20.4%) had side-effects: two discontinued atorvastatin due to side-effects; two patients had rashes; six had myalgia and two had diarrhoea. Gastrointestinal side-effects were described in 16 (30.1%) patients on simvastatin-cholestyramine therapy and four cases of myalgia (11.2%) were seen with simvastatin-fenofibrate. In nine patients on atorvastatin (20.4%) a 30% or greater fall in HDL was observed, compared to five patients with resin therapy (9.2%) and two with fibrate therapy (5.5%). There were no significant differences in liver or muscle biochemistry between the regimens, but atorvastatin did raise transaminase and creatine kinase concentrations significantly compared to pre-treatment values (p = 0.001). Atorvastatin significantly improves the lipid profile in most patients compared with other regimens. It has a comparable incidence of side-effects to combination therapy regimens.

Adolescent↗
PubMed1997

Fenofibrate plus simvastatin therapy versus simvastatin plus cholestyramine therapy for familial hypercholesterolaemia.

Combination therapy is routinely used to achieve improved cholesterol reduction in familial hypercholesterolaemia. We compared the standard simvastatin plus bile-acid sequestrant (cholestyramine) therapy with simvastatin plus fenofibrate in 29 patients with severe familial hypercholesterolaemia. The fibrate regimen resulted in an 35.1 +/- 10.7% reduction in total cholesterol, a 40.6 +/- 20.5% in LDL cholesterol, 17.2 +/- 56.5% reduction in triglycerides and a 20.3 +/- 52.0% increase in HDL cholesterol. The cholestyramine regimen produced reductions of 29.3 +/- 13.2% in cholesterol, 37.1 +/- 21.9% in LDL cholesterol, and 12.5 +/- 48.9% in triglycerides, and a 5.0 +/- 25.4% rise in HDL cholesterol. The fibrate regimen was significantly more effective in reducing total cholesterol (p < 0.001) and LDL-cholesterol (p = 0.004), and also reduced triglycerides significantly (p = 0.05), compared to the cholestyramine regimen. There were significant improvements in the LDL:HDL cholesterol ratio (3.62 +/- 1.54 vs. 4.00 +/- 1.36; p = 0.05) and in the apolipoprotein B:A1 ratio (1.13 +/- 0.036 vs. 1.20 +/- 0.34; p = 0.05). Gastrointestinal side-effects occurred in 10 patients on cholestyramine therapy, and four patients on fibrate therapy had myalgia. There were no cases of rhabdomyolysis with either regime. No significant differences in liver biochemistry or creatine kinase were seen with either regimen.

Adolescent↗
PubMed1997

Serum sialic acid and its relationship to various haematological parameters, including erythrocyte sedimentation rate.

Serum total sialic acid (TSA) has been reported to be a marker or risk factor for cardiovascular disease. The reason for this is not clear, although it has been suggested that serum TSA is a marker of the acute phase response. We measured serum TSA and various haematological parameters in 40 subjects. Significant correlations of serum TSA with erythrocyte sedimentation rate (ESR) (r = 0.65, P < 0.0001), platelet count (r = 0.65, P < 0.0001) and neutrophil count (r = 0.33, P < 0.05) were found. There was an inverse correlation with haemoglobin concentration (r = -0.62, P < 0.0001) and erythrocyte count (r = -0.42, P < 0.01).

Adolescent↗
PubMed1996

Serum sialic acid and the long-term complications of insulin-dependent diabetes mellitus.

Elevated serum sialic acid (SSA) predicts cardiovascular disease in the non-diabetic population and is also associated with the presence of microalbuminuria and clinical proteinuria in patients with insulin-dependent diabetes (IDDM). We have studied 121 patients with IDDM of long duration (mean duration 25.2 years) to investigate the relationship of SSA concentrations to the presence of retinopathy, nephropathy, and neuropathy. SSA levels were elevated in patients with retinopathy (0.578 +/- 0.161 gl-1, n = 98) when compared with those without retinopathy (0.468 +/- 0.145 gl-1, n = 23, p = 0.002). Patients with nephropathy (urinary albumin:creatinine ratio of > 3 mg mmol-1 in all of three early morning specimens of urine) also had raised SSA levels (0.625 +/- 0.169 gl-1, n = 30) compared with those without nephropathy (0.533 +/- 0.160 gl-1, n = 91, p = 0.006). There was a significant correlation of SSA with urinary albumin:creatinine ratio (correlation coefficient 0.33, p < 0.001). SSA levels were not related to the presence or absence of neuropathy (0.567 +/- 0.181 gl-1, n = 28, vs 0.533 +/- 0.160 gl-1, n = 93, p = 0.92, respectively). In conclusion, retinopathy and nephropathy but not neuropathy are associated with increased SSA levels in patients with IDDM. The significance of this is not yet clear but it is possible that sialic acid is involved in the pathophysiology of microvascular disease in IDDM.

Adult↗
PubMed1996

Plasma fibrinogen and its relationship to plasma sialic acid in non-insulin-dependent diabetes mellitus.

Serum or plasma sialic acid (SA) has been shown to be a possible risk factor for cardiovascular disease and to be elevated in diabetes mellitus. We postulated that plasma SA may be related to plasma fibrinogen, another reputed cardiovascular risk factor. We decided to test this hypothesis in 27 patients with non-insulin-dependent diabetes mellitus (NIDDM) and 27 age- and sex-matched control subjects. Plasma fibrinogen was significantly elevated in the diabetic patients compared with the control subjects (3.4 +/- 1.5 g/l versus 2.2 +/- 0.6 g/l, P < 0.001). Similarly, plasma SA was elevated in the diabetic patients in comparison with the control subjects (0.74 +/- 0.14 g/l versus 0.62 +/- 0.08 g/l, P < 0.001). There was a strong univariate correlation between plasma fibrinogen and plasma SA in both NIDDM patients (r = 0.80, P < 0.001) and control subjects (r = 0.54, P < 0.01).

Aged↗
PubMed1996

Serum sialic acid in patients with multiple myeloma.

Serum sialic acid (SA) has been reported recently to be elevated in a number of malignant conditions. To test the hypothesis that serum SA may be elevated in patients with multiple myeloma we looked at 34 myeloma patients (17 females and 17 males) and 22 controls (11 females and 11 males). The mean age of the myeloma patients was 61.2 +/- 10.9 years versus 58.9 +/- 12.6 years for the control group. There was a highly significant difference between the serum SA in the myeloma patients compared to the control group; 103.5 +/- 32.8 mg/dL versus 78.9 +/- 10.2 mg/dL respectively (P < 0.001). There was a significant correlation between serum SA and serum total protein and globulin concentration in the IgA myeloma patients, and a significant correlation between serum paraprotein quantity and globulin concentration in the IgM patients.

Adult↗
PubMed1995

Serum sialic acid as an indicator of change in coronary artery disease.

We measured serum levels of total sialic acid (TSA) by an enzymatic method in 74 men who completed the St Thomas' Atherosclerosis Regression Study (STARS). Coronary artery disease (CAD) was assessed as the change (delta) in mean absolute width of coronary segments (MAWS) over 3 years by a computerized technique. Delta TSA was significantly correlated with delta MAWS (r = -.50, P < .001) after adjusting for age, blood pressure, smoking status, and plasma low-density lipoprotein (LDL) cholesterol. The relative risk of progression of CAD for a delta TSA exceeding 10 mg/dL as compared with a delta TSA not exceeding 10 mg/dL was 4.6 (95% confidence interval, 2.4 to 8.7). We conclude that serial measurement of serum TSA levels may be a useful indicator of the progression of CAD.

Age Factors↗