PubMed Health⌕ Search

Biomedical subjects

M Seed

Publications and source records attributed to M Seed.

At least 19 recordsLinked to original sources
PubMed2006

Genetic causes of familial hypercholesterolaemia in patients in the UK: relation to plasma lipid levels and coronary heart disease risk.

AIMS: To determine the relative frequency of mutations in three different genes (low-density lipoprotein receptor (LDLR), APOB, PCSK9), and to examine their effect in development of coronary heart disease (CHD) in patients with clinically defined definite familial hypercholesterolaemia in UK. PATIENTS AND METHODS: 409 patients with familial hypercholesterolaemia patients (158 with CHD) were studied. The LDLR was partially screened by single-strand conformational polymorphism (SSCP) (exons 3, 4, 6-10 and 14) and by using a commercial kit for gross deletions or rearrangements. APOB (p.R3500Q) and PCSK9 (p.D374Y) were detected by specific assays. Coding exons of PCSK9 were screened by SSCP. RESULTS: Mutations were detected in 253 (61.9%) PATIENTS: 236 (57.7%) carried LDLR, 10 (2.4%) carried APOB p.Q3500 and 7 (1.7%) PCSK9 p.Y374. No additional mutations were identified in PCSK9. After adjusting for age, sex, smoking and systolic blood pressure, compared to those with no detectable mutation, the odds ratio of having CHD in those with an LDLR mutation was 1.84 (95% CI 1.10 to 3.06), for APOB 3.40 (0.71 to 16.36), and for PCSK9 19.96 (1.88 to 211.5; p = 0.001 overall). The high risk in patients carrying LDLR and PCSK9 p.Y374 was partly explained by their higher pretreatment cholesterol levels (LDLR, PCSK9 and no mutation, 10.29 (1.85), 13.12 and 9.85 (1.90) mmol/l, respectively, p = 0.001). The post-statin treatment lipid profile in PCSK9 p.Y374 carriers was worse than in patients with no identified mutation (LDL-C, 6.77 (1.82) mmol/l v 4.19 (1.26) mmol/l, p = 0.001, HDL-C 1.09 (0.27) mmol/l v 1.36 (0.36) mmol/l, p = 0.03). CONCLUSIONS: The higher CHD risk in patients carrying PCSK9 p.Y347 or a detected LDLR mutation supports the usefulness of DNA testing in the diagnosis and management of patients with familial hypercholesterolaemia. Mutations in PCSK9 appear uncommon in patients with familial hypercholesterolaemia in UK.

Adult↗
PubMed2004

Comparison of the effects of dietary plant sterol and stanol esters on lipid metabolism.

BACKGROUND AND AIM: To compare the cholesterol-lowering efficacy and other metabolic effects of plant sterol and stanol esters, both of which are commonly used in the dietary management of hypercholesterolaemia. METHODS AND RESULTS: The cholesterol-lowering efficacy of equivalent intakes of sterol and stanol esters and of different intakes of stanol esters were compared at 1 and 2 months, both in normal subjects and treated patients with familial hypercholesterolaemia. Systemic effects were assessed by measuring serum levels of plant sterols and of lathosterol and 7alpha-hydroxy-cholestenone, indices of sterol absorption and of cholesterol and bile acid synthesis respectively. There were no significant differences during the study between 1.6g daily of sterol and stanol esters in reducing total cholesterol (by 3-7%) or low density lipoprotein cholesterol (by 4-8%), nor between 1.6 and 2.6 g daily of stanol. However, the cholesterol-lowering effect of plant sterol esters was attenuated between 1 and 2 months. This was accompanied by increased serum plant sterols and decreased levels of 7alpha-hydroxy-cholestenone, especially in statin-treated hypercholesterolaemic patients not taking bile acid sequestrants. CONCLUSIONS: These findings suggest that absorption of dietary plant sterols suppressed bile acid synthesis, thereby diminishing their cholesterol-lowering efficacy. In contrast, plant stanols reduced plant sterol absorption and maintained their cholesterol-lowering efficacy.

Adult↗
PubMed2004

Established and emerging coronary risk factors in patients with heterozygous familial hypercholesterolaemia.

OBJECTIVES: To assess the clinical and biochemical factors associated with inter-individual variation in susceptibility to coronary artery disease (CAD) in treated heterozygous familial hypercholesterolaemia. DESIGN: A cross sectional study was conducted of 410 patients recruited from six lipid clinics in the UK. RESULTS: CAD was documented in 104 of the 211 men and in 55 of the 199 women with mean ages of onset of 43.1 and 46.5 years, respectively. CAD was significantly more common in men (49% v 28%, p < 0.001) and in patients who had smoked cigarettes versus patients who had never smoked (51% v 28%, p < 0.001). After adjusting for age, sex, and current smoking status, there were no significant differences between patients with or without CAD in lipoprotein(a), homocysteine, fibrinogen, plasminogen activator inhibitor-1, white blood cell count, body mass index, glucose, triglyceride or total cholesterol. However, high density lipoprotein (HDL) cholesterol concentrations were significantly lower in those with CAD (6%, 95% confidence interval (CI) 1% to 11%, p = 0.03) and this difference was greater in women than men (12% v 2%, p = 0.041). CONCLUSIONS: These results indicate that emerging coronary risk factors appear not to be associated with CAD in adults with treated familial hypercholesterolaemia, but the strong association with smoking suggests that patients should be identified early in childhood and discouraged from ever starting to smoke.

Adult↗
PubMed2001

Lipoprotein (a) as a predictor of myocardial infarction in middle-aged men.

PURPOSE: Whether serum lipoprotein (a) [Lp(a)] levels are an independent risk factor for coronary heart disease has been controversial. We have investigated its status in a prospective population survey, the Second Northwick Park Heart Study. METHODS: We recruited 2,616 men 50 to 61 years old from nine primary care practices in the United Kingdom. Baseline serum Lp(a) levels were measured by enzyme-linked immunosorbent assay (ELISA) and were analyzed in 3 groups (<25th percentile, 25th to 75th percentile, and >75th percentile) to overcome the problem of some measurements falling below the threshold of the assay. Coronary end points included sudden cardiac death, acute myocardial infarction, silent myocardial infarction on the electrocardiogram, and coronary artery bypass surgery. RESULTS: During a mean of 6 years of follow-up, 121 men had coronary events. In a multivariate analysis that also adjusted for fibrinogen, Apo-A1, Apo-B, and triglyceride levels, we identified several independent risk factors for coronary events, including cholesterol level (hazard ratio [HR] = 1.5 per SD 95% confidence interval [CI] 1.3 to 1.8), diabetes (HR = 4.1, 95% CI: 2. 0 to 8.4), current versus never smoking (HR = 2.5, 95% CI: 1.5 to 4.1), diastolic blood pressure (HR = 1.4 per SD, 95% CI: 1.1 to 1.7), Apo-A1 (HR = 0.8 per SD, 95% CI: 0.6 to 0.9), age (HR = 1.3 per SD, 95% CI: 1.1 to 1.6), and Lp(a) (>26.3 mg/dL [75th percentile] versus <2.9 mg/dL [25th percentile], HR = 1.9, 95% CI: 1.1 to 3.3]. There was a statistically significant (P = 0.01) difference in risk between the three levels of Lp(a). CONCLUSIONS: We found that a high Lp(a) level was an independent predictor of the development of coronary heart disease in middle-aged men.

Apolipoprotein A-I↗
PubMed2001

Glycaemic control and plasma lipoproteins in menopausal women with Type 2 diabetes treated with oral and transdermal combined hormone replacement therapy.

AIMS: To compare the effect of a fixed combination of an oestrogen (17-beta oestradiol) with a cyclical progestagen (norethisterone) on glycaemic control, plasma lipoproteins and haemostatic factors in women with Type 2 diabetes. METHODS: Oral and transdermal hormone replacement therapy (HRT) were compared to no HRT treatment in 33 postmenopausal women with Type 2 diabetes, in a 12-week randomised prospective open parallel group study. RESULTS: In the 11 women who received 12 weeks of oral HRT, there was a significant fall in total cholesterol (5.9+/-1.0 (S.D.) to 4.7+/-1.0 mmol l(-1), P=0.005), low density lipoprotein cholesterol (3.44+/-0.89 to 2.77+/-0.92 mmol l(-1), P=0.005) and triglyceride values (median (range)), (2.46 (0.96-5.52) to 2.29 (1.00-3.87) mmol l(-1), P<0.05). Oral HRT improved glycated haemoglobin (HbA(1c)) (7.4+/-1.4 to 6.8+/-1.2%, P< or =0.005). Oral HRT additionally reduced the cell adhesion factor E-selectin (82+/-33 to 60+/-20 microg l(-1), P<0.01) and factor VII (143+/-25 to 109+/-24% pooled plasma activity, P<0.01). No improvement in any of these parameters, except E-selectin (65+/-19 to 58+/-18 microg l(-1), P<0.01), occurred in the nine women receiving transdermal HRT, and no improvement occurred in the 13 controls randomised to no treatment. CONCLUSION: In women with Type 2 diabetes, cyclical oestrogen and progestagen taken orally for 12 weeks significantly improved glycaemic control and lipoprotein concentrations. These metabolic benefits were not apparent when a similar HRT preparation was administered transdermally.

Administration, Cutaneous↗
PubMed2000

The effect of hormone replacement therapy and route of administration on selected cardiovascular risk factors in post-menopausal women.

BACKGROUND: There is increasing use of hormone replacement therapy (HRT) by post-menopausal women. Observational epidemiological studies have shown reductions in cardiovascular risk factors in HRT users in the USA, but no randomized controlled trials of HRT have been carried out in the primary practice setting. Previous studies of cardiovascular risk factors have shown a variety of responses according to type of progestagen and oral or topical administration. None has examined the effect of route using an identical progestagen. OBJECTIVES: Our aim was to establish differences, if any, in alteration in cardiovascular risk factors with HRT in post-menopausal women according to route of administration of HRT, oral, transdermal and implant, using first oestrogen alone then oestrogen plus norethisterone, or testosterone for implant. METHODS: Subjects were recruited by letter of invitation to women aged 50-65 years from lists in general practices local to the Charing Cross Hospital Lipid Clinic in West London. Their menopausal status was confirmed and they were randomized to one of three treatment groups or acted as controls. They attended for three visits; at baseline, HRT was initiated as oestrogen alone, oral or transdermal. At the 3-month visit, HRT with the progestagen, norethisterone, was given cyclically, continuously or transdermally until the final visit at 6 months. A separate group of women from the menopause clinic at Chelsea and Westminster Hospital were studied on oestrogen implant then on implanted oestrogen and testosterone. The outcome measures studied were the separate effects of the four regimes as compared with controls on lipoproteins, glucose, insulin, fibrinogen, factor VII and E-selectin, together with weight, waist:hip ratio and blood pressure. RESULTS: The continuous combined oestrogen-progestagen therapy had similar effects on cardiovascular risk factors as oestrogen with cyclical progestagen. All regimes lowered low-density lipoprotein cholesterol, the oral route being more potent than the parenteral; the effect of transdermal HRT was similar to the implant. Lp(a) was reduced only with the oral route. Reductions in factor VII and E-selectin were observed in both the oral and transdermal routes. There was no increase in body mass index, waist:hip ratio, blood pressure or glucose and insulin levels with any of the HRT regimes used. Systolic blood pressure was reduced with the transdermal route. CONCLUSIONS: This study supports the evidence that oestrogen-progestagen HRT, both oral and transdermal, although attenuating some of the benefit of oestrogen alone on fibrinogen and high-density lipoprotein, significantly reduces cardiovascular risk factors, which should diminish post-menopausal risk of coronary disease.

Cardiovascular Diseases↗
PubMed1999

The type of mutation in the low density lipoprotein receptor gene influences the cholesterol-lowering response of the HMG-CoA reductase inhibitor simvastatin in patients with heterozygous familial hypercholesterolaemia.

In a genetically heterogeneous group of 109 patients with a clinical diagnosis of heterozygous familial hypercholesterolaemia (FH), the influence of gender, apolipoprotein (apo) E genotype and the type of molecular defect in the LDL-receptor (LDLR) gene on the reduction of plasma LDL-cholesterol levels to treatment with a HMG-CoA reductase inhibitor (simvastatin) were studied. Response was determined as the percentage fall in LDL-cholesterol from untreated levels and as the proportion of patients where levels fell below 4.9 or 4.1 mmol/l. Of the patients, 86 individuals had tendon xanthomata (TX+) and a diagnosis of 'definite' FH and these individuals presented with a significantly higher untreated LDL-cholesterol compared to the 23 individuals who did not have xanthomas (TX-) and a diagnosis of 'probable' FH (8.14+/-0.19 vs. 6.81+/-0.25, P= 0.001). Overall, HMG-CoA reductase inhibitor doses of 10, 20 or 40 mg/day resulted in a significant fall of LDL-cholesterol levels of 29, 39 and 49%, but at all doses those with TX had significantly higher levels than those without, and significantly fewer TX + patients achieved LDL-cholesterol levels below 4.9 or 4.1 mmol/l than the TX - group (P < 0.05 at each dose). In the TX+ group the response to treatment was of similar magnitude in men and women and in patients with different apoE genotype. In the 'probable' FH probands only three mutations were identified (detection rate 13%), one in the LDLR gene and two in the APOB gene, a detection rate significantly lower (P= 0.02) than in the 'definite' FH probands where 28 mutations were detected (detection rate 37%). In the TX + patients where no mutation was detected, treatment resulted in a greater proportion achieving LDL-cholesterol levels below 4.9 and 4.1 mmol/l compared to those with any LDLR mutation, this difference was close to statistical significance at the 4.9 mmol/l threshold at 10 mg/day (41 vs. 13%, P = 0.058). For the 14 patients with an LDLR mutation that was predicted to be 'severe', fewer achieved LDL-cholesterol levels below 4.9 or 4.1 mmol/l at each dosage compared to the 16 individuals with 'mild' mutations, and this difference was statistically significant at the maximal dosage of 40 mg/day (P = 0.018). Thus although characterisation of the molecular defect in FH patients may not be relevant to their immediate clinical management, those with a particular mutation may need more aggressive lipid-lowering treatment to reach LDL-cholesterol levels recommended to reduce the risk of coronary heart disease (CHD).

Adult↗
PubMed1999

Double-masked comparison of the quality of life of hypercholesterolemic men treated with simvastatin or pravastatin. International Quality of Life Multicenter Group.

The efficacy, safety, and impact on quality of life of once-daily treatment with simvastatin 20 mg and pravastatin 40 mg were compared in a multinational, randomized, double-masked trial involving 387 men 21 to 72 years of age with primary mild-to-moderate hypercholesterolemia. The trial consisted of a 12-week baseline period, which included 6 weeks of single-masked placebo administration, and a 12-week double-masked active treatment period. Throughout the trial, patients were maintained on a standard lipid-lowering diet. Efficacy variables were plasma lipid levels and a measurement of health-related quality of life evaluated by means of a self-administered questionnaire (the Nottingham Health Profile [NHP]) and other questionnaires related to general health, sexual function, and stress/life events. Clinic visits were scheduled at study entry (week -12), at initiation and week 5 of placebo (weeks -6 and -1, respectively); at randomization (week 1, day 1); and after 4, 8, and 12 weeks of active treatment. At each visit, blood samples were collected for determination of lipid levels and the NHP, the principal measure of health-related quality of life, was administered. Primary safety measures were adverse events and laboratory test results. All statistical comparisons were two-sided, and significance was defined as P< or =0.05 except for the NHP questionnaire, which was P< or =0.01. Treatment with simvastatin 20 mg/d for 12 weeks (n = 194) resulted in significantly greater reductions in plasma total cholesterol and low-density lipoprotein cholesterol levels (25.7% and 33.6%, respectively) compared with pravastatin 40 mg/d for 12 weeks (n = 193) (19.0% and 26.3%, respectively) (P<0.001). No detrimental effects on health-related quality-of-life measurements were reported with either drug. A small but statistically significant improvement in emotional reaction from baseline (P<0.001) was observed after 12 weeks of treatment with simvastatin. At least 75% of simvastatin-treated patients indicated no change in response from baseline on NHP domain scores; these findings were similar to those for pravastatin-treated patients. The differences in the changes in lipid profiles between the 2 treatment groups were not associated with any observed differences in tolerability or health-related quality-of-life measures.

Adult↗
PubMed1999

Hormone replacement therapy and cardiovascular disease.

This year's work on hormone replacement therapy (HRT) and cardiovascular disease has been remarkable for the publication of the first randomised controlled trial of HRT use, the Heart Estrogen Replacement Study (HERS). The findings go against not only the trend of previous observational epidemiological studies, but also against findings in the very many studies which have previously shown and continue to show this year a beneficial effect of HRT on a large variety of cardiovascular risk factors, including endothelial function, here reviewed. The aspect of the effect of HRT on clotting variables is clearly crucial given the increased risk of venous thrombosis, and also increased number of cardiac events in the first 4 months of the HERS. Prothrombotic factors increase with age in women, and HRT alters these, particularly fibrinogen, factor VII, and PAI (less change with transdermal HRT) and antithrombin III. In normal women therefore the balance should be towards fibrinolysis rather than coagulation. Work has been presented in abstract for clarifying the effects of HRT on coagulation markers and grasping the problem of differences according to its route of administration. The full publications on this work are expected shortly. We are still awaiting evidence from randomized controlled trials of HRT in primary prevention; one is now recruited but will not report until 2005.

Cardiovascular Diseases↗
PubMed1999

Elevated levels of sE-selectin in post-menopausal females are decreased by hormone replacement therapy to levels observed in pre-menopausal females.

Observational epidemiological studies have shown that mortality from coronary heart disease is reduced in post-menopausal women by hormone replacement therapy (HRT). The aim of this study was to measure sE-selectin levels in post-menopausal females before and after HRT and to compare these with pre-menopausal females and aged matched males. Post-menopausal females (n = 70) were given HRT or no treatment to act as a control group. sE-selectin levels were significantly lower in the pre-menopausal (n = 36) when compared with the post-menopausal females (n = 70) (p = 0.027), whereas no difference between two age matched male groups was found (n = 40). Oral and transdermal HRT significantly decreased sE-selectin levels (p<0.0001 and p = 0.0005 respectively) with no change in the control group. The reduction in the levels of this marker of endothelial activation after HRT, may reflect a decrease in leucocyte/endothelial interaction which may reduce atherosclerotic risk in post-menopausal females.

Adult↗
PubMed1998

Lipoprotein(a) as a risk predictor for cardiac mortality in patients with acute coronary syndromes.

AIMS: Raised lipoprotein(a) concentrations are considered to be a risk factor for atherothrombotic diseases. We examined whether baseline concentrations were a risk factor for an adverse outcome in patients admitted with acute coronary syndromes. METHODS AND RESULTS: Five hundred and nineteen patients admitted with suspected acute coronary syndromes were studied and followed prospectively for a median of 3 years. The prognostic significance of a baseline lipoprotein(a) concentration of > or = 30 mg x dl(-1) or lower for subsequent cardiac death was assessed in patients with myocardial infarction (266) and unstable angina (197) and compared with other variables in regression models. In patients with myocardial infarction, a baseline lipoprotein(a) concentration of > or =30 mg x dl(-1) was associated with a 62% increase in subsequent cardiac death compared to the lower concentration group (29.8% vs 18.6%, Log rank P=0.04). In a multivariate regression model a baseline lipoprotein(a) concentration of > or = 30 mg x dl(-1) retained its significance as an independent predictor of cardiac death (P=0.037). In patients with unstable angina, baseline concentrations of > or = 7.9 mg x dl(-1) were found to be significant predictors of cardiac death in univariate (P=0.021) and multivariate (P=0.035) regression models. CONCLUSION: Baseline lipoprotein(a) concentrations in patients admitted with acute coronary syndromes are associated with an increased risk of cardiac death. For patients with myocardial infarction a concentration of > or = 30 mg x dl(-1) appears appropriate as a risk discriminator; for patients admitted with unstable angina, however, much lower concentrations of lipoprotein(a) appear to be prognostically important.

Acute Disease↗
PubMed1998

Mechanism for elevated plasma lipoprotein(a) concentrations in patients on dialysis: turnover studies.

Plasma concentrations of lipoprotein (a) [Lp(a)] are increased in patients on renal replacement therapy. Lipoprotein (a) is increasingly being recognized as an independent cardiovascular risk factor. In an effort to explore the mechanism for elevation of Lp(a) in patients on dialysis we have performed turnover studies of Lp(a) with radioactive iodine. Lp(a) was isolated from 1 patient on hemodialysis (HD) and 1 patient on continuous ambulatory peritoneal dialysis (CAPD); the protein was labeled with 125I and returned to each patient. Lipoprotein (a) was subsequently isolated from the patients over a 15-day period and the decay of the specific radioactivity of Lp(a) was used to determine the fractional catabolic rate (FCR), which was 0.27 (pool/day) for the HD patient and 0.28 (pool/day) for the CAPD patient. These rates are indistinguishable from those measured in 4 patients with hypercholesterolemia (0.29, SEM = 0.01) and in 4 other familial hypercholesterolemic patients (0.29, SEM = 0.02) studied previously using the same method by Knight et al. (7). We found no difference in the FCR of patients on dialysis when compared to patients with hyperlipidemia and normal renal function. Increased plasma concentration of Lp(a) in our patients on renal replacement therapy is not due to decreased catabolism, but is caused by increased synthesis.

Adult↗
PubMed1997

The depletion of substance P by diclofenac in the mouse.

Diclofenac in hyaluronan is analgesic and angiostatic. The depletion of substance P may be a common mechanism. Mice received diclofenac, diclofenac in hyaluronan, or saline i.v. for 5 days and snout substance P assessed: saline 2.80 +/- 0.23; 0.5 mg/kg diclofenac 2.03 +/- 0.20 (P < 0.05); diclofenac in hyaluronan 1.88 +/- 0.21 (P < 0.02); capsaicin 1.45 +/- 0.26 fmol/mg tissue (P < 0.005). Substance P recovered by 5 days (diclofenac in hyaluronan, capsaicin) and 24 h (diclofenac). Diclofenac may deplete substance P in analgesia, and hyaluronan prolong the depletion.

Analgesics↗
PubMed1997

A prospective study of the role of lipoprotein(a) in the pathogenesis of unstable angina.

AIM: Lipoprotein(a) is considered to be a risk factor for atherothrombotic diseases. The aim of the study was to examine the potential role of lipoprotein(a) concentrations in patients admitted with unstable angina with particular reference to their cardiac Troponin T concentrations, which identifies a subgroup at high risk of subsequent cardiac events. METHODS AND RESULTS: Consecutive patients admitted with chest pain to a single coronary care unit were studied. One hundred and sixty-seven patients had a final diagnosis of unstable angina, of whom 56 were cardiac Troponin T-positive. Admission lipoprotein(a) concentrations were significantly higher in the cardiac Troponin T-positive unstable angina group as compared to the cardiac Troponin T-negative unstable angina group: median and interquartile ranges 22.25 mg.dl-1 (6.25, 32.0) vs 6.0 mg.dl-1 (2.22, 14.8) respectively) P = 0.0004. A highly significant correlation was also found between the level of cardiac Troponin T at diagnosis and the lipoprotein(a) concentration: rs = 0.2798, P = 0.0001. CONCLUSION: This study provides the first evidence in man of a significant role for lipoprotein(a) in unstable angina. The correlation between lipoprotein(a) concentration and cardiac Troponin T concentration suggests that lipoprotein(a) may be significantly involved in the early failure of plaque rupture stabilization.

Adult↗
PubMed1997

Gastric outflow obstruction caused by gall stones and leading to death by complex metabolic derangement.

A 67 year old woman was admitted with a three week history of vomiting, having become increasingly confused for three days. Investigations revealed deranged serum biochemistry consistent with a combination of a diabetic non-ketotic hyperosmolar state and a metabolic alkalosis consistent with gastric outflow obstruction. She was treated with intravenous saline, intravenous insulin, and subcutaneous heparin, but did not improve clinically and had an asystolic cardiac arrest the following day; she was transferred to the intensive care unit and despite treatment with inotropes she died 40 hours after admission. Necropsy revealed that the stomach was massively dilated with gas and stomach contents, and contained many small black faceted gall stones. In addition a large nonfaceted brown-yellow gall stone was wedged in the pyloric antrum causing total obstruction. The patient had died from a complex metabolic derangement including non-ketotic hyperosmotic diabetic coma and metabolic alkalosis precipitated by the acute gastric outflow obstruction complicated by previously undiagnosed type II diabetes mellitus.

Aged↗
PubMed1997

The effect of change of renal replacement therapy on serum lipoprotein (a) concentration.

Lipoprotein (a) [Lp(a)] is an independent atherogenic risk factor. Lp(a) levels are elevated in patients on renal replacement therapy (RRT). This study looked at the effect of change of RRT on serum lipid and Lp(a) levels. Three groups were identified: (1) patients on dialysis who were transplanted; (2) those who had lost their transplants through immunorejection; (3) those who changed from continuous ambulatory peritoneal dialysis (CAPD) to hemodialysis (HD). All Lp(a) measurements were taken at least 3 months after the change of therapy. Our results were as follows: Group A (n = 21): 8 CAPD and 13 HD patients were transplanted. Median Lp(a) levels fell posttransplantation in the CAPD group (15.6 mg/dL vs 11.4 mg/dL, p = 0.04). The HD group showed a rise in cholesterol, low-density (LDL) and high-density lipoprotein (HDL) levels, with no change in Lp(a) levels. Group B (n = 11): 7 patients started CAPD and 4 HD. Overall, there was a marked increase in Lp(a) levels: median 38.2 mg/dL vs 55.9 mg/dL (p = 0.04), reflecting an increase in those starting CAPD (27.8 mg/dL vs 60.0 mg/dL, p = 0.01), with little change in the HD group (40.45 mg/dL vs 40.05 mg/dL). However, there was a decrease in cholesterol (7.4 mmol/L vs 5.1 mmol/L, p = 0.002) and LDL (5.5 mmol/L vs 3.3 mmol/L, p = 0.004). Group C (n = 16): 16 patients changed from CAPD to HD. Lp(a) levels were higher while on CAPD, as compared to when on HD (58.9 mg/dL vs 49 mg/dL, p = 0.03). Cholesterol (6.62 mmol/L vs 5.26 mmol/L, p = 0.006) and LDL (4.48 mmol/L vs 3.40 mmol/L, p = 0.004) were also higher when on CAPD. In conclusion, serum Lp(a) levels are clearly affected by the mode of the RRT, being highest in CAPD, and decline after transplantation or conversion to HD. Atherogenic risk is thus likely to differ between the modes of RRT and may be greatest for those on CAPD.

Adult↗