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Biomedical subjects

M S Elisaf

Publications and source records attributed to M S Elisaf.

At least 37 records · Page 2Linked to original sources
PubMed2001

Hyperosmolar syndrome in a patient with uncontrolled diabetes mellitus.

Nonketotic hyperglycemic hyperosmolar syndrome (HHS) is found mostly in type 2 diabetic patients with marked hyperglycemia. HHS is a metabolic emergency and is associated with a high mortality rate. It is characterized by extreme dehydration and neurologic symptoms, which are related directly to the degree of hyperosmolality. We describe a 65-year-old patient who was admitted because of impaired consciousness caused by HHS. The relevant clinical and laboratory findings are discussed, and a brief overview of the pathophysiology and therapeutic management is provided.

Aged↗
PubMed2001

Effect of letrozole on the lipid profile in postmenopausal women with breast cancer.

Hormonal therapy plays a central role in the overall treatment of breast cancer. Aromatase inhibitors can inhibit the aromatase enzyme system resulting in a reduction of oestrogens. Letrozole is a non-steroidal aromatase inhibitor that effectively blocks aromatase activity without interfering with adrenal steroid biosynthesis. The drug can significantly reduce the levels of plasma oestrogens, which remain suppressed throughout the treatment. Data are scarce concerning the influence of these drugs on serum lipid levels. In the present study, we evaluated the effects of letrozole on the serum lipid profile in postmenopausal women with breast cancer. A total of 20 patients with breast cancer were treated with letrozole, 2.5 mg once daily. After an overnight fast, serum lipid parameters (total cholesterol, high density lipoprotein (HDL) cholesterol, low density lipoprotein (LDL) cholesterol, triglycerides, apolipoproteins A1, B and E and lipoprotein (a)) were measured before treatment and at 8 and 16 weeks afterwards. A significant increase in total cholesterol (P=0.05), LDL cholesterol (P<0.01) and apolipoprotein B levels (P=0.05) in the serum, as well as in the atherogenic risk ratios total cholesterol/HDL cholesterol (P<0.005) and LDL cholesterol/HDL cholesterol (P<0.005) was noticed after letrozole treatment. We conclude that letrozole administration in postmenopausal women with breast cancer has an unfavourable effect on the serum lipid profile.

Aged↗
PubMed2001

Serum uric acid levels: a useful but not absolute marker of compliance with fenofibrate treatment.

The purpose of our study was to investigate whether measurement of serum uric acid levels is a reliable method to assess adherence to fenofibrate treatment. This was a 21 week, open-label study conducted in our lipid clinic. After an 8 week dietary baseline phase, we implemented a treatment phase, during which patients received 200 mg/day micronized fenofibrate for 3 months. Serum lipid profiles, including levels of lipoprotein(a) and fibrinogen, serum uric acid, as well as muscle and liver enzymes, were measured after the dietary phase, and at the end of the 3 month treatment period. Compliance was assessed using a clinical interview. A significant decrease in serum uric acid levels was observed in the compliant, while no significant change was noticed in the non-compliant. The compliant had lower serum uric acid concentrations compared to the non-compliant (P < 0.01) after fenofibrate treatment. Furthermore, they demonstrated lower levels of triglycerides and higher high-density lipoprotein (HDL) cholesterol concentrations (P < 0.05 for both parameters). The results show that serum uric acid concentrations may be used as a useful tool to assess compliance with fenofibrate therapy.

Adult↗
PubMed2001

Serum lipoprotein(a) concentrations and apolipoprotein(a) isoforms: association with the severity of clinical presentation in patients with coronary heart disease.

OBJECTIVE: The aim of this study was to investigate the possible associations between lipoprotein(a) [Lp(a)] concentrations or apolipoprotein(a) isoforms and the mode of clinical presentation of coronary heart disease (CHD) (acute thrombotic event or not). METHODS: A total of 131 CHD patients and 71 age- and gender-matched individuals without known CAD (free of symptoms of heart disease) were enrolled in the study. CHD patients were classified into patients with a history of an acute coronary syndrome (ACS, n=94) and patients with stable angina (SA, n=37). Lp(a) levels were measured with an ELISA method, whereas apolipoprotein(a) isoform analysis was performed (in all patients and 33 controls) by electrophoresis in 1.5% SDS-agarose gels followed by immunoblotting. Isoform size was expressed as the number of kringle 4 (K4) repeats. RESULTS: ACS patients had higher Lp(a) plasma levels 121.9 (0.8-84.1) mg/dl] and a greater proportion of elevated (> or = 30 mg/dl) Lp(a) concentrations (25.5%) compared with SA patients [9.2 (0.8-50.5) mg/dl, P < 0.01 and 10.8%, P < 0.05] and controls [8.0 (0.8-55.0) mg/dl, P < 0.01 and 11.2%, P < 0.05], while there were no differences between SA patients and controls. The median apolipoprotein(a)-isoform size was 26 K4. In 17 (10%) patients we could not detect any apolipoprotein(a) isoform bands by immunoblotting. ACS patients had a higher proportion of isoforms < 26 K4 (low molecular weight) than SA patients (56/85 vs. 12/33, P < 0.005) and controls (10/29, P < 0.005). CONCLUSIONS: CAD patients with a history of ACS have higher Lp(a) plasma levels and a significantly higher proportion of low molecular weight apolipoprotein(a) isoforms compared with patients with SA or to controls.

Acute Disease↗
PubMed2001

The effect of atorvastatin on serum lipids, lipoprotein(a) and plasma fibrinogen levels in primary dyslipidaemia--a pilot study involving serial sampling.

We conducted an open-label study to test the effects of atorvastatin on serum lipids, lipoprotein(a) [Lp(a)] and plasma fibrinogen levels. A total of 90 dyslipidaemic, non-smoking patients (45 patients with primary hypercholesterolaemia and 45 patients with primary mixed hyperlipidaemia) aged 48 +/- 11 years were studied. The patients were treated with 20 mg of atorvastatin for 24 weeks, in a single nocturnal dose. At baseline and every eight weeks, the fasting lipid profile, together with serum Lp(a) and plasma fibrinogen levels (Clauss method), were measured. Atorvastatin was highly effective in normalising the serum lipid profile. No significant change in median serum Lp(a) levels was observed in the whole group of patients (0.14 g/l before, vs. 0.16 g/l after, treatment) as well as in patients with raised (> 0.30 g/l) baseline levels (n = 32). A small non-significant increase of plasma fibrinogen was found (3.04 g/l vs. 3.14 g/l) after 24 weeks of atorvastatin administration. The effects of atorvastatin on both these variables did not differ in patients with hypercholesterolaemia or mixed hyperlipidaemia. In conclusion, our findings suggest that the effect of atorvastatin on plasma fibrinogen levels in dyslipidaemic patients without evident vascular disease is not clinically relevant. Furthermore, any rise in fibrinogen levels that may occur is likely to be transient in nature. Further studies are necessary to clarify this issue. There was no evidence that atorvastatin influences serum Lp(a) levels.

Analysis of Variance↗
PubMed2001

Lipid profile in subclinical hypothyroidism: is L-thyroxine substitution beneficial?

OBJECTIVE: The significance of dyslipidemia in subclinical hypothyroidism (SH) and the effect of thyroid substitution on lipids remain controversial. The present study aimed to assess the association of SH with lipid abnormalities and to quantify the effect of L-thyroxine therapy on serum lipid profiles. DESIGN: Serum lipid parameters of 66 patients with SH and 75 age- and sex-matched euthyroid controls were evaluated in a cross-sectional study. RESULTS: Patients with SH had higher total cholesterol (TC) (222+/-45 (s.d.) vs 190+/- 32 mg/dl), low-density lipoprotein cholesterol (LDL-C) (139+/-28 vs 118+/-39 mg/dl), apolipoprotein B (149+/-21 vs 139+/-18 mg/dl) and lipoprotein (a) (Lp(a)) (median 12.5 (0.8-101) mg/dl vs 7 (0.8-44) mg/dl) levels compared with euthyroid controls (P<0.05 for all comparisons). In a follow-up study including 37 patients with SH, all measurements were repeated after restoration of a euthyroid state with incremental doses of l-thyroxine. No significant changes in serum lipid profiles were observed except for a decrease in high-density lipoprotein cholesterol (59+/-15 to 55+/-14 mg/dl, P<0.05). However, patients with high pre-treatment TC (> or =240 mg/dl) showed a significant reduction in both TC (278+/-28 vs 257+/-36 mg/dl, P<0.05) and LDL-C (192+/-23 vs 173+/-28 mg/dl, P<0.01) levels. Similar but more pronounced changes were observed in a subgroup of patients with pre-treatment levels of TSH > or =10 microU/ml. Thyroid autoimmunity had no effect on either the baseline or the post-treatment lipid profile. CONCLUSION: Although patients with subclinical hypothyroidism exhibit increased levels of the atherogenic parameters (mainly LDL-C and Lp(a)), thyroid substitution therapy does not seem to significantly improve dyslipidemia in the whole group of patients.

Adult↗
PubMed2001

Tamoxifen-induced hypertriglyceridemia in association with diabetes mellitus.

Several pharmacological agents are associated with hyperlipidemia. Tamoxifen is an example of a drug-induced increase of serum triglyceride levels. However, there are only scarce reports on how inborn errors in lipid metabolism as well as secondary dyslipidemias, including diabetes mellitus, influence the hypertriglyceridemic effect of tamoxifen. Herein, we describe a case of a breast cancer patient receiving tamoxifen who presented with remarkable hypertriglyceridemia in the context of diabetes mellitus. We also provide a brief review of the relevant literature and discuss the mechanisms underlying the pathogenesis of hypertriglyceridemia related to tamoxifen.

Antineoplastic Agents, Hormonal↗
PubMed2000

Efficacy of combination of atorvastatin and micronised fenofibrate in the treatment of severe mixed hyperlipidemia.

OBJECTIVES: In patients with mixed lipid disorders, monotherapy may not effectively control all lipid abnormalities. We undertook this study to assess the efficacy of fenofibrate in combination with atorvastatin in patients with severe mixed dyslipidemia. METHODS: This was an 18-week, open-label study conducted in our lipid clinic. After a 6-week dietary baseline phase, patients received 200 mg/day micronised fenofibrate for 6 weeks. At the end of this period the subjects discontinued this treatment and received 40 mg/day atorvastatin for 6 weeks. Finally 200 mg/day of micronised fenofibrate was added to the statin therapy. RESULTS: Administration of micronised fenofibrate reduced serum triglycerides (P < 0.01) and total cholesterol and low-density lipoprotein (LDL) cholesterol (P < 0.05 for both parameters), while it evoked a significant increase in serum high-density lipoprotein (HDL) cholesterol levels (P < 0.05). Atorvastatin monotherapy induced a more pronounced decrease of total and LDL cholesterol. However, plasma triglycerides, although significantly lower than baseline values (P < 0.05), were higher than the values observed during treatment with fenofibrate. Moreover, serum HDL cholesterol concentrations were higher during fibrate therapy than during the statin one. During the combination therapy, the decrease in triglycerides was greater than that observed with fenofibrate alone, while the decrease in LDL cholesterol was more pronounced than that observed with atorvastatin alone. CONCLUSION: The combination of atorvastatin with micronised fenofibrate in patients with severe mixed dyslipidemia may have a favourable effect on some major coronary artery disease risk factors.

Adolescent↗
PubMed2000

Tamoxifen-induced severe hypertriglyceridemia and pancreatitis.

Tamoxifen exhibits favorable effects on the lipid and lipoprotein profile since it decreases the total and LDL cholesterol levels as well as the Lp(a) levels. Additionally, a small increase in serum triglycerides is commonly found after tamoxifen administration. However, severe hypertriglyceridemia which can sometimes be associated with life-threatening complications is occasionally noticed. Herein, we describe a patient who developed tamoxifen-induced severe hypertriglyceridemia and pancreatitis. An analysis of the underlying pathogenetic mechanisms as well as a review of the relevant literature is also provided.

Antineoplastic Agents, Hormonal↗