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Biomedical subjects

S M Carlsen

Publications and source records attributed to S M Carlsen.

13 recordsLinked to original sources
PubMed2003

Androgen levels in pregnant women decrease with increasing maternal age.

BACKGROUND: To investigate a possible effect of age on maternal androgen levels in uncomplicated pregnancies. METHODS: A study of 134 parous women with uncomplicated pregnancies was carried out at three university hospitals in Norway and Sweden. Maternal levels of androstenedione, dehydroepiandrosterone sulphate, testosterone and the free testosterone index were measured during weeks 17 and 33 of pregnancy. RESULTS: Maternal levels of androstenedione and testosterone had a negative association with maternal age in weeks 17 and 33 of pregnancy, while dehydroepiandrosterone sulphate and the free testosterone index were associated negatively in week 33 only. Adjustment for maternal parity, pre-pregnancy body mass index, smoking and fetal gender did not affect the results. CONCLUSIONS: Maternal androgen levels decrease with increasing maternal age. The cause and possible implication of this finding remain unknown.

Adolescent↗
PubMed2000

[Beta blockers or ACE inhibitors following myocardial infarction in patients with diabetes?].

BACKGROUND: Total mortality after myocardial infarction is about twice as high for diabetic as for non-diabetic subjects. ACE inhibitors are regarded as a first drug for all diabetics, also for post-infarction treatment. MATERIAL AND METHODS: We have reviewed the literature with an emphasis on the effect on hard end points in diabetic subjects treated for at least six weeks with beta blockers or ACE inhibitors after myocardial infarction. RESULTS: We identified eight post-infarction studies for which subgroup analyses of diabetic subjects were available, four with beta blockers and four with ACE inhibitors. We found that beta blockers without intrinsic sympathetic activity probably reduce total mortality more than ACE inhibitors do. The reduction of total mortality after treatment with beta blockers was 56-63%, compared to 12-35% after treatment with ACE inhibitors. INTERPRETATION: Beta blockers should be the preferred choice in post-infarction treatment of diabetics. ACE inhibitors and beta blockers used together give no further reduction in mortality.

Adrenergic beta-Antagonists↗
PubMed1998

Metformin increases circulating tumour necrosis factor-alpha levels in non-obese non-diabetic patients with coronary heart disease.

Metformin reduces insulin resistance and hyperinsulinaemia, as well as lipid levels and body weight. The mechanisms behind these effects are likely to involve intracellular insulin signalling. Recent evidence implicates tumour necrosis factor-alpha (TNF-alpha) as a modulatory factor on insulin resistance. The present investigation was undertaken to clarify whether metformin affects TNF-alpha and soluble TNF receptor levels. Sixty non-diabetic men with coronary heart disease were treated with diet and lifestyle advice and lovastatin 40 mg/day during a 4-week run-in period. During this period TNF-alpha and soluble TNF receptor p75 remained unchanged, whereas soluble TNF receptor p55 increased by 8% (P < 0.05). Twelve weeks of metformin treatment increased TNF-alpha by 33% (P < 0.05). This effect was restricted to non-obese patients in whom TNF-alpha increased by 68% (P < 0.01). Soluble TNF receptors p55 and p75 remained unchanged in the whole group, whereas soluble TNF receptor p55 increased by 11% (P < 0.05) in non-obese patients. Since metformin reduces insulin resistance both in obese and non-obese subjects but increases TNF-alpha levels only in the latter, it is concluded that the drug does not exert its effect on insulin resistance through regulation of circulating TNF-alpha levels.

Adult↗
PubMed1998

Evidence for dissociation of insulin- and weight-reducing effects of metformin in non-diabetic male patients with coronary heart disease.

Metformin effects on insulin resistance and insulin/glucose relationships during an oral glucose tolerance test (OGTT) were investigated in 60 non-diabetic male patients previously treated with coronary artery bypass surgery or angioplasty in an open, 12 week prospective study. During a 4 week run-in period, all patients were treated with diet and lifestyle advice and lovastatin 40 mg daily. Lovastatin treatment was continued in all the patient throughout the study. After randomization, the metformin group got additional treatment with metformin up to 2000 mg/day. Fasting plasma glucose levels and glucose area during OGTT remained unaffected by metformin treatment. Insulin resistance, assessed as the insulin area/glucose area ratio during OGTT decreased by 24% (P = 0.028) in the whole group and by 30% in obese subjects (P = 0.049). Notably, the reduction in body weight by metformin treatment did not correlate with amelioration of insulin resistance or changes in lipid levels. However, changes in insulin resistance correlated with changes in lipid levels. Hence, metformin effects on insulin resistance and body weight appear to be mediated, at least partly, by different mechanisms, while metformin effects on insulin resistance and lipid metabolism are associated in non-diabetic subjects.

Adult↗
PubMed1998

Folate administration reduces circulating homocysteine levels in NIDDM patients on long-term metformin treatment.

OBJECTIVES: Metformin treatment increases circulating homocysteine levels. We studied whether administration of folate reduces serum total homocysteine levels in patients on long-term metformin treatment. DESIGN: A prospective, randomized, double-blind, placebo-controlled study lasting for 12 weeks and taking place in a university hospital setting. SUBJECTS: Thirty patients treated with a metformin dose of at least 1000 mg day-1 for a minimum of 1 year were included. At baseline serum total homocysteine levels were within the reference range. One patient who withdrew and one who died were excluded from the statistical evaluation. Twenty-six of the remaining patients suffered from NIDDM, the other two from hyperlipidaemia. INTERVENTION: Patients were randomized into two groups at week 0. The folate group received 0.25 mg day-1 of folate in addition to 60 mg day-1 of Fe2+, while the placebo group received only 60 mg day-1 of Fe2+. MAIN OUTCOME MEASURES: Fasting homocysteine, cysteine, cysteinylglycine, vitamin B12 and folate were measured at week 0, 4 and 12. Changes from week 0 to week 4 and from week 0 to week 12 were calculated. RESULTS: Folate administration reduced serum levels of total homocysteine in the folate group as compared with the placebo group by 13.9% (P < 0.01) and 21.7% (P < 0.001) at week 4 and 12, respectively. In the folate group versus the placebo group serum levels of vitamin B12 increased by 9.9% (P = 0.010) and 9.6% (P = 0.043) while folate levels increased by 96.9 and 89.9% at week 4 and 12, respectively. CONCLUSION: The present study indicates that the homocysteine-increasing effect of metformin can be counteracted by folate administration.

Cardiovascular Diseases↗
PubMed1997

[Sulfonylurea-induced hypoglycemia. An iatrogenic and potentially fatal condition].

Sulfonylureas are the most frequently used peroral antidiabetic drugs in Norway. Five cases of serious sulfonylurea-induced hypoglycemia are described. In one of these cases glibenklamid-induced hypoglycemia was thought to be the direct cause of death. A review of the literature indicates that glibenclamide induces more frequent and serious hypoglycemias than other sulfonylureas do. The author discusses the possible mechanisms behind these differences, and the conditions predisposing to sulfonylurea-induced hypoglycemia. It is recommended to check blood glucose whenever a patient's diagnosis has not been adequately clarified.

Aged↗
PubMed1997

Metformin increases total serum homocysteine levels in non-diabetic male patients with coronary heart disease.

It is known that the metabolism of homocysteine (Hcy) depends on the vitamins B6, B12 and folate, and furthermore that metformin reduces serum vitamin B12 levels. In order to investigate whether metformin treatment affects serum total Hcy (tHcy) levels we performed an open, prospective, randomised study in 60 non-diabetic male patients with cardiovascular disease. After a 4-week run-in period with lovastatin 40 mg day-1, and diet and lifestyle advice, patients were randomised into two groups, both continuing the run-in treatment. One group received metformin up to 2000 mg day-1, whereas the control group got no additional treatment. After 12 and 40 weeks of metformin treatment, tHcy levels increased moderately but significantly by 7.2% (p < 0.05) and 13.8% (p < 0.05) in the metformin group relative to the control group, whereas serum vitamin B12 levels decreased by 13.4% (p < 0.0005) and 17.7% (p < 0.0005), respectively. Serum folate levels did not change after 12 weeks, but decreased by 8.0% after 40 weeks (p = 0.061) relative to the control group. Serum levels of total cysteine and methylmalonic acid (MMA) did not change. In conclusion, metformin treatment increased tHcy levels and decreased levels of vitamin B12 and folate. Since MMA levels were unchanged, it remains an open question whether the increase in tHcy levels is secondary to reduced vitamin B12 levels, folate levels or a combination of both.

Adult↗
PubMed1996

Metformin improves blood lipid pattern in nondiabetic patients with coronary heart disease.

OBJECTIVES: To study whether the addition of metformin further improves the blood lipid pattern in non-diabetic patients with coronary heart disease already treated with lovastatin, diet and lifestyle advice. DESIGN: An open, prospective, randomized study in a university hospital setting. SUBJECTS: Sixty non-diabetic male patients previously treated with coronary artery bypass surgery or angioplasty and with serum cholesterol > or = 6.0 mmol L-1 and/or HDL-cholesterol < or = 1.2 mmol L-1. INTERVENTIONS: After a 4-week run-in period with lovastatin (40 mg day-1), and diet and lifestyle advice, patients were randomized into two groups, both continuing the run in treatment. One group received metformin up to 2000 mg day-1; the control group got no additional treatment. MAIN OUTCOME MEASURES: Fasting serum lipids, glucose and weight were registered at entrance (= week-4), and at weeks 0, 4 and 12. Changes from week 0 to week 4 and from week 0 to week 12 were compared. Side-effects of the treatment were also registered. RESULTS: Metformin lowered the LDL/HDL-cholesterol ratio by 12 and 6% at weeks 4 and 12, respectively, and reduced body weight by 1.8 kg at week 12. There was also a transient lowering effect on LDL-cholesterol and apolipoprotein B. In the normal weight subgroup of patients (body mass index < 27 kg m-2), metformin induced a decrease in total cholesterol (-9%). LDL-cholesterol (-12%). LDL/HDL-cholesterol ratio (-10%) and apolipoprotein B (-7%), as compared to the control group. In this subgroup, body weight and fasting glucose were unaffected by metformin. Thus, the lipid lowering effect in normal weight patients was not secondary to changes in body weight or fasting glucose. In overweight patients (body mass index > 27 kg m-2), metformin had no significant effects on blood lipids, but induced a weight loss of -3.0 kg and a transient reduction of fasting glucose. No side-effects were registered apart from those expected from each individual drug. CONCLUSIONS: Metformin given for 12 weeks as a supplement to lovastatin, diet and lifestyle advice to non-diabetic male patients with coronary heart disease further improves the lipid pattern in normal weight patients, and reduces weight in the overweight patients. Because metformin is cheap and other lipid lowering drugs are expensive, the potential of metformin as a lipid lowering agent should be further investigated.

Blood Glucose↗
PubMed1995

[Should insulin treatment be avoided? Blood sugar is not everything in type 2 diabetes].

Cardiovascular disease is frequent and is the main cause of death in type 2-diabetic patients. Hyperinsulinaemia is a risk factor for cardiovascular disease, and insulin accelerates many of the processes leading to atherosclerosis. Studies in type 2-diabetic patients show that high insulin levels correlate with cardiovascular disease and overall mortality. A recent pilot study showed that intensive versus traditional insulin treatment increased the incidence of cardiovascular disease. Therefore treatment regimens that reduce insulin levels should be preferred, at least when equal glucose levels are achieved. In this perspective metformin is the drug of choice. Insulin treatment should be considered only when combined treatment with metformin and sulfonylurea is contraindicated or leads to insufficient blood glucose control. Special caution should be shown with insulin treatment in patients with cardiovascular disease.

Arteriosclerosis↗
PubMed1994

[Metformin reevaluated--time for rehabilitation?].

The consumption of metformin in Norway is low. Most probably this is caused by poorly based impressions of small effects and frequent and serious side effects. A review of the literature shows that metformin and sulfonylurea lower average blood glucose values equally well, both in obese and non-obese type 2 diabetic patients. In sulfonylurea failure, addition of metformin lowers the glucose values to the same extent as a shift to insulin monotherapy does. Metformin is anti-hyperglycaemic only, and therefore does not cause hypoglycaemia. The risk of drug-related deaths is no higher with metformin than with sulfonylurea. Metformin improves the lipid profile, and has other effects which could lower risk of cardiovascular complications. The place of metformin in the treatment of type 2 diabetic patients should be reconsidered.

Drug Evaluation↗