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Query: UMLS:C0004153 (atherosclerosis)
 77,401 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Eight subjects, belonging to a large family kindred repeatedly showing the electrophoretic pattern of the "double pre-beta lipoproteinemia", were studied. In seven of them thyroid function, serum lipids and apolipoprotein A-I were determined before and after treatment with dextro-thyroxine, preparation almost free of levo-thyroxine. In most of the patients, total-T4 levels and free-T4 Index were in the lower normal range, but basal TSH levels and the TSH response to TRH were normal. Dextro-thyroxine was effective in reducing both serum total cholesterol and triglycerides, but the percentage decrease in serum triglycerides was definitely greater than that of serum total cholesterol. This marked, unexpected hypotriglyceridemic effect is similar to that observed in a group of obese, hypertriglyceridemic hypothyroid patients treated with levo-thyroxine. Besides serum total cholesterol and triglycerides, the VLDL cholesterol/triglycerides ratio and the electrophoretic "slow moving" pre-beta component were also significantly reduced after treatment, suggesting that dextro-thyroxine can remove efficiently "remnant" VLDL particles from the plasma. Following dextro-thyroxine therapy, the relatively low pretreatment values of apolipoprotein A-I were significantly increased, being restored to normal.
Atherosclerosis 1984 Feb
PMID:Effects of dextro-thyroxine, a preparation almost free of levo-thyroxine, on thyroid function, serum lipids and apolipoprotein A-I in "double pre-beta lipoproteinemia". 642 87

Hypophysectomy was found to increase low density lipoprotein (LDL) cholesterol in rats from 0.18 to 1.18 mmol/l in 1 week, while very low density lipoprotein (VLDL) and high density lipoprotein (HDL) cholesterol decreased simultaneously from 0.08 to 0.03 mmol/l and from 2.12 to 1.01 mmol/l, respectively. Serum total cholesterol levels remained unchanged. Thyroid supplementation (T3 or T4) with doses causing a euthyroid state did not fully correct the lipoprotein pattern. The increase of LDL caused by hypophysectomy was significantly rectified, but the normal level could not be maintained, whilst the HDL level was not at all affected by thyroid hormones. Serum total cholesterol was markedly reduced in all groups with thyroid supplementation, indicating increased cholesterol catabolism. These results suggest that TSH and peripheral thyroid hormones modulate LDL but no effect on HDL could be detected. Other hormones, notably ACTH, growth hormone, lipotropins and gonadotropins are also involved in the control of lipoproteins at the pituitary level. Their exact impact cannot at present be assessed.
Atherosclerosis
PMID:Failure of thyroid hormones to maintain the normal lipoprotein pattern in rats after removal of the pituitary gland. 747 Jan 94

The results of hypothyreosis therapy with thyroideum (dried thyroid gland) were assessed in 40 patients. The study aimed at establishing proper dosage and assaying blood serum T4, T3, and TSH levels. Daily dose of 1 tablet (0.2 mg of iodine) improved clinical status but did not cover the daily requirement of the body for thyroid hormones. An increase in daily dose to 2 tablets (0.4 mg of iodine) produced nearly complete compensation of hypothyreosis. However, such a daily dose was often associated with adverse reactions, especially in patients with arterial hypertension or atherosclerosis. Thyroid hormones assay has shown that dried thyroid gland administered in daily dose of 0.4 mg normalizes serum T3 levels whereas serum T3 levels remained constantly low, and TSH increased as in non-treated disease. An increase of the daily dose to 0.6 mg of iodine produces excessive increase in serum T3 levels with clinical symptoms of T3 toxicity.
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PMID:[Outcome of treating hypothyroidism with thyreoideum]. 809 Jun 51

Hypothyroidism promotes both significant diastolic hypertension and hypercholesterolemia and, as a consequence, their combination has been suggested to accelerate atherosclerosis. Prevalence of elevated LDL-cholesterol is significantly increased not only in overt hypothyroidism, but also in subclinical hypothyroidism. Serum TSH will be determined in all the patients, as a first line test and only the patients with TSH values over 5 microU/ml will be further investigated: serum T4, FT4 and antimicrosomal and antithyroglobulin antibodies. In the study group were not included severe nonthyroid illness, major depression, untreated Addison's disease and the patients using some drugs that interfere with serum TSH level.
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PMID:Overt and subclinical hypothyroidism and atherosclerotic arteriopathy of the lower limbs (clinical and subclinical). 817 76

Secondary causes of hyperlipidemia are important to recognize. In fact, hyperlipidemia may be a clue to the presence of an underlying systemic disorder. It may greatly heighten the risk of atherosclerosis with a raised LDL-c, triglyceride-rich lipoprotein excess, and increased lipoprotein(a) as well as lowered HDL-c. The search for secondary causes may provide a clue as to why patients with primary lipid disorders suddenly develop worsening lipid profiles. The point is a crucial one because some acquired causes of hyperlipidemia, such as alcohol, estrogens, steroids, or pregnancy, when superimposed on a primary familial form of hypertriglyceridemia can result in a saturated removal system and a buildup of chylomicrons, which can lead to life-threatening pancreatitis. A convenient way to remember secondary causes is to think of the four D's of diet, drugs, disorders of metabolism, and diseases. Although diets rich in saturated fats and cholesterol are a common cause of the mild hypercholesterolemia seen in our society, alcohol excess and weight gain can explain much of the tendency toward hypertriglyceridemia. Interestingly anorexia nervosa has long been associated with severe but reversible hypercholesterolemia. Several classes of drugs need to be considered as common causes of altered lipid profiles. Glucocorticoids and estrogens elevate triglycerides and raise levels of HDL-c. Anabolic steroids taken orally markedly reduce levels of HDL-c in contrast to injectable testosterone, which does not adversely affect the LDL-to-HDL ratio. Oral contraceptives affect atherosclerotic risk depending on the kind and doses of progestin/estrogen. In those with an underlying primary hypertriglyceridemia and associated obesity, estrogenic medications can depress triglyceride removal mechanisms, leading to the chylomicronemia syndrome and pancreatitis. Antihypertensives have variable effects on lipids and lipoproteins. Although short-term thiazide usage raises cholesterol, triglycerides, and LDL-c, long-term usage is not necessarily associated with significant alterations in lipid levels. Alpha blockers may cause an increase in HDL-c, whereas beta blockers raise triglycerides and lower HDL-c. Sympatholytics, angiotensin converting enzyme inhibitors, and calcium channel blockers are essentially lipid neutral. Retinoids can be associated with increased LDL-to-HDL ratios and occasionally striking elevations in triglycerides. Cyclosporine raises LDL-c and lipoprotein(a). Classes of drugs that may raise HDL-c include cimetidine, antiepileptic drugs, and tamoxifen, but the effect may be seen primarily in women. Hypothyroidism is the most common secondary cause of hyperlipidemia after dietary causes are considered. A thyroxine and TSH level should be obtained on all new cases of clinically important hyperlipidemia.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Secondary causes of hyperlipidemia. 828 27

Disorders in lipoprotein metabolism (dyslipidemia) can result in premature atherosclerosis or pancreatitis. Dyslipidemias can be classified as hypercholesterolemia, hypertriglyceridemia, combined hyperlipidemia, and low levels of high density lipoprotein (HDL) cholesterol. All of the dyslipidemias can be primary or secondary. Both elevated levels of low density lipoprotein cholesterol and decreased levels of HDL cholesterol predispose to premature atherosclerosis. Triglyceride levels greater than 1,000 mg/dL increase the risk for pancreatitis. In the appraisal of the dyslipidemias, measurement of serum cholesterol, triglycerides, HDL-cholesterol and obtaining the LDL cholesterol by Friedewald equation is usually sufficient in the majority of patients. However, in some cases, such as the diagnosis of the Type III dyslipidemia and when triglycerides are > or = 400 mg/dL, ultracentrifugation is required to determine the VLDL or LDL cholesterol. Lipoprotein electrophoresis can be useful in the diagnosis of Type III dyslipidemia (broad beta band) and also to detect chylomicrons. In young subjects with coronary artery disease with a normal LDL cholesterol an apolipoprotein B-100 level may be a useful test. In children and young adults with severe hypertriglyceridemia, measurement of lipoprotein lipase activity or assaying apolipoprotein C-II levels can be useful in elucidating the cause. Also, laboratory tests are useful in excluding a secondary cause of dyslipidemia (urinalysis, plasma creatinine, TSH, glucose, protein electrophoresis, alkaline phosphatase and transaminases). Thus, laboratory investigations play an important role in the management of dyslipidemia.
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PMID:A practical approach to the laboratory diagnosis of dyslipidemia. 870 23

Patients with hypothyroidism are considered to have an increased risk of developing atherosclerosis; because endothelial dysfunction is an early sign of atherosclerosis, we investigated whether endothelial dysfunction is present in patients with hypothyroidism. Thirty-five subjects with various TSH levels were investigated by high-resolution ultrasound imaging of the brachial artery to assess endothelial and smooth muscle responses. Flow-mediated, endothelium-dependent vasodilatation was significantly higher in subjects with TSH 0.4-2 microIU/mL (11.8 +/- 2.7%), compared with subjects with TSH 2.01-4 microIU/mL (6.8 +/- 2.9%), 4.01-10 microIU/mL (5.2 +/- 6.3%) and >10 microIU/mL (4.0 +/- 4.4%); TSH levels correlated inversely to endothelium-dependent dilatation. Thus, flow-mediated vasodilatation, a marker of endothelial function, is impaired not only in patients with mild hypothyroidism but also in subjects with "high-normal" serum TSH levels (ie, 2.01-4.0 microIU/mL) that may be characterized as possibly abnormal.
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PMID:Flow-mediated, endothelium-dependent vasodilation is impaired in subjects with hypothyroidism, borderline hypothyroidism, and high-normal serum thyrotropin (TSH) values. 922 12

Hypothyroidism leads to an increase of plasma low-density lipoprotein (LDL) cholesterol levels. Oxidation of LDL particles changes their intrinsic properties, thereby enhancing the development of atherosclerosis. T4 has three specific binding sites on apolipoprotein B; furthermore it inhibits LDL oxidation in vitro. We therefore hypothesized that T4 deficiency not only results in elevated LDL-cholesterol levels but also in increased LDL oxidation. Ten patients with overt hypothyroidism were studied when untreated (TSH 76 +/- 13 mU/L, T4 40 +/- 6 nmol/L) and again when they were euthyroid for at least 3 months during T4 treatment (TSH 2.7 +/- 0.5 mU/L, T4 115 +/- 11 nmol/L). Plasma lipids and lipoproteins and the oxidizability and chemical composition of LDL were determined. The transition from the hypothyroid to the euthyroid state was associated with a decrease (mean +/- SE) of plasma total cholesterol (5.8 +/- 0.3 vs. 4.8 +/- 0.2 mmol/L, P < 0.005), LDL cholesterol (3.8 +/- 0.3 vs. 2.9 +/- 0.2 nmol/L, P < 0.005) and apolipoprotein B (1.2 +/- 0.1 vs. 0.9 +/- 0.1 g/L, P < 0.005); plasma high-density lipoprotein cholesterol, apolipoprotein A-1, and triglycerides did not change. The actual content of dienes in LDL particles was increased in hypothyroidism, with a decrease after T4 suppletion [median (range) = 257 (165-346) vs. 188 (138-254) nmol/mg LDL protein, P < 0.005; reference range 140-180]. The lag time, an estimate of the resistance of LDL against oxidation in vitro, was shortened when hypothyroid but normalized after T4 treatment [29 (19-90) vs. 77 (42-96) min, P < 0.005; reference range 67-87]. The density, the relative fatty acid content, and the vitamin E content of LDL particles did not change. In conclusion, the hypothyroid state is not only associated with a quantitative increase of LDL particles, but it also changes their quality by increasing LDL oxidizability.
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PMID:Increased oxidizability of low-density lipoproteins in hypothyroidism. 958 87

In 18 patients with pernicious anaemia (PA) the authors assessed the blood glucose level, C-peptide level and immunoreactive insulin (IRI) during the oral glucose tolerance test (o-GTT). They calculated the body mass index (BMI), assessed the level of the thyroid-stimulating hormone (s-TSH), free thyroxine (fT4), triiodothyronine (T3) and took repeatedly blood pressure readings. In one female patient they confirmed the diagnosis of insulin dependent diabetes mellitus (IDDM), in another six subjects they detected non-insulin dependent diabetes mellitus (NIDDM), incl. two persons where it was detected newly. In four patients impaired glucose tolerance was revealed. In the remaining seven patients non-classifiable glucose tolerance was found, none of the patients had a quite normal o-GTT. In five patients, hitherto not diagnosed latent hypothyroidism was detected. Eleven subjects were obese, four patients suffered from hypertension, another six from systolic hypertension, in eight patients a significantly elevated C-peptide level on fasting was found, in the majority of patients an elevated, or protracted response of C-peptide and insulin to orally administered glucose was found. Patients with pernicious anaemia must be considered subjects with cumulation of risk factors for atherosclerosis; these risk factors must be actively sought and treated.
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PMID:[Occurrence of diabetes, hyperinsulinism and other risk factors for atherosclerosis in patients with pernicious anemia]. 982 Jan 7

Turner's syndrome is associated with a high incidence of cardiovascular disease and hypothyreosis; conditions which are associated with abnormal lipid metabolism. To test whether alterations of lipid metabolism is present in healthy Turner's women, we compared lipids in a group of adult women with Turner's syndrome with an age matched group of healthy women. In addition the impact of sex steroid replacement therapy was studied in the women with Turner's syndrome. Patients were studied before and during treatment with hormonal replacement therapy, consisting of either oral 17beta-estradiol or transdermal 17beta-estradiol, and oral norethisterone. Control subjects were studied once in the early follicular stage of the menstrual cycle. The study group consisted of 26 (33.2+/-7.9 years) patients with Turner's syndrome and an age matched control group of 24 (32.7+/-7.6 years) normal women. Body composition measures, apolipoprotein (apo) B and apo A-I, Lp(a), cholesterol, HDL, LDL, triglycerides, thyroxine (TT4), free thyroxine (FT4), triiodothyronine (TT3), free triiodothyronine (FT3), TSH, and leptin were determined. Apo A-I levels were higher in Turner's patients (P45 g/l) Lp(a), more women with Turner's syndrome had high levels of Lp(a) than controls (P=0.024), while all other measures of lipid metabolism were comparable to controls. The level of TSH, FT3, and FT4 were significantly higher in Turner's patients, while TT4, TT3 and adjusted 24h energy expenditure were comparable to controls. Lp(a) (P=0.005), HDL (P=0.045) and apo A-I (P=0.039) decreased significantly, while there was a tendency towards a decrease in apo B (P=0.063) during treatment with sex hormones. In conclusion more women with Turner's syndrome than controls have high levels of apolipoprotein A-I and Lp(a), but only after dichomitization, while other markers of lipid metabolism are normal. Replacement therapy with female sex hormones lowered Lp(a), HDL cholesterol and apolipoprotein A-I.
Atherosclerosis 2000 May
PMID:Lp(a) and lipids in adult Turner's syndrome: impact of treatment with 17beta-estradiol and norethisterone. 1078 52


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