Regression of Achilles Tendon Xanthomas Evaluated by CT Scan After Hypolipidemic Treatment with Simvastatin

Kolovou, Genovefa; Daskalova, Deliana; Mastorakou, I.; Anagnostopoulou, Katherine K.; Cokkinos, Dennis V.

doi:10.1177/000331970405500314

Cited by 16 publications

(13 citation statements)

References 25 publications

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“…Familial hypercholesterolaemia (FH) is a monogenic disorder associated with hypercholesterolaemia due to reduced low‐density lipoprotein (LDL) receptor activity (1). FH is clinically characterised by elevated LDL cholesterol (>4.9 mmol/l), a positive family history of dyslipidaemia and early coronary heart disease (CHD), as well as the presence of tendon xanthomas and pre‐mature atherosclerosis (1–4). The heterozygote (h) frequency is estimated to be 1/500 in most populations (1,3,5,6).…”

Section: Introductionmentioning

confidence: 99%

Heterozygote men with familial hypercholesterolaemia may have an abnormal triglyceride response post-prandially. Evidence for another predictor of vascular risk in familial hypercholesterolaemia

Kolovou

Anagnostopoulou

Pilatis

et al. 2004

International Journal of Clinical Practice

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Familial hypercholesterolaemia (FH) is associated with premature coronary heart disease (CHD). Post-prandial hypertriglyceridaemia has also been associated with cardiovascular disease. Thus, an abnormal post-prandial triglyceride (TG) clearance may contribute to the heterogeneity in the risk of CHD in heterozygous (h) FH. Therefore, we investigated the response of TG levels to a fatty meal in men with hFH. We studied 26 Greek men divided into two groups: the hFH group of 14 men, mean age 39 (SD = 11) years and the control group of 12 healthy men, mean age 43 (50:5) years. An increased TG response to the fatty meal was defined as a post-prandial TG concentration (at 4, 6 or 8 h) greater than the highest TG concentration in any hour in any control individual. All hFH patients had normal baseline fasting TG levels. However, seven hFH men showed an abnormal TG response after the fatty meal; these patients had higher baseline fasting TG levels than others [1.5 (0.2) vs. 1.0 (0.4) mmol/l, p = 0.005]. The hFH men constituted a heterogeneous group regarding their TG response to the fatty meal compared with healthy men because 50% with higher, but nevertheless 'normal' basal TG levels, had an abnormal post-prandial TG response. The reduced activity of low-density lipoprotein receptors in hFH together with other defects in TG handling may explain the abnormal rise of TG levels post-prandially.

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Section: Introductionmentioning

confidence: 99%

Heterozygote men with familial hypercholesterolaemia may have an abnormal triglyceride response post-prandially. Evidence for another predictor of vascular risk in familial hypercholesterolaemia

Kolovou

Anagnostopoulou

Pilatis

et al. 2004

International Journal of Clinical Practice

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“…Noteworthy to mention, most of the patients, referred to us, were already presented with clinical manifestations of atherosclerosis [16–18]. In the study by Masaki et al [19], the event-free survival with respect to a major cardiac event (cardiac death and myocardial infarction) was 94.4% for 6 years.…”

Section: Discussionmentioning

confidence: 99%

Changes in Lipids and Lipoproteins after Selective LDL Apheresis (7-Year Experience)

et al. 2012

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Background. The aim of the study was to investigate the changes in plasma lipids and lipoproteins and the cardiovascular events after selective LDL apheresis.Methods and Results. Two pediatric patients with familial hypercholesterolemia aged 11 and 13 years and 19 dyslipidemic adults aged 41 ± 14 years underwent direct adsorption of lipoproteins (DALI) sessions. The mean follow-up period was 47 ± 23 months. The total cholesterol (TC) values before and after treatment were 8.2 ± 2.2 and 3.1 ± 1.6 mmol/l (318 ± 86 and 122 ± 62 mg/dL), respectively. The interval mean of TC was 6.9 ± 1.9 mmol/l (268 ± 75 mg/dL). The LDL cholesterol concentrations before and after treatment were 6.6 ± 2.1 and 1.7 ± 1.1 mmol/l, (256 ± 82 mg/dL and 65 ± 41 mg/dL), respectively. The percentage of acute LDL cholesterol reduction was 75 ± 11%. Cardiovascular events were observed in seven patients. The average annual event rate was 5.51%.Conclusion. LDL apheresis is a very important therapeutic tool in managing patients at high risk for premature CAD or with aggressive CAD, despite adequate medical treatment.

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Section: Detection Of Achilles Tendon Xanthomas (Table 1)mentioning

confidence: 99%

“…Computed tomography (CT) scan, which is a cross‐sectional method, depicts the Achilles tendon as a soft tissue structure surrounded by the very low‐density subcutaneous fat [52–54]. The good contrast between the Achilles tendon and the surrounding fat tissue offers the possibility to perform accurate size measurements [52–54]. Although size measurements are useful for the initial evaluation of ATX and for controlling the response to treatment, density measurements of the Achilles tendon fail to demonstrate differences between normocholesterolaemic and hypercholesterolaemic subjects [52,54].…”

Section: Detection Of Achilles Tendon Xanthomas (Table 1)mentioning

confidence: 99%

Pathogenesis, detection and treatment of Achilles tendon xanthomas

Tsouli

Kiortsis

Argyropoulou

et al. 2005

Eur J Clin Investigation

121

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Tendon xanthomatosis often accompanies familial hypercholesterolaemia, but it can also occur in other pathologic states. Achilles tendons are the most common sites of tendon xanthomas. Low-density lipoprotein (LDL) derived from the circulation accumulates into tendons. The next steps leading to the formation of Achilles tendon xanthomas (ATX) are the transformation of LDL into oxidized LDL (oxLDL) and the active uptake of oxLDL by macrophages within the tendons. Although physical examination may reveal Achilles tendon xanthomas (ATX), there are several imaging methods for their detection. It is worth mentioning that ultrasonography is the method of choice in everyday clinical practice. Although several treatments for Achilles tendon xanthomas (ATX) have been proposed (LDL apheresis, statins, etc.), they target mostly in the treatment of the basic metabolic disorder of lipid metabolism, which is the main cause of these lesions. In this review we describe the formation, detection, differential diagnosis and treatment of ATX as well as the relationship between tendon xanthomas and atheroma.

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Regression of Achilles Tendon Xanthomas Evaluated by CT Scan After Hypolipidemic Treatment with Simvastatin

Cited by 16 publications

References 25 publications

Heterozygote men with familial hypercholesterolaemia may have an abnormal triglyceride response post-prandially. Evidence for another predictor of vascular risk in familial hypercholesterolaemia

Heterozygote men with familial hypercholesterolaemia may have an abnormal triglyceride response post-prandially. Evidence for another predictor of vascular risk in familial hypercholesterolaemia

Changes in Lipids and Lipoproteins after Selective LDL Apheresis (7-Year Experience)

Pathogenesis, detection and treatment of Achilles tendon xanthomas

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