Hyperlipidemia Xanthoma

The nurse takes a dietary history, focusing on the types of foods normally included in the diet. Vital signs and weight are recorded. The skin and eyelids are inspected for evidence of xanthomas (flat or elevated yellowish deposits) that may be seen in the more severe forms of hyperlipidemia. 

A complete history and physical examination should assess (1) presence or absence of cardiovascular risk factors or definite cardiovascular disease in the individual (2) family history of premature cardiovascular disease or lipid disorders (3) presence or absence of secondary causes of hyperlipidemia, including concurrent medications and (4) presence or absence of xanthomas, abdominal pain, or history of pancreatitis, renal or liver disease, peripheral vascular disease, abdominal aortic aneurysm, or cerebral vascular disease (carotid bruits, stroke, or transient ischemic attack). 

Many patients treated for primary hyperlipidemia have no symptoms or clinical manifestations of a genetic lipid disorder (e.g., xanthomas), so monitoring is solely laboratory based. 

In patients treated for secondary intervention, symptoms of atherosclerotic cardiovascular disease, such as angina or intermittent claudication, may improve over months to years. Xanthomas or other external manifestations of hyperlipidemia should regress with therapy. 

Hyperlipidemia with skin xanthomas elevation of triglycerides (VLDL)... 

W5. Watanabe, Y., Serial inbreeding of rabbits with hereditary hyperlipidemia (WHHL-rabbit) Incidence and development of atherosclerosis and xanthoma. Atherosclerosis 36, 261-268 (1980). 

Type TV hyperlipoproteinemia is common and occurs in adulthood primarily in patients who are obese, diabetic, and hyperuricemic and do not have xanthomas. It may be secondary to alcohol ingestion and can be aggravated by stress, progestins, oral contraceptives, thiazides, or 8-blockers. Two genetic patterns occur in type IV hyperlipoproteinemia familial hypertriglyceridemia, which does not carry a great risk for premature CAD, and familial combined hyperlipidemia, which is associated with increased risk of cardiovascular disease. 

First of all, the typing of hyperlipemias seems to be essential requirement inasmuch as the responses of the Types to diet or drugs are substantially different. Several of the lipoprotein abnormahties appear to lead to vascular disease at an accelerated rate. In Lebanon, for example, there are relatively more cases of hyperlipidemia of Type II. These patients are predominantly children, who have xanthomas in their pre-teen years, angina and typical coronary artery disease in their teens, and an outlook for an average life-expectancy of 25 years [447]. Hyperlipidemia appears to be the primary disease in these children and apparently, leads to the secondary and fatal coronary artery disease. A thorough study of the abnormal lipoproteins of these children is obviously a necessity. 

Of the secondary hyperlipidemias those of hypothyroidism and biliary cirrhosis deserve particular attention, since they may show considerable elevation of cholesterol without hyperglyceridemia. In addition, xanthomas may occur in both with long duration. While biliary cirrhosis is characterized by the presence of jaundice, a very low ester cholesterol to free cholesterol ratio, and significant elevation of the phospholipid level, the exclusion of hypothjrroidism is not always as simple and may require appropriate thyroid function tests. 

Studies with dextrothyroxine in patients with hyperlipidemias including EFH were performed by Kuo and Bassett (1963), by Stbisower and Strisower (1964), by Duncan and Best (1964) and others, with a good hypocholesterolemic effect. Lowering of Sf 0—20 (beta) lipoproteins in the study of Strisower and Strisower averaged 21% and exceeded the effect of Atromid (see page 431). Decrease in size of xanthomas or their disappearance with dextrothyroxine therapy has been reported by Owen et al. (1962), Bernheim et al. (1963) and others. 

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