Talk:Combined hyperlipidemia

Requested move

Combined hyperlipidemia → Mixed hyperlipidaemia — The WHO CHD10 code for Type IIb is E78.2 which is clearly to be called "Mixed hyperlipidaemia". The only "combined" form in E78 group is for "Familial combined hyperlipidaemia" of E78.4. So should not this article be renamed to more correct Mixed hyperlipidaemia ? David Ruben ^Talk 22:18, 28 May 2009 (UTC)

It seems like you probably know better than anyone else at WP:RM. I've created a redirect from the proposed title to this one. Please go ahead and perform the move if you feel confident about it. Dekimasuよ! 09:39, 6 June 2009 (UTC)

I'd only suggest using Mixed hyperlipidemia instead to avoid running afoul of WP:ENGVAR. Dekimasuよ! 09:41, 6 June 2009 (UTC)

Commonality of disorder

From Harrison's: Rader Daniel J, Hobbs Helen H, "Chapter 350. Disorders of Lipoprotein Metabolism" (Chapter). Fauci AS, Braunwald E, Kasper DL, Hauser SL, Longo DL, Jameson JL, Loscalzo J: Harrison's Principles of Internal Medicine, 17e: http://www.accessmedicine.com/content.aspx?aID=2882429.

Familial Combined Hyperlipidemia

"FCHL is generally characterized by moderate elevations in plasma levels of triglycerides (VLDL) and cholesterol (LDL) and reduced plasma levels of HDL-C. It is the most common inherited lipid disorder, occurring in approximately 1 in 200 persons. Approximately 20% of patients who develop CHD under age 60 have FCHL. The disease is autosomal dominant in inheritance, and affected family members typically have one of three possible phenotypes: (1) elevated plasma levels of LDL-C, (2) elevated plasma levels of triglycerides due to elevation in VLDL-C, or (3) elevated plasma levels of both LDL-C and VLDL-C. A classic feature of FCHL is that the lipoprotein profile can switch among these three phenotypes over time and may depend on factors such as diet. FCHL can manifest in childhood but is usually not fully expressed until adulthood. A cluster of other metabolic risk factors are often found in association with this hyperlipidemia, including obesity, glucose intolerance, insulin resistance and hypertension (the so-called metabolic syndrome, Chap. 236). These patients do not develop xanthomas.

Patients with FCHL almost always have significantly elevated plasma levels of apoB. The levels of apoB are disproportionately high relative to the plasma LDL-C concentration, indicating the presence of small, dense LDL particles, which are characteristic of this syndrome. Hyperapobetalipoproteinemia, which has been used to describe the state of elevated plasma levels of apoB with normal plasma LDL-C levels, is probably a form of FCHL. Individuals with FCHL generally share the same metabolic defect, which is overproduction of VLDL by the liver. The molecular etiology of FCHL remains poorly understood, and it is likely that defects in several different genes can cause the phenotype of FCHL.

The presence of a mixed dyslipidemia (plasma triglyceride levels between 200–800 mg/dL and total cholesterol levels between 200–400 mg/dL, usually with HDL-C levels <40 mg/dL in men or <50 mg/dL in women) and a family history of hyperlipidemia and/or premature CHD strongly suggests the diagnosis of FCHL. The finding of an elevated plasma level of apoB level or the finding of an increased number of small, dense LDL particles in the plasma through advanced lipoprotein testing supports this diagnosis. FDBL should be considered and ruled out by beta quantification in suspected patients with a mixed hyperlipidemia.

Individuals with FCHL should be treated aggressively due to significantly increased risk of premature CHD. Decreased dietary intake of saturated fat and simple carbohydrates, aerobic exercise, and weight loss can all have beneficial effects on the lipid profile. Patients with diabetes should be aggressively treated to maintain good glucose control. Most patients with FCHL require lipid-lowering drug therapy to reduce lipoprotein levels to the recommended range and reduce the high risk of ASCVD. Statins are effective in this condition, but many patients will need a second drug (cholesterol absorption inhibitor, niacin, or fibrate) for optimal control of lipoprotein levels."

I added the commonality information in the introduction but do not know how to format a proper citation. Thanks! Ryan Pedigo (talk) 21:04, 3 April 2010 (UTC)