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Goldenberg N, Glueck C. · Cholesterol and Metabolism Center of Jewish Hospital, Cincinnati, Ohio, USA. · Vasc Health Risk Manag. · Pubmed #19475774 links to  free full text

Abstract: Statins became available for the treatment of hypercholesterolemia in 1987. Multiple, well-designed, placebo-controlled, double-blind studies revealed that each 1% reduction in serum cholesterol level was associated with about 1% reduction in risk of cardiovascular events. Low-density lipoprotein (LDL) cholesterol reduction to less than 78 mg/dL may be associated with reduction of atheroma burden. Patients with high levels of high specificity C-reactive protein and having LDL cholesterol less than 3.4 mmol/L (130 mg/dL) in primary prevention settings benefited from aggressive LDL cholesterol reduction with rosuvastatin over a 2-year period. However, in real life practice, about half of patients who are prescribed statins discontinue the medication by the end of the year. Medication adherence is lower in younger patients, women, and absence of known coronary heart disease. Personal features of the prescribing physician and dispensing pharmacies also affect patients' compliance. More studies are needed to evaluate if "compliance packets" would benefit patients in a real life situation.

Glueck CJ, Rawal B, Khan NA, Yeramaneni S, Goldenberg N, Wang P. · Cholesterol Center, Jewish Hospital, Cincinnati, OH 45229, USA. · Metabolism. · Pubmed #19154957 No free full text.

Abstract: Patients with high low-density lipoprotein cholesterol (LDLC) and asymptomatic high creatine kinase (CK) (>or=250 but <2500 IU/L, 10x the laboratory upper normal limit [UNL]) are often not started on statins or have statins stopped because of concern about myositis-rhabdomyolysis. In the current report, we prospectively examined the hypothesis that asymptomatic patients with high CK (>or=250 but <2500 IU/L) tolerate statins well at doses reducing LDLC to target, less than 100 mg/dL, without development of myalgia-myositis. We assessed outcomes of 3 groups of patients referred to us because of asymptomatic high CK (>or=250 but <2500 IU/L)--1 group (n = 29) on statins at referral and continued on statins, 1 group (n = 20) not on statins and started on statins, and 1 group (n = 19) not on statins and not given statins--all restudied 1 month after entry and then every 3 months. Of the 68 patients, 59 (87%) had CK greater than 1 to 3 times the UNL, 7 (10%) had CK greater than 3 to 5 times the UNL, and 2 (3%) had CK greater than 5 to 10 times the UNL. After 1.2 months of follow-up in 29 statin-->statin patients, median CK fell from 353 to 301 (P = .0018) and was 287 (P = .015) after 4 months. After 1.3 months of follow-up in 20 no statin-->statin patients, median CK fell from 397 to 292 (P = .0094) and was 419 after 4.1 months. After 1.1 months of follow-up in 19 no statin-->no statin patients, median CK fell from 392 to 323 (P = .14) and was 271 (P = .029) after 4.2 months. By repeated-measures analysis, there were no differences in entry CK among the 3 treatment groups; CK fell (P = .04) in the no statin-->no statin patients. Despite high baseline CK (48 patients with CK 1-5x the UNL, 1 with CK 5-10x UNL), no patients during follow-up on statins developed CK greater than 10 times the UNL (2500 IU/L), none discontinued statins or reduced statin dose because of myalgia-myositis, and there was no rhabdomyolysis. High pretreatment CK, particularly 1 to 5 times the UNL, should not be an impediment to start or continue statins to lower LDLC.

Ahmed W, Khan N, Glueck CJ, Pandey S, Wang P, Goldenberg N, Uppal M, Khanal S. · Cholesterol Center, Jewish Hospital of Cincinnati, Cincinnati, OH 45229, USA. · Transl Res. · Pubmed #19100953 No free full text.

Abstract: Our specific aims were to determine whether low serum 25 (OH) vitamin D (D2 + D3) (<32 ng/mL) was associated with myalgia in statin-treated patients and whether the myalgia could be reversed by vitamin D supplementation while continuing statins. After excluding subjects who took corticosteroids or supplemental vitamin D, serum 25 (OH) D was measured in 621 statin-treated patients, which consisted of 128 patients with myalgia at entry and 493 asymptomatic patients. The 128 myalgic patients had lower mean +/- standard deviation (SD) serum vitamin D than the 493 asymptomatic patients (28.6 +/- 13.2 vs 34.2 +/- 13.8 ng/mL, P < 0.0001), but they did not differ (p > 0.05) by age, body mass index (BMI), type 2 diabetes, or creatine kinase levels. By analysis of variance, which was adjusted for race, sex, and age, the least square mean (+/- standard error [SE]) serum vitamin D was lower in the 128 patients with myalgia than in the 493 asymptomatic patients (28.7 +/- 1.2 vs 34.3 +/- 0.6 ng/mL, P < 0.0001). Serum 25 (OH) D was low in 82 of 128 (64%) patients with myalgia versus 214 of 493 (43%) asymptomatic patients (chi(2) = 17.4, P < 0.0001). Of the 82 vitamin-D-deficient, myalgic patients, while continuing statins, 38 were given vitamin D (50,000 units/week for 12 weeks), with a resultant increase in serum vitamin D from 20.4 +/- 7.3 to 48.2 +/- 17.9 ng/mL (P < 0.0001) and resolution of myalgia in 35 (92%). We speculate that symptomatic myalgia in statin-treated patients with concurrent vitamin D deficiency may reflect a reversible interaction between vitamin D deficiency and statins on skeletal muscle.