Medication Induced Changes in Lipids and Lipoproteins

Megan C. Herink

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Medication Induced Changes in Lipids and Lipoproteins

Megan C. Herink, Pharm.D., BCPS.

Author Information and Affiliations

Last Update: September 2, 2025.

ABSTRACT

Several medications and medication classes have been reported to affect the lipid profile. This should be considered when evaluating patients with elevated levels of total cholesterol (TC), low-density lipoproteins cholesterol (LDL-C), non-high-density lipoprotein cholesterol (Non-HDL-C), triglycerides (TG), and reductions in high-density lipoprotein cholesterol (HDL-C). Glucocorticoids, atypical antipsychotics, anticonvulsants, hormones, and certain immunosuppressives are just some of the more commonly known medications to have a negative impact on the lipid profile. In some cases, this is a class effect and in others it might depend on dose and specific drug. However, how this translates to atherosclerotic cardiovascular disease (ASCVD) risk remains unknown, as there is insufficient evidence on the impact of these metabolic changes on overall risk of ASCVD. While for many of these medications, there is an abundance of literature and comprehensive reviews discussing the potential harmful effects on lipoprotein metabolism there remains much debate about the actual long-term implications, if any, of these changes. A thorough risk-benefit analysis of each treatment associated with an adverse effect on the lipid profile should be done based on individual patient factors. In general, if negative changes in the lipid profile are observed during therapy, replacement with an equivalent alternative therapy can be recommended. If no equivalent therapy is available and treatment must be initiated, then monitoring of serum lipid levels and initiating treatment for dyslipidemia is vital. The use of existing guidelines for the management of dyslipidemia in the general population can be referred to and in extreme cases when benefits do not outweigh the risks the use of the suspected medication should be reassessed. For complete coverage of all related areas of Endocrinology, please visit our on-line FREE web-text, WWW.ENDOTEXT.ORG.

INTRODUCTION

Secondary causes of dyslipidemia are important to identify as treatment of the underlying cause may alleviate the dyslipidemia and ultimately reduce the need for drug treatment or the need for combination pharmacotherapy (1). Guidelines recommend that providers should evaluate for underlying conditions that could be causing dyslipidemias before initiating treatment in patients (2,3). One such secondary cause of abnormally altered lipid or lipoprotein levels is medications used for other indications (4). Serum lipid levels can be affected both positively and negatively by certain medications. Medications can affect lipid levels either directly or indirectly through effects on weight or glucose metabolism. This should be considered when evaluating patients with elevated levels of total cholesterol (TC), low-density lipoproteins cholesterol (LDL-C), non-high-density lipoprotein cholesterol (Non-HDL-C), triglycerides (TG) and reductions in high-density lipoprotein cholesterol (HDL-C) (5).

There have also been reports of various medications causing severe drug-induced hypertriglyceridemia that leads to acute pancreatitis (6-8). While there is a paucity of data describing the exact mechanism of drug-induced pancreatitis, it is known that severe hypertriglyceridemia (TG > 1000 mg/dl) can cause acute pancreatitis. Therefore, in the absence of other causes, medications should be evaluated in the presence of acute pancreatitis and severe hypertriglyceridemia.

Several medications and medication classes have been reported to affect the lipid profile (Table 1). In some cases, this is a class effect, and some instances agents belonging to the same class can have significantly different actions on lipid levels (e.g. beta blockers) (9). This is a consideration to appreciate when selecting a specific agent for high-risk patients and concurrent medications known to induce lipid abnormalities should be evaluated for discontinuation or dosage reduction prior to initiating long-term lipid lowering agents. How this translates to atherosclerotic cardiovascular disease (ASCVD) risk remains unknown, as there is insufficient evidence on the impact of these metabolic changes on overall risk of ASCVD.

Table 1.

Drugs That May Cause Dyslipidemias

	LDL Cholesterol	Triglycerides	HDL Cholesterol
*Cardiovascular*
Amiodarone	↑Variable	↔	↔
β-Blockers^***	↔	↑10-40%	↓5-20%
Loop diuretics	↑5-10%	↑5-10%	↔
Thiazide diuretics (high dose)	↑5-10%	↑5-15%	↔
*Hormones*
Estrogen	↓7-20%	↑40%	↑5-20%
Select progestins	↑Variable	↓Variable	↓15-40%
Selective Estrogen Receptor Modulators	↓10-20%	↑0-30^*	↔
Danazol	↑10-40%	↔	↓50%
Anabolic steroids	↑20%	↔	↓20-70%
Corticosteroids	↑Variable	↑Variable	↔
Growth Hormone	↑10-25%	↔	↔↑7%
*Antiviral Therapy*
Protease inhibitors	↑15-30%	↑15-200%	↔
Direct Acting Antivirals	↑12-27%	↔	↑14-20%
I *mmunosuppressants*
Cyclosporine and tacrolimus	↑0-50%	↑0-70%	↑0-90%
*Centrally Acting Medications*
First Generation antipsychotics	↔	↑22%	↓20%
Second Generation antipsychotics	↔	↑20-50%	↔
Anticonvulsants	↑Variable	↔	↑Variable
*Other Medications*
Retinoids	↑15%	↑35-100%	↔^**
Janus Kinase Inhibitors	↑10-15%	↑Variable	↑10-15%

*: Raloxifene has not been shown to increase triglyceride levels, while reported increases of up to 30% have been reported with use of tamoxifen. **Data remains conflicting, and some evidence shows a decrease, no effect, or increase. ***Varies based on individual drug.

ANTIHYPERTENSIVE DRUGS

There is an abundance of literature and comprehensive reviews discussing the potential harmful effects of antihypertensive drugs on lipoprotein metabolism and there remains much debate about the actual long term implications, if any, of these changes (10). The diuretics and β-

adrenergic blockers have the most data to support their adverse effects on lipid levels (11-16).

Diuretics

Thiazide and loop diuretics have been associated with increases in plasma cholesterol in studies of patients with hypertension. Guidelines from the American College of Cardiology/American Heart Association recommend thiazide diuretics as one of four specific medication classes to be considered as initial therapy for hypertension (17). In view of these recommendations and widespread use of diuretics, it is important to review the adverse metabolic effects. Use of high-dose thiazide diuretics (≥50 mg/day) may negatively affect lipoprotein levels, as seen in small studies, and some investigators have suggested that as a result, diuretics could worsen coronary artery disease (CAD) (13). Total cholesterol levels can be increased by approximately 4% and LDL-C levels by approximately 10% (10,16,18). HDL-C levels are not affected, while TG concentrations can also be elevated by 5-15% (10). Low dose hydrochlorothiazide (12.5 – 25 mg/day) has been shown not to effect plasma lipids in otherwise healthy men and women (13). The dose appears to be a factor in resulting cholesterol levels (19); however, there are conflicting data regarding whether the effects on lipid levels is primarily caused by higher doses (13). Long term effects beyond one year remain undetermined as more recent studies showed that effects are short term and serum lipid levels return to initial levels (20). Additionally, thiazide diuretics have been shown to decrease the risk of cardiovascular (CV) events despite this effect on lipid levels (21).

Loop diuretics have similarly been shown to increase LDL-C and TG levels with some studies showing changes of comparable magnitude and some showing effects that are less than thiazide diuretics (22,23). However, the effects appear to be acute and not expected at time intervals longer than the duration of action of furosemide (6 to 8 hours). One possibility is that hormones stimulated in response to decreased intravascular volume are responsible for some changes in lipid and lipoprotein levels (23). The effects of monotherapy with potassium-sparing diuretics on lipid levels are largely unknown, but the combination of a potassium-sparing diuretic and a thiazide show similar changes as monotherapy with a thiazide diuretic, suggesting no impact from potassium-sparing diuretics.

The mechanism of increased lipid levels and TGs caused by diuretics remains unclear. One theory is that a reduction in insulin sensitivity may cause an increase in hepatic production of cholesterol (18,24). It has been recently suggested that they may modulate adipocyte differentiation leading to accumulation of plasma TGs in susceptible patients with a particular genetic polymorphism in the NELL1 gene (25). It is also thought that there are sex differences, as diuretics were shown to produce a greater short-term increase in TC and LDL-C in postmenopausal women than in men. Premenopausal women may have a protective effect from estrogens and have demonstrated no changes in lipid levels (16). Estrogens have been theorized to increase the number of hepatic LDL binding sites and stimulate the hepatic uptake of lipoproteins (18).

β-Blockers

The metabolic adverse effects of β-blockers depend on dose and the specific drug. While β-blocking agents have a negligible effect on serum TC or LDL-C, they can increase TG levels from 10 to 40% and decrease HDL-C levels by approximately 5 to 20% (10). The evidence on duration of effect remains conflicting with studies citing effects to last less than 1 year (20), and other studies reporting increased levels after several years of treatment (25). The alterations in lipoprotein levels from β-blockers does not appear to be a class effect, and agents with intrinsic sympathomimetic activity (ISA), β1-selectivity, or vasodilatory effects (Table 2) are associated with a less pronounced effect (10,26). Non-selective β-blockers which cause peripheral vasoconstriction through peripheral β-adrenergic receptors seem to increase insulin resistance, leading to lowering of HDL-C and increased TG (27). Agents that are cardioselective and/or have alpha-1-adrenoreceptor blocking activity do not appear to increase insulin resistance. Other potential mechanisms of β-blocker induced lipid changes are from β-blocker associated weight gain, a decreased lipid metabolism through a reduction in the muscle lipoprotein lipase enzyme, and endothelial dysfunction from peripheral vasoconstriction (Table 3) (28). The beneficial effects of carvedilol compared to metoprolol and atenolol on lipid parameters has been demonstrated in several small studies (14,27,29). Carvedilol has selective α -1-adrenoreceptor blocking activity, causing vasodilation and a reduction in insulin resistance with no effect on lipid levels. Conversely, selective α-blocking agents (prazosin) have a beneficial effect on the lipid profile and have been shown to increase HDL-C and decrease TG (30,31).

Table 2.

Pharmacological Properties of β-Blockers

	Beta Selectivity	Intrinsic sympathomimetic (ISA) or α-blocking	Vasodilating Properties
More pronounced effect on lipid levels
Atenolol	β1 selective	-	-
Betaxolol	β1 selective	-	-
Bisoprolol	β1 selective	-	-
Metoprolol	β1 selective	-	-
Nadolol	Nonselective	-	Vasoconstricting
Propanolol	Nonselective	-	Vasoconstricting
Timolol	Nonselective	-	Vasoconstricting
Less pronounced effect on lipid levels
Acebutolol	Nonselective	ISA	Vasoconstricting
Penbutolol	Nonselective	ISA	Vasoconstricting
Pindolol	Nonselective	ISA	Vasoconstricting
No effect on Lipid levels
Carvedilol	Nonselective	α-blocking	Vasodilating
Labetolol	Nonselective	α-blocking	Vasodilating
Nebivolol	β1 Selective	-	Vasodilating

Table 3.

Potential Mechanism of β-blocker Induced Dyslipidemia

Inhibition of insulin release

Insulin resistance

Weight gain

Inhibition of lipolysis

Reduced activity of lipoprotein lipase enzyme

Endothelial dysfunction

Thiazide diuretics and β-blockers are important agents for other cardiovascular indications. β-blockers are effective in reducing cardiovascular morbidity and mortality in congestive heart failure and diuretics are vital for symptomatic management of many CV comorbidities. While it is important to assess for increased lipid levels caused by these agents, with other compelling indications, it remains prudent to continue them while continuing to monitor serum lipid levels. For patients with dyslipidemia and a compelling indication for a β-blocker, carvedilol may be the best choice.

OTHER CARDIOVASCULAR MEDICATIONS

Amiodarone

Amiodarone, a potent antiarrhythmic drug, increases plasma cholesterol levels, reported in case reports (32,33). Amiodarone increases LDL-C levels because of a decreased expression of the LDL-receptor gene (32,34,35). In addition, amiodarone induced hypothyroidism can cause alterations in lipid metabolism as hypothyroidism is one of the most common causes of secondary hyperlipidemia. Amiodarone contains 39.4% iodine on weight basis which may cause hyperthyroidism or hypothyroidism (35). Research demonstrates that long-term amiodarone treatment induces a dose-dependent increase in plasma cholesterol, in part due to thyroid hormone deficiency and a decrease in the number of LDL receptors (36,37).

DIABETES MEDICATIONS

Sodium-Glucose Co-Transporter 2 (SGLT2) Inhibitors

The SGLT2 inhibitors lower blood glucose and hemoglobin A1c (HgA1c) through inhibiting SGLT2 in the proximal tubule, thereby blocking reabsorption of glucose and increasing the renal excretion of glucose (38). There are currently several SGLT2 inhibitors available and approved for the treatment of type 2 diabetes mellitus. Although data is mixed and the individual agents appear to affect the lipid profile to a varying degree, these agents have been shown to increase LDL-C while also increasing HDL-C with variable effects (decreasing or no effect) on TG. A meta-analysis of 60 randomized studies showed that as a class, SLGT2 inhibitors can increase TC by a mean difference of 3.65 mg/dl (95% CI 2.4 to 4.89), LDL-C by 2.92 mg/dl (95% CI 1.92 to 3.92), HDL-C by 2.23 mg/dl (95% CI 1.85 to 2.61), and reduce TG by a mean difference of -8.78 mg/dl (95% CI -12.46 to -5.10) (39). While a decrease in weight could explain the favorable effects seen on HDL-C and TG, it remains unclear what the mechanism behind the modest dose-related increase in LDL-C is (40). One possibility is that SGLT2 inhibitors cause a switch from carbohydrate to lipid utilization causing an increase in hepatic fatty acid levels to induce ketone production and hepatic total cholesterol levels (40). They may also increase lipoprotein lipase mediated conversion of VLDL to LDL (39). Despite this small increase in LDL-C, SGLT2 inhibitors have proven CV benefits in patients with diabetes and heart failure. To date, canagliflozin, dapagliflozin and empagliflozin have demonstrated an improvement in CV outcomes (composite of CV mortality, nonfatal myocardial infarction (MI), or nonfatal stroke) and a reduction in heart failure hospitalizations in subjects with high CV risk (41). While additional lipoprotein monitoring may be necessary, the CV benefits of SGLT-2 inhibitors outweigh the potential for slight increases in LDL-C.

Metformin

Metformin may decrease serum TG levels and LDL-C levels without altering HDL-C levels (42). In a meta-analysis of 37 trials with 2,891 patients, metformin decreased TG by 11.4mg/dL when compared with control treatment (p=0.003) (43). In an analysis of 24 trials with 1,867 patients, metformin decreased LDL-C by 8.4mg/dL compared to control treatment (p<0.001) (43). In contrast, metformin did not significantly alter HDL-C levels (43). It should be noted that in the Diabetes Prevention Program 3,234 individuals with impaired glucose metabolism were randomized to placebo, intensive lifestyle, or metformin therapy. In the metformin therapy group no significant changes were noted in TG, LDL-C, or HDL-C levels compared to the placebo group (44). Thus, metformin may have small effects on lipid levels.

Thiazolidinediones

The effect of thiazolidinediones depends on which agent is used. Rosiglitazone increases serum LDL-C levels, increases HDL-C levels, and only decreases serum TG if the baseline TG levels are high (42). In contrast, pioglitazone has less impact on LDL-C levels, but increases HDL-C levels, and decreases TG (42). In the PROactive study, a large randomized cardiovascular outcome study, pioglitazone decreased TG levels by approximately 10%, increased HDL-C levels by approximately 10%, and increased LDL-C by 1-4% (45). It should be noted that reductions in the small dense LDL subfraction and an increase in the large buoyant LDL subfraction are seen with both thiazolidinediones (42). In a randomized head-to-head trial, it was shown that pioglitazone decreased TG levels and increased serum HDL-C levels to a greater degree than rosiglitazone treatment (46,47). Additionally, pioglitazone increased LDL-C levels less than rosiglitazone. In contrast to the differences in lipid parameters, both rosiglitazone and pioglitazone decreased A1c and C-reactive protein to a similar extent. The mechanism by which pioglitazone induces more favorable changes in lipid levels than rosiglitazone despite similar changes in glucose levels is unclear, but differential actions of ligands for nuclear hormone receptors are well described.

Incretins

Glucagon-like peptide-1 (GLP-1) receptor agonists can favorably affect the lipid profile by inducing weight loss (decreasing TG and very modestly decreasing LDL-C levels) (42). In a review by Nauck and colleagues it was noted that GLP-1 receptor agonists lowered TG levels by 18 to 62mg/dL depending upon the specific GLP-1 receptor agonist while decreasing LDL-C by 3-8mg/dL and increasing HDL-C by less than 1mg/dL (48). In a meta-analysis of the effect of semaglutide in obese or overweight patients without diabetes on lipid levels LDL-C and TG levels were decreased by 5.16% and 16.5% respectively while HDL-C levels increased by 2.08% (49). Additionally, GLP-1 receptor agonists reduce postprandial TG by reducing circulating chylomicrons by decreasing intestinal lipoprotein production (42,48). DPP4 inhibitors have a similar effect on postprandial TG levels as GLP-1 receptor agonists while having minimal effects on fasting lipid levels (48).

In the SURPASS tirzepatide studies TG levels were consistently decreased by 13-25% (50). In most studies except for SURPASS 5, HDL cholesterol levels increased by 3-11% (50). Total cholesterol and LDL cholesterol levels were modestly decreased in most studies (50). Not unexpectedly given the decrease in TG levels small LDL particles were decreased. In a head-to-head trial comparing the effect of tirzepatide 10-15mg vs. semaglutide 1.7-2.4mg on lipid levels in adults with obesity a slightly greater effect was observed with tirzepatide (TG -34.9 vs. -27.5mg/dL; LDL-C -7.8 vs. -5.9mg/dL; HDL 5.7 vs. 2.9mg/dL) (51).

Table 4.

Effect of Glucose Lowering Drugs on Lipid Levels (52)

Metformin	Modestly decrease TG and LDL-C
Sulfonylureas	No effect
DPP4 inhibitors	Decrease postprandial TG
GLP1 analogues	Decrease fasting and postprandial TG, increases HDL-C, modestly decrease LDL-C
Tirzepatide	Decrease TG, modestly decrease LDL-C, increase HDL-C
Acarbose	Decrease postprandial TG
Pioglitazone Rosiglitazone	Decrease TG and increase HDL-C. Small increase LDL-C but a decrease in small dense LDL
SGLT2 inhibitors	Small increase in LDL-C and HDL-C. Variable effect on TG
Colesevelam	Decrease LDL-C. May increase TG
Bromocriptine-QR	Decrease TG
Insulin	No effect

HORMONES

Glucocorticoids

In patients without inflammatory disorders, the administration of glucocorticoids has variable effects on the lipid profile; HDL-C levels are typically increased with the magnitude of change in plasma triglyceride and LDL-C varying among studies (53-55). In patients with inflammatory diseases, the effect of glucocorticoids on lipids is confounded by the marked anti-inflammatory effects of glucocorticoids. Inflammation affects lipid and lipoprotein levels and thus reducing inflammation per se can affect the lipid response to glucocorticoid treatment (56). Similarly, the effect of glucocorticoids on lipids following transplantation or the treatment of other medical conditions is also difficult to interpret due to the simultaneous use of other medications and the response of the underlying medical conditions. Furthermore, the dose and route of administration of the glucocorticoids can be an important variable, as low doses often have minimal effects on triglyceride, LDL-C, and HDL-C levels while high doses tend to increase serum triglyceride, LDL-C, and HDL-C levels.

The precise mechanisms by which glucocorticoids alter lipid levels is unclear. Glucocorticoids increase the activity of acetyl CoA carboxylase and fatty acid synthase resulting in an increase in hepatic fatty acid synthesis (57). Additionally, in acute experimental models’ glucocorticoids also increase adipose tissue lipolysis resulting in an increase in circulating free fatty acid levels, which will deliver fatty acids to the liver (57). Glucocorticoids also stimulate the enzymes required for the synthesis of triglyceride in the liver and the increase in hepatic triglyceride levels decreases the degradation of Apo B and increases the formation and secretion of VLDL (57). Moreover, in patients with Cushing’s syndrome VLDL production rates are increased, while VLDL clearance is not altered, indicating that hepatic overproduction of VLDL accounts for the increase in serum triglyceride levels (58). This increase in VLDL production could also contribute to the increase in LDL-C levels in patients with Cushing’s syndrome (58). Glucocorticoids increase the synthesis and secretion of Apo A-I by direct effects on the Apo A-I promoter that are mediated via the glucocorticoid receptor (59,60). The increased production of Apo A-I could lead to an increase in HDL-C.

DRUGS USED TO TREAT CUSHING’S SYNDROME

Ketoconazole is an anti-fungal imidazole derivative that blocks several steps in cortisol biosynthesis thereby lowering serum cortisol levels. However, ketoconazole is also an inhibitor of cholesterol biosynthesis, acting directly by blocking the conversion of methyl sterols to cholesterol and indirectly by suppressing cholesterol synthesis via feedback inhibition of HMG-CoA reductase by sterol intermediates (61,62). In the past, ketoconazole had been used to treat patients with familial hypercholesterolemia before the widespread use of statins, as it reduced total, intermediate density cholesterol, LDL-C, and apo B levels by approximately 25% (63). Levoketoconazole, also decreases total cholesterol and LDL-C levels by approximately 25% and slightly increases HDL-C levels (64).

Mitotane is used for treatment of adrenal carcinoma or intractable Cushing’s disease. Mitotane raises circulating cholesterol, LDL-C, Apo B, and HDL-C levels (65-67). Increases in triglyceride levels have also occurred (66,67). Mitotane increases HMGCoA reductase activity, which may contribute to the increase in LDL-C (68). In a case report mitotane increased LDL-C levels as high as 300mg/dl (69). Because mitotane induces CYP3A4 activity one should use a statin that is not metabolized by this enzyme (for example pravastatin or rosuvastatin) (66).

Mifepristone, a potent antagonist of glucocorticoid and progesterone receptors, lowers HDL-C and Apo AI levels (70). The mechanism for this decrease in HDL-C is unknown. In a small study short-term administration of mifepristone reduced serum TG levels, which correlated with increases in adipose tissue lipoprotein lipase activity (71).

Pasireotide, a somatostatin analog, targets corticotroph tumors and is used for Cushing’s disease when surgery is unsuccessful or not accessible. Despite causing hypergylcemia, pasireotide has a positive impact on the lipid profile and leads to small decreases in TC and LDL-C and increases in HDL-C levels (72).

Estrogens and Progestins

Estrogen administration increases HDL-C levels by 5-15% and decreases LDL-C levels by 5-20% (73-76). In addition, estrogens also increase triglycerides but in patients with genetic or acquired abnormalities in triglyceride metabolism estrogen therapy can precipitate marked hypertriglyceridemia and even the chylomicronemia syndrome (77,78). In women with normal baseline triglycerides an approximate 10-15mg/dl increase in triglycerides occurs with estrogen therapy (73-76). If the increase in triglycerides is substantial, it leads to a decrease in LDL size (i.e., formation of small dense LDL). Not unexpectedly, estrogens induce an increase in Apo A-I levels and a decrease in Apo B levels. Lp(a) levels are also decreased by 20-25% by estrogen therapy (73-76). The effects of oral estradiol are similar to that of oral conjugated equine estrogens (Premarin).

Transdermal estrogen administration has less of an effect on lipids and lipoproteins (73-76,79). The increase in HDL-C and the decrease in LDL-C are markedly blunted (73-76,79). Importantly, the effect of transdermal estrogen on triglycerides is minimal and therefore in patients with baseline abnormalities in triglyceride metabolism, the use of transdermal estrogen therapy is preferred (73-76,79). The lack of a robust effect on lipids with transdermal estrogen preparations is likely due to decreased exposure of the liver to estrogens compared with oral therapy.

Selective estrogen-receptor modulators, including raloxifene and tamoxifen, appear to have less impact on lipids, but can still elevate TG levels (80). There have been several case reports in the literature describing tamoxifen-induced hypertriglyceridemia causing acute pancreatitis (7,8,81,82).

Progestins generally have androgen-like effects on lipid and lipoproteins and therefore progestin administration decreases HDL-C and TG levels but has little or no effect on LDL-C levels (73-76). Thus, when combined with estrogen therapy, the estrogen/progesterone preparation blunts the characteristic estrogen induced increase in HDL-C levels without affecting the estrogen induced reduction in LDL-C levels (73-76). In many but not all studies, progesterone also blunts the estrogen induced increase in TG levels (73-76,83). In contrast, progesterone appears to either slightly augment or have no effect on the ability of estrogens to decrease Lp(a) levels (75). It is important to note that the effect of adding progesterone is dependent on both the dose and the androgenicity of the particular progesterone used. Godsland analyzed a large number of studies and found in order of least to most potent progesterone affecting lipid levels the following; dydrogesterone and medrogestone, progesterone, cyproterone acetate, medroxyprogesterone acetate, transdermal norethindrone acetate, norgestrel, and oral norethindrone acetate (75). Progestins with more androgenic effects, such as levonorgestrel, have larger effects on lipid levels than those with less androgenic effects (84). Newer, “third generation” progestins (desogestrel, gestodene) with higher specificity have been developed to reduce this risk and have demonstrated favorable effects on LDL-C levels and HDL-C levels, but they can also increase TGs (85,86).

In recent years, the dose of ethinyl estradiol in oral contraceptives has been decreased from 50 down to just 20-30 mcg in current formulations to reduce adverse metabolic changes. Therefore, the effect varies with oral contraceptives based on their estrogen and progestin content and more specifically the potency of the estrogen and the androgenicity of the progestin. The American Heart Association recommends that lower estrogen-containing preparations or other forms of contraception should be considered in women who develop hypertriglyceridemia while taking therapy (80). Oral contraceptives with low doses of estrogen should be used in women with dyslipidemia, as studies of low dose triphasic oral contraceptives have resulted in no significant changes or only mild elevations in TC, LDL-C, and TG levels. Contraceptives that can be considered for women with uncontrolled LDL-C levels or multiple CV risk factors, include using non-androgenic or anti-androgenic progestins as they have minimal influence on the lipid profile (87).

There are several effects of estrogen that could lead to an increase in HDL-C levels (for review see (57). First, studies have shown that estrogens stimulate the expression of Apo A-I, which will lead to an increased synthesis of Apo A-I and the increased formation of HDL. Second, estrogen therapy decreases hepatic lipase activity, which will decrease the hydrolysis of triglyceride and phospholipids on HDL particles, which could potentially result in a decrease in the catabolism of HDL. Finally, estrogens suppress the expression of SR-B1 in the liver, which will decrease the transfer of cholesterol from HDL particles into the hepatocyte increasing plasma HDL-C levels. Based on kinetic studies it is likely that the predominant effect of estrogens is to increase the production of HDL, which is mediated by an increase in Apo A-I production. The net result may be protective from atherosclerosis.

The decrease in LDL-C induced by estrogen treatment is accounted for by an increase in LDL clearance (57). Studies have shown that estrogens increase the expression of hepatic LDL receptors (57). Additionally, estrogens reduce PCSK9 levels, which would decrease the degradation of LDL receptors (57). Together, this would increase the number of hepatic LDL receptors leading to the accelerated clearance of LDL and a reduction in plasma LDL-C levels.

The increase in plasma triglyceride levels induced by estrogen treatment is due to the increased production and secretion of VLDL particles (57). The mechanism by which estrogens decrease Lp(a) levels is unknown.

Anabolic Steroids

DANAZOL

Danazol is a synthetic steroid indicated for endometriosis and for prophylaxis in patients with hereditary angioedema (HAE) (88,89). A review of data for the treatment of endometriosis showed that danazol treatment can result in a rapid reduction in HDL-C by up to 50% and increase in LDL-C by 10-40% (90). However, these levels return to baseline levels after stopping therapy and there is only a concern in prolonged therapy for 12 months or greater or in patients with a high risk of ASCVD (89). This effect is consistent in the literature (91-94). The mechanism is likely from its effects on hepatic lipase, LDL receptor, and lecithin cholesterol acyl transferase activity. Data supports an altering of lipoprotein levels in women treated for endometriosis, but there may not be an effect in the treatment of HAE (95). Some possible explanations for this difference are that HAE doses are lower than doses used for the treatment of endometriosis, the duration of therapy is longer and often lifelong versus 2-6 months for endometriosis, and men are also treated for HAE. A randomized trial evaluated danazol on HDL-C in healthy volunteers and patients with HAE. Patients with ASCVD or significant risk factors for ASCVD were excluded in this healthy volunteer study. Short-term use in healthy subjects (n=15) demonstrated a 23% decrease in HDL-C levels; however, these were normalized after 4 weeks of treatment. There was no effect seen on LDL-C or TG. Longer-term use in patients with HAE did not appear to decrease HDL-C levels compared to matched healthy controls. This study supports the belief that the differences in study populations as well as varying duration and doses of danazol impact the effect danazol has on the lipid profile. However, other studies have shown conflicting results and also demonstrated a decrease in HDL-C (as well as apolipoprotein Apo A-I; the major protein component of the HDL particle) and increase in LDL-C in long term use for the prevention of HAE (95,96). However, this negative effect was not shown to translate into an increased risk of atherosclerosis (96).

Androgens

The changes in lipid and lipoprotein levels induced by testosterone treatment are relatively small and variable depending upon the patient population studied, the route and dose of testosterone administration, the duration of therapy, the specific testosterone preparation (whether or not it can undergo aromatization to estrogens), and perhaps other unrecognized factors (57). For example, the reductions in HDL-C appear to be greater in patients whose baseline HDL-C levels are high (97,98). Additionally, transdermal testosterone treatment appears to have less effect on HDL-C levels than intramuscular administration (99). High dose testosterone treatment appears to more consistently lower HDL-C levels than low dose treatment (100). For example, testosterone enanthate 200mg IM every week used in a contraception study resulted in a relatively robust 13% decrease in HDL-C levels (101). Similarly, raising serum testosterone levels to higher levels produces greater decreases in LDL-C levels (100). Finally, using testosterone preparations that are not converted to estrogens or simultaneously blocking aromatization can lead to more profound decreases in HDL-C and LDL-C levels, which can be attributed to estrogens having effects on lipid and lipoprotein levels that counterbalance the effects of androgens (estrogens increase HDL-C and decrease LDL-C) (102,103). The important clinical point is that in the typical androgen deficient patients that we treat with the usual testosterone therapy there will only be a modest or no changes in plasma lipid and lipoprotein levels. The minimal effect of testosterone therapy was clearly demonstrated in a large randomized double-blind trial of 788 males over the age of 65 with low testosterone levels who were treated with either testosterone gel to normalize testosterone levels or placebo for 1 year (104). In this trial HDL-C (adjusted mean difference, -2.0 mg/dL; P < 0.001), and LDL-C were both slightly decreased (adjusted mean difference, -2.3 mg/dL; P = 0.051) from baseline with no change in triglyceride levels in the testosterone treated individuals.

Several studies have shown that testosterone administration decreases Lp(a) levels and the effect is more robust in individuals who have high baseline Lp(a) levels (101,105,106). Moreover, it has been shown that simultaneously administering testosterone with an aromatase inhibitor does not markedly reduce the ability of testosterone to decrease Lp(a) levels, indicating that the conversion of testosterone to estrogens does not account for this effect suggesting a direct action of testosterone (105). Lp(a) is a pro-atherogenic lipoprotein so testosterone induced decreases should be beneficial.

While treatment of typical older hypogonadal men with testosterone therapy has only modest to no effects on plasma lipids and lipoproteins, the use of high dose androgenic steroids in young men for the purpose of increasing muscle mass and strength can have profound effects. Studies of bodybuilders and weight lifters using anabolic steroids have revealed reductions in HDL-C levels by 20-70% accompanied by decreases in apo A-I levels, as well as elevations in LDL-C by approximately 20% (107-110). In a study by Webb and colleagues of 14 individuals taking high dose androgenic steroids, HDL-C levels were markedly reduced to 29mg/dl, which was less than 50% of the mean HDL-C when exogenous steroids were not used (61mg/dl) (110). Additionally in these individuals LDL-C levels were also higher on androgenic steroids (150mg/dl) than off of androgenic steroids (125mg/dl) (110). Similarly, Hurley and colleagues demonstrated that androgen use by eight bodybuilders and four powerlifters lowered HDL-C levels by 55% and raised LDL-C levels by 61% (111). In a double-blind cross-over study anabolic steroids, which may not have androgenic effects, induced a 25-27% decrease in HDL-C levels, which returned towards normal 6 weeks after cessation of drug use (112). A literature review described 49 reports of 1,467 athletes using anabolic-androgenic steroids corroborating the link and reports that these changes can occur within 9 weeks of self-administration and the effects seem to be reversible and normalize within 5 months after discontinuation (113). Thus, if one sees an athletic male with unexpectedly low HDL-C levels one should suspect androgen and/or anabolic steroid use, which is often obtained as a dietary supplement or as a pharmaceutical from an unregulated source.

There are a number of potential explanations why the changes in lipid and lipoprotein levels are greater in athletes using androgenic steroids. First, the doses used by the athletes are much higher than used in typical testosterone replacement. Second, the androgenic steroids used are often different and more potent (for example nandrolone-decanoate and oxandrolone). Often the compounds used are not converted to estrogen by aromatase and therefore their effects on serum lipid levels will not be counterbalanced by estrogen formation. Lastly, young athletes are often lean and have little adipose tissue and thus low aromatase activity. There can be individual patient variation in aromatase activity with obese older individuals having increased aromatase activity compared to young athletic individuals (114). The conversion of testosterone to estrogens by aromatase may blunt the effects of testosterone as estrogens will increase HDL-C levels and decrease LDL-C levels. Together it is likely that these factors account for the more robust changes in lipids and lipoprotein levels induced by androgens in young athletes.

ANDROGEN DEPRIVATION THERAPY

Androgen deprivation therapy (ADT) is hormone therapy with gonadotropin-releasing hormone (GnRH) agonists used for the treatment of prostate cancer and is associated with a variety of metabolic adverse events, including lipid alterations (115). Studies of androgen deprivation therapy have shown an increase in plasma HDL-C and Apo A-I levels (116-123). This increase occurs very rapidly within 2 weeks of lowering serum testosterone levels (116). Furthermore, this increase in HDL-C is inhibited if one simultaneously administers testosterone demonstrating that this increase is due to the suppression of testosterone levels (121). In addition, androgen deprivation therapy is also associated with an elevation of LDL-C, non-HDL-C, Lp(a), and triglyceride levels (117-120,122,124-127). The increase of Lp(a) is notable as the metabolism of Lp(a) often does not parallel the metabolism of LDL.

Growth Hormone

Adults with growth hormone deficiency frequently have lipid abnormalities, decreased insulin sensitivity and an increased CV morbidity and mortality. Treatment with recombinant human growth hormone, or somatropin, for adults with growth hormone deficiency has contributed to positive lipid changes, including decreased levels of TC and LDL-C by 10-25% (128-133). A meta-analysis by Newman and colleagues reported on the effect of low dose GH replacement (<0.7mg/day; seven studies) and high dose GH replacement (>0.7mg/day; sixteen studies) involving over 1000 subjects (134). In both the low dose and high dose groups, GH replacement therapy decreased total and LDL-C levels but did not significantly affect either HDL-C or triglyceride levels. LDL-C levels decreased by 11.3%. A meta-analysis of 37 trials by Maison et al also found that total and LDL-C levels were decreased with no significant changes in triglycerides or HDL-C by GH treatment (135). In a few studies, HDL-C levels have been observed to increase with GH therapy (136-138). For example, in a 15 year long term perspective study GH therapy reduced LDL-C and increased HDL-C levels, while having no significant effect on triglyceride levels (129). This long observational study demonstrates that treatment of growth hormone deficiency in adults results in sustained improvements in the serum lipid profile. The decrease in LDL-C levels with GH treatment correlates with baseline LDL-C levels (i.e. the higher the LDL-C the greater the decrease with GH treatment) (139). Interestingly GH treatment increases Lp(a) levels (138,140-143). There is some data to suggest that individual response to growth hormone on lipid metabolism is partly influenced by genetic polymorphisms in genes related to lipid metabolism (144).

Studies have shown that GH increases the expression of hepatic LDL receptors (145,146). Additionally, GH decreases circulating PCSK9 levels, which would also increase hepatic LDL receptors (147). As a consequence, the clearance of LDL-C is accelerated by GH treatment (148,149). Thus, the increase in total cholesterol and LDL-C levels in GH deficient patients is likely due to a decrease in hepatic LDL receptors and therefore with GH administration the number of LDL receptors increases leading to a decrease in plasma LDL-C levels. Notably, in a patient with homozygous familial hypercholesterolemia, devoid of functional LDL receptors, GH treatment did not result in a decrease in LDL-C levels, whereas in GH deficient patients, normal subjects, and patients with heterozygous familial hypercholesterolemia treatment with GH resulted in a decrease in LDL-C levels (148). This observation further demonstrates the importance of LDL receptors in mediating the decrease in LDL-C levels in response to GH administration.

In transgenic mice expressing the human Apo (a) gene, GH administration increases the mRNA levels of Apo (a) and plasma levels of Apo (a) (150). The increased production of Apo (a) induced by GH could account for the increase in Lp(a) levels induced by GH treatment.

Thyroid Hormone

A meta-analysis by Kotwal et al demonstrated that the treatment of hypothyroidism with levothyroxine resulted in a decrease in TC by -58 mg/dL, LDL-C by -41 mg/dL, HDL-C by -4.1 mg/dL, TG by -7.3 mg/dL, apo A by -12.6 mg/dL, apo B by -34.0 mg/dL, and Lp(a) by -5.6 mg/dL (151). The decrease in LDL-C levels is primarily due to an increase in hepatic LDL receptors resulting in the accelerated clearance of circulating LDL (152). This increase in LDL receptors is due to thyroid hormone stimulating the increased expression of LDL receptors (152,153). In addition, hyperthyroidism leads to a decrease in PCSK9, which will lead to a decrease in the degradation in LDL receptors contributing to the increase in LDL receptors (154). Thyroid hormone induces other alterations in cholesterol metabolism that could contribute to the decrease in LDL-C levels including stimulating the elimination of cholesterol from the body by increasing the conversion of cholesterol into bile acids and increasing the biliary secretion of bile acids and cholesterol, decreasing intestinal absorption of dietary cholesterol, and decreasing Apo B production (57).

A number of key proteins involved in HDL metabolism and reverse cholesterol transport are regulated by thyroid hormone. Specifically, CETP, hepatic lipase, LCAT, and SR-B1 are increased by thyroid hormone (57). An increase in CETP, hepatic lipase, LCAT, and SR-B1 would be anticipated to result in a decrease in HDL-C and an increase in reverse cholesterol transport. The mechanism for the decrease in Lp(a) is unknown.

RESMETIROM

Resmetirom is a liver-directed, thyroid hormone receptor beta (THR-β)–selective agonist approved for the treatment of metabolic dysfunction–associated steatohepatitis (MASH). In a large randomized trial LDL-C levels at 24 weeks decreased by 13.6% in the 80-mg resmetirom group and 16.3% in the 100-mg resmetirom group compared with 0.1% in the placebo group (P<0.001 for both comparisons with placebo) (155). Additionally, TG (~20%) (in patients with baseline TG >150 mg/dL), non–HDL-C (15-18%), and Lp(a) (30-35%) levels also decreased in the resmetirom groups compared to the placebo group. HDL-C levels did not change in this study. The differences in the effect of thyroid hormone and resmetirom on lipid levels are due to resmetiron only activating the thyroid hormone receptor in the liver.

RETINOIDS

Retinoids are synthetic analogues of Vitamin A effective for the treatment of psoriasis, severe acne, and other related skin disorders caused by abnormal keratinization. Oral isotretinoin was first reported to cause hypertriglyceridemia most likely due to a reduction in the clearance of VLDL particles secondary to decreasing lipoprotein lipase-mediated lipolysis (156,157). Retinoids have also been shown to increase plasma apo C-III concentrations by increasing the transcriptional activity of the human apo C-III gene via the retinoid X receptor (RXR), ultimately contributing to the development of hypertriglyceridemia (158,159). Isotretinoin has been reported to cause a variety of adverse events with some potential serious consequences, including case reports of pancreatitis (160). Patients with significantly elevated TG levels are more likely to develop pancreatitis and therefore, patients with preexisting hypertriglyceridemia should avoid retinoid therapy or use with extreme caution until TG levels can get better controlled. In addition, a baseline lipid profile should be obtained in all patients and TG levels checked at least once after four weeks of therapy. Patients with a higher risk of developing hypertriglyceridemia should be monitored more frequently.

Studies with isotretinoin have demonstrated a rise in VLDL-C, TG, LDL-C, and TC with a slight decrease in HDL-C (4). A large retrospective cohort study including 12,140 adults exposed to isotretinoin found no significant association between isotretinoin and cardiovascular outcomes (161).

ANTIPSYCHOTICS

Antipsychotic medications can be highly effective in controlling psychiatric illnesses. However, some of these are also associated with metabolic adverse events that can increase the risk for ASCVD (162-165). One such adverse event includes dyslipidemia, with increases primarily occurring in TG levels. Phenothiazines, which are first generation or ‘typical’ antipsychotics, were found to elevate serum TG and TC levels soon after their approval, with a greater effect on TG levels. Studies have shown an increase of up to 22% after a year of treatment with chlorpromazine (4). Further studies have observed similar effects with trifluronated phenothiazines and haloperidol. The possibility that these drugs contribute to lipoprotein abnormalities should be considered in patients with dyslipidemia or high CV risk.

Second generation, or ‘atypical’ antipsychotics were later developed to reduce relapse rates and adverse events. Compared to first generation antipsychotics, they have lower affinity for the D₂ receptors and instead act namely on serotonin and norepinephrine. They have become first line treatment due to a lower potential risk of extrapyramidal symptoms. However, metabolic side effects including an increase in serum TG levels as well as minor increases in TC, have also been demonstrated with the use of second-generation antipsychotics. The exact mechanism of their impact on lipoprotein metabolism remains uncertain. Clozapine, a second-generation antipsychotic, was the first agent shown to increase serum TG levels (166). A retrospective study reviewed patients on clozapine and found that men on clozapine had an average 48.13% increase in TG level and women a 35.38% increase and there was a significant interaction between drug and gender over time (166).

Weight gain is a common adverse effect of using atypical antipsychotics which can lead to an increase in TG levels (167). The 5-HT2c receptor-blocking and/or histamine antagonism action of these medications is a possible cause of the related weight gain. One study demonstrated a significant increase in weight and serum TG with olanzapine and clozapine, with minimal and moderate changes in those on risperidone and quetiapine, respectively (167). However, this was an extremely small study (n=56) and it is difficult to translate these results to the general population. This is consistent with the overall evidence, and it appears that clozapine and olanzapine have the greatest effect on the risk of dyslipidemia, followed by quetiapine. Risperidone, ziprasidone, lurasidone and aripiprazole have a relatively low risk of dyslipidemia associated with their use (166,168). As access to general and preventive care remains a limitation for patient populations with schizophrenia, these adverse effects can be of great concern for a population already at increased risk of CV complications. Therefore, checking baseline lipid levels and screening for the duration of therapy may be necessary in patients receiving therapy with atypical antipsychotics. If a patient develops elevated TG levels or dyslipidemia, they should be offered lipid-lowering therapy or if possible, switched to a less offending agent.

ANTICONVULSANTS

Changes in serum lipid levels have been reported with the use of various anticonvulsants with variability and inconsistency in the literature. Some observational studies have reported elevated levels of LDL-C and HDL-C while others have shown no significant effects. TG levels are not influenced by treatment with anticonvulsants. Since most anticonvulsants induce the hepatic cytochrome P450 (CYP) enzymes, it is theorized that competition between the medication and cholesterol for the enzyme occurs which results in a decreased breakdown of cholesterol to bile acids and an increase in TC (10). This inconsistency has been noted in studies in both adults and pediatrics with epilepsy and it appears differences may exist based on the individual anticonvulsant used. In addition, the influence of therapy on the development of atherosclerosis remains debatable.

Carbamazepine and phenobarbital have been shown to cause alterations in the lipid profile. In children and adolescents with epilepsy, carbamazepine has demonstrated a consistent increase in TC and LDL-C levels, while some individual studies have also shown an increase in HDL-C as well as TG levels (169,170). Treatment of epilepsy in children with phenobarbital has also shown increased TC, LDL-C, and HDL-C, as well as lower TG levels. Valproic acid appears to have little effect, or even a slightly favorable effect, on the lipid profile (169).

IMMUNOSUPPRESSIVES AND IMMUNE MODULATORS

Cyclosporine and Tacrolimus

Cyclosporine and tacrolimus are immunosuppressant agents used as mainstay therapy for solid organ transplant recipients. Several metabolic abnormalities are associated with the use of both medications, including glucose intolerance, bone loss, and elevations in TC and LDL-C and apo B-100 levels. Effects on HDL-C levels are inconsistent, but trials have also demonstrated increases in HDL-C (10). Hyperlipidemia can occur in up to 60% in post-transplant patients (171). This is due to a combination of factors, including post-transplant obesity, multiple drug therapy (including steroids and other immunosuppressants), and diabetes. These adverse effects are much greater with cyclosporine than tacrolimus, which has minimal effects on TC and LDL-C, and smaller effects on TG levels than cyclosporine (172). A randomized prospective trial compared a tacrolimus-based regimen to a cyclosporine-based regimen in patients undergoing a cardiac transplant. After 12 months of therapy, serum TC, LDL-C, HDL-C, and TG were significantly higher in the cyclosporine group compared to tacrolimus and more patients received medical treatment for elevated lipids (71% vs. 41%; p=0.01) (172). The impact of cyclosporine on lipid levels appears to be dose dependent and trough blood levels correlate with the elevations in TC and LDL-C, as well as reductions in HDL-C levels (173). The mechanisms by which cyclosporine causes hyperlipidemia are unclear, as the effects in humans are confounded by many other factors in transplant patients.

Conversion from cyclosporine to tacrolimus can be considered if post-transplant hyperlipidemia occurs, and several studies have demonstrated this (174-176). Statins are recommended as first line treatment for dyslipidemia in transplant recipients. However, drug interactions need to be accounted for. Concomitant use of cyclosporine and HMG-CoA reductase inhibitors metabolized by CYP3A4 has been shown to increase the risk of myopathy and rhabdomyolysis due to a potential drug-drug interaction through inhibition of the CYP3A-mediated metabolism of simvastatin, lovastatin, and atorvastatin. Cyclosporine also inhibits the organic anion transporter protein (OATP1B1)-mediated hepatic uptake of simvastatin (177,178). Statins metabolized by other cytochromes (e.g. fluvastatin or rosuvastatin) or statins not significantly metabolized by CYP enzymes (pravastatin), may be a favorable choice in this patient population due to the decreased risk of drug-drug interactions (179). However, pravastatin and fluvastatin doses should still be lowered due to cyclosporine inhibition of the OATP1B1-mediated hepatic uptake and patients should be monitored for statin associated muscle symptoms. Furthermore, fluvastatin has been shown to reduce CV events and lower LDL-C concentrations in transplant recipients receiving immunosuppressive therapy with cyclosporine (180).

mTOR Kinase Inhibitors

Sirolimus and everolimus inhibit the mammalian target of rapamycin (mTOR) and are immunosuppressants used to prevent rejection following organ transplantation. The mTOR complex is involved in lipoprotein synthesis and insulin resistance. Inhibitors of mTOR increase triglycerides, VLDL, and LDL through inhibition of LDL function and inhibition of the breakdown of apolipoproteins apoB100 and apoCIII (21). Dyslipidemia can occur in more than half of patients taking these medications. Everolimus has been shown to increase total cholesterol by 47.4 mg/dl (95% CI 37.5-57.3) and triglycerides by 28.9 mg/dl (95% CI 20.7-37.1) and sirolimus resulted in higher levels of TG and LDL compared to cyclosporine and tacrolimus (181).

Transplant patients are at an increased risk of ASCVD for a number of reasons, including the effect on immunosuppressants on the lipid profile. Therefore, it is important to monitor lipid levels and initiate lipid lowering therapy when appropriate, while taking into account pharmacological drug interactions.

Kinase Inhibitors

Janus kinase (JAK) inhibitors are immune modulating drugs that inhibit cell proliferation, differentiation, and immune regulation (182). These drugs were originally developed and approved for rheumatoid arthritis (RA) but there are now used for many other chronic inflammatory conditions (Table 5) (182,183). There have been safety signals concerning for an increased risk of major adverse cardiovascular events (MACE) and venous thromboembolic events (VTE) (183). Data supporting these risks comes mostly from older patient populations with RA and at least 1 CV risk factor and a meta-analysis of JAK inhibitors in a younger patient population with dermatologic indications did not find an increased risk of MACE or VTE (184).

Some of the JAK inhibitors cause a dose-dependent increase in TC, LDL-C, and HDL-C (Table 5). Inflammation is well known to decrease TC, LDL-C, and HDL-C and drugs that reduce inflammation may lead to an increase in TC, LDL-C, and HDL-C (56). This is known as the ‘lipid paradox’ in which a reduction in systemic inflammation and disease activity can result in elevations of lipid levels that represent a return to baseline levels. JAK inhibitors may also influence hepatic lipid metabolism and there may be specific polymorphisms in JAK genes that result in higher lipid levels in some individuals.(185)

One systematic review found that the JAK inhibitors used in RA result in a pooled increase in LDL-C from baseline of 11.37 mg/dl (95% CI 7.84-14.91) and an increase in HDL-C from baseline of 8.11 mg/dl (95% CI 6.65-9.58) (182). These increases were observed within the first few weeks of therapy and stabilized by the third month. This study did not find a significant difference in ASCVD risk between JAK inhibitors and placebo or other active agents.

Patients on JAK inhibitors should regularly be monitored for dyslipidemia and a lipid profile should be checked at baseline, 4-12 weeks after initiating a JAK inhibitor, and periodically thereafter. Lipid-lowering agents may be necessary, especially in patients with a history of ASCVD or at high risk for CVD.

Table 5:

FDA Approved Janus Kinase Inhibitors

JAK Inhibitor	FDA Approved Indications	Effect on Lipid Profile
		LDL-C	HDL-C	TG
Abrocitinib	Atopic dermatitis	↑	↑	↑
Baricitinib	Alopecia areata Rheumatoid arthritis	↑	↑	↔
Deucravacitinib*	Plaque psoriasis	↔	↔	↑
Deuroxolitinib	Alopecia areata	↑	↑	↑
Fedratinib*	Myelofibrosis	↔	↔	↔
Momelotinib	Myelofibrosis	↔	↔	↔
Pacritinib*	Myelofibrosis	↔	↔	↔
Ritlecitinib***	Alopecia areata	↔	↔	↔
Ruxolitinib	Myelofibrosis Polycythemia vera	↑	↑	↑
Tofacitinib	Ankylosing spondylitis Psoriatic arthritis Rheumatoid arthritis Ulcerative colitis	↑	↑	↑
Upadacitinib	Ankylosing spondylitis Atopic dermatitis Crohn disease Psoriatic arthritis Rheumatoid arthritis Ulcerative colitis	↑	↑	↑

*: Selective for Janus kinase2 (JAK 2).
**: Selective for Janus kinase 3 (JAK3).

ANTIVIRAL THERAPY

Protease Inhibitors

Protease inhibitors (PIs) are potent antiretroviral drugs used in combination with other drugs as part of a antiretroviral regimen for the treatment of human immunodeficiency virus (HIV) (186). These PIs have substantial clinical benefits, but can also produce lipodystrophy, hyperlipidemia, and insulin resistance (187,188). The hyperlipidemia is thought to be caused by increases in VLDL production and intermediate density lipoproteins (IDL) with the potential to cause endothelial dysfunction and atherosclerosis. Enzymes imperative for the removal of triglyceride rich lipoproteins are also decreased in HIV patients. This includes lipoprotein lipase and hepatic lipase. PI associated insulin resistance and abnormal expression of the apolipoprotein C-III gene may also induce dyslipidemia (189).

Studies evaluating PIs have shown increases in TC as well as TG with little to no effects on HDL-C and inconsistent increases in LDL-C levels (190). The main increase being in triglyceride-containing lipoproteins supports the mechanism of a release of free fatty acids and resulting increase in synthesis of VLDL causing these changes. While all PIs can change lipid levels, ritonavir appears to have the greatest effects and has also been reported to cause cases of extreme hyperlipidemia. During a randomized, 4-week double blind study, ritonavir was associated with at least a doubling of the serum TG level in 24 (61%) patients compared to only 4 (19%) patients on placebo (p=0.003) and seven subjects had TG levels exceeding 1000 mg/dL (191). Patients with high serum TG levels are at a higher risk of pancreatitis, which has been reported after protease inhibitor therapy (192). Therefore, the long-term complications of elevated lipids in the setting of HIV should be taken into consideration in patients treated with PIs. Guideline supported lipid lowering therapy and efforts to modify other CV risk factors should be initiated in patients (193). Recently, pitavastatin 4mg daily was associated with a 36% relative risk reduction in major adverse cardiovascular events over 5.6 years in a phase 3 study of adults with HIV receiving antiretroviral therapy (194). In this study, subjects had low-to-intermediate 10-year ASCVD risk and those with known ASCVD were excluded, indicating a lower risk population. For a detailed discussion of the lipid abnormalities in patients living with HIV see the Endotext chapter entitled “Lipid Disorders in People with HIV” (195).

Direct Acting Antivirals

Regimens of direct acting antivirals (DAAs) have vastly changed the treatment of chronic hepatitis C (CHC) since the approval of sofosbuvir in 2014. The DAAs have shown to be more effective than previous standard of care (interferon-based treatments such as pegylated interferon and ribavirin) in producing sustained virologic response (SVR) of ≥90% and are associated with fewer side effects (196). There are currently four classes of DAAs, defined by their mechanism of action and therapeutic target (NS3/4A inhibitors, protease inhibitors [PIs], NS5B inhibitors and NS5A inhibitors) (196). Recommended regimens today consist of multiple antivirals that target different sites to improve efficacy and decrease resistance rates.

While the hepatitis C virus itself can impact lipid metabolism, treatment with a DAA regimen has been associated with short term increases in LDL-C, TC, and HDL-C (197). There do not appear to be any significant effects on TG’s. This effect may result from a cancellation of the suppressive effect from HCV viral replication or from direct pharmacologic activity of the DAA’s themselves (198). The magnitude of effect does seem to vary based on DAA regimen with an increase in LDL-C of up to 27% reported. A pooled analysis of observational studies found an increase in total cholesterol of 15.86 mg/dl (95% CI 9.68 to 22.05) after 4 weeks of treatment with a DAA regimen and a similar increase in LDL-C of 13.77 mg/dl (95% CI 9.30 to 18.24) (199). Furthermore, a meta-analysis found that these results may be sustained and that total cholesterol and LDL-C levels were still increased a year after treatment compared with before treatment with no effect on TGs (200). Additional studies are needed to elucidate the exact mechanism of action and which regimens have the greatest impact.

Elimination of HCV can lead to improved cardiovascular outcomes and reduced risk of diabetes and insulin resistance and the benefit of treating HCV likely outweighs the modest changes in TC and LDL-C. Patients with ASCVD or high CV risk should be educated about potential alterations in lipid parameters and more monitoring in these individuals is prudent. However, it is important to acknowledge that many of these agents have pharmacokinetic drug-drug interactions with statins. Clinicians may elect to temporarily hold statin therapy which may also contribute to changes in the lipid profile during the treatment period.

INTERFERONS

Interferons are associated with a wide range of systemic complications including neuropsychiatric changes, fatigue, and bone marrow suppression. Although metabolic side effects are less frequent, α interferon is known to inhibit lipoprotein lipase, stimulate hepatic lipogenesis, and is associated with an increase in TG (201,202). A cohort study of patients with chronic hepatitis C on treatment with various forms of α interferon were evaluated for changes in TG and TC (202). Overall, mean serum TG levels rose 40% at 12 weeks and returned to baseline by 24 weeks after stopping therapy. However, the effect on individual patients was variable and 41 patients (27%) experienced TGs that more than doubled from baseline. There was no significant change in TC noted. The long-term complications of this have not been evaluated and no patients in the study developed acute pancreatitis. It appears that any significant clinical consequence from this rise in TG is extremely rare. There did not seem to be a difference in change in levels based on the specific form of α interferon that was used, including the long-acting PEGylated forms.

As the landscape for the treatment of chronic hepatitis C has transitioned to interferon-free regimens with DAAs, this is irrelevant in these patients. However, this effect on TG has been seen in the treatment with interferons for other illnesses, including chronic myelogenous leukemia and other cancers (203,204). Patients receiving interferon treatment for the treatment of cancer can be considered for anti-dyslipidemic medications to manage secondary hypertriglyceridemia (205).

OTHER DRUGS THAT AFFECT LIPOPROTEIN LEVELS

Various other drugs have been reported to affect lipid and/or lipoprotein levels (Table 6). Lipid changes from these drugs are based on limited data, are reported inconsistently, and could be due to other disease related aspects. Thus, the effects on serum lipid levels cannot fully be substantiated.

Table 6.

Other Drugs that Affect Lipid and/or Lipoproteins

Aminosalicylic acid

Antacids

Ascorbic Acid

Aspirin

Cimetidine/ranitidine

Danicopan

Elacestrant

L-asparaginase

Mitapivat

Neomycin

Olezarsen

Omaveloxolone

Ponesimod

Revumenib

MANAGEMENT

Several medication classes or individual medications can affect the lipid profile, both positively and negatively. Risk factors include elevated lipid levels at baseline and high cardiovascular risk patients. Identifying potential medications as the cause of these changes and monitoring the lipid profile while on therapy can provide value to the care of the patient. However, the long-term implications of these drugs on ASCVD mortality and morbidity remains unknown and there is limited evidence on the overall impact of these drug-induced changes.

A thorough risk-benefit analysis of each treatment should be done based on individual patient factors. In general, if negative changes in the lipid profile are observed during therapy, replacement with an equivalent alternative therapy can be recommended. If no equivalent therapy is available and treatment must be initiated, then monitoring of serum lipid levels is vital. The use of existing guidelines for the management of dyslipidemia in the general population can be referred to and in extreme cases; the use of the suspected medication should be reassessed.

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Herink MC. Medication Induced Changes in Lipids and Lipoproteins. [Updated 2025 Sep 2]. In: Feingold KR, Ahmed SF, Anawalt B, et al., editors. Endotext [Internet]. South Dartmouth (MA): MDText.com, Inc.; 2000-.

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ABSTRACT
INTRODUCTION
ANTIHYPERTENSIVE DRUGS
OTHER CARDIOVASCULAR MEDICATIONS
DIABETES MEDICATIONS
HORMONES
RETINOIDS
ANTIPSYCHOTICS
ANTICONVULSANTS
IMMUNOSUPPRESSIVES AND IMMUNE MODULATORS
ANTIVIRAL THERAPY
INTERFERONS
OTHER DRUGS THAT AFFECT LIPOPROTEIN LEVELS
MANAGEMENT
REFERENCES

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Medication Induced Changes in Lipids and Lipoproteins

ABSTRACT

INTRODUCTION

Table 1.

ANTIHYPERTENSIVE DRUGS

Diuretics

β-Blockers

Table 2.

Table 3.

OTHER CARDIOVASCULAR MEDICATIONS

Amiodarone

DIABETES MEDICATIONS

Sodium-Glucose Co-Transporter 2 (SGLT2) Inhibitors

Metformin

Thiazolidinediones

Incretins

Table 4.

HORMONES

Glucocorticoids

DRUGS USED TO TREAT CUSHING’S SYNDROME

Estrogens and Progestins

Anabolic Steroids

DANAZOL

Androgens

ANDROGEN DEPRIVATION THERAPY

Growth Hormone

Thyroid Hormone

RESMETIROM

RETINOIDS

ANTIPSYCHOTICS

ANTICONVULSANTS

IMMUNOSUPPRESSIVES AND IMMUNE MODULATORS

Cyclosporine and Tacrolimus

mTOR Kinase Inhibitors

Kinase Inhibitors

Table 5:

ANTIVIRAL THERAPY

Protease Inhibitors

Direct Acting Antivirals

INTERFERONS

OTHER DRUGS THAT AFFECT LIPOPROTEIN LEVELS

Table 6.

MANAGEMENT

REFERENCES

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