Treatment Guidelines w/Low HDL – Low HDL is an independent risk factor

on 9.6.08 with 0 comments



If HDL <>

If HDL < id="m11t10397" class="western">


These drugs are all cost-effective based on cost of preventive treatment vs cost of treatment of vascular disease.

Drug / Indications

Pharm

MOA

Effectiveness

Side Effects

HMG-CoA Reductase Inhibitors

Lovastatin (Mevacor)

Pravastatin (Pravachol)

Simvistatin (Zocor)

Fluvastatin (Lescol)


Atorvastatin (Lipitor)

Elevated LDL


Oral doses at supper time

Peak action occurs at 6 hrs or sooner

Duration extends to ~12 hrs

Drugs have roughly equivalent efficacy & side effects w/different potency and pharmacokinetics

Competitive inhibitors of HMC-CoA reductase (rate-limiting enzyme of C synthesis)

Lower [C]i \ increase LDL Rs ® increased uptake \ decreases [LDL] in serum

¯¯ VLDL

¯¯¯ LDL

¯¯¯ Total C

¯ TG

­ HDL


­­­­­­¯¯¯¯¯¯¯

Reversible ­ LFTs

Check LFTs every 6 wks in 1st few mths

Myositis – flu-like muscle pain

May be associated w/­ CK levels – measure them & change drug if needed

Do not combine w/fibrates – increased change of myositis
Bile-acid binding resins

Cholestyramine (Questran)

Colestipol (Colestid)

Colesevelam (WelChol)

Elevated LDL

Non-absorbable granular powder taken orally

Response apparent w/in 3-4 wks; max usually seen at 6-8 wks

Package doses, tablets, bulk (much lower cost)

Bind bile acids in the SI – ¯enterohepatic return of bile acids to liver \ accelerate hepatic bile acid synthesis ® ¯of [pre-C]i & up-regulation of LDL Rs in liver Þ ­LDL R mediated removal of LDL \ decrease [LDL]circulating

¯¯¯ LDL

¯¯¯ Total C

® ¯ TG

® ­ HDL


® ­ VLDL

Constipation

Abdominal discomfort

Bloating

Flatulence


At high doses, may induce malabsorption of fat-soluble vitamins

Nicotinic acid


Elevated TG, elevated LDL-C, and/or low HDL


Natural vitamin available in unaltered and slow release form

Completely absorbed and hepatically detoxified

Usual dose is 1-3g/day

Very inexpensive
Inhibits VLDL synthesis and release in 2 ways:

Inhibits peripheral lipolysis \ decreasing available FFAs as substrate for hepatic TG synthesis

Inhibits VLDL synthesis directly

¯VLDL ® ¯LDL

¯¯¯ LDL

¯¯¯ Total C

¯¯¯TG

­ HDL


¯¯¯ VLDL

Facial flushing – treat w/aspirin

Gastric irritation

Exacerbation of glucose intolerance

Hyperuricemia / gout

Reversible increase LFT (w/old extended release form)


Contraindications:

PUD

Asthma

Cardiac dysrhythmias

Hyperuricemia

DM
Fibric Acid Derivatives

Gemfibrozil (Lopid)

Fenofibrate (Tricor)

Elevated TG, elevated LDL-C, and/or low HDL

Max response usually seen @ 4 wks

Usually taken ĉ breakfast


¯ [VLDL]plasma \ ¯ [LDL]plasma

¯ Synthesis & release hepatic VLDL

Also, stimulate TG-rich lipoprotein clearance by ­ LPL activity

­ [HDL]plasma

Stimulate the synthesis of apo- A-1 (primary apo-lipoprotein associated ĉ HDL)

¯ LDL

¯ Total C

¯¯¯TG

­ HDL


¯¯¯ VLDL

Myalgia

Skin rash

GI bloating or cramping

Drug interations:

Potentiates warfarin action

Its absorption is diminished by bile acid resins


Lowers cyclosporine levels in transplant patient

Omega 3 Fatty Acids


HyperTG pts who cannot tolerate or do not respond to 1st line drugs


Capsules of fish oil containing eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA)

Unknown, but reported decrease synthesis of LDL in the liver


Also have anti-platelet activity that can inhibit formation of platelet thrombi


¯¯¯TG


¯¯¯ VLDL

Bloating

Flatulence

Diarrhea

Deterioration of glycemic control in diabetics

Potential hemostasis effect

Antioxidants

(Vitamins – E, C, beta carotene)



Decrease oxidation of LDLs \ decrease formation of atherosclerotic plaques

Results are not conclusive of any definite protection

No known side effects, except for mega dosing…May as well take them.

Category: Endocrinology Notes , Pharmacology Notes

POST COMMENT

0 comments:

Post a Comment