wallenberg syndrome

http://www.medscape.org/viewarticle/730607?src=cmemp 

HyperTAG

• The serum triglyceride concentration can be stratified in terms of population percentiles and/or coronary risk (see 'Definitions, epidemiology, and detection' above):

• Normal <150 mg/dL (1.7 mmol/L)
• Borderline high — 150 to 199 mg/dL (1.7 to 2.2 mmol/L)
• High — 200 to 499 mg/dL (2.3 to 5.6 mmol/L)
• Very high — ≥500 mg/dL (≥5.7 mmol/L)

• Although the contribution of triglycerides to cardiovascular risk has been debated in the past, it now seems clear that elevated triglyceride levels are independently associated with cardiovascular risk, particularly coronary risk. It remains uncertain, however, whether this association is causal, such that hypertriglyceridemia, independent of associated lipoprotein, inflammatory and hemostatic abnormalities, causes atherosclerosis. It is also uncertain whether lowering triglyceride levels reduces risk. (See 'Triglycerides and atherosclerosis' above.)
• There are only limited data regarding which patients with hypertriglyceridemia require treatment and on the choice of therapies. (See 'Management' above.)
• Nonpharmacologic interventions such as weight loss in obese patients, aerobic exercise, avoidance of concentrated sugars and medications that raise serum triglyceride levels, and strict glycemic control in diabetics should be first-line therapy in patients with mild-to-moderate hypertriglyceridemia. Other risk factors for cardiovascular disease, such as hypertension and smoking, should also be addressed. (See 'Nonpharmacologic therapy' above.)
  
  In patients with severe hypertriglyceridemia (fasting triglyceride levels above 1000 mg/dL [11.3 mmol/L]), we suggest a very low fat diet (Grade 2C). (See 'Nonpharmacologic therapy' above.)
• Options for pharmacologic therapy directed at reducing triglycerides include fibrates, nicotinic acid, and fish oil. (See 'Pharmacologic therapy (including fish oil)' above.)
• For patients with mild to moderate hypertriglyceridemia (150 to 500 mg/dL [1.7 to 5.7 mmol/L]), and even in patients with triglyceride levels as high as 1000 mg/dL (11.3 mmol/L), the main indication for therapy is reduction of cardiovascular (CV) risk. In patients where the goal of therapy is CV risk reduction:

• Decisions about initiating pharmacologic therapy should be based on global cardiovascular risk. Nearly all patients with known coronary heart disease (CHD) or a CHD risk equivalent (table 4) will require therapy. (See "Treatment of lipids (including hypercholesterolemia) in primary prevention", section on 'Deciding whom to treat' and "Treatment of lipids (including hypercholesterolemia) in secondary prevention", section on 'Identification of patients at risk'.)
• For patients with a triglyceride level below 500 mg/dL (5.7 mmol/L) in whom pharmacologic therapy is indicated, we suggest treatment with a statin rather than an agent targeted at reduction of triglycerides (Grade 2B). Given the lack of high quality evidence directly comparing statin therapy with other treatment options, a reasonable alternative in such patients would be to treat them with fibrates, nicotinic acid, or fish oil. (See 'Mild to moderate hypertriglyceridemia' above.)
• In patients with CHD or a CHD risk equivalent (table 4) who have moderate hypertriglyceridemia (200 to 500 mg/dL [2.3 to 5.7 mmol/L]) and are intolerant of statin therapy, we suggest treatment with nicotinic acid or a fibrate (Grade 2C). Treatment with fish oil is a reasonable alternative. (See 'Mild to moderate hypertriglyceridemia' above.)
• For patients with a triglyceride level above 500 mg/dL (5.7 mmol/L) in whom pharmacologic therapy is indicated, we suggest treatment with a fibrate (such as fenofibrate), followed by the addition of a statin once the triglyceride levels are brought down (Grade 2C). Fish oil therapy is also an option. A reasonable alternative would be to treat lower-risk patients with a statin alone and to only add triglyceride-directed therapy in patients with CHD or a CHD risk equivalent (table 4). (See 'Severe hypertriglyceridemia' above.)

• In patients without a prior episode of pancreatitis, we suggest initiating pharmacologic therapy to reduce triglycerides with a goal of preventing pancreatitis when the level exceeds 1000 mg/dL (11.3 mmol/L) (Grade 2C). Even at this level of triglyceride elevation, the risk of pancreatitis appears to be quite small. Patients being treated for prevention of pancreatitis will often require combinations of triglyceride-lowering medications (ie, a fibrate, fish oil, nicotinic acid) to reduce the triglyceride level below 1000 mg/dL (11.3 mmol/L). (See 'Severe hypertriglyceridemia' above.)
• The management of patients with hypertriglyceridemia and acute pancreatitis and/or a prior episode of pancreatitis is discussed separately. (See "Hypertriglyceridemia-induced acute pancreatitis".)

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HyperTAg causing Pancreatitis

Proposed approach to hypertriglyceridemic pancreatitis

Apheresis — Apheresis should be considered to remove triglycerides from serum if the patient does not have concurrent hyperglycemia and there are no contraindications, such as unstable vital signs or inability to tolerate central venous access.

Many case reports and series have described apheresis for HTGP [28-40]. One series of seven patients with an average level of 1406 mg/dL reported a 41 percent decrease in triglyceride levels after one plasma exchange session [35]. In another case report, triglycerides were lowered from 2410 to 138 mg/dL after three days of apheresis [40]. Neither report described the use of adjunctive therapy such as intravenous insulin, intravenous heparin, or oral statins.
The most common anticoagulant used during apheresis is heparin, but there are no data to recommend the appropriate apheresis replacement fluid (albumin versus fresh frozen plasma). When plasma exchange is compared with double membrane filtration apheresis, rates of removal of serum lipids have been lower with double membrane filtration apheresis [41].
The main concerns surrounding apheresis include cost and availability. After one cycle, serum triglyceride levels are re-checked and, if less than 500 mg/dL, apheresis is stopped. If the triglyceride rises (above 500 mg/dL), we generally re-treat with apheresis.
Early initiation of apheresis is likely to be beneficial. We generally proceed with apheresis as soon as possible. In a review of 10 patients with HTGP, nine patients received apheresis with IV heparin and insulin within 48 hours of the diagnosis of HTGP with successful outcomes [42].

Insulin — If apheresis is unavailable, if the patient cannot tolerate apheresis, or if the patient's serum glucose level is >500 mg/dL, we use intravenous insulin. Insulin decreases serum triglyceride levels by enhancing lipoprotein lipase activity, an enzyme that accelerates chylomicron metabolism to glycerol and fatty free acids [43,44]. Because HTGP often presents in patients with uncontrolled diabetes, insulin can decrease both triglyceride and glucose levels.

Intravenous insulin may be more effective than subcutaneous insulin in severe cases of HTGP [25,26]. Many regimens have been reported to lower triglyceride levels to less than 500 mg/dL over 3.5 to 4 days [25-27]. We typically initiate an intravenous infusion of regular insulin in 5 percent dextrose at a rate of 0.1 to 0.3 units/kg/hour to maintain blood sugar levels between 150 and 200 mg/dL.
Fingerstick glucose levels every four hours are suggested to ensure glucose control, and triglyceride levels should be monitored every 12 to 24 hours with adjustment of the insulin dosage as needed. Intravenous insulin should be stopped when triglyceride levels are <500 mg/dL, which typically occurs within several days.

Insulin and heparin — The role of heparin is controversial. Heparin stimulates the release of endothelial lipoprotein lipase into the circulation [45] and has been used without insulin to manage HTG [42,46,47]. Multiple case reports and series have described the use of heparin and insulin to lower HTG [21-24,48].

Studies have used varying doses of insulin and heparin administered by various routes [21,22,48]. As an example, in two reports subcutaneous heparin at 5000 units twice daily was used with intravenous insulin [22,48]. In both healthy volunteers and dialysis patients, low molecular weight heparin has been found to deplete lipoprotein lipase stores as efficiently as heparin and to retard the metabolism of triglyceride [49,50].
Despite the reported success of intravenous heparin in combination with insulin in HTG management, the use of heparin to treat HTGP has come under greater scrutiny. Heparin causes an initial rise in circulating lipoprotein lipase levels that is quickly followed by increased hepatic degradation of heparin [51]. This degradation contributes to further depletion of plasma stores of lipoprotein lipase and results in an increase of levels of chylomicrons [52]. The transient nature of the benefit seen with heparin raises question as to its use as monotherapy or in combination with insulin.

Antihyperlipidemic therapy — Antihyperlipidemic agents (eg, oral gemfibrozil 600 mg twice daily) should be initiated as adjuvant therapy in patients with HTGP. (See "Lipid lowering with fibric acid derivatives" and "Lipid lowering with diet or dietary supplements" and "Treatment of lipids (including hypercholesterolemia) in secondary prevention".)

Long-term therapy — Oral antihyperlipidemic agents and dietary fat restriction may be needed long-term to prevent recurrences of AP and prevent other complications of HTG. Periodic apheresis has been used with some success as continuing therapy after patients have recovered from their initial episode of AP, and particularly in patients who are noncompliant with diet and oral drug therapy [53]. (See "Lipid lowering with fibric acid derivatives" and "Lipid lowering with diet or dietary supplements" and "Treatment of lipids (including hypercholesterolemia) in secondary prevention".)

Pregnancy — The treatment of HTGP does not differ in pregnancy. Several case reports of gestational HTGP have described the use of apheresis [54,55], intravenous insulin and glucose with enteral restriction of triglyceride [56], intravenous heparin [42,46], low fat diet [57], and gemfibrozil. All resulted in the successful control of HTG and delivery of a healthy neonate

heart blog

http://blogs.theheart.org/private-practice/2011/8/24/adopting-dabigatran-pradaxa-the-pros-and-the-cons

Statin comparision

There are very good reasons to use rosuvastatin over atorvastatin.  Crestor is not a CYP3A4 substrate (Lipitor is), Crestor has only minor actitive metabolites (Lipitor has several very active metabolites), and Crestor is hydrophilic whereas Lipitor is not; hydrophilicity appears to minimize entry into muscles and minimizes muscle pain complaints.

Lipitor differs from simvastatin only in efficacy.  If you don't like simva you shouldn't like Lipitor.  Pravastatin, although the least potent, is not a 3A4 suThere are very good reasons to use rosuvastatin over atorvastatin.  Crestor is not a CYP3A4 substrate (Lipitor is), Crestor has only minor acbstrate and is hydrophilic.  It is a good first choice for many.

 with all the publicity over rhabdomyolysis at the 80 mg dose, the fact that simvastatin is markedly inferior to atorvastatin (both in hard endpoint trials like IDEAL and in 'softer' surrogate marker studies), and that simvastatin is by far and away the most prone to drug interactions through CYP3A4 of all the statins (witness the labelling revisions for amiodarone, verapamil, diltiazem on top of the previous litany of azole antifungals, antivirals, etc). Quite simply, this statin sucks! It is also the most myopathic of all the statins and the dose-response curve and renal clearance are worrisome. More than 40% of patients in SHARP discontinued it.