Omega-3 Fatty Acids and Nonalcoholic Fatty Liver Disease

A recent study (Janczyk W. J Pediatr 2015; 166: 1358-63; editorial 1335-6) examines whether omega-3 fatty acid supplement would be helpful for overweight/obese children with nonalcoholic fatty liver disease (NAFLD).  This randomized controlled trial had 64 patients complete the study; the median age of enrolled patients was 13 years.

Free Full Text Article: Omega-3 Fatty Acids Therapy in Children with Nonalcoholic Fatty Liver Disease: A Randomized Controlled Trial

The treatment cohort received doscosahexaenoic acid (DHA) and eicosapenatenoic acid (EPA) at a dose of 450-1300 mg/day.

Key finding:

  • After 6 months, omega-3 fatty acid supplementation did not increase the number of patients with decreased ALT levels and it did not affect liver steatosis on ultrasound.

The editorial reviews a previous positive study for DHA supplementation from Italy (n=60) but notes that other larger trials in adults have not shown efficacy of omega-3 fatty acids (Gastroenterol 2014; 147: 377-84.e1, Hepatology 2014; 60: 1211-21). It could be that much longer studies will be needed to determine whether omega-3 fatty acids will be helpful.

Take-home message: Overall, the sum of these studies indicates that supplementation with omega-3 fatty acids has not been shown to be effective for NAFLD and it is not likely to be a significant breakthrough.  Even if it were shown to help modestly, would pediatric patients be placed on therapy indefinitely?

Briefly noted:

Kusters DM et al. “Efficacy and Safety of Ezetimibe Monotherapy in Children with Heterozygous Familial and Nonfamilial Hypercholesterolemia” J Pediatr 2015; 166: 1377-84.  Ezetimbe (10 mg), a cholesterol absorption inhibitor, lowered LDL by 27% after 12 weeks from baseline. It was well-tolerated

“This Is A Stick Up — Your Money or Your Life”

When I read a recent Hepatology editorial (Hepatology 2015; 61: 1106-8), I could not help think of the aforementioned title of this blog.

Here’s the scoop:

The two most commonly used medications for Wilson’s disease are trientine (Syprine) and D-penicillamine (Cupramine). For about 20 years, the original manufacturer of these medications kept the consumer cost at ~$1 per 250 mg tablet.  Currently the cost of Syprine is ~$200 per 250 mg tablet and Cuprimine costs ~$55 per 250 mg tablet.  This 200-fold increase translates into a yearly cost of ~$300,000.

How did this happen?

  • Little competition
  • Profit motive
  • Patients are reluctant to protest (they need this medication to be manufactured)

Why is this outrageous?

This increase in cost was not driven by any new discovery or research innovation.

Are there options?

Zinc is inexpensive and may be an option after initial period of chelation/normalization of liver biochemistries.  Zinc needs to be taken two to three times per day and “well away from meals for best absorption.”

Bottomline: These medication prices are outrageous.

Briefly noted:

  • “Molecular pathophysiology of portal hypertension”  Hepatology 2015; 61: 1406-15. Terrific review with excellent figures.
  • “Ezetimibe for the treatment of Nonacloholic Steatohepatitis” (MOZART trial) Hepatology 2015; 61: 1239-50. This randomized double-blind, placebo-controlled trial with 50 patients (biopsy-proven NASH) showed that Ezetimbe was not significantly different from placebo in histologic response rates, serum aminotransferases, or in magnetic resonance elastography findings.
  • Van Biervliet et al. “Clinical Zinc Deficiency as Early Presentation of Wilson Disease” JPGN 2015; 60: 457-9. Case report.

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