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The Role of an Intravenous Fat Emulsion Composed of Fish Oil in a Parenteral Nutrition-Dependent Patient With Hypertriglyceridemia
Kathleen Gura, PharmD*
Robbert Strijbosch, MD*
Sarah Arnold, PharmD*
Christopher McPherson, PharmD
Mark Puder, MD, PhD*
* Children's Hospital Boston, Boston,
Massachusetts; and the University of North
Carolina, Chapel Hill, North Carolina
Correspondence: Correspondence: Kathleen Gura, PharmD, Children's Hospital Boston, 300
Longwood Avenue, Boston, MA 02115. Electronic mail may be sent to
kathleen.gura{at}childrens.harvard.edu.
Hypertriglyceridemia is a common complication in patients receiving
parenteral nutrition (PN). Management typically involves withholding the IV
fat emulsion (IVFE) until serum triglyceride levels normalize. In some
instances, this practice may predispose patients to the development of
essential fatty acid deficiency (EFAD) unless alternative therapies such as
oral or topical oils are used. This is especially true in patients unable to
tolerate enteral intake. We describe the management of hypertriglyceridemia in
a 12-year-old boy dependent on PN who developed EFAD due to prolonged use of
fat-free PN. His course was further complicated by PN-associated liver
disease. Treatment involved the use of an IVFE derived from fish oils. Within
3 weeks, there was clinical improvement in EFAD and hypertriglyceridemia. The
patient's triene:tetraene ratio decreased from 0.207 to 0.044 (normal:
0.013–0.05). Similarly, his serum triglyceride levels decreased from 628
mg/dL to 183 mg/dL (normal: <200 mg/dL). After 2 months of treatment, he
was successfully transitioned to enteral feedings; hepatic function
normalized, as did the essential fatty acid profile and serum triglycerides
levels. This suggests that using fish-oil-based IVFE may be an effective
alternative to conventional IVFE in PN-dependent patients whose clinical
course is complicated by hypertriglyceridemia.
Parenteral nutrition (PN) provides the necessary nutrition requirements for
patients who are unable to absorb sufficient nutrients due to intestinal
abnormalities or in which there is a contraindication to using the
gastrointestinal (GI) tract. Typically, PN is administered in conjunction with
IV fat emulsion (IVFE) to provide an alternative to carbohydrates as a source
of nonprotein calories and to prevent essential fatty acid deficiency (EFAD).
In some instances, patients are unable to tolerate IVFE due to allergy to one
of its components or due to an inability to clear the fats efficiently.
Hypertriglyceridemia occurs in up to 33% of patients receiving
PN.1 In most cases,
the treatment for PN-induced hypertriglyceridemia is to reduce the dose or
discontinue the IVFE infusion for 4–6 hours to allow for clearance. In
some instances, the IVFE may be held for several days and only resumed to
provide sufficient fat calories to prevent EFAD. PN therapy typically includes
the avoidance of excessive carbohydrates; thus, optimum calories may not be
administered if additional calories cannot be provided as fat. Further, the
discontinuation of lipids for a prolonged period of time in response to
hypertriglyceridemia can predispose patients to biochemical and clinical
evidence of EFAD.
Orally administered fish oil supplements are often used to reduce serum
triglyceride levels. More recently, case reports using parenteral fish oils
have emerged for the treatment of PN-associated liver disease. We report a
PN-dependent patient with hypertriglyceridemia and his management using a
lipid formulation of fish oils and its potential new role as an alternative to
soy-based IVFEs.
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Case Report
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The patient was a 12-year-old boy with cerebral palsy, neurofibromatosis,
seizure disorder, and severe gastroesophageal reflux. On admission, his
medications included clonazepam, baclofen, and metoclopramide. For >9
years, his seizures were successfully controlled with valproic acid. When he
was an infant, a Nissen fundoplication was performed for his reflux. This was
later revised at age 11. A year after his revision, he developed a gangrenous
small bowel obstruction that required a small bowel resection. This was
complicated by an enterocutaneous fistula located at the proximal jejunum. His
postoperative course was further complicated by pseudomonas urosepsis,
resulting in hemodynamic instability. He also developed diabetes insipidus,
fluid and electrolyte imbalances, cholestasis, and abdominal ascites.
Nutrition History
The patient's admission weight was 22 kg (<3rd percentile, 54%
standard). His estimated basal energy expenditure (BEE) using World Heath
Organization (WHO) criteria was 1140 kcal/d (1036 kcal x 1.1 stress
activity factor). His recommended dietary intake was estimated to be 55
kcal/kg/d, with 1 g/kg/d as protein. Initially, the admitting team used a goal
intake of 1200 kcal/d. This was considerably lower than his preadmission
intake. Before his hospitalization, his diet consisted of Nutren 1.5
(Nestlé Nutrition, Glendale, CA), 6 cans/d. This provided 2160 kcal/d
and 3.9 g protein/kg. Per the transfer notes from the referring facility, this
high-calorie, high-protein diet was necessary to allow for growth, given his
high degree of seizure activity and frequency of muscle spasms.
At the time the intestinal obstruction developed, he underwent a
laparotomy; a central venous catheter was placed for the provision of PN. On
postoperative day 8, he returned to the operating room for surgical repair of
an anastomotic breakdown and the placement of a jejunostomy feeding tube. He
was unable to tolerate adequate enteral nutrition due to the development of a
jejunal fistula, and PN was continued.
Initially, his PN consisted of 144 g/d of dextrose, 21.6 g/d of amino acids
(Aminosyn; Hospira, Lake Forest, IL) that infused at 60 mL/h x 24 hours,
along with 22 g/d IVFE (Intralipid; Baxter Health-care/Fresenius Kabi,
Deerfield, IL). The PN formula provided 801 kcal, 1 g/kg/d protein, and 1
g/kg/d fat. Approximately 61% of his total calories were provided as
carbohydrates (6.5 g/kg/d) with a glucose infusion rate (GIR) of 4.5
mg/kg/min. Several days later, his PN regimen reached a goal rate that
provided 216 g of dextrose and 28.8 g of amino acids at 1440 mL/d, with 1
g/kg/d provided as fat and 1.3 g/kg/d protein. This delivered a total of 1069
kcal/d, with 68% of total calories provided as carbohydrate, 11% as protein,
and 21% as fat. His carbohydrate intake was determined to be 9.8 g/kg/d, with
a glucose infusion rate of 6.8 mg/kg/min, higher than the usual 5 mg/kg/min
used in adults but not unusual for a child of this age. The distribution of
nonprotein calories to g nitrogen was 207:1, which was considered acceptable
by team members given the patient's age and clinical condition. This regimen
was well tolerated for several weeks, and there was no evidence of
hyperglycemia or hypertriglyceridemia.
Indirect calorimetry (IC) was conducted 1 week after the second operation,
using the Vmax V29 metabolic monitor (SensorMedics, Yorba Linda, CA). The
results showed that the patient was moderately hypermetabolic. His resting
energy expenditure (REE) was determined to be 1517 kcal/d (140% of predicted
REE level of 1080 kcal/d 67 using the Schofield norms) and his respiratory
quotient (RQ) was 0.69, suggesting that he was not being overfed and perhaps
even underfed (500 kcal less than measured). Further, the RQ of 0.69 was
indicative that he was actually breaking down his fat stores.
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Figure 1. Serum triglyceride levels in a 12-year-old boy receiving parenteral
nutrition improved after initiation of IV fish oil emulsion therapy. Before
the discontinuation of conventional soy-containing lipid emulsions, the
patient's serum triglyceride levels peaked at 628 mg/dL. Initial management
involved holding further administration of fat emulsion until the triglyceride
levels were <200 mg/dL. Although serum triglyceride levels did improve,
this practice resulted in the patient developing biochemical evidence of
essential fatty acid deficiency (EFAD) 6 weeks after the development of
hypertriglyceridemia. When Omegaven (Fresenius Kabi, Bad Homburg, Germany) was
started, serum triglyceride levels were still slightly elevated; however, the
patient now also had evidence of EFAD. Within 10 days of receiving this
alternative lipid source, serum triglyceride levels markedly improved, as did
his essential fatty acid profile.
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After 4 weeks of PN, his nutrition course was complicated by worsening
hypertriglyceridemia (defined as a serum triglyceride level >200 mg/dL).
The initial management of the hypertriglyceridemia was to reduce the infusion
time of the fat emulsion from 24 to 20 hours. This allowed 4 hours for
triglyceride clearance. When this failed to decrease triglyceride levels
(Figure 1), IVFE administration
was then reduced to every other day and subsequently held indefinitely until
triglyceride levels returned to an acceptable level (ie, <200 mg/dL). His
highest serum triglyceride level was 628 mg/dL approximately 2 months after
starting PN (Table 1). After
withholding IVFE, biochemical evidence of EFAD occurred within 6 weeks of
developing hypertriglyceridemia (Table
2; day 0). An essential fatty acid (FA) profile was obtained that
showed an elevated serum triene:tetraene (T:T) ratio of 0.207 µmol/L
(normal, 0.013–0.05), along with an elevated Mead acid of 114 µmol/L
(normal, 7–30 µmol/L). He did not have any clinical symptoms
associated with EFAD.
In addition to biochemical evidence of EFAD, the patient had elevated serum
transaminases, including an aspartate amino transferase (AST) of 581 units/L
(normal, 2–40 units/L) and alanine amino transferase (ALT) of 291
units/L (normal, 3–30 units/L; Table
1). He then became jaundiced, with his serum total bilirubin level
peaking at 9.4 mg/dL (normal, 0.3–1.2 mg/dL) and direct serum bilirubin
reaching 6.3 mg/dL (normal, 0–0.4 mg/dL). Due to concerns of overfeeding
and his worsening clinical state, a second IC measurement was obtained and
showed that he had become moderately hypocatabolic, with an REE of 877 kcal/d
(75% of predicted REE level of 1162 kcal/d), with an RQ of 0.95. At that time,
he was receiving 100% of his calories parenterally, ranging from 899 to 1069
kcal/d, depending on fat intake. He was still unable to tolerate any enteral
feedings. According to the IC findings, the dextrose content in the PN was
reduced to 144 g/d. Despite having evidence of hyperglycemia, no insulin was
added to his regimen.
On day 87 of hospitalization (day 42 of PN), in response to his worsening
hepatic function and continued hypertriglyceridemia, coupled with biochemical
evidence of EFAD, an alternative IVFE (Omegaven; Fresenius Kabi AG, Bad
Homburg, Germany), was added to his PN regimen. The rationale for the use of
this product was based on our previous experience using a fish-oil-based IVFE
in an adolescent boy with EFAD secondary to soy allergy and our recently
published findings that  -3 rich lipid emulsions may prevent or treat
PN-associated liver
disease.2,3
Unlike the more commonly used IVFEs, such as Intralipid (Kabi Pharmacia,
Clayton, NC) and Liposyn, both of which contain soybean oils, this product
contains only fish oils (Table
3). Because it is not commercially available in the United States,
compassionate approval for its use was obtained from both the FDA and the
Children's Hospital Boston Investigational Review Board and informed consent
from the child's parent. Intralipid was discontinued and he received 200 mL
(20 g,  0.7–1 g/kg/d) Omegaven daily for 71 days in addition to his
PN. The fish-oil–based fat emulsion was administered via y-site
administration into his PN line and infused over 12 hours. He continued to
receive 144 g/d dextrose, 28.8 g/d of amino acids in his PN, providing an
average of 830 kcal/d. Within 2 weeks of starting the fish-oil–based
IVFE, his biochemical evidence of EFAD improved and eventually normalized by 5
weeks, with a T:T ratio of 0.035 and a decreased Mead acid of 30 µmol/L.
His hypertriglyceridemia and hyperglycemia also normalized by day 18 of
therapy. Likewise, his hepatic function improved and his jaundice resolved,
despite the fact that he continued to receive all of his nutrition
parenterally. Before starting parenteral fish oil, he had several serious
wound infections and fistulas that would not close. Although he did not
experience any further wound infections after starting parenteral fish oil, he
did have 2 bloodstream infections in the first month of therapy, both of which
quickly resolved. The first, due to Enterobacter cloacae, occurred in
conjunction with a urinary tract infection and resolved upon removal of the
central venous catheter; the second bloodstream infection, due to
Staphylococcus species, was successfully managed with appropriate
antibiotic therapy. After 29 days of parenteral fish oil therapy, the
patient's biochemical evidence of cholestasis resolved, despite remaining NPO
before closure of the fistula at the jejunostomy feeding tube site. On
postoperative day 53, the patient returned to the operating room for resection
of the enterocutaneous fistula and a jejunojejunostomy. A liver biopsy showed
diffuse hepatocellular damage, with ballooning giant cell transformation,
pseudoacinar transformation, and cholestasis and mild portal chronic
inflammatory infiltrate and mild portal fibrosis. Once bowel sounds returned,
he was slowly transitioned back to his home nasogastric tube feeding regimen
of 240 mL of Nutren (Nestle Nutrition, Glendale, CA) 1.5 6 times daily. He was
discharged to home 3 weeks after his last operation and has remained
stable.
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Discussion
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Iatrogenic Hypertriglyceridemia
In the pediatric patient, hypertriglyceridemia is defined as a serum
triglyceride level >200 mg/dL. It develops from a confluence of risk
factors, including infection or inflammation, hypothyroidism, renal and liver
failure, insulin resistance, diet, or
drugs.4,5
Nutrition factors associated with hypertriglyceridemia include excessive
macronutrients (either as carbohydrates or fat), poor glycemic control, and
carnitine
deficiency.1 If left
untreated, patients with severe hypertriglyceridemia (ie, serum triglyceride
levels >1000 mg/dL) may develop complications such as pancreatitis, lipid
pneumonitis, and neurologic
changes.6
Medications including corticosteroids, estrogens, retinoids, cyclosporine,
antihypertensives, interferon  -2-b, L-asparaginase,
antiretroviral agents, meropenem, rapamycin, and antiepileptic drugs are known
to cause
hypertriglyceridemia.4,7
Common mechanisms of drug-induced hypertriglyceridemia include decreased
clearance of triglycerides, increased triglyceride and very-low-density
lipoprotein (VLDL) production, or a combination of
both.4,8
Soybean-oil–based IVFE can also predispose patients to
hypertriglyceridemia. In addition to oil, IVFEs provide about 20% of their
calories as glycerin (glycerol) and egg emulsifier. These products are
formulated as an emulsion in which the long-chain FAs are suspended in a
superficial layer of phospholipids. Depending upon concentration of IVFE (10%,
20%, or 30%) and the volume of IVFE administered, the amount of phospholipids
will vary dramatically. For this reason, the use of 10% IVFE is discouraged in
children because of the high phosphospholipid content per g of
fat.9 Further, high
lipid infusion rates, >0.15 g/kg/h, may exceed the rate of metabolism and
can lead to accumulation and further increase in serum
triglycerides.10
This accumulation of lipids in the hepatic Kupffer cells and hepatocytes may
further impair liver
function.11
Although massive hypertriglyceridemia associated with fatty liver and
abdominal pain is uncommon, it is a clinically important and underrecognized
complication. Pancreatitis, lipemia retinalis, lipid pneumonitis, neurologic
changes, consumption coagulopathy, and xanthoma have all been associated with
hypertriglyceridemia.12
Treatment Options
Treatment of pediatric hypertriglyceridemia in the PN-dependent patient
should begin at the source of the disorder. Traditional nonpharmacologic
recommendations such as lifestyle modification clearly would be minimally
practical or beneficial in this patient. Nutrition factors associated with
hypertriglyceridemia are mentioned above and should be addressed with initial
therapy. Guidelines for the administration of specialized nutrition support in
pediatrics offer recommendations for the management of hypertriglyceridemia in
patients requiring IVFE, including use of 20% IVFE and avoidance of
overfeeding.13 If a
serum triglyceride level exceeds 200 mg/mL, the lipid emulsion may be held.
Because of its ability to induce lipoprotein lipase, heparin is often added to
PN at a dose of 1 unit/mL of PN to enhance the lipid
clearance.14
Insulin can also promote clearing of triglycerides as it promotes both fat
storage and its
mobilization.15 The
hormone prompts glycogenesis, the formation of glyceride and glycerol, and FA
synthesis from glucose, and inhibits the release of FAs by forming
-glycerophosphate, resulting in triglyceride
formation.16
Carnitine, a derivative of the amino acid lysine, has also been added to PN
for this purpose.17
Carnitine is essential for the transport of free FAs from the cytosol to the
mitochondrial matrix, where FAs are
oxidized.18 In
addition to lowering serum triglycerides, carnitine also lowers total
cholesterol levels while increasing concentrations of high-density
lipoproteins
(HDL).19
In this case, our patient was already receiving carnitine supplementation
because of its theoretical role as a hepatoprotective agent in patients
treated with valproic acid, a medication with known hepatotoxic
properties.20
Valproic acid can also deplete carnitine
stores.21 By
accepting and shuttling unmetabolized acyl groups from the mitochondria,
carnitine is able to eliminate acyl drugs or acyl metabolites of a drug and
thus effect the detoxification of the
agent.22,23
Although unlikely, valproic acid use was considered a plausible cause of
this patient's increased transaminases. Hepatotoxic effects associated with
valproic acid use typically occur during the first 6 months of therapy,
although they can occur at any time. In a retrospective review of reported
cases, children under the age of 2 years seem to be at greatest risk for
developing fatal
hepatotoxicity.24
In this case, the patient was 12 years old at the onset of his transaminase
elevations and had been treated with valproic acid for over 9 years. Further,
clinical improvement in hepatic function occurred despite continuing to
receive the medication, suggesting that PN use may have been the cause for his
hepatic dysfunction.
Failure of these interventions may require the use of pharmacologic agents
(ie, statins or gemfibrozil) or plasma pheresis. Experience with pharmacologic
therapies in pediatric patients is limited and should be used with caution. In
most cases, successful therapy arises from proper management of the underlying
cause of hypertriglyceridemia. In this case, initial management involved
holding the IVFE until the serum triglyceride level decreased to an acceptable
level, minimizing overfeeding, and continuing carnitine supplements.
EFAD
Essential fatty acids (EFAs) cannot be synthesized in human tissues and
must be obtained from the
diet.25 EFAs are
needed for processes including maintaining the integrity of the skin and the
structure of cell membranes, and the synthesis of prostaglandins and
leukotrienes.24
EFAs include linoleic (LA, an -6) and -linolenic (ALA, an
-3) acids. -3 FAs are found most abundantly in green plants,
ocean microalgae, and soybeans. -6 FAs are found in nuts, seeds, and
vegetable and seed oils. The body can derive other FAs, such as arachidonic
acid (AA, another -6) from LA and eicosapentaenoic (EPA, another
-3) and docosahexaenoic acid (DHA, also an -3) from ALA, but
fish oil is a more efficient source as it does not rely on the conversion of
ALA to DHA and EPA or LA to AA. In fact, fish oils contain mainly EPA and DHA,
whereas vegetable oils predominantly contain LA or ALA. EPA and DHA may
decrease hypertension, reduce elevated cholesterol and triglycerides, prevent
atherosclerosis, and improve skin
disorders.26–29
Requirements of EFAs are 1%–2% of dietary calories for children and
4%–5% for infants. The suggested ratio of -6 to -3 FAs is
variable, without
consensus.30
Previous recommendations suggest a balance of 10:1, but emerging data indicate
that a ratio as low as 2:1 would be beneficial in ill
patients.31,32
Soybean and olive-oil-based emulsions contain a ratio of approximately 7:1 and
9:1,
respectively.33
Deficiency can develop when intake of EFAs is inadequate (<1%–2%
of total
calories).34,35
This condition occurs with malabsorption syndromes, increased physical
requirements, chronic malnutrition, or the use of PN with inadequate fat
intake.34 Patients
with EFAD may show adverse effects, including skin lesions, reproductive
failure, growth retardation, reduced learning, impaired vision, and
polydipsia, as well as susceptibility to
infections.34,35
The decline in -3 and -6 FA concentrations that is
characteristic of EFAD is accompanied by a corresponding increase in the
percentage of -9 FAs (Mead acid), which the body produces as a result
of the elongation and desaturation of oleic acid that is produced by de
novo lipogenesis. As Mead acid typically accumulates in conditions of
EFAD, the ratio of this compound to AA (ie, the T:T ratio) is used as a
diagnostic marker for EFAD. Until recently, plasma values of T:T above 0.2
were considered abnormal, whereas levels >0.4 were considered diagnostic
for EFAD.36 Siguel
et al37 have since
developed more sensitive age-based range criteria that suggest T:T ratios
>0.05 and Mead acid to AA ratios >0.2 are more reflective of EFAD. It
must also be noted that the T:T ratio does not reflect -3 FA status.
Physical signs and symptoms of EFAD can vary, depending on the specific FA
that is deficient. Biochemical abnormalities appear in 1–2 weeks in
children, whereas physical signs and symptoms may not appear for 4–6
weeks.35
EFAD may be treated with a variety of modalities that may be administered
topically, orally, or IV. In the absence of IVFE, donor plasma has even been
administered to patients with
EFAD.38 Topical
products, including safflower and corn oils (both of which do not provide
adequate linolenic acid), have been used with slow and unpredictable results
and may take 2–3 weeks to take
effect.39,40
In the absence of enteral feedings, the most reliable therapy for EFAD
consists of IVFE. The products used in the United States are rich in -6
FAs derived from soybean oil with or without safflower oils. An alternative
lipid emulsion, available in Europe and Asia and not FDA approved, is
Omegaven, which consists of 100% fish oil and is rich in -3 FAs with
very little -6 FAs. This lipid emulsion, when dosed at approximately 1
g/kg/d, provides sufficient EFAs to prevent EFAD, although this dose is
considerably higher than the 0.2 g/kg/d recommended by its
manufacturer.41
Unlike other IVFEs, Omegaven is not intended to be used as monotherapy but
rather as a supplement added to conventional lipid emulsions as an additional
source of -3 FAs.
-3 FAs
-3 FAs have been used for the treatment of inflammatory bowel
disease (IBD), autoimmune disorders, peripheral vascular disease, adult
respiratory distress syndrome, cardiovascular disease, and
psychosis.42–47
These agents are proposed to provide benefit by attenuating the immune or
inflammatory response. Additionally, unsaturated FAs are necessary for normal
growth and development. Several studies suggest that -3 FAs may
increase cell-mediated immune responses through the action of
prostaglandins.43–48
The inhibitory effects of FAs on immune function seem to be mediated by
changes in surface adhesion on leukocytes and lymphocytes. -3 FAs also
have hypolipidemic activity, primarily reducing triglyceride concentrations by
reducing VLDL.49
The mechanism of action is not entirely understood; however, possible
mechanisms include the inhibition of acyl coenzyme A: 1,2-diacylglycerol
acyltransferase and increased peroxisomal β-oxidation in the
liver.50
Furthermore, these esters may diminish the synthesis of triglycerides in the
liver because EPA and DHA are poor substrates for the enzymes responsible for
triglyceride synthesis and because they inhibit esterification of other FAs.
Recently, the FDA approved the use of a purified oral fish oil capsule
(Omacor; Reliant Pharmaceuticals, Liberty Corner, NJ) for the management of
hypertriglyceridemia and mixed lipoprotein
disorders.51 There
is currently no parenteral product approved for use in the United States.
The FDA regards -3 FAs as "generally recognized as safe"
in dosages of <3
g/d.52 There are
several theoretical adverse effects associated with -3 FAs, including
increased LDL-cholesterol levels and deterioration of glycemic control in
patients with type 2 diabetes
mellitus.53
Critical analysis of these previously published studies, however, has since
concluded that glycemic control is not adversely impacted and -3 FAs
may actually be beneficial in the diabetic
patient.54–56
Excessive bleeding has been thought to be a risk associated with -3
use, but to date, there has been no clinical evidence of this complication. In
this case report, our patient's hyperglycemia resolved despite not receiving
any insulin, and he had no evidence of bleeding.
Studies in surgical patients and septic patients have displayed the utility
of increased intake of -3 FAs in patients with inflammation or
infection.57
Several randomized, controlled trials showed an increased immune cytokine
production and suppressed monocyte generation of proinflammatory cytokines and
decreased C-reactive protein
levels.57–60
This is similar to our experience. Before starting therapy with Omegaven, the
patient's serum C-reactive protein level was as high as 8.78 mg/dL (<0.5
mg/dL). Soon after starting Omegaven, it began to drop and eventually returned
to normal within 1 month. This is similar to reports by Weiss and colleagues,
who showed a down-regulation of the inflammatory response and decreased
postoperative immunosuppression with parenteral fish oil
therapy.61 In our
case, the patient did have a transient increase in his C-reactive protein
levels after starting to receive fish oil IVFE, but this occurred after he
returned to the operating room for resection of the enterocutaneous fistula.
Unlike the patient's course prior to infusion of fish oil, however, his
C-reactive protein increase was not accompanied by a corresponding increased
in serum bilirubin levels. Likewise, there is some evidence that IV fish oil
may reduce complication rates. One study showed a significant decrease in
reoperation rates in patients with abdominal
sepsis.62 Other
clinical studies have shown a tendency toward numerous benefits in surgical
patients, including infection, thrombosis, length of hospital stay, and
mortality.63
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Summary
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A novel approach of using of fish-oil-based IVFE for the treatment of
hypertriglyceridemia in a PN-dependent patient is described. In addition to
correcting EFAD, it also helped improve serum triglyceride levels and provided
an important source of nonprotein calories in a patient who could not tolerate
other forms of conventional fat emulsions.
Further, by switching to an alternative lipid source, it may have
contributed to the improvement of the patient's PN-associated liver disease,
as evidenced by normalization of serum bilirubin levels and resolution of
jaundice. This suggests that better alternatives to currently available
parenteral fat emulsions are needed. A randomized clinical trial evaluating
these alternatives to conventional practice is warranted.
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lipid emulsion to treat essential fatty acid deficiency in a soy allergic
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DOI: 10.1177/0115426507022006664
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