Published online Jul 26, 2026. doi: 10.12998/wjcc.123291
Revised: June 3, 2026
Accepted: June 26, 2026
Published online: July 26, 2026
Processing time: 68 Days and 21.7 Hours
Prolonged parenteral nutrition (PN) is a major risk factor for intestinal failure-associated liver disease (IFALD), particularly in preterm infants. Plant-derived lipid emulsions, rich in phytosterols and ω-6 fatty acids, are considered key con
We report three preterm infants (gestational age, 31-36+2 weeks) with severe IFALD who were transitioned from soybean oil-based or multi-oil emulsions to FO-ILE. Fish oil was administered at a dose of 2 g/kg/day, a dosing approach for which limited data are available in this population. Prior to the transition, peak direct bilirubin (DB) levels ranged from 191.9 μmol/L to 356 μmol/L, with one patient exhibiting severe cholestasis and marked hepatosplenomegaly. Following 29-63 days of treatment, DB levels decreased to 30.7-89.9 μmol/L, resulting in a faster DB decline than that observed with the conventional 1 g/kg/day dosage. Full enteral feeding was achieved after 69-105 days of PN. The regimen was well tolerated, with no evidence of essential fatty acid deficiency, growth im
FO-ILE up to 2 g/kg/day was well tolerated and improved liver function, which supports further investigation in PN-dependent infants.
Core Tip: Prolonged parenteral nutrition in preterm infants can lead to intestinal failure-associated liver disease (IFALD). We describe three preterm infants with severe IFALD who were treated with pure fish oil lipid emulsion (FO-ILE) at 2 g/kg/day—higher than conventional protocols. This approach was associated with a rapid decline in direct bilirubin levels and was well tolerated without evidence of essential fatty acid deficiency, growth impairment, or bleeding complications. To the best of our knowledge, this report is among the first reports of high-dose FO-ILE for severe IFALD in preterm infants, a vulnerable population because of hepatic immaturity.
- Citation: Chen HJ, Danzeng ZG, Ye PF, Xu XM, Liang J, Zhang L. Fish oil emulsion for reversal of intestinal failure-associated liver disease in preterm infants: Three case reports and review of literature. World J Clin Cases 2026; 14(21): 123291
- URL: https://www.wjgnet.com/2307-8960/full/v14/i21/123291.htm
- DOI: https://dx.doi.org/10.12998/wjcc.123291
Parenteral nutrition (PN) is essential for the growth and survival of preterm infants; however, prolonged PN use can lead to intestinal failure-associated liver disease (IFALD), which adversely affects clinical outcomes. IFALD is characterized by cholestasis, hepatic steatosis, and fibrosis and can progress to advanced liver disease, including cirrhosis, potentially requiring liver transplantation or resulting in death[1]. Although no uniform diagnostic criteria currently exist, a typical case in infants is defined by PN use for more than 14 days and a serum direct bilirubin (DB) level of ≥ 2 mg/dL (34.2 μmol/L) on two consecutive measurements obtained at least 1 week apart, after exclusion of other causes of liver injury[2]. Based on DB levels, IFALD severity is classified as mild (2-4.9 mg/dL), moderate (5-9.9 mg/dL), or severe (≥ 10 mg/dL)[3]. In pediatric short bowel syndrome, cholestasis (i.e., DB ≥ 2.5 mg/dL) is the strongest predictor of mortality[4]. The incidence of IFALD is approximately 40%-60% in children receiving long-term PN[1] and up to 50% in neonates[5].
Although the pathogenesis of IFALD is not fully understood, plant-derived lipid emulsions (e.g., soybean oil) have been identified as major contributing factors[6]. These emulsions are associated with impaired bile acid secretion and proinflammatory responses mediated by ω-6 polyunsaturated fatty acids and phytosterols[7]. Therefore, an ideal lipid emulsion should contain minimal phytosterols, possess antioxidant properties, and meet the nutritional requirements of infants.
In recent years, the use of intravenous lipid emulsions in preterm infants has evolved, with a gradual shift from soybean oil-based lipid emulsions (SO-ILE) to fish oil-containing composite lipid emulsions and pure fish oil formula
| Case 1 | Case 2 | Case 3 | ||
| Sex | Male | Female | Male | |
| Gestational age | 31 weeks | 35 weeks | 36+2 weeks | |
| Birth weight | 1320 g | 920 g | 2750 g | |
| Condition | Necrotizing enterocolitis, septic shock, meconium intestinal obstruction | Hemodynamically significant patent ductus arteriosus, heart failure, neonatal pneumonia | Complex small bowel atresia, neonatal sepsis | |
| Medications that may cause cholestasis | Cefoperazone-sulbactam, vancomycin | Cefoperazone-sulbactam, meropenem, ibuprofen | Cefoperazone-sulbactam, meropenem | |
| Direct bilirubin (μmol/L) | At FO-ILE start | 229.2 | 191.9 | 38.4 |
| Peak value | 229.2 | 191.9 | 356 | |
| At FO-ILE cessation | 89.9 | 19.9 | 30.7 | |
| Peak total bilirubin (μmol/L) | 300.9 | 298.3 | 451.9 | |
| Duration of PN before FO-ILE | 69 days | 22 days | 42 days | |
| Duration of FO-ILE therapy | 29 days | 47 days | 63 days | |
| Duration of PN after FO-ILE | 0 days | 0 days | 0 days | |
| Duration of PN | 98 days | 69 days | 105 days | |
| Peak triglyceride level (borderline high: 1.7-2.25 mmol/L) | 2.00 mmol/L | 2.06 mmol/L | 3.39 mmol/L | |
| Peak prothrombin time value (9.0-15.0 seconds) | 14.7 seconds | 15.7 seconds | 16.5 seconds | |
| Peak APTT value (18.3-38.3 seconds) | 45.9 seconds | 48.3 seconds | 37.2 seconds | |
| Peak INR value (0.8-1.5) | 1.43 | 1.53 | 1.65 | |
| Triene:Tetraene | Normal | Normal | Normal | |
| Outcome | Resolved | Resolved | Resolved | |
Case 1: A preterm infant was admitted 18 minutes after delivery and subsequently developed abdominal distention and poor stooling.
Case 2: Tachypnea for 3 days following preterm birth.
Case 3: Suspected small intestinal atresia or stenosis based on fetal magnetic resonance imaging (MRI) at 30+6 weeks of gestation. The infant was admitted immediately after birth.
Case 1: A male infant born at 31 weeks of gestation with a birth weight of 1320 g presented with abdominal distension and poor stooling shortly after birth due to meconium intestinal obstruction. Following feeding, he developed recurrent bilious vomiting, abdominal distension, and hypoactive bowel sounds, accompanied by hyponatremia, acidosis, and portal venous gas. Neonatal necrotizing enterocolitis with perforation and septic shock were diagnosed. Ileostomy was performed, and cefoperazone-sulbactam and vancomycin were administered.
Intraoperatively, the small intestine measured 140 cm in length; the distal 40 cm showed severe necrosis, whereas the proximal 100 cm was less severely affected. During reintroduction of feeding, the patient received a SO-ILE (maximum 3.5 g/kg/day), amino acids (3-3.5 g/kg/day), and carbohydrates (9-16 g/kg/day). Over time, the skin gradually deve
Case 2: A female infant born at 35 weeks of gestation with a birth weight of 920 g was treated with ibuprofen for hemodynamically significant patent ductus arteriosus and associated heart failure. The patient received cefoperazone-sulbactam followed by meropenem for neonatal pneumonia. As the patient was small for gestational age and presented with generalized edema, hepatomegaly, and ascites, prolonged PN was required.
The patient was started on a lipid emulsion containing soybean oil, medium-chain triglycerides, olive oil, and fish oil (SMOF), administered at a maximum dose of 3.5 g/kg/day, along with amino acids and carbohydrates, as in Case 1. After 20 days of PN, the patient developed feeding intolerance, worsening jaundice, and progressive hepatomegaly.
Case 3: A male infant born at 36+2 weeks of gestation with a birth weight of 2750 g underwent fetal MRI, which sug
Intraoperatively, multiple atresias were identified, leading to a diagnosis of complex small bowel atresia (types IIIB and IV). Feeding was resumed after a 10-day postoperative fast, during which he received a SMOF at a maximum dose of 3 g/kg/day. Over time, his stools became pale, and his skin developed a dull yellow hue.
Case 1: No relevant past medical history.
Case 2: After birth, the infant, who was the smaller of twins, received mechanical ventilation and anti-infective treatment at an outside hospital for preterm birth and tachypnea; however, respiratory irregularities persisted.
Case 3: No relevant past medical history.
Case 1: No relevant personal or medical history.
Case 2: No significant personal or medical history.
Case 3: No relevant personal or medical history.
Case 1: Progressive jaundice and hepatosplenomegaly were observed.
Case 2: Worsening jaundice and hepatomegaly were noted.
Case 3: Dull yellow discoloration of the skin, marked abdominal distension, and hepatosplenomegaly were observed.
Case 1: Baseline DB was 13.5 μmol/L. Peak values included alanine aminotransferase (ALT) 220 U/L, aspartate amino
Case 2: Baseline DB was 22.5 μmol/L. DB increased to 191.9 μmol/L, and TBA reached 264.3 μmol/L after 22 days of SMOF therapy.
Case 3: Baseline DB was 16.9 μmol/L. DB increased to 38.4 μmol/L after 42 days of SMOF therapy.
Cases 1 and 2: No imaging examinations specific to IFALD were performed.
Case 3: Computed tomography demonstrated marked hepatosplenomegaly (Figure 1).
(1) Very low birth weight (1320 g); (2) Neonatal necrotizing enterocolitis; (3) Postoperative status: Ileostomy, adhesiolysis, and reduction of intestinal volvulus; (4) Septic shock; (5) Meconium intestinal obstruction; (6) Very preterm infant (31 weeks); (7) Functional short bowel syndrome; and (8) IFALD.
(1) Extremely low birth weight (920 g); (2) Hemodynamically significant patent ductus arteriosus; (3) IFALD; (4) Ascites; (5) Preterm infant (35 weeks); and (6) Neonatal pneumonia.
(1) Complex small intestinal atresia (types IIIB and IV); (2) IFALD; (3) Splenomegaly with hypersplenism; (4) Preterm infant (36+2 weeks); (5) Intestinal adhesions; (6) Ascites; and (7) Neonatal sepsis.
The lipid emulsion was switched to pure fish oil, initiated at 0.5 g/kg/day and gradually increased to a maximum of 2 g/kg/day. L-carnitine and glutathione were administered as adjunctive therapy.
Initial treatment with ursodeoxycholic acid and probiotics was ineffective. The patient was subsequently switched to pure fish oil, starting at 0.8 g/kg/day and gradually increasing to 2 g/kg/day.
The patient was switched to pure fish oil, initiated at 1.3 g/kg/day and increased to a maximum of 2 g/kg/day. The patient had concurrent sepsis and received sequential treatment with meropenem and cefoperazone-sulbactam. Peak laboratory values, observed after 30 days of pure fish oil therapy, included TBA 74.9 μmol/L, ALT 363 U/L, AST 261 U/L, total bilirubin 451.9 μmol/L, and DB 356 μmol/L. L-carnitine and glutathione were added. The patient subsequently underwent stoma closure, enterolysis, and peritoneal drainage. Intraoperatively, the liver was markedly enlarged and dark brown. Fish oil therapy was continued for 63 days.
In all three cases, an individualized dose-escalation regimen was used. Due to fluid restrictions from the underlying disease, the starting dose of fish oil was not uniform. Tolerability was assessed every 1-3 days, after which the dose was increased by 0.5 g/kg/day when appropriate. Assessment was based on biochemical tolerance indicators, including regular monitoring of DB, transaminases, and lipid levels, as well as clinical signs of bleeding tendency or lipid overload. No fixed escalation intervals were used, and dose adjustments were individualized. None of the infants experienced adverse reactions requiring dose reduction or treatment interruption during dose titration.
DB and TBA decreased to 89.9 μmol/L and 60.4 μmol/L, respectively, representing reductions of 62.9% and 71.7% from peak values. After 98 days of PN, near-full enteral feeding was achieved. Following discharge, oral fish oil supplementation was continued until liver function normalized (Figure 2A).
After 69 days of PN, the patient successfully transitioned to full enteral feeding. At the time of PN discontinuation, DB and TBA levels had decreased to 19.9 μmol/L and 14.3 μmol/L, respectively (Figure 2B).
Liver function improved after reaching peak levels. At cessation of fish oil therapy, DB had decreased to 30.7 μmol/L (91.4% reduction from the peak value of 356 μmol/L), and TBA had decreased to 11.7 μmol/L (84.3% reduction). By discharge, DB had further decreased to 15.3 μmol/L (95.7% reduction), accompanied by normalization of liver enzyme levels. After 105 days of PN, full enteral feeding was achieved, and the patient was discharged (Figure 2C).
In Case 1, antibiotic therapy had been completed before initiation of fish oil treatment. In Case 2, no increase in DB levels was observed during ibuprofen administration. DB levels subsequently increased following initiation of PN and continued to rise despite infection control and completion of antibiotic therapy. Following initiation of fish oil treatment, DB levels gradually declined. In Case 3, DB levels continued to increase despite resolution of infection; however, a decline in DB was observed after initiation of fish oil therapy, even while antibiotic treatment was ongoing.
All three infants tolerated fish oil therapy well. Monitoring of coagulation function, blood glucose, and renal function revealed no abnormalities. No persistent lipid overload was observed. In Case 3, triglyceride levels were only mildly and transiently elevated and normalized shortly after enteral feeding volume increased and the requirement for lipid emul
Case 1 was followed until 6 years and 3 months of age, Case 2 until 6 years of age, and Case 3 until 1 year and 1 month of age. At the latest follow-up, all three infants had normal liver function with no recurrence of IFALD. All achieved and maintained full enteral feeding, and none required liver transplantation.
Neuromotor developmental assessments demonstrated normal neurological development in all cases. In Case 1, General Movements (GMs) assessment was normal at a corrected age of 4 months, the Gesell Developmental Quotient (DQ) was 96 (normal range, 85-115) at a corrected age of 12 months, and 105 at 6 years of age. In Case 2, GMs assessment was normal at a corrected age of 4 months, and the DQ was 110 at 6 years of age. In Case 3, GMs assessment was normal at a corrected age of 5 months, and the Gesell DQ was 102 at 1 year and 1 month of age. All three infants showed normal development in the domains of gross motor, fine motor, language, and social interaction.
IFALD is a serious complication in patients receiving long-term PN, with established risk factors including prematurity, low birth weight, gastrointestinal immaturity, inflammation, and sepsis[2]. Its pathogenesis is multifactorial and involves lipid emulsion composition, intestinal barrier dysfunction, gut microbiota dysbiosis, and activation of hepatic innate immunity[9].
Plant-derived lipid emulsions are considered major contributing factors to IFALD and warrant efforts to minimize PN duration and lipid exposure where possible. Doses exceeding 1 g/kg/day may increase exposure to ω-6 polyunsaturated fatty acids and phytosterols while decreasing α-tocopherol levels[10]. Excess ω-6 fatty acids promote inflammation, whereas phytosterols inhibit hepatic farnesoid X receptor (FXR) signaling and disrupt the FXR/fibroblast growth factor-19 pathway[8]. This disruption impairs bile acid flow and promotes oxidative stress and inflammatory liver injury, ultimately leading to cholestasis[11]. Conversely, α-tocopherol enhances antioxidant capacity and lipid metabolism, whereas ω-3 fatty acids reduce liver inflammation and may improve cholestasis and fibrosis[10].
Based on these mechanisms, fish oil-based lipid emulsions provide a rich source of ω-3 fatty acids, including eicosapen
MOILEs have demonstrated hepatoprotective effects and may improve growth and development in infants receiving long-term PN[14]. However, findings have been inconsistent, with some studies reporting no significant difference between MOILEs and SO-ILE[15,16]. Additionally, certain fish oil-containing preparations have not been associated with significant improvements in liver function parameters despite their anti-inflammatory properties[17]. These findings suggest that even small amounts of soy-based lipids may contribute to liver injury, whereas complete replacement with fish oil may provide greater therapeutic benefit.
Accordingly, the United States Food and Drug Administration approved the fish oil-based emulsion Omegaven for the treatment of IFALD in 2018[1]. Clinical studies have reported improved outcomes with fish oil compared to SMOF (56% vs 38%) in patients with newly diagnosed IFALD[18]. In neonates and one young infant who developed cholestasis while receiving MOILEs[19,20] or SO-ILEs[21], switching to 100% fish oil has been associated with reductions in bilirubin levels. A dose of 1 g/kg/day has been associated with resolution of cholestasis and improvement in biochemical markers of IFALD in many infants[22], potentially reducing the need for liver transplantation[23]. Omegaven has been associated with more rapid resolution of cholestasis and lower mortality than SO-ILE in previous studies[24]. In our three patients, DB and TBA levels decreased following the transition from SO-ILE or SMOF to fish oil therapy, further supporting its therapeutic potential[25].
Fish oil exerts multiple biochemical and cellular hepatoprotective effects[26]. Its ω-3 fatty acids possess anti-inflammatory properties and promote the generation of specialized pro-resolving mediators, such as resolvins and protectins. ω-3 fatty acids also inhibit nuclear factor κB signaling, reduce leukocyte chemotaxis[27], and suppress cytokine release[1]. Additionally, ω-3 fatty acids modulate innate and adaptive immune responses and inhibit the secretion of profibrotic mediators, including transforming growth factor-beta 1 (TGF-β1) and matrix metalloproteinase-9[28]. These effects may be partially attributable to reduced phytosterol exposure[29].
Although fish oil is rich in polyunsaturated fatty acids (PUFAs) and high PUFA intake may theoretically increase the risk of lipid peroxidation, available evidence suggests that fish oil enhances antioxidant capacity. Animal studies have shown that fish oil reduces DNA damage[30], enhances antioxidant defenses in the brain[31], and alleviates hepatic oxidative stress[32]. Similarly, a study of adolescents with depression found that ω-3 PUFAs reduced lipid peroxidation and enhanced membrane antioxidant capacity[33]. Mechanistically, ω-3 fatty acids increase total antioxidant capacity and the activity of glutathione peroxidase (GPx), superoxide dismutase (SOD), and heme oxygenase-1, while reducing malondialdehyde (MDA) levels. These effects may result from alterations in membrane structure and lipid composition, inhibition of cyclooxygenase-2, and activation of the nuclear factor erythroid 2-related factor 2 (Nrf2) pathway, a key regulator of antioxidant responses. Consistent with these findings, fish oil supplementation reduced hepatic F2-isoprostane levels, a recognized marker of lipid peroxidation, while increasing Nrf2, GPx, SOD, and catalase levels in animal models[34].
Moreover, ω-3 fatty acids may directly neutralize reactive oxygen species and modulate endogenous antioxidant systems, including glutathione. In patients receiving home-based PN, higher fish oil doses have been associated with normalization of SOD1 activity without significant cholestasis[35]. Omegaven has been reported to modulate cytokine levels and increase paraoxonase 1 activity, thereby reducing oxidative stress[26]. Beyond their antioxidant effects, ω-3 fatty acids modulate Toll-like receptor 4 signaling and influence hepatic β-oxidation through peroxisome proliferator-activated receptor-α[36], contributing to reduced inflammation. DHA and EPA promote an anti-inflammatory microenvironment and may provide protection against sepsis and viral replication[37], potentially through modulation of immune responses, reduction of C-reactive protein levels, and lower infection rates following hepatectomy[38]. Fur
At the molecular level, fish oil modulates multiple signaling pathways, including the TGF-β-mediated Mothers Against Decapentaplegic Homolog-2/3 pathway, which has been implicated in inflammatory processes[41]. It affects the miR-122/FXR axis, which regulates oxidative stress, inflammation, and metabolic pathways[36]. These mechanisms may contribute to the anti-inflammatory, antioxidant, and anti-fibrotic effects of fish oil in IFALD.
Safety concerns regarding fish oil include essential fatty acid deficiency (EFAD), insufficient caloric intake, and bleeding risk. However, existing evidence generally supports its safety. Although fish oil contains relatively low levels of LA and ALA, studies suggest that EFAD is uncommon, even with long-term use of up to 10 years[42-46]. A dose of 1 g/kg/day may be sufficient to prevent or even treat EFAD[22]. Fish oil contains small amounts of EFAs, and its ARA content is higher than that of SO-ILE; In addition, ARA and DHA can be retroconverted to upstream fatty acids. As ARA, EPA, and DHA serve as precursors for bioactive eicosanoids involved in numerous physiological processes[8], the high EPA and DHA content of fish oil may reduce dependence on ω-6 fatty acids, while still meeting EFA requirements.
With respect to growth and development, some studies suggest that fish oil administered at 1 g/kg/day may provide insufficient caloric intake, necessitating adjustments in carbohydrate provision[18]. However, other studies have reported comparable or improved growth outcomes relative to soybean oil, accompanied by fewer metabolic abnormalities[22,47].
Although ω-3 fatty acids may theoretically increase bleeding risk through effects on platelet function, clinical evidence does not support a significant increase in bleeding events[37]. Improved liver function and platelet counts in patients receiving fish oil may reduce bleeding risk compared with SO-ILE[37]. Consistent with these findings, none of the infants in the present study developed EFAD, growth impairment, or bleeding complications[40].
Optimization of fish oil dosing remains an area of ongoing investigation. Most studies have focused on doses ≤ 1 g/kg/day; however, higher doses may provide additional benefits in selected patients. For example, increasing the dose to 1.5 g/kg/day has been associated with improved weight gain and maintenance of EFA status[48]. Additionally, normal T:T ratios and Mead acid levels have been reported, indicating adequate EFA reserves[49]. Nevertheless, in patients with poor weight gain and elevated glucose infusion rates, increasing the fish oil dose to 1.5 g/kg/day has been shown to improve weight Z-scores, although only a modest reduction in glucose infusion rates (GIRs) was observed, suggesting that higher doses may be required to reduce carbohydrate dependence[49]. Moreover, resolution of cholestasis may be slow, potentially prolonging hospital stays and increasing infection risk and healthcare costs.
All three infants in the present study had impaired glucose tolerance associated with liver dysfunction and required high GIRs. However, IFALD limited the use of conventional lipid emulsions. Increasing glucose delivery alone was insufficient to meet growth requirements, and persistent hyperglycemia is associated with adverse outcomes. Increasing the fish oil dose to 2 g/kg/day reduced glucose infusion requirements while providing additional non-protein calories to support growth. Prior to dose escalation, hypertriglyceridemia (baseline TG > 2.25 mmol/L) and bleeding tendency were excluded. Therefore, fish oil was administered at doses up to 2 g/kg/day to balance efficacy and safety. This approach was associated with improved weight gain and reductions in DB levels, without evidence of EFAD or coagulation abnormalities.
The decline in DB appeared more rapid than that reported in historical studies using fish oil at 1 g/kg/day[20,50,51], suggesting that higher doses may provide additional benefit when standard dosing is insufficient. To explore this observation, DB reduction rates were compared with those reported in 20 previously published cases with comparable baseline characteristics treated with 1 g/kg/day fish oil. Among these historical cases, DB reduction rates ranged from 0.13 μmol/L/day to 2.64 μmol/L/day, whereas those in Cases 1 and 2 of the present study were 3.66 μmol/L/day and 4.80 μmol/L/day, respectively (Table 2). Case 3 was excluded from this comparison because fish oil therapy was initiated when DB was only slightly above 2 mg/dL. Instead, the rate of DB decline was assessed from the peak DB value. Peak DB decline rates were 3.66 μmol/L/day, 4.80 μmol/L/day, and 9.86 μmol/L/day in Cases 1-3, respectively. In contrast, peak DB decline rates reported in studies using 1 g/kg/day fish oil ranged from 0.93 μmol/L/day to 2.06 μmol/L/day (Table 3).
| Cases | DB at fish oil initiation (μmol/L) | DB at fish oil cessation (μmol/L) | Duration of fish oil therapy | DB reduction rates (μmol/L/day) |
| This Case 1 | 229.2 | 89.9 | 29 days | 4.80 |
| This Case 2 | 191.9 | 19.9 | 47 days | 3.66 |
| Case 2[20] | 44.5 | 23.9 | 27 days | 0.76 |
| Case 4[20] | 51.3 | 22.2 | 39 days | 0.75 |
| Case 5[20] | 70.1 | 41.0 | 33 days | 0.88 |
| Case 7[20] | 148.8 | 22.2 | 54 days | 2.34 |
| Case 8[20] | 162.5 | 12.0 | 57 days | 2.64 |
| Case 9[20] | 160.7 | 25.7 | 82 days | 1.65 |
| Case 10[20] | 109.4 | 17.1 | 59 days | 1.56 |
| Case 11[20] | 90.6 | 85.5 | 26 days | 0.20 |
| Case 12[20] | 198.4 | 112.9 | 112 days | 0.76 |
| Case 13[20] | 212.0 | 159.0 | 38 days | 1.39 |
| Case 1[50] | 58.1 | 23.9 | 90 days | 0.38 |
| Case 2[50] | 99.2 | 32.5 | 21 weeks | 0.45 |
| Case 1[51] | 186.4 | 1.7 | 41 weeks | 0.64 |
| Case 2[51] | 59.9 | 22.2 | 5 weeks | 1.08 |
| Case 3[51] | 70.1 | 1.7 | 12 weeks | 0.81 |
| Case 4[51] | 46.2 | 1.7 | 17 weeks | 0.31 |
| Case 6[51] | 42.8 | 1.7 | 16 weeks | 0.37 |
| Case 7[51] | 42.8 | 5.1 | 40 weeks | 0.13 |
| Case 8[51] | 145.4 | 41.0 | 32 weeks | 0.47 |
| Case 10[51] | 167.6 | 95.8 | 13 weeks | 0.79 |
| Cases | Peak DB (μmol/L) | DB at fish oil cessation (μmol/L) | Duration of fish oil therapy from peak | DB reduction rate (μmol/L/day) |
| This Case 1 | 229.2 | 89.9 | 29 days | 4.80 |
| This Case 2 | 191.9 | 19.9 | 47 days | 3.66 |
| This Case 3 | 356 | 30.7 | 33 days | 9.86 |
| Case 1[50] | 109.4 | 23.9 | 90 days | 0.95 |
| Case 2[50] | 136.8 | 32.5 | 16 weeks | 0.93 |
| Case 5[51] | 212.0 | 10.3 | 14 weeks | 2.06 |
To the best of our knowledge, this case series is among the first reports describing fish oil administration at 2 g/kg/day in preterm infants with severe IFALD, with favorable outcomes and no apparent safety concerns.
The route, timing, and duration of administration are important considerations. Oral fish oil has limited absorption in patients with intestinal failure, whereas parenteral administration may produce more rapid effects[26]. One infant with IFALD did not respond to oral therapy but experienced a 69.9% reduction in DB within 7 days of switching to intrave
DB levels may initially increase after treatment initiation before subsequently declining[54]. Additionally, ω-6 fatty acid levels decrease during the first few weeks of treatment and typically stabilize after approximately 8 weeks. These observations support continued therapy until cholestasis resolves[45]. In the present study, fish oil was initiated pro
This study has limitations, including a small sample size, the absence of a control group, and the potential for residual confounding. Oxidative stress markers (e.g., MDA, SOD, and F2-isoprostane) were not directly measured because these assays are not routinely performed at our center and require specialized sample collection. However, liver function and coagulation parameters remained stable or improved during treatment in all three infants, erythrocyte fatty acid profiles demonstrated normal T:T ratios, and no clinical signs of hemolysis or lipid peroxidation (e.g., worsening jaundice or thrombocytopenia) were observed. These findings provide indirect evidence supporting the safety of high-dose fish oil therapy. Future studies should include direct measurement of oxidative stress markers to further evaluate the safety of high-dose fish oil in preterm infants.
This case series describes three preterm infants with IFALD secondary to long-term PN, in whom plant-derived lipid emulsions were a major contributing factor. FO-ILE demonstrated therapeutic potential and was associated with improvements in biochemical markers of IFALD, likely through its anti-inflammatory, antioxidant, lipid-modulating, and anti-fibrotic properties. Compared with SMOF or SO-ILE, fish oil monotherapy may be associated with a more rapid decline in DB levels and resolution of cholestasis. Determining the optimal fish oil dose remains important for improving treatment outcomes.
In this case series, administration of fish oil at doses up to 2 g/kg/day was well tolerated and was not associated with evidence of EFAD, growth impairment, or coagulation abnormalities. Long-term follow-up demonstrated normal growth and development and no recurrence of IFALD. To the best of our knowledge, this case series is among the first reports describing the use of pure fish oil emulsion at 2 g/kg/day in preterm infants (gestational age, 31-36+2 weeks) with severe IFALD. Although the long-term outcomes were favorable, larger prospective studies are needed to establish optimal dosing strategies and further evaluate the efficacy and safety of fish oil in improving outcomes in PN-dependent infants.
We would like to thank Sang Ba for collecting data.
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