Does Long‐Term Home Parenteral Nutrition in Adult Patients Cause Chronic Liver Disease?

Bowyer, Brad A.; Fleming, C. Richard; Ludwig, Jürgen; Petz, Janice L.; McGill, Douglas B.

doi:10.1177/014860718500900111

Cited by 144 publications

(37 citation statements)

References 36 publications

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“…9,22 Hyperinsulinemia is common in the conditions with which NASH is most frequently associated: obesity, 22,39-41 type 2 diabetes mellitus, 39 and parenteral nutrition. 42 In our study, type 2 diabetes mellitus was diagnosed in half the patients with end-stage liver disease secondary to NASH.…”

Section: Discussionmentioning

confidence: 64%

Frequency of nonalcoholic steatohepatitis as a cause of advanced liver disease

Charlton

2001

Liver Transplantation

242

147

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Although nonalcoholic steatohepatitis (NASH) has generally been considered a benign condition, the increasing prevalence and severity of obesity has heightened concerns about the frequency with which NASH progresses to end-stage liver disease. The aim of this study is to determine the frequency, clinical features, and posttransplantation history of decompensated liver disease secondary to NASH. The frequency of NASH as a cause of end-stage liver disease was prospectively determined in patients evaluated for liver transplantation. NASH was considered to be the primary cause of liver disease in patients who had histological evidence of steatohepatitis and in whom chronic liver diseases other than NASH were excluded. Posttransplantation histological characteristics were also determined in patients with NASH and compared with those of patients with pretransplantation diagnoses of cholestatic liver diseases, alcoholic disease, and hepatitis C. Of 1,207 patients evaluated for liver transplantation during the study period, 31 patients (2.6%) had NASH as the primary cause of liver disease. In the same period, 546 liver transplantations were performed, 16 of which (2.9%) were for end-stage disease secondary to NASH. Posttransplantation steatosis was seen in 60% of transplant recipients with NASH versus 5% of those with cholestatic disease, 15% of those with alcoholic disease, and 15% of those with hepatitis C. Steatohepatitis recurred in 33% of transplant recipients with NASH, with progression to cirrhosis in 12.5%. NASH can progress to end-stage liver disease in a minority of affected patients and was the primary cause of liver disease in 2.9% of patients evaluated for liver transplantation at our center. Recurrence of steatosis and NASH is frequent and can be severe after liver transplantation. (Liver Transpl 2001;7:608-614.)

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Section: Discussionmentioning

confidence: 64%

Frequency of nonalcoholic steatohepatitis as a cause of advanced liver disease

Charlton

2001

Liver Transplantation

242

147

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“…Finally, we cannot exclude that a longer time may be necessary for a measurable depletion in liver triglyceride; for example, the buildup of liver steatosis due to parenteral nutrition with lipid emulsions requires weeks (6,22), but our findings showed no trend while prolonging the suppression of fatty acids from 1 day to 1 wk.…”

Section: Ajp-endocrinol Metabmentioning

confidence: 59%

The lowering of hepatic fatty acid uptake improves liver function and insulin sensitivity without affecting hepatic fat content in humans

Rigazio

Lehto

Tuunanen

et al. 2008

American Journal of Physiology-Endocrinology and Metabolism

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Iozzo P. The lowering of hepatic fatty acid uptake improves liver function and insulin sensitivity without affecting hepatic fat content in humans. Am J Physiol Endocrinol Metab 295: E413-E419, 2008. First published May 27, 2008 doi:10.1152/ajpendo.00744.2007.-Lipolysis may regulate liver free fatty acid (FFA) uptake and triglyceride accumulation; both are potential causes of insulin resistance and liver damage. We evaluated whether 1) systemic FFA release is the major determinant of liver FFA uptake in fasting humans in vivo and 2) the beneficial metabolic effects of FFA lowering can be explained by a reduction in liver triglyceride content. Sixteen healthy subjects were subdivided in two groups of similar characteristics to undergo positron emission tomography with [11 C]acetate and [ 11 C]palmitate to quantify liver FFA metabolism (n ϭ 8), or magnetic resonance spectroscopy (MRS) to measure hepatic fat content (n ϭ 8), before and after the acute lowering of circulating FFAs by using the antilipolytic agent acipimox. MRS was again repeated after a 1-wk treatment period. Acipimox suppressed FFA levels while stimulating hepatic fractional extraction of FFAs (P Ͻ 0.05). As a result, fasting liver FFA uptake was decreased by 79% (P ϭ 0.0002) in tight association with lipolysis (r ϭ 0.996, P Ͻ 0.0001). The 1-wk treatment induced a significant improvement in systemic (ϩ30%) and liver (ϩ70%) insulin sensitivity (P Ͻ 0.05) and decreased circulating triglycerides (Ϫ20%, P ϭ 0.06) and liver enzymes (ALT Ϫ20%, P ϭ 0.03). No change in liver fat content was observed after either acute or sustained FFA suppression. We conclude that acute and sustained inhibitions of lipolysis and liver FFA uptake fail to deplete liver fat in healthy human subjects. Liver FFA uptake was decreased in proportion to FFA delivery. As a consequence, liver and systemic insulin sensitivity were improved, together with liver function, independently of changes in hepatic triglyceride accumulation. lipolysis; liver metabolism; positron emission tomography; magnetic resonance; acipimox; insulin resistance ACCORDING TO THE OVERFLOW HYPOTHESIS, the provision of fatty acids, as released from adipose tissue to the liver, is responsible for the regulation of liver fat accumulation via hepatic fatty acid uptake (7,14). In turn, liver fat content is proportional to indicators of liver damage such as liver enzymes, suggesting a cause-effect relationship (7,9,14,32). This view implicates that substrate delivery from the circulation plays a dominant, and the intrinsic organ response has a minor, role in the regulation of liver fatty acid uptake. This passive response of the liver remains to be proven in humans in vivo.Lipolysis is not the only source of fatty acids. Lipodystrophy represents an unphysiological state associated with liver steatosis in which endogenous fatty acids may be one major source of triglyceride precursors (25, 27). However, in the normal situation, the meal provides nutrients, suppressing their endogenous release during a time in which hi...

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“…Although providing good nutritional recovery, the complex technology of HPN reduces the quality of life, 26 and serious side effects, such as sepsis, venous thrombosis, and liver disease may occur. [27][28][29][30] Small bowel transplantation is an exciting alternative, but many still consider it experimental for most short-bowel patients until it has proven superior to parenteral nutrition in terms of quality of life and mortality. 27 Therefore, the search for factors to enhance small bowel adaptation and to increase the assimilation of macronutrients and absorption of water and electrolytes, thereby decreasing the need for parenteral nutrition, has been intensive.…”

Section: Discussionmentioning

confidence: 99%

Glucagon-like peptide 2 improves nutrient absorption and nutritional status in short-bowel patients with no colon

et al. 2001

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Background & Aims: Glucagon-like peptide 2 (GLP-2) is intestinotrophic, antisecretory, and transit-modulating in rodents, and it is mainly secreted from the intestinal mucosa of the terminal ileum and colon after food ingestion. We assessed the effect of GLP-2 on the gastrointestinal function in patients without a terminal ileum and colon who have functional short-bowel syndrome with severe malabsorption of wet weight (>1.5 kg/day) and energy (>2.3 MJ/day) and no postprandial secretion of GLP-2. Methods: Balance studies were performed before and after treatment with GLP-2, 400 g subcutaneously twice a day for 35 days, in 8 patients (4 -17 years from last bowel resection; 6 with Crohn's disease). Four patients received home parenteral nutrition (mean residual jejunum, 83 cm), and 4 did not (mean ileum resection, 106 cm). Biopsy specimens were taken from jejunal/ileal stomas, transit was measured by scintigraphy, and body composition was measured by dual-energy x-ray absorptiometry. Results: Treatment with GLP-2 improved the intestinal absorption of energy 3.5% ؎ 4.0% (mean ؎ SD) from 49.9% to 53.4% (P ‫؍‬ 0.04), wet weight 11% ؎ 12% from 25% to 36% (P ‫؍‬ 0.04), and nitrogen 4.7% ؎ 5.4% from 47.4% to 52.1% (P ‫؍‬ 0.04). Body weight increased 1.2 ؎ 1.0 kg (P ‫؍‬ 0.01), lean body mass increased 2.9 ؎ 1.9 kg (P ‫؍‬ 0.004), fat mass decreased 1.8 ؎ 1.3 kg (P ‫؍‬ 0.007), and 24-hour urine creatinine excretion increased (P ‫؍‬ 0.02). The time to 50% gastric emptying of solids increased 30 ؎ 16 minutes from 89 to 119 minutes (P < 0.05). Small bowel transit time was not changed. Crypt depth and villus height were increased in 5 and 6 patients, respectively. Conclusions: Treatment with GLP-2 improves intestinal absorption and nutritional status in short-bowel patients with impaired postprandial GLP-2 secretion in whom the terminal ileum and the colon have been resected.

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Does Long‐Term Home Parenteral Nutrition in Adult Patients Cause Chronic Liver Disease?

Cited by 144 publications

References 36 publications

Frequency of nonalcoholic steatohepatitis as a cause of advanced liver disease

Frequency of nonalcoholic steatohepatitis as a cause of advanced liver disease

The lowering of hepatic fatty acid uptake improves liver function and insulin sensitivity without affecting hepatic fat content in humans

Glucagon-like peptide 2 improves nutrient absorption and nutritional status in short-bowel patients with no colon

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