scholarly journals Parenteral Nutrition in Liver Resection

2012 ◽  
Vol 2012 ◽  
pp. 1-5 ◽  
Author(s):  
Carlo Chiarla ◽  
Ivo Giovannini ◽  
Felice Giuliante ◽  
Francesco Ardito ◽  
Maria Vellone ◽  
...  

Albeit a very large number of experiments have assessed the impact of various substrates on liver regeneration after partial hepatectomy, a limited number of clinical studies have evaluated artificial nutrition in liver resection patients. This is a peculiar topic because many patients do not need artificial nutrition, while several patients need it because of malnutrition and/or prolonged inability to feeding caused by complications. The optimal nutritional regimen to support liver regeneration, within other postoperative problems or complications, is not yet exactly defined. This short review addresses relevant aspects and potential developments in the issue of postoperative parenteral nutrition after liver resection.

2020 ◽  
Vol 318 (4) ◽  
pp. G772-G780
Author(s):  
Joonyong Lee ◽  
Veronica Garcia ◽  
Shashank Manohar Nambiar ◽  
Huaizhou Jiang ◽  
Guoli Dai

Liver resection induces robust liver regrowth or regeneration to compensate for the lost tissue mass. In a clinical setting, pregnant women may need liver resection without terminating pregnancy in some cases. However, how pregnancy affects maternal liver regeneration remains elusive. We performed 70% partial hepatectomy (PH) in nonpregnant mice and gestation day 14 mice, and histologically and molecularly compared their liver regrowth during the next 4 days. We found that compared with the nonpregnant state, pregnancy altered the molecular programs driving hepatocyte replication, indicated by enhanced activities of epidermal growth factor receptor and STAT5A, reduced activities of cMet and p70S6K, decreased production of IL-6, TNFα, and hepatocyte growth factor, suppressed cyclin D1 expression, increased cyclin A1 expression, and early activated cyclin A2 expression. As a result, pregnancy allowed the remnant hepatocytes to enter the cell cycle at least 12 h earlier, increased hepatic fat accumulation, and enhanced hepatocyte mitosis. Consequently, pregnancy ameliorated maternal liver regeneration following PH. In addition, a report showed that maternal liver regrowth after PH is driven mainly by hepatocyte hypertrophy rather than hyperplasia during the second half of gestation in young adult mice. In contrast, we demonstrate that maternal liver relies mainly on hepatocyte hyperplasia instead of hypertrophy to restore the lost mass after PH. Overall, we demonstrate that pregnancy facilitates maternal liver regeneration likely via triggering an early onset of hepatocyte replication, accumulating excessive liver fat, and promoting hepatocyte mitosis. The results from our current studies enable us to gain more insights into how maternal liver regeneration progresses during gestation. NEW & NOTEWORTHY We demonstrate that pregnancy may generate positive effects on maternal liver regeneration following partial hepatectomy, which are manifested by early entry of the cell cycle of remnant hepatocytes, increased hepatic fat accumulation, enhanced hepatocyte mitosis, and overall accelerated liver regrowth.


1985 ◽  
Vol 249 (5) ◽  
pp. R563-R569 ◽  
Author(s):  
R. P. Cornell

The influence of restricting gut-derived endotoxin availability on liver regeneration after partial hepatectomy was evaluated. Partial hepatectomy was performed by 67% liver resection of ether-anesthetized rats. Liver regeneration was quantified after partial hepatectomy by [3H]thymidine incorporation into hepatic DNA; endotoxemia due to absorption of endogenous endotoxin from the gut into the portal circulation was determined by qualitative lysate assay of perchloric acid-extracted plasma samples, and plasma levels of the hepatotrophic factors insulin and glucagon were measured by radioimmunoassay. Treatments to restrict gut-derived endotoxin included chronic gavage with neomycin and cefazolin for gut sterilization, chronic gavage with cholestyramine to bind endotoxin within the gut, subcutaneous administration of polymyxin B to neutralize the lipid A portion of circulating endotoxin, intraperitoneal induction of endotoxin tolerance by progressively higher doses of endotoxin, and experimentation with isolator-reared defined flora Fisher rats that were Gram-negative bacteria deficient and therefore endotoxin deficient. All treatments to restrict endogenous endotoxin impaired DNA synthesis in regenerating livers particularly 21 h posthepatectomy when replication was increasing most rapidly in normal rats. We hypothesize that impairment of DNA synthesis after partial hepatectomy in endotoxin-restricted animals was due to the observed lack of normal systemic endotoxemic as well as hyperinsulinemic and hyperglucagonemic responses to 67% liver resection.


2013 ◽  
Vol 33 (3) ◽  
pp. 469-475 ◽  
Author(s):  
Petra G. Kele ◽  
Eric J. van der Jagt ◽  
Annette S. H. Gouw ◽  
Ton Lisman ◽  
Robert J. Porte ◽  
...  

2019 ◽  
Vol 9 (1) ◽  
Author(s):  
Florencia Lorenzetti ◽  
Marina Cecilia Vera ◽  
María Paula Ceballos ◽  
María Teresa Ronco ◽  
Gerardo Bruno Pisani ◽  
...  

AbstractRegeneration is the unmatched liver ability for recovering its functional mass after tissue lost. Leukotrienes (LT) are a family of eicosanoids with the capacity of signaling to promote proliferation. We analyzed the impact of blocking LT synthesis during liver regeneration after partial hepatectomy (PH). Male Wistar rats were subjected to two-third PH and treated with zileuton, a specific inhibitor of 5-lipoxygenase (5-LOX). Our first find was a significant increment of intrahepatic LTB4 during the first hour after PH together with an increase in 5-LOX expression. Zileuton reduced hepatic LTB4 levels at the moment of hepatectomy and also inhibited the increase in hepatic LTB4. This inhibition produced a delay in liver proliferation as seen by decreased PCNA and cyclin D1 nuclear expression 24 h post-PH. Results also showed that hepatic LTB4 diminution by zileuton was associated with a decrease in NF-ĸB activity. Additionally, decreased hepatic LTB4 levels by zileuton affected the recruitment of neutrophils and macrophages. Non-parenchymal cells (NPCs) from zileuton-treated PH-rats displayed higher apoptosis than NPCs from PH control rats. In conclusion, the present work provides evidences that 5-LOX activation and its product LTB4 are involved in the initial signaling events for liver regeneration after PH and the pharmacological inhibition of this enzyme can delay the initial time course of the phenomenon.


2009 ◽  
Vol 24 (1) ◽  
pp. 1-8 ◽  
Author(s):  
S. C. Schmidt ◽  
G. Schumacher ◽  
N. Klage ◽  
S. Chopra ◽  
P. Neuhaus ◽  
...  

2014 ◽  
Vol 3 (9) ◽  
pp. 1233-1237
Author(s):  
Shinn Young Kim ◽  
◽  
Dong-Goo Kim ◽  
Jong-Young Choi ◽  
Eun Sun Chung ◽  
...  

2011 ◽  
Vol 171 (1) ◽  
pp. 259-265 ◽  
Author(s):  
Kensuke Miyazaki ◽  
Susumu Eguchi ◽  
Tetsuo Tomonaga ◽  
Takamitsu Inokuma ◽  
Koji Hamasaki ◽  
...  

2012 ◽  
Vol 27 (7) ◽  
pp. 460-464 ◽  
Author(s):  
Maria de Lourdes Pessole Biondo-Simões ◽  
Camila Gadens Zamboni ◽  
Evelise Martins ◽  
Luka David Lechinewski ◽  
Sérgio Ossamu Ioshii ◽  
...  

PURPOSE: To determine the impact of hypertension in liver regeneration, in rats by examining gain in liver mass and the replication of hepatocytes and stellate cells. METHODS: Forty Wistar rats were allocated into two groups of twenty, the control and experiment group. The experiment group animals were submitted to induction of renovascular hypertension. A week later, all the animals underwent a partial hepatectomy. Measurements were taken after 24 hours and seven days, when ten animals in each group were euthanized. Thus, four subgroups were obtained. The livers were excised and sent for histopathological analysis. RESULTS: The control group had a greater gain in liver mass than the experiment group seven days after partial hepatectomy (p=0.0051). The difference in the activate stellate cell count was not statistically significant following analysis after both 24 hours and seven days (p=1.0). A higher number of dividing hepatocytes was observed in the control group seven days after partial hepatectomy (p=0.0014). CONCLUSION: In rats, hypertension had no direct influence on stellate cell replication, but led to a delay in liver mass gain and were shown to be a reduction factor on hepatocyte replication seven7 days after partial hepatectomy.


2020 ◽  
Author(s):  
Mihai-Calin Pavel ◽  
Raquel Casanova ◽  
Laia Estalella ◽  
Robert Memba ◽  
Erik Llàcer ◽  
...  

Abstract Introduction The primary objective of this systematic review is to assess the effect of neoadjuvant chemotherapy on liver regeneration after liver resection (LR) or portal vein embolization (PVE) in patients with liver metastasis from colo-rectal cancer. The secondary objectives are to evaluate the impact of the type of chemotherapy, number of cycles and time between end of treatment and procedure (LR or PVE) and to investigate whether there is an association between degree of hypertrophy and postoperative liver failure. Methods The design of this systematic review will follow the current recommendations of PRISMA. After an exhaustive literature search with pre-established criteria, two researchers will individually screen the identified records, according to a list of inclusion and exclusion criteria. Primary outcome will be future liver remnant regeneration rate. All data will be registered in a predesigned database. In the event of a substantial heterogeneity of selected articles, a narrative systematic review will be performed. Discussion The results of this systematic review may help to better identify the patients affected by liver metastasis that could present low regeneration rates after neoadjuvant chemotherapy. These patients are at risk to develop liver failure after extended hepatectomies and therefore are not good candidates for such aggressive procedures. Systematic Review Registration PROSPERO registration number: CRD42020178481 (July 5th 2020).


Blood ◽  
2019 ◽  
Vol 133 (11) ◽  
pp. 1245-1256 ◽  
Author(s):  
Dafna Groeneveld ◽  
David Pereyra ◽  
Zwanida Veldhuis ◽  
Jelle Adelmeijer ◽  
Petra Ottens ◽  
...  

AbstractPlatelets play a pivotal role in stimulating liver regeneration after partial hepatectomy in rodents and humans. Liver regeneration in rodents is delayed when platelets are inhibited. However, the exact mechanisms whereby platelets accumulate and promote liver regeneration remain uncertain. Thrombin-dependent intrahepatic fibrin(ogen) deposition was recently reported after partial hepatectomy (PHx) in mice, but the role of fibrin(ogen) deposits in liver regeneration has not been investigated. We tested the hypothesis that fibrin(ogen) contributes to liver regeneration by promoting intrahepatic platelet accumulation and identified the trigger of rapid intrahepatic coagulation after PHx. PHx in wild-type mice triggered rapid intrahepatic coagulation, evidenced by intrahepatic fibrin(ogen) deposition. Intrahepatic fibrin(ogen) deposition was abolished in mice with liver-specific tissue factor deficiency, pinpointing the trigger of coagulation after PHx. Direct thrombin activation of platelets through protease-activated receptor-4 did not contribute to hepatocyte proliferation after PHx, indicating that thrombin contributes to liver regeneration primarily by driving intrahepatic fibrin(ogen) deposition. Fibrinogen depletion with ancrod reduced both intrahepatic platelet accumulation and hepatocyte proliferation after PHx, indicating that fibrin(ogen) contributes to liver regeneration after PHx by promoting intrahepatic platelet accumulation. Consistent with the protective function of fibrin(ogen) in mice, low postoperative plasma fibrinogen levels were associated with liver dysfunction and mortality in patients undergoing liver resection. Moreover, increased intrahepatic fibrin(ogen) deposition was evident in livers of patients after liver resection but was remarkably absent in patients displaying hepatic dysfunction postresection. The results suggest a novel mechanism whereby coagulation-dependent intrahepatic fibrin(ogen) deposition drives platelet accumulation and liver regeneration after PHx.


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