Clinical outcome of intestinal transplantation at the University of Miami

Misiakos, Evangelos P.; Weppler, D.; Bakonyi, Alexandre; Nery, Jose; Pinna, Antonio D.; Kato, Tomoaki; Rodríguez, Miguel; Ruiz, Phil; Thompson, John F.; Ricordi, Camillo; Tzakis, Andreas G.

doi:10.1016/s0041-1345(98)01558-9

Cited by 20 publications

(10 citation statements)

References 4 publications

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“…10,29 Also, it relieves these patients from the expenses of chronic home intravenous hyperalimentation, which may reach $150 000 to $200 000 per patient per year. 9 However, these patients must be carefully assessed before transplantation to exclude conditions that preclude transplantation.…”

Section: Discussionmentioning

confidence: 99%

“…30 Intestinal rejection is still a major cause of early mortality and graft loss. 10,18 Two of 4 deaths and 3 graft losses were attributable to severe acute graft rejection resistant to treatment.…”

Section: Discussionmentioning

confidence: 99%

“…The donor pancreas was implanted in 3 cases of liver-intestinal or isolated intestinal transplants for technical reasons. 9,10,14 One patient received 2 kidneys with the multivisceral graft because of concomitant end-stage renal disease attributable to chronic glomerulonephritis (Table 1). Grafts were obtained from ABO-compatible donors; lymphocytotoxic cross-match was negative in all cases except the patient who had retransplantation.…”

Section: Transplant Surgerymentioning

confidence: 99%

“…One patient received triple therapy of tacrolimus, steroids, and daclizumab (Zenapax, Roche Laboratories Inc). 10 The patients received Gancyclovir and CMV-specific immune globulin (Cytogam, MedImmune Inc, Gaithersburg, MD) to prevent CMV infection. Standard antifungal (amphotericin) and antiprotozoal (trimethoprim-sulfamethoxazole) and antibacterial (ampicillin/sulbactam) agents also were administered.…”

Section: Immediate Postoperative Periodmentioning

confidence: 99%

“…5,6 However, a small proportion of patients develops chronic dependence on total parenteral nutrition (TPN) and associated life-threatening complications, such as liver failure, recurrent catheter sepsis, and loss of intravenous access, and they require intestinal transplantation as an extreme life-saving option. [7][8][9][10][11] This article reviews our experience with intestinal transplantation for SGS attributable to NEC focusing on the mode of presentation, natural history, timing, and outcome.…”

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confidence: 99%

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Intestinal Transplantation for Short Gut Syndrome Attributable to Necrotizing Enterocolitis

et al. 2000

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ABSTRACT. Background. Necrotizing enterocolitis (NEC) is a life-threatening condition of the neonatal age, which frequently requires surgical intervention. After extensive bowel resection, a small proportion of these patients may develop chronic short gut syndrome (SGS) and require chronic total parenteral nutrition (TPN) use. Intestinal transplantation has been performed in these patients as a life-saving option.This study reviews our experience with intestinal transplantation for SGS attributable to NEC emphasizing the mode of presentation, natural history, timing, and outcome.Methods. A retrospective chart review was performed for all pediatric patients who underwent small bowel transplantation for NEC at the University of Miami between August 1994 and March 1999.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Section: Transplant Surgerymentioning

confidence: 99%

Section: Immediate Postoperative Periodmentioning

confidence: 99%

mentioning

confidence: 99%

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Intestinal Transplantation for Short Gut Syndrome Attributable to Necrotizing Enterocolitis

et al. 2000

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The effect of hepatocyte growth factor on intestinal adaption in an experimental model of short bowel syndrome

et al. 2023

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Nowadays, the standard therapy for patients with short bowel syndrome is parenteral nutrition (PN). Various growth factors have been tested in order to achieve weaning from prolonged PN administration.We evaluated the effect of hepatocyte growth factor (HGF) on structural intestinal adaptation and cell proliferation in a rat model of SBS. MethodsThirty Sprague-Dawley rats were divided into three groups; group A rats (sham) underwent bowel transection, group B rats underwent a 75% bowel resection and group C rats underwent the same procedure but were treated postoperatively with HGF. Histopathologic parameters of intestinal adaptation were determined, while a microarray and a rt-PCR analyses of ileal RNA was also performed. ResultsTreatment with HGF resulted in signi cant increase in body weight, while the jejunal and ileal villus height and crypt depth were increased in HGF rats (36%, P < 0.05 and 27%, P < 0.05 respectively). Enterocyte proliferation was also signi cantly increased in HGF rats (21% P < 0.05). Microarray and quantitative rt-PCR analyses showed that the genes hgfac, rac 1, cdc42 and akt 1 were more than two-fold up-regulated after HGF treatment. ConclusionHGF emerges as a growth factor that enhances intestinal adaptation. The future use of HGF may potentially reduce the requirement for PN in SBS patients.

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