22. Workshop für experimentelle und klinische Lebertransplantation ...

Transplantationsmedizin
Supplement I – 2011, S. 35
Sleeve Gastrectomy after Liver
Transplantation
T. Meile, M. Küper, M. Feilitzsch,
M. Kramer, M. Zdichavski,
A. Königsrainer, S. Nadalin
Universitätsklinikum Tübingen
One important risk after sleeve gastrectomy
is the ability to drink. This is especially
important after renal transplant, not to
endanger graft function. Therefore patient
preparation and education prior to bariatric
surgery is highly important.
Obesity increases the risk of graft loss
after organ transplantation and survival
statistics for obese patients are very poor.
Hepatitis C is a very common reason for
liver transplantation. Treatment of hepatitis
C is very difficult in obese patients.
The aim of this report is to describe the
outcome of two patients who underwent
sleeve gastrectomy after liver transplantation
or combined liver and kidney transplantation.
A retrospective chart review
was conducted to analyze outcome of morbidly
obese patients after liver transplantation
that underwent laparoscopic sleeve
gastrectomy.
Patient 1, a 60 years old female, was combined
liver and kidney transplanted for
chronic hepatitis C infection with cirrhosis
and diabetic nephropathy in December
2008. Co morbidities were diabetes mellitus
type 2, intermittent atrial fibrillation,
arterial hypertension and osteoporosis.
After transplantation she had a rapid
weight gain due to corticosteroids with stable
graft function. In August 2010 she got
a sleeve gastrectomy without complications
weighting 123 kg at a BMI of 49
kg/m 2 . Until December 2010 she lost 25
kg, weighting 98 kg which corresponds to
a BMI of 39 kg/m 2 . This represents an excess
weight loss (EWL) of 38% within 4
months. Organ functions are stable, insulin
doses have been cut into thirds.
Patient 2, a 60 years old male, was liver
transplanted for chronic hepatitis C infection
with cirrhosis and hepatocellular carcinoma
in January 2008. Co-morbidities were
diabetes type 2, arterial hypertension
and a huge incisional hernia. In July 2009
he got a sleeve gastrectomy without complications
weighting 120 kg at a BMI of 43
kg/m 2 . Until September 2010 he lost 34 kg,
weighting 86 kg which corresponds to a
BMI of 31 kg/m 2 . This represents a EWL
of 64% within about one year. Organ
functions are stable and the incisional hernia
was successfully close in February
2010. Chronic hepatitis C infection was
successfully treated with Interferon and
Ribavirin and the patient’s HCV RNA
PCR is negative since February 2010.
We can report two successful cases of bariatric
surgery after liver transplantation.
Acute Liver Failure by
α-Amanitin Intoxication:
Liver Transplantation or
Spontaneous Regeneration
M. Schenk 1 , Ch. Thiel 1 , K. Thiel 1 ,
M. H. Morgalla 2 , A. Königsrainer 1
1
Allgemeine, Viszeral- und Transplantationschirurgie,
Universitätsklinikum Tübingen
2
Neurochirurgie, Universitätsklinikum Tübingen
Introduction: Acute liver failure caused
by drug ingestion, viral hepatitis or poisoning
is still associated with an extremely
high mortality rate. Liver transplantation
remains the life-saving therapy for all affected
individuals, but worldwide shortage
of donor organs remains the limiting factor.
Aim of the present study was to simulate
the clinical course of α-amanitin intoxication
in a pig model of acute liver
failure. Prognostic indicators for spontaneous
liver regeneration were evaluated.
Methods: 8 male German landrace pigs
received 5 mg (0.15 mg/kg body weight)
(n=4) α-amanitin intravenously or 10 mg
(0.35 mg/kg body weight) (n=8) intraportally.
Pigs remained under deep general
anesthesia until conclusion of the study
protocol. Ventilation and vital parameters
were recorded continuously, laboratory
values including TNF-α as a potential regeneration
marker were analyzed every 8
hours, liver biopsies were taken every 24
hours.
Results: All pigs 100% (8/8) developed
acute liver failure, which was defined by a
prothrombin time below 30% within 40±8
hours. All pigs receiving 10 mg amanitin
died due to multiorgan failure. Pigs which
received 5 mg amanitin survived poisoning.
They recovered spontaneously after
50±14 hours in acute liver failure and were
euthanized after 112 hours, when prothrombin
time returned to levels above
50%. Clinical, biochemical and histological
signs of liver regeneration were recorded.
Laboratory values started to recover
96±7 hours after intoxication paralleled by
clinical stabilization. TNF-α levels in the