O.42 Liver damage in total parenteral nutrition (TPN) in infants and children

[ S T U D I E S ON L I P O P R O T E I N X /LPX/ A P P E A R A N C E D U R I N G P A R E N T E R A L NU[/PN/.M.PERTKIEWICZ,D.Bobilewicz,T.Korta,J.Kotlicka./Clinic of n t e s t i n a l S u r g e r y and A n a e s t h e s i a D e p t . , M e d i c a l A c a d e m y and Dept. ~ratory D i a g n o s t i c , M e d . C e n t r e of P o s t g r a d . E d u c . , W a r s a w , P o l a n d . known to be present in most of PN p a t i e n t s r e c e i v i n g fat e m u l s i o n )wing no c l i n i c a l signs of c h o l e s t a s i s . T h e a i m of this study was >are some a n t i g e n i c p r o p e r t i e s of c h o l e s t a t i c and f a t - i n d u c e d LPX b i o c h e m i c a l c o n d i t i o n s a s s o c i a t e d w i t h their a p p e a r a n c e . M e t h o d s : LPX p o s i t i v e PN patients and m a t c h e d c o n t r o l group of c h o l e s t a t i c ~s total c h o l e s t e r o l / C h o l / b y c o l o r i m e t r i c m e t h o d , p h o s p h o l i p i d s by ~ t r i c or e n z y m a t i c m e t h o d were m e a s u r e d . 2 . P r e s e n c e of LPX w a s by agar e l e c t r o p h o r e s i s f o l l o w e d by C a C l o / h e p a r i n e p r e c i p i t a t i o n t w o - d i m e n s i o n a l i m m u n o e l e c t r c p h o r e s l s a g a i n s t a n t i - L P X . I n 15 PN LPX was p r e c i p i t a t e d from the serum by p h o s p h o t u n g s t a t e a f t e r preremoval A p o - L p B by a n t i - A p o B , d i s s o l v e d in 0 , 9 % NaCI and r e e s t i m a L i p o p r o t e i n f r a c t i o n s were o b t a i n e d by c h e m i c a l p r e c i p i t a t i o n and [mated by e n z y m a t i c m e t h o d ~ R e s u l t s : l . B i l i r u b i n , C h o l and p h o s p h o l i acreased in j a u n d i c e d were d e c r e a s e d or n o r m a l in PN patients.2. out of 15 cases we failed to show LPX by a g a r e l e c t r o p h o r e s i s and ery low p r e c i p i t a t l a n peak was found on e l e c t r o i m m u n o d i f f u s i o n , o n atrary to the c h o l e s t a t i c L P X , w h l c h was a l w a y s clearly v i s i b l e . 3 . se of LDL-TG and decrease of V L D L - T G w a s the most s t r i k i n g a b n o r ,which a c c o m p a n i e d the LPX a p p e a r a n c e .

NES INDUCED BY TPN IN ACUTELY ILL CHILDREN: A CLINICAL STUDY. M. van Caillie d, G. Janssens, A. Bochner, A.Verhelst,H.Peeters,W.Van Herreweghe, R. Clara en Kinderziekenhuis Antwerpen, U.I.A., Antwerpen,Belgium) atic

liver

disease

i s a w e l l known c o m p l i c a t i o n

o f TPN i n

children

(1).

rant gallstones formation is not yet fully recognised in this young age Since Januari 1982, a biliary ultrasonographic study was systematically ~d on children with persistent disturbance in liver function tests while on onal support (N 4). We found gallstones in 3 children: a 10 year old girl L high gastrointestinal fistula after an abdominal trauma, a premature baby i0 gr) with necrotising enterocolitis, and a I0 month old infant with a bronchopneu~onia secondary to adenovirus infection. All were girls and only Id icterus. In each child, the clinical course was characterised by I) rebouts of sepsis with disseminated intravascular coagulation 2) hemolytic with hepatosplenomegaly, requiring repeated transfusions 3) interruption of =ralipid infusions without vitamine E supplementation during septicaemias and 3ence of enteral feeding from 14 days up to 4 months. Outpatient follow up resolution of the stone in one child 6 months after discharge. In another who developed 2 episodes of abdominal colic, the cholelitbiasis was still t 15 months later. sions: Cholelithiasis has to be suspected in children with liver dysfunction and after TPN. This may cause ascending cholangitis,sepsis and abdominal These observations suggest that the formation of gallstones is more prohae to the combination of multiple factors. • Hughes e t a l . :

Gut 24:

241,1983.