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D I S C U S S I O N   A N D   V A L O R I Z A T I O N   A D D E N D U M     Small  for  gestational  age  children   Besides  the  evidence  of  the  origin  of  the  metabolic  syndrome  in  SGA  children,  it  is   also  remarkable  that  their  growth  in  length  and  height  often  stay  behind  the  norm.   One   of   the   factors   mentioned   with   respect   to   the   stunted   growth   SGA   children   is   reduced   sensitivity   for   the   insulin-­‐like   growth   factor   1   (IGF-­‐1)8.   IGF-­‐1   is   mainly   secreted   by   the   liver   as   a   result   of   stimulation   by   growth   hormone.   IGF-­‐1   expres-­‐ sion   is   required   for   achieving   maximal   growth.   Short   SGA   children   show   plasma   IGF-­‐1  levels  that  are  in  the  lower  normal  range9.    For  that  reason  these  children  are   treated   with   recombinant   human   growth   hormone   (rhGH)   nowadays.   In   general   they   respond   very   good   on   this   treatment   and   correct   their   height   towards   their   genetically  defined  percentile.  At  the  same  time  it  is  known  from  that  treatment  of   growth  hormone  deficient  (GHD)  children  with  rhGH  results  in  a  change  of  the  me-­‐ tabolism10.  This  change  is  assumed  to  be  an  effect  of  IGF-­‐I  what  is  a  primary  regula-­‐ tor  of  systemic  anabolism  and  muscle  growth11.  Growth  hormone  deficiency  is  as-­‐ sociated   with   increased   body   fat   and   a   lower   lean   body   mass.   These   changes   in   body   composition   are   associated   with   metabolic   derangements   including   insulin   resistance.  They  normalize  with  growth  hormone  replacement  therapy12.     In   this   thesis   we   showed   that   treatment   with   rhGH   has   also   a   positive   metabolic   effect  on  body  composition  of  SGA  children.  The  treatment  with  rhGH  causes  a  shift   in  body  composition  of  FM  towards  FFM.  After  treatment  with  rhGH,  SGA  children   show   an   increase   in   height   but   also   in   weight.   The   detected   increase   in   weight   is   based  on  an  increase  in  FFM  and  not  in  FM.  This  means,  as  mentioned  before,  that   the  body  composition  in  SGA  children  improves  after  receiving  rhGH  treatment.  In   SGA  children  rhGH  treatment  prevents  overweight  and  thereby  the  metabolic  syn-­‐ drome.     To  evaluate  adequate  and  inadequate  responders  to  rhGH  therapy,  with  respect  to   height,  changes  in  body  composition  can  be  measured.  The  change  in  body  compo-­‐ sition  is  an  actual  tool  in  predicting  the  individual  response  on  rhGH  treatment.  By   using  this  method  rhGH  therapy  can  be  given  only  to  adequate  responders  and  it  is   possible  to  prevent  aimless  administration.       In  obese  children  there  exists  a  decrease  in  growth  hormone  (GH)  secretion  what  is   fully   reversible   when   body   weight   is   normalized13.   A   decrease   in   spontaneous   GH   release   in   obesity   has   been   confirmed   in   several   comparative   studies   on   the   24-­‐ hour  secretion  of  GH  in  normal  weight14  and  obese  children13,  15.  In  obese  children,   GH   secretion   may   be   as   low   as   in   poorly   growing   children   with   classical   GHD16.   Investigation   of   the   pattern   of   factors   potentially   influencing   GH   secretion   con-­‐ firmed  a  significant  and  independent  impact  of  fat  mass.  Relative  adiposity  acts  as  a   negative  determinant  of  the  frequency  and  amplitude  of  GH  secretory  bursts.  They   are  associated  with  an  increased  GH  clearance  leading  to  a  lower  GH  half-­‐life  time,     109  


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