In one of our first patients with severely disabling and fluctuating Parkin
son's disease (PD) we observed a transient pancreatic enzymes increase 6 mo
nths after continuous apomorphine therapy. Since this adverse effect had no
t been previously reported, we systematically investigated the course of pa
ncreas and liver functions in response to apomorphine: laboratory and neuro
logical assessments were conducted before initiation of apomorphine therapy
, during the increment phase up to the optimal motor effective level and at
all follow-up visits.
We found in five out of 29 PD patients a transient increase of pancreatic e
nzymes during the initial phase of continuous subcutaneous apomorphine appl
ication. Peaks of pathological plasma levels were apparent fi-om the first
day up to the fifth day after apomorphine initiation, and returned to norma
l levels within 10 days in all 5 patients. Otherwise, this pancreatic enzym
es increase was not accompanied by any raising in plasma levels of correspo
nding liver enzymes. No pathological signs in the endoscopic-retrograde cho
langiopancreatography, the abdominal ultrasonography and the computed tomog
raphy of the abdomen were found in any of the affected PD patients. Further
more, there was no evidence of pancreato-hepatal risk factors in the previo
us history in any of the PD patients studied. With respect to the course of
PD, no differences were obtained upon comparison of affected and non-affec
ted PD patients.
Considering the patients' history, clinical course and current knowledge ab
out the effect of apomorphine on pancreato-hepatal function, we conclude th
at a possible cumulative pathomechanism between transient pancreato-hepatal
enzymes and continuous applied apomorpine, especially in the titrating pha
se, might cause this adverse event in about 20% of PD patients treated with
apomorphine continuously.