Summary.
In one of our first patients with severely disabling and fluctuating Parkinson's disease (PD) we observed a transient pancreatic enzymes increase 6 months after continuous apomorphine therapy. Since this adverse effect had not been previously reported, we systematically investigated the course of pancreas and liver functions in response to apomorphine: laboratory and neurological 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 enzymes during the initial phase of continuous subcutaneous apomorphine application. Peaks of pathological plasma levels were apparent from the first day up to the fifth day after apomorphine initiation, and returned to normal levels within 10 days in all 5 patients. Otherwise, this pancreatic enzymes increase was not accompanied by any raising in plasma levels of corresponding liver enzymes. No pathological signs in the endoscopic-retrograde cholangiopancreatography, the abdominal ultrasonography and the computed tomography of the abdomen were found in any of the affected PD patients. Furthermore, there was no evidence of pancreato-hepatal risk factors in the previous 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-affected PD patients.
Considering the patients' history, clinical course and current knowledge about the effect of apomorphine on pancreato-hepatal function, we conclude that a possible cumulative pathomechanism between transient pancreato-hepatal enzymes and continuous applied apomorpine, especially in the titrating phase, might cause this adverse event in about 20% of PD patients treated with apomorphine continuously.
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Received March 12, 1996; accepted May 19, 1998
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Pinter, M., Helscher, R., Mundsperger, N. et al. Transient increase of pancreatic enzymes evoked by apomorphine in Parkinson's disease. J Neural Transm 105, 1237–1244 (1998). https://doi.org/10.1007/s007020050126
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DOI: https://doi.org/10.1007/s007020050126