Klara Coello1, Brian V Broberg2, Nikolaj Bak2, Anna Madsen3, Henrik B Mortensen4, Birgitte Søgaard5, Pal B Szecsi6, Filip K Knop7, Henrik Lublin3, Bjørn H Ebdrup8. 1. Centre for Neuropsychiatric Schizophrenia Research, CNSR, Psychiatric Centre Glostrup, Copenhagen University Hospitals, Mental Health Services, Capital Region of Denmark, Glostrup, Denmark; Psychiatric Centre Copenhagen, Department O, Copenhagen University Hospitals, Mental Health Services, Capital Region of Denmark, Copenhagen, Denmark. 2. Centre for Neuropsychiatric Schizophrenia Research, CNSR, Psychiatric Centre Glostrup, Copenhagen University Hospitals, Mental Health Services, Capital Region of Denmark, Glostrup, Denmark; Centre for Clinical Intervention and Neuropsychiatric Schizophrenia Research, CINS, Copenhagen University Hospitals, Mental Health Services, Capital Region of Denmark, Glostrup, Denmark. 3. Centre for Neuropsychiatric Schizophrenia Research, CNSR, Psychiatric Centre Glostrup, Copenhagen University Hospitals, Mental Health Services, Capital Region of Denmark, Glostrup, Denmark. 4. Department of Pediatrics, Herlev Hospital, Faculty of Health and Medical Sciences, University of Copenhagen, Copenhagen, Denmark. 5. Department of Clinical Pharmacology, Lundbeck A/S, Valby, Denmark. 6. Department of Clinical Biochemistry, Gentofte Hospital, University of Copenhagen, Hellerup, Denmark. 7. Center for Diabetes Research, Gentofte Hospital, University of Copenhagen, Hellerup, Denmark; NNF Center for Basic Metabolic Research and Department of Biomedical Sciences, Faculty of Health Sciences, University of Copenhagen, Copenhagen, Denmark. 8. Centre for Neuropsychiatric Schizophrenia Research, CNSR, Psychiatric Centre Glostrup, Copenhagen University Hospitals, Mental Health Services, Capital Region of Denmark, Glostrup, Denmark; Centre for Clinical Intervention and Neuropsychiatric Schizophrenia Research, CINS, Copenhagen University Hospitals, Mental Health Services, Capital Region of Denmark, Glostrup, Denmark. Electronic address: bebdrup@cnsr.dk.
Abstract
INTRODUCTION: Hyperprolactinemia is a common side-effect of antipsychotic treatment. Antipsychotics and hyperprolactinemia are both considered risk factors of metabolic disturbances and diabetes. Investigations on prolactin response to meal ingestion in antipsychotic-treated patients are missing. MATERIAL AND METHODS: In a case-control design, 49 antipsychotic-treated, clinically stable, non-diabetic, schizophrenia spectrum male patients were compared with 93 healthy male controls by age (33.1, SD 7.4 vs. 32.9, SD 6.6 years), body mass index (26.2, SD 4.6 vs. 26.1, SD 3.9 kg/m(2)) and waist circumference (96.4, SD 13.0 vs. 96.7, SD 11.9 cm). Serum-prolactin was measured in the morning and 90 min after ingestion of a standardized liquid meal (2268 kJ). RESULTS: Fasting prolactin levels varied considerably, and mean fasting prolactin levels did not significantly differ between patients and controls (12.33, SD 11.58 vs. 10.06, SD 8.67 ng/ml, p = 0.623). In the controls, postprandial serum prolactin was significantly reduced (Δ -2.53, SD 9.75 ng/ml, p = 0.016). In antipsychotic-treated patients postprandial serum prolactin tended to increase (Δ 2.62, SD 10.96 ng/ml, p = 0.081). Analyses of subgroups based on the prolactinogenic liability of their antipsychotic treatment indicated 22 to 65% higher postprandial prolactin levels with high and intermediate prolactinogenic antipsychotics. DISCUSSION: A physiological postprandial suppression of serum prolactin appears absent in antipsychotic-treated males. Marked variability in fasting prolactin levels may reflect individual variations in the diurnal cycle. Uniform acquisition procedures accounting for diurnal variation and food intake may enhance reliability of prolactin levels in antipsychotic-treated male patients.
INTRODUCTION:Hyperprolactinemia is a common side-effect of antipsychotic treatment. Antipsychotics and hyperprolactinemia are both considered risk factors of metabolic disturbances and diabetes. Investigations on prolactin response to meal ingestion in antipsychotic-treated patients are missing. MATERIAL AND METHODS: In a case-control design, 49 antipsychotic-treated, clinically stable, non-diabetic, schizophrenia spectrum male patients were compared with 93 healthy male controls by age (33.1, SD 7.4 vs. 32.9, SD 6.6 years), body mass index (26.2, SD 4.6 vs. 26.1, SD 3.9 kg/m(2)) and waist circumference (96.4, SD 13.0 vs. 96.7, SD 11.9 cm). Serum-prolactin was measured in the morning and 90 min after ingestion of a standardized liquid meal (2268 kJ). RESULTS: Fasting prolactin levels varied considerably, and mean fasting prolactin levels did not significantly differ between patients and controls (12.33, SD 11.58 vs. 10.06, SD 8.67 ng/ml, p = 0.623). In the controls, postprandial serum prolactin was significantly reduced (Δ -2.53, SD 9.75 ng/ml, p = 0.016). In antipsychotic-treated patients postprandial serum prolactin tended to increase (Δ 2.62, SD 10.96 ng/ml, p = 0.081). Analyses of subgroups based on the prolactinogenic liability of their antipsychotic treatment indicated 22 to 65% higher postprandial prolactin levels with high and intermediate prolactinogenic antipsychotics. DISCUSSION: A physiological postprandial suppression of serum prolactin appears absent in antipsychotic-treated males. Marked variability in fasting prolactin levels may reflect individual variations in the diurnal cycle. Uniform acquisition procedures accounting for diurnal variation and food intake may enhance reliability of prolactin levels in antipsychotic-treated male patients.
Authors: Olga B Baltzersen; Herbert Y Meltzer; Vibe G Frokjaer; Jayachandra M Raghava; Lone Baandrup; Birgitte Fagerlund; Henrik B W Larsson; H Christian Fibiger; Birte Y Glenthøj; Gitte M Knudsen; Bjørn H Ebdrup Journal: Front Pharmacol Date: 2020-04-30 Impact factor: 5.810