Cholecystokinin, β-endorphin and vasoactive intestinal peptide in peripheral blood mononuclear cells of drug-naive schizophrenic patients treated with haloperidol compared to healthy controls

Mauri, Massimo C.; Rudelli, Renata; Panza, Gabriele; Sicaro, Aldo; Audisio, Daniele; Sacerdote, Paola; Panerai, Alberto E.

doi:10.1016/s0165-1781(97)00145-5

Cited by 19 publications

(12 citation statements)

References 19 publications

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“…This result is consistent to a previous study that failed to find an association of schizophrenia to either the T allele or a second polymorphism at the intron near the second exon of the CCK gene [Bowen et al, 1998]. Based on a previous report [Mauri et al, 1998], which showed a negative correlation between CCK level in peripheral blood mononuclear cell and SANS baseline score, we further analyzed our sample along the dimensions of positive and negative symptoms. Though the analysis in the patients with prominent negative symptoms seem to present some signals for association, it quickly faded away after the Bonferroni correction.…”

Section: Discussionsupporting

confidence: 89%

“…Though there was a higher frequency of the T variant in the schizophrenia sample, the association between the T variant and schizophrenia was not statistically significant (odds ratio [OR] = 1.59, χ 2 = 2.77, P > 0.1). Based on the previous report of negative correlation between CCK and Scale for Assessment of Negative Symptoms (SANS) baseline score, which suggested that lower CCK basal level relate to patients with a prevalence of negative symptomatology [Mauri et al, 1998], we analyzed the schizophrenia sample further along the dimensions of positive and negative symptoms based on the score of Scale for Assessment of Positive Symptom (SAPS) and SANS [Andreasen, 1983, 1984]. The sample was subdivided by SAPS scores into subgroups with prominent (SAPS ≥ 7) and less prominent (SAPS < 7) positive symptoms.…”

Section: Resultsmentioning

confidence: 99%

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Possible association of a cholecystokinin promoter variant to schizophrenia

et al. 2002

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Several lines of research indicate a cholecystokinin (CCK) deficit in schizophrenia patients. A C to T substitution was found in the promoter region of the CCK gene. We investigated this promoter variant in patients with schizophrenia and geographically-matchedcontrols. The T allele was detected in 24% of the 85 schizophrenics and 16% of the 247 controls. No significant difference in the T allele frequency was found between patients and controls (chi(2) = 2.77, P > 0.1). The schizophrenia sample was analyzed further along the dimensions of positive and negative symptoms. The patients with prominent negative symptoms presented a statistically significant association to the T allele (chi(2) = 4.13, P < 0.04). However, the significance disappeared after the Bonferroni correction (P > 0.15). Since the case-control analysis may present incorrect ethnic match between cases and controls, we applied the family-based tests to verify the above findings. Both transmission disequilibrium test (TDT; chi(2) = 5.33, P < 0.025 in 12 trios) and haplotype relative risk (HRR; chi(2) = 3.844, P < 0.05 in 60 trios) indicated a significantly high transmission of T allele to schizophrenia offspring probands from their parents. While our family-based tests seem to support the CCK involvement in schizophrenia, no definite conclusion can be drawn based on such a small sample size. This preliminary finding is subjected to future investigations.

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Section: Discussionsupporting

confidence: 89%

Section: Resultsmentioning

confidence: 99%

Possible association of a cholecystokinin promoter variant to schizophrenia

et al. 2002

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“…Some of them failed to find significant differences in BE concentration between drug-naïve schizophrenics and controls, although there was a trend toward higher values in the patients. 6 The majority of previous studies on pharmacologically treated patients included very small and non-homogeneous patient samples. 7,8 The study methodology also varied in terms of the biological material used to assess BE content, i.e.…”

Section: Introductionmentioning

confidence: 99%

<p>The Relationship Between Course of Illness and β-Endorphin Plasma Levels in Patients with Schizophrenia</p>

Urban-Kowalczyk

Kotlicka-Antczak

Strzelecki

et al. 2020

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Objective: Extensive investigations have been conducted into predictors of schizophrenia outcome. The heterogeneity of the illness implies that many factors should be taken into account. Some studies have reported the relationship between increased β-endorphin concentration and predominant negative symptoms. Methods: We included 77 outpatients with schizophrenia and 74 healthy controls. Data referring to duration and course of illness, hospitalization number and treatment were collected on the basis of clinical interviews and medical documentation analysis. The β-endorphin concentrations were assessed once in all participants, at the onset of the study. Results: A chronic course of illness was found in 44 of the 77 schizophrenics. Patients with schizophrenia, especially those with a chronic course of illness, revealed significantly higher β-endorphin concentrations than those with an episodic course and controls (mean 29.70 vs 19.86 pmol/L; p=0.0001). Increased levels of β-endorphin were related to longer duration of illness (R=0.294, p=0.009) and frequent psychiatric hospitalization (R=0.346, p=-0.002). Conclusion: Endorphins may be potential biological predictors of persistent negative symptoms and final outcome in schizophrenia.

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“…Postoji povezanost gena za CCK receptore sa patogenezom slusnih halucinacija kod obolelih od shizofrenije [25]. Oboleli od shizofrenije, koji su lose reagovali na terapiju haloperidolom, pokazuju negativnu korelaciju izmedu CCK u mononuklearnim celijarna krvi i rezultata na skali za procenu negativnih simptoma, sto ukazuje na cinjenicu da nize bazalne vrednosti CCK potpomazu pojavu negativnih simptoma shizofrenije [26]. Nalazi strukturnih abnormalnosti u kori LPI ukazuju da patogeneza shizofrenije ukljucuje poremecaje neurotransmisije impulsa interneurona kore, tj.…”

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