Serum hepcidin / ferroportin levels in bipolar disorder and schizophrenia.

BACKGROUND: Despite several alternatives for cellular iron influx, the only mechanism for cellular iron efflux is ferroportin mediated active transport. In cases of ferroportin dysfunction, iron accumulates in the cell and causes ferroptosis. Hepcidin suppresses ferroportin levels and inflammatory activation increases hepcidin production. Mild inflammation in schizophrenia and bipolar disorder may alter hepcidin and ferroportin. METHODS: The study included a total of 137 patients aged 18-65 years, 57 diagnosed with schizophrenia and 80 with bipolar disorder, according to the DSM-IV diagnostic criteria, and a control group (HC) of 42 healthy individuals. Biochemical analyses, thyroid function tests, hemogram, serum iron level, iron-binding capacity, and ferritin levels were examined. Serum levels of hepcidin and ferroportin were measured with enzyme-linked immunosorbent assay (ELISA) method. RESULTS: A statistically significant difference was determined between the groups in terms of the serum ferroportin levels (F = 15.69, p < 0.001). Post-hoc analyses showed that the schizophrenia group had higher ferroportin levels than in the bipolar group (p < 0.001) and HCs (p < 0.001). Hepcidin levels did not differ between the groups. Chlorpromazine equivalent doses of antipsychotics correlated with ferroportin levels (p = 0.024). CONCLUSION: Ferroportin levels were increased in the schizophrenia group, although iron and hepcidin levels were within normal ranges. Antipsychotics may alter the mechanisms which control ferroportin levels. Further studies are needed to examine the relationships between antipsychotics and iron metabolism for determination of causal relationship.

[Relationship between Childhood Adversities, Emotion Dysregulation and Cognitive Processes in Bipolar Disorder and Recurrent Depressive Disorder]. / Bipolar Bozukluk ve Yineleyici Depresif Bozuklukta Çocukluk Çagi Travmalari ve Duygu Düzenleme Güçlükleri ile Bilissel Süreçler Arasindaki Iliski.

OBJECTIVE: Cognitive development is susceptible to environmental distress, leading to cognitive distortions. Cognitive distortions may affect clinical course of psychiatric disorders. We aimed to assess whether childhood maltreatment and emotion dysregulation impair automatic thoughts (ATs) and meta-cognitions (MCs) in Bipolar Disorder (BD) and Major Depressive Disorder - Recurrent (MDB-RE) in this study. METHOD: 85 patients with BD, 81 MDD-RE in remission and 86 healthy participants were enrolled. Automatic Thoughts Scale (ATS), Metacognition Questionnaire (MCQ-30), Childhood Trauma Questionnaire (CTQ- 28), Difficulties in Emotion Regulation Strategies Scale (DERS) were the measures used. RESULTS: ATs were determined by CTQ physical abuse (ß=0.34, p<0.01), DERS goals (ß=-0.37, p<0.01), impulse (ß=0.53, p<0.01) and non-accept (ß=0.23, p<0.05) subscales in BD (F=21.08, p<0.01) and CTQ emotional neglect (ß=0.22, p<0.05), DERS strategies (ß=0.39, p<0.05) in MDD-RE (F=9.97, p<0.05). MCs were predicted by sexual abuse (ß=0.46, p<0.01) in BD (F=4.88, p<0.01), and emotional abuse (B=-0.30, p<0.05) in MDD-RE (F= 7.02, p<0.01). CONCLUSION: These results suggest that emotion dysregulation and childhood adversities are associated with cognitive processes such as MCs and ATs in MDD-RE and BD. Cognitive processes can cause various clinical manifestations and emotion dysregulation and childhood traumas should be considered as psychopathological components that can affect the course of mood disorders via various components. Further follow-up studies and larger samples are needed to better understand the effects of these components.