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Bipolar disorder (BD) is related to high prevalence of somatic comorbidities, health care costs, and premature mortality [1]. Some evidence supports the view of BD as chronic, progressive and multisystem disorder in which not only mental system, but also somatic systems are involved [2].
Aim
To investigate differences in physical health in patients with bipolar disorder at different stages (early vs. late) of the disease.
Methods
Cross-sectional, naturalistic, multicenter study. Sample: 110 outpatients with BD [68 early stage (diagnosed at least 5 years earlier) and 42 late stage (at least 20 years earlier)]. Assessment: demographic and clinical variables; psychopathology: HDRS, YMRS and CGI; biological information: anthropometric, vital signs and lab results.
Results
Early stage group: mean age 40.1 (11.9), 66.2% females and CGI = 3.6 (1.4). Late stage group: mean age 55.8 (8.2), 69.0% females and CGI = 4.0 (1.4). Patients in early stage have significantly higher levels of glucose (t = −4.007, P < 0.001), urea (t = −2.724, P = 0.008), creatinine (F = 0.560, P = 0.022), triglycerides (t = −3.501, P = 0.001), Fe (t = 2.871, P = 0.005) and insulin (t = −3.223, P = 0.002). Moreover, they have higher Body Max Index (BMI) (t = −3.728, P < 0.000), abdominal circumference (t = −4.040, P < 0.000) and greater number of somatic comorbidities (t = −2.101, P = 0.041).
Conclusions
– patients with bipolar disorders in late stages have worse physical health than those in early stage.
– these results could be an indication that bipolar disorder might better viewed as a multisystem disorder.
Disclosure of interest
The authors have not supplied their declaration of competing interest.
Immune-inflammatory processes have been implicated in schizophrenia (SCH), but their specificity is not clear.
Main aim
To identify potential differential intra-/intercellular biochemical pathways controlling immune-inflammatory response and their oxidative-nitrosative impact on SCH patients, compared with bipolar disorder (BD) patients and healthy controls (HC).
Methods
Cross-sectional, naturalistic study of a cohort of SCH patients (n=123) and their controls [BD (n=102) and HC (n=80)].
Statistical analysis
ANCOVA (or Quade test) controlling for age and gender when comparing the three groups, and controlling for age, gender, length of illness, cigarettes per day, and body mass index (BMI) when comparing SCH and BD.
Results
Pro-inflammatory biomarkers: Expression of COX-1 was statistically higher in SCH and BD than HC (P<0.0001; P<0.0001); NFκB and PGE2 were statistically higher in SCH compared with BD (P=0.001; P<0.0001) and HC (P=0.003; P<0.0001); NLRP3 was higher in BD than HC (P=0.005); and CPR showed a gradient among the three groups. Anti-inflammatory biomarkers: BD patients had lower PPARγ and higher 15d-PGJ2 levels than SCH (P=0.005; P=0.008) and HC (P=0.001; P=0.001). Differences between SCH and BD: previous markers of SCH (NFκB and PGE2) and BD (PPARγ and 15d-PGJ2) remained statistically significant and, interestingly, iNOS and COX-2 (pro-inflammatory biomarkers) levels were statistically higher in SCH than BD (P=0.019; P=0.040).
Conclusions
This study suggests a specific immune-inflammatory biomarker pattern for established SCH (NFκB, PGE2, iNOS, and COX-2) that differentiates it from BD and HC. In future, their pharmacological modulation may constitute a promising therapeutic target.
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