A Multivariate Analysis of Depression Prevalence in Psoriasis Patients: A Cohort Study.

The literature reported higher depression rates in psoriasis patients compared to the general population. Our study aimed to verify whether variability in depression prevalence was due to using different diagnostic tools. We also aimed to determine whether dysfunctional coping strategies might increase the depression burden. We assessed psoriasis severity by the Psoriasis Area Severity Index (PASI) and PSOdisk. We analyzed mental alterations of 120 outpatients by Hamilton Depression and Anxiety Rating Scales (HAM-D and HAM-A), Symptom Checklist-90-Revised (SCL-90-R), plus coping strategies and quality of life by Coping Orientation to Problems Experienced (COPE) Inventory and 36-Item Short Form Health Survey (SF-36). We divided our cohort into five subgroups from minimal to severe psoriasis using the PSOdisk total score. Depression prevalence varied according to the assessment criteria for specificity, frequency, and severity. Different mood disorders other than major depression emerged when we used DSM-IV-TR criteria. Correlation analysis of the criteria we used to diagnose depression or depressed mood indicated that a dysfunctional coping strategy was highly and positively correlated only in patients of the severe subgroup. Differently, a negative correlation emerged between the SF-36 Mental Summary Component (MSC) and behavioral disengagement, thus suggesting that psychopathological distress might induce patients with a marked/severe psoriasis to adopt dysfunctional coping strategies. Dermatologists are fundamental in detecting comorbid depression, referring psoriasis patients to mental health specialists to achieve adequate treatments, and preventing suicide risk.

A hypothesis on Cotard's syndrome as an evolution of obsessive-compulsive disorder.

Cotard's syndrome usually presents as combined symptoms occurring in a broad series of neurological, psychiatric, and medical disorders, being severe depression the most frequent. The syndrome is not classified as a distinct clinical entity in the nosological systems but appears solely as a clinical condition in case reports. Thus, the diagnosis of Cotard's syndrome mainly centres on the psychiatric interview and the ability of the clinician to recognise specific symptoms due to the absence of both clinical instruments and diagnostic criteria. Cotard's syndrome has never been described to date in patients with a history of obsessive-compulsive disorder (OCD). We report a case of a 49-year-old woman presenting obsessive symptoms and related compulsions for more than 30 years. Cotard's syndrome appeared after 3 years from a tragic event that had caused a psychological trauma. Such an occurrence may have contributed to worsening OCD and leading to a second major depressive episode followed by a suicidal attempt. Since then, the subject of our patient's obsessive thoughts changed, and the belief of being dead appeared. The repetitive and stereotyped thoughts caused severe distress, and accompanied the compulsive nature of reassurance seeking, temporarily beneficial to the anxiety arousing. The transition from obsession to delusion occurred when resistance was abandoned, and insight was lost. Once Cotard's syndrome had stabilised, OCD was no longer present. Additional distinctive features were the absence of psychiatric family history and the persistent nature of the affective psychosis. We concluded that Cotard's syndrome represented the evolution of the initial obsessive-compulsive disorder. Furthermore, we differentiated the clinical condition of our patient from other psychiatric diseases with similar clinical features. Larger-scale research is needed to consider topics other than comorbidity and also to explore significant elements of the patient's clinical history to discover what may influence the evolution and/or the persistence of the diseases.

The unmasking of hidden severe hyponatremia after long-term combination therapy in exacerbated bipolar patients: a case series.

Hyponatremia is occasionally unmasked in psychiatric patients during hospitalization after routine blood and urinary tests, and correlates in most cases with an inappropriate secretion of antidiuretic hormone, mainly due to iatrogenic factors. Only a few studies have regarded the combination of psychotropic drugs as triggers of chronic, asymptomatic hyponatremia in bipolar patients, who require to be hospitalized because of the exacerbation of their mental illness. We presented three clinical cases of patients affected by a long-term psychiatric disorder and under polypharmacotherapy for several months. After excluding other potential factors, we hypothesized that pharmacological treatment with a mood stabilizer (oxcarbazepine) associated with a benzodiazepine (delorazepam), a second-generation antipsychotic (olanzapine) or an antidepressant (fluvoxamine), triggered severe hyponatremia ([Na+] ≤125 mEq/L), serum hypo-osmolarity, and elevated inappropriate urine osmolarity added to more diluted sodium concentration. When we discontinued the treatment, clinical conditions of our patients improved, despite the previous administration of hypertonic saline jointly with water restriction. Psychiatrists should consider that bipolar patients on long-term polypharmacotherapy may present a higher risk of severe hyponatremia not clinically detectable. Consequently, routine laboratory tests should be periodically repeated as they represent the only available tool to unmask such electrolyte imbalances.