Associations of internalized stigma with psychosocial functioning and quality of life in people with schizophrenia.

BACKGROUND: Schizophrenia is associated with poor functional recovery. Internalized stigma is one of the factors related to the functioning of individuals with schizophrenia. We aimed to investigate whether internalized stigma was associated with subjective and objective recovery-related outcomes after controlling for neurocognition and other important confounders in individuals with schizophrenia. METHOD: We assessed the socio demographic background, psychopathology, neurocognition, internalized stigma, psychosocial functioning, and quality of life of 86 patients who had schizophrenia. Correlation analyses and multiple linear regression were used to investigate the association of internalized stigma and other variables with recovery-related outcomes. RESULTS: We found that the negative symptom scores of the Positive and Negative Syndrome Scale but not internalized stigma was associated with psychosocial functioning as measured by the Personal and Social Performance global score. In contrast, internalized stigma was associated with the Psychological, Social relationships, and Environment scores of the World Health Organization Quality of Life Scale Brief Version (WHOQOL-BREF). Depression was also associated with the Physical health, Psychological, and Social relationships sores of the WHOQOL-BREF. CONCLUSIONS: While internalized stigma was associated with several domains of quality of life, it was not associated with clinician-rated psychosocial functioning. The effects of internalized stigma on the subjective and objective recovery-related outcomes of individuals with schizophrenia might be divergent.

Patients who complain of autonomic dysregulation: A cross-sectional study of patients with somatic symptom disorder.

BACKGROUND: Somatic symptom disorder (SSD) is common in medical settings but has been underdiagnosed. Stigma related to psychiatric illness was one of the barriers to making the diagnosis. More and more SSD patients who visited psychiatric clinics with physical complaints identify themselves as having 'autonomic dysregulation' in Taiwan. AIMS: This study aimed to investigate the characteristics of patients with a subjective diagnosis of 'autonomic dysregulation'. METHOD: We assessed the sociodemographic profile, medical/psychiatric diagnoses, subjective psychiatric diagnoses, perceived psychiatric stigma, help-seeking attitude, and healthcare utilization of 122 participants with SSD. Participants who identified themselves as having 'autonomic dysregulation' (n = 84) were compared to those who did not (n=38). RESULTS: Participants with a subjective diagnosis of 'autonomic dysregulation' were younger and had a higher education level than those who did not have such a subjective diagnosis. They also had higher scores on the Patient Health Questionnaire-15 (PHQ-15) and Health Anxiety Questionnaire (HAQ), whereas comorbid psychiatric diagnoses were similar in the two groups. Participants with and without a subjective diagnosis of 'autonomic dysregulation' did not have a significant difference in perceived psychiatric stigma and help-seeking attitude/behaviors. In a multiple logistic regression model, only age was associated with having a subjective diagnosis of 'autonomic dysregulation'. CONCLUSION: Among SSD patients, those who identify themselves as having 'autonomic dysregulation' tend to have higher somatic distress and health anxiety than those who do not. 'Autonomic dysregulation' is not associated with perceived psychiatric stigma.

Parasympathetic activity as a potential biomarker of negative symptoms in patients with schizophrenia.

INTRODUCTION: Autonomic dysfunction in patients with schizophrenia has raised concern considering the higher cardiovascular mortality and morbidity rate. This phenomenon has been demonstrated using various measurements and is inferred to be associated with demographics, medical treatment, and psychopathology. However, few have targeted the role of negative symptoms within schizophrenia. METHODS: Schizophrenia patients with stationary psychopathology were recruited from a chronic ward, a daycare center, and a nonintensive case management program. Demographic data, medication history, the Positive and Negative Syndrome Scale (PANSS) score, the Personal and Social Performance Scale (PSP) score, and the five-minute resting-state heart rate variability (HRV) were collected at trial initiation (Time 1) and a year later (Time 2). The relationships between variables and HRV indices were evaluated using correlation and regression analyses. RESULTS: A total of 63 participants were recruited at Time 1, with 29 participants remaining at Time 2. Correlation analyses showed a negative correlation between the PANSS negative score (PANSS-N) and total power (TP), low-frequency power (LF), and high-frequency power (HF) at Time 1. The results were further examined with multiple linear regression analysis and remained significant between the PANSS-N score and HF (ß = -0.306, P = .012). A generalized estimating equation model revealed the above negative association to be significant considering both timepoints. DISCUSSION: The negative association between negative symptom severity and parasympathetic activity was significant, which may inspire further research into the corresponding treatment, the mechanisms, and the use of HRV as an applicable biomarker for treatment response.

Is severity a clinically meaningful specifier of somatic symptom disorder?

OBJECTIVE: Few existing studies have investigated the clinical relevance of Diagnostic and Statistical Manual of Mental Disorders, Fifth Edition (DSM-5) somatic symptom disorder (SSD) severity rated by clinicians. We examined the association of SSD severity with psychiatric and medical comorbidity, psychological features and help-seeking attitude and behaviours. METHODS: A total of 123 patients with SSD were prospectively recruited and completed several types of self-report instrument. Information about medical comorbidity and healthcare use was gathered from the participants and medical record review. Common comorbid psychiatric diagnoses of SSD were assessed by psychiatrists. Group differences of patients with SSD of varying severity were assessed with ANOVA and chi-square tests. Multiple linear regression models were used to examine the relationships between SSD severity and psychological features. RESULTS: Prevalence of medical comorbidity and comorbid psychiatric diagnoses of SSD was not significantly different among patients with varying SSD severity. Patients with severe SSD had the highest Patient Health Questionnaire-15 (PHQ-15), Health Anxiety Questionnaire (HAQ), Beck Depression Inventory-II (BDI-II) and Beck Anxiety Inventory (BAI) scores. Help-seeking behaviour was not associated with SSD severity. After controlling for demographic variables, the associations between 'severe SSD' and the PHQ-15, HAQ, BDI-II and BAI scores were significant. CONCLUSION: SSD severity rated by clinicians was not associated with comorbid medical or psychiatric diagnoses. Compared to patients with mild/moderate SSD, patients with severe SSD not only had higher somatic distress and health anxiety but also higher levels of anxiety/depression. However, SSD severity was not associated with help-seeking attitude and behaviour.

Functional analyses indicate a pathogenic role of factor H autoantibodies in atypical haemolytic uraemic syndrome.

BACKGROUND: Atypical haemolytic uraemic syndrome (aHUS) is associated with defective complement regulation. Recently, an autoimmune aHUS form has been described that is associated with complement factor H (CFH) autoantibodies. The aim of this study was to address the pathologic relevance of CFH autoantibodies in aHUS. METHODS: CFH autoantibodies were identified and antibody levels were analysed in three aHUS patients during the disease course by the ELISA method. Epitope mapping was performed using recombinant factor H fragments and domain-mapped monoclonal antibodies. The effect of the antibodies on cell-protective activity of CFH was measured by haemolytic assays. CFH:autoantibody complexes were analysed by ELISA. RESULTS: All three autoantibodies bound to the C-terminal domain of CFH, which is essential for CFH binding to cell surfaces. In patient 1, plasma exchanges and immune adsorption temporarily reduced the autoantibody titre and led to temporary clinical improvement. In patient 2, plasma exchanges and long-term immunosuppression strongly reduced the CFH autoantibody level, and induced a stable remission of aHUS. Patient 3 had lower autoantibody levels that decreased during the follow-up and is in good clinical condition. The patients' plasma samples caused enhanced lysis of sheep erythrocytes, and the degree of lysis correlated with the CFH autoantibody titre and the amount of CFH:autoantibody complexes. An addition of purified CFH to aHUS plasma or removal of IgG inhibited the haemolytic activity. CONCLUSION: These results support a direct role of the autoantibodies in aHUS pathology by inhibiting the regulatory function of CFH at cell surfaces and suggest that reduction of the autoantibody titre is beneficial for the patients.

Anti factor H autoantibodies block C-terminal recognition function of factor H in hemolytic uremic syndrome.

The atypical form of the kidney disease hemolytic uremic syndrome (aHUS) is associated with defective complement regulation. In addition to mutations in complement regulators, factor H (FH)-specific autoantibodies have been reported for aHUS patients. The aim of the present study was to understand the role of these autoantibodies in aHUS. First, the binding sites of FH autoantibodies from 5 unrelated aHUS patients were mapped using recombinant FH fragments and competitor antibodies. For all 5 autoantibodies, the binding site was localized to the FH C-terminus. In a functional assay, isolated patient IgG inhibited FH binding to C3b. In addition, autoantibody-positive patients' plasma caused enhanced hemolysis of sheep erythrocytes, which was reversed by adding FH in excess. These results suggest that aHUS-associated FH autoantibodies mimic the effect of C-terminal FH mutations, as they inhibit the regulatory function of FH at cell surfaces by blocking its C-terminal recognition region.