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Severely malnourished patients with anorexia nervosa (AN) are reported to show fewer symptomatic viral infections and a poorer response to bacterial infection than controls. They are also reported to show mild immune system changes, although the relevance of these to altered infection disease presentation in AN and AN pathophysiology is unknown. Thus, in this paper, we suggest a range of immune system changes that might underpin these altered responses to common pathogens, and review a number of recent infectious disease findings for their utility in explaining the pathophysiology of AN.
A systematic review of the literature pertaining to immunity and infectious disease in AN was performed.
AN is associated with leucopenia, and the increased spontaneous and stimulated levels of proinflammatory cytokines [i.e. interleukin (IL)-1β, IL-6 and tumour necrosis factor α). A range of less consistent findings are also reviewed. Most of these data were not controlled for length of illness, degree of malnutrition, micronutrient or vitamin deficiencies or recent refeeding and starvation.
Cytokine disturbances have been suggested to be causally related to AN symptomatology and pathophysiology of AN, although the evidence supporting this assertion is lacking. Immune and cytokine changes in AN do, however, occur in association with a decreased incidence of symptomatic viral infection, decreased clinical response to bacterial infection leading to delayed diagnosis and increased morbidity and mortality associated with the infections.
Schizophrenia has been associated with limited abilities to interact effectively in social situations. Face perception and ability to recognise familiar faces are critical for social interaction. Patients with chronic schizophrenia are known to show impaired face recognition. Studying first-episode (FE) patients allows the exclusion of confounding effects of chronicity, medication and institutionalisation in this deficit.
To determine brain (dys)functions during a face encoding and recognition paradigm in FE schizophrenia.
Thirteen antipsychotic-naïve FE schizophrenia patients and 13 age- and sex-matched healthy controls underwent functional magnetic resonance imaging during a face encoding and recognition paradigm. Behavioural responses were recorded on line.
Patients recognised significantly fewer of previously presented faces than the controls (p = 0.008). At the neural level, both groups activated a network of regions including the fusiform area, occipital, temporal and frontal regions. In brain activity, the two groups did not differ in any region during encoding or recognition conditions (p > 0.05, corrected or uncorrected).
Our findings show impaired face recognition without a significant alteration of related brain activity in FE schizophrenia patients. It is possible that neural changes become more strongly evident with progression of the illness, and manifest themselves as behavioural impairments during the early course.
The present study aims to investigate the association of unipolar depression (UPD) with six serotonergic gene polymorphisms in Han Chinese.
One hundred and thirty-two UPD patients and 180 healthy controls were genotyped for polymorphisms of six serotonergic genes, including tryptophan hydroxylase (TPH1 A218C), serotonin transporter promoter region (5-HTTLPR), serotonin receptor 2A (5-HT2AR −1438G/A), serotonin receptor 2C (5-HT2CR Cys23Ser), serotonin receptor 6 (5-HT6R C267T) and serotonin receptor 1Dβ (5-HT1DβR T371G). Symptomatic clusters were evaluated by the 24-item Hamilton Rating Scale for Depression (HAMD).
The frequencies of S/S genotype and S allele in 5-HTTLPR polymorphism were significantly higher in UPD patients than in healthy controls. There was a significant difference in distributions of genotypes in 5-HT2CR Cys23Ser polymorphism between UPD patients and control subjects, but the difference became no significant when the data were further stratified by gender. The patients with genotypes G/G and T/G of 5-HT1DβR T371G polymorphism had significantly lower scores of diurnal variation evaluated by HAMD than those with genotype T/T, while the patients with genotype T/G had significantly higher scores of hopelessness than those with genotypes G/G and T/T. There were no significant differences in genotypic and allelic distributions of TPH1 A218C, 5-HT2AR −1438G/A or 5-HT6R C267T polymorphisms between the case and control groups.
The study demonstrates that 5-HTTLPR and 5-HT2CR Cys23Ser polymorphisms might contribute to susceptibility of UPD, and the genotype T/T in 5-HT1DβR T371G polymorphism might be a risk factor for diurnal variation, while T/G might be a protective factor against hopelessness in Han Chinese populations.
Neuropsychiatric disturbances are common among patients with genital herpes simplex virus (HSV) infection. To date, no studies have examined the possible role of immune activation in the aetiology of these disturbances. The aim of this study was to examine the relationship between markers of immune activation and measures of emotional and somatic dysfunction among patients with symptomatic genital herpes.
Twenty-two patients with documented genital herpes were assessed when herpetic lesions were present and when they were not. Each assessment included a clinical examination, self-reported symptom measures as well as a blood and urine collection. Markers of immune activation [neopterin and interleukin (IL)-6] in serum and urine were quantified by enzyme-linked immunoassay. These measures were also obtained from a group of healthy control subjects.
Urine, but not serum, levels of neopterin and IL-6 correlated significantly with measures of reported psychological distress and fatigue. These associations were not confined to periods of overt clinical lesions.
HSV-related neuropsychiatric morbidity correlates selectively with regional, but not systemic, measures of immune activation. We hypothesise that communication between the local inflammatory site in the pelvis and the brain occurs through autonomic afferent pathways.
Delirium tremens (DT) is one of the most serious complications of alcohol withdrawal, affecting 5–10% of in-patients with a mortality rate up to 15%. DT, characterised by delirium and tremors, appears within 48–72 h of abstinence and persists for about 5–10 days.
We report a case of DT in a young man with delayed onset on the 15th day after the cessation of alcohol use, despite an uncomplicated detoxification with benzodiazepine treatment.
We hypothesise that the intake of country liquor in our patient, which contains higher percentages of alcohol, causes a prolonged imbalance of N-methyl-d-aspartic acid and glutamate receptor activity, leading to the picture of delayed-onset DT and that an atypical presentation at the time of admission and atypicality in early course are clinical pointers to the subsequent development of delayed-onset DT.