Long-term outcomes in treated males with anorexia nervosa and bulimia nervosa-A prospective, gender-matched study.

OBJECTIVE: We report on the long-term outcome of males compared to females treated for anorexia nervosa (AN) or bulimia nervosa (BN). METHODS: A total of 119 males with AN and 60 males with BN were reassessed 5.8 ± 4.6 and 7.5 ± 5.9 years (respectively) after treatment and compared to matched female patients. RESULTS: At follow-up, males with AN had a higher body weight than females. For AN, remission rates (40% males vs. 41% females) did not differ at follow-up. And at follow-up, more males (34%) than females (19%) had an eating disorder not otherwise specified (ED-NOS; p < .01). At follow-up of AN, there was no binge-eating disorder (BED) and obesity was rare. For BN, remission rates (44% males vs. 50% females) and frequency of AN, BN, BED and ED-NOS did not differ at follow-up. Males with AN scored lower than females at follow-up on most subscales of the Eating Disorder Inventory (EDI) and on somatization, obsessive-compulsive symptoms, and depression (Brief Symptom Inventory). Males with BN scored lower than females with BN on perfectionism and higher on interpersonal distrust (EDI) at follow-up. DISCUSSION: Results from the scarce literature on males with ED are inconclusive regarding longer term outcome. In the present study, males with AN showed a slightly better outcome than females. In BN, outcome was about the same in males and females. According to our study, existing treatment is equally effective in both males and females. Additional research on the need of gender-specific diagnosis and therapy is required.

Mortality in males treated for an eating disorder-A large prospective study.

OBJECTIVE: To report on the long-term mortality of eating disorders in male inpatients. METHOD: Crude mortality rates (CMR) and standardized mortality ratios (SMR) were computed for a large sample of males (147 anorexia nervosa [AN], 81 bulimia nervosa [BN], 110 eating disorder not otherwise specified [ED-NOS]; DSM-IV). In addition, a survival analysis from onset of eating disorder to death or end of observation was computed. RESULTS: CMR was 12.9% in AN, 11.1% in BN, and 6.4% in ED-NOS. Standardized mortality was significantly elevated in males with AN (SMR = 5.91; 95% confidence interval 3.56-9.23) as well as ED-NOS (SMR = 3.40; 95% confidence interval 1.37-7.01) but not in males with BN (SMR = 1.88; 95% confidence interval 0.86-3.58). Males with AN died sooner after onset of eating disorder than males with BN or ED-NOS. DISCUSSION: Mortality in male inpatients with eating disorder is high, especially in AN. There is need for developing more effective treatments to achieve better outcome.

Pre-Sleep Arousal Scale (PSAS) and the Time Monitoring Behavior-10 scale (TMB-10) in good sleepers and patients with insomnia.

OBJECTIVES: Pre-sleep arousal and time monitoring behavior are two putative factors involved in the development and maintenance of insomnia. We investigate two questionnaires measuring these factors in good sleepers and patients with insomnia. PARTICIPANTS: A sample of 96 patients with non-organic insomnia according to ICD-10 and 208 good sleepers completed the Pre-Sleep Arousal Scale (PSAS), the Time Monitoring Behavior-10 scale (TMB-10), the Beck Depression Inventory (BDI)-II, the Pittsburgh Sleep Quality Index (PSQI), the Insomnia Severity Index (ISI) and the State-Trait Anxiety Inventory (STAI). METHODS: In this study, 95% quantile cut-off scores were determined for good sleeper in the age and gender mathed subgroups of the insomnia group. Multiple logistic regression analysis was used to determine variables predicting above-threshold values in the two target questionnaires. Included predictors were age, gender as well as ISI, BDI-II, STAI-1 and -2 total scores. RESULTS: Good sleepers showed 95% quantiles between 12.2 and 23.8 for PSAS and between 7.5 and 12.7 for TMB-10. Approximately 40% of patients with insomnia had scores above these cut-offs for PSAS and ca. 25% for TMB-10. Female gender and anxiety were variables associated with scores above cut-off on the PSAS. Insomnia severity and anxiety were associated with scores above cut-off on the TMB-10. CONCLUSIONS: These findings underline the importance of PSAS and TMB-10 in the diagnostic investigation of insomnia and indicate that time monitoring is related to increased insomnia severity. Further research may investigate the impact of the corresponding two constructs on response rates to cognitive-behavioral treatment for insomnia.

Short- and long-term outcome of males treated for anorexia nervosa: a review of the literature.

PURPOSE: To give an overview of existing studies on the short- and long-term outcome for males treated for anorexia nervosa and to compare the outcome between adolescents and adults as well as between males and females. METHODS: A systematic literature search was conducted in PubMed, PsycINFO and PSYNDEX and complemented by a manual search of the references from all relevant studies. RESULTS: Out of 1064 search results, 18 studies met our inclusion criteria. A combined total of 1129 males of varying age groups were followed 0.5-27 years post-treatment. For 1009 individuals, only vital status was ascertained. Length of follow-up and outcome definitions varied considerably. Limited data-especially in adults-prevented adequate age comparisons. In both adolescents and adults outcome and mortality differed widely across studies with no firm evidence for gender differences. Outcome in mixed samples of adolescents and adults was inconsistent. Studies rarely compared the genders statistically, and when they did, the results were nonsignificant. CONCLUSIONS: Knowledge on the outcome of males treated for anorexia nervosa is scarce. Only few studies comprising insufficient numbers of males exist. Results based on these findings are inconclusive and in part contradicting. Further research is needed, including large sample sizes of reliably diagnosed males, adequate follow-up intervals, follow-up assessments with carefully defined outcome criteria, and comparisons to matched female patient samples. LEVEL OF EVIDENCE: Level I, Systematic review.

Anti-LcrV antibody inhibits delivery of Yops by Yersinia pestis KIM5 by directly promoting phagocytosis.

LcrV of Yersinia pestis is a major protective antigen proposed for inclusion in subunit plague vaccines. One way that anti-LcrV antibody is thought to protect is by inhibiting the delivery of toxins called Yops to host cells. The present study characterizes the relation between this inhibition and the phagocytosis of the bacteria. J774A.1 cells were infected with Y. pestis KIM5 in the presence of a protective polyclonal anti-LcrV antibody or a nonprotective polyclonal anti-YopM antibody, and delivery of YopH and YopE into the cytoplasm was assayed by immunoblotting. The ability to inhibit the delivery of these Yops depended upon having antibody bound to the cell surface; blocking conditions that prevented the binding of antibody to Fc receptors prevented the inhibition of Yop delivery. Anti-LcrV antibody also promoted phagocytosis of the yersiniae, whereas F(ab')(2) fragments did not. Further, anti-LcrV antibody could not inhibit the delivery of Yops into cells that were unable to phagocytose due to the presence of cytochalasin D. However, Yops were produced only by extracellular yersiniae. We hypothesize that anti-LcrV antibody does not directly inhibit Yop delivery but instead causes phagocytosis, with consequent inhibition of Yop protein production in the intracellular yersiniae. The prophagocytic effect of anti-LcrV antibody extended to mouse polymorphonuclear neutrophils (PMNs) in vitro, and PMNs were shown to be critical for protection: when PMNs in mice were ablated, the mice lost all ability to be protected by anti-LcrV antibody.

Antibody against V antigen prevents Yop-dependent growth of Yersinia pestis.

The V antigen (LcrV) of the plague bacterium Yersinia pestis is a potent protective antigen that is under development as a vaccine component for humans. LcrV is multifunctional. On the bacterial surface it mediates delivery of a set of toxins called Yops into host cells, and as a released protein it can cause production of the immunosuppressive cytokine interleukin-10 (IL-10) and can inhibit chemotaxis of polymorphonuclear neutrophils. It is not known how these mechanisms of LcrV operate, what their relative importance is, when they function during plague, and which are critical to protection by antibody. This study investigated several of these issues. C57BL/6 mice, mice unable to express IL-10, or mice with the macrophage lineage eliminated were treated with a protective anti-LcrV antibody or a nonprotective antibody against YopM and infected intravenously by Y. pestis KIM5 or a strain that lacked the genes encoding all six effector Yops. Viable bacterial numbers were determined at various times. The data indicated that Yops were necessary for Yersinia growth after the bacteria had seeded liver and spleen. Anti-LcrV antibody prevented this growth, even in IL-10-/- mice, demonstrating that one protective mechanism for anti-LcrV antibody is independent of IL-10. Anti-LcrV antibody had no effect on persistence in organs of Y. pestis lacking effector Yops, even though the yersiniae could strongly express LcrV, suggesting that Yops are necessary for building sufficient bacterial numbers to produce enough LcrV for its immunosuppressive effects. In vitro assays showed that anti-LcrV antibody could partially block delivery of Yops and downstream effects of Yops in infected macrophage-like J774A.1 cells. However, cells of the macrophage lineage were found to be dispensable for protection by anti-LcrV antibody in spleen, although they contributed to protection in liver. Taken together, the data support the hypothesis that one protective effect of the antibody is to block delivery of Yops to host cells and prevent early bacterial growth. The findings also identified the macrophage lineage as one host cell type that mediates protection.

LcrQ and SycH function together at the Ysc type III secretion system in Yersinia pestis to impose a hierarchy of secretion.

LcrQ is a regulatory protein unique to Yersinia. Previous study in Yersinia pseudotuberculosis and Yersinia enterocolitica prompted the model in which LcrQ negatively regulates the expression of a set of virulence proteins called Yops, and its secretion upon activation of the Yop secretion (Ysc) type III secretion system permits full induction of Yops expression. In this study, we tested the hypothesis that LcrQ's effects on Yops expression might be indirect. Excess LcrQ was found to exert an inhibitory effect specifically at the level of Yops secretion, independent of production, and a normal inner Ysc gate protein LcrG was required for this activity. However, overexpression of LcrQ did not prevent YopH secretion, suggesting that LcrQ's effects at the Ysc discriminate among the Yops. We tested this idea by determining the effects of deletion or overexpression of LcrQ, YopH and their common chaperone SycH on early Yop secretion through the Ysc. Together, our findings indicated that LcrQ is not a negative regulator directly, but it acts in partnership with SycH at the Ysc gate to control the entry of a set of Ysc secretion substrates. A hierarchy of YopH secretion before YopE appears to be imposed by SycH in conjunction with both LcrQ and YopH. LcrQ and SycH in addition influenced the deployment of LcrV, a component of the Yops delivery mechanism. Accordingly, LcrQ appears to be a central player in determining the substrate specificity of the Ysc.