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Generalized anxiety disorder (GAD) is highly co-morbid with depression. Depression is associated with elevated levels of the inflammation marker C-reactive protein (CRP), cross-sectionally and over time. To date, no studies have looked at the association between CRP and GAD. A total of nine waves of data from the prospective population-based Great Smoky Mountains Study (n=1420) were used, covering children in the community aged 9-16, 19 and 21 years old. Structured interviews were used at each assessment to assess GAD symptoms, diagnosis and cumulative episodes. Blood spots were collected and assayed for high-sensitivity CRP levels. GAD was associated with increased levels of CRP in bivariate cross-sectional analyses. These bivariate associations, however, were attenuated after accounting for demographic, substance-use and health-related covariates. In longitudinal models, there was little evidence that CRP predicted later GAD. Associations from GAD to later CRP were attenuated in models adjusted for health-related coavariates and there was evidence that the GAD-CRP association was mediated by body mass index (BMI) and medication use. Similar to depression, GAD was associated with elevated levels of CRP, but the effect of GAD on CRP levels was explained by the effect of GAD on health-related behaviors such as BMI and medication use. This study suggests differences in the association between inflammation and depression and GAD.

▪ Abstract  This review addresses the importance of studies of human psychoneuroimmunology in understanding the role of psychological factors in physical illness. First, it provides psychologically and biologically plausible explanations for how psychological factors might influence immunity and immune system–mediated disease. Second, it covers substantial evidence that factors such as stress, negative affect, clinical depression, social support, and repression/denial can influence both cellular and humoral indicators of immune status and function. Third, at least in the case of the less serious infectious diseases (colds, influenza, herpes), it considers consistent and convincing evidence of links between stress and negative affect and disease onset and progression. Although still early in its development, research also suggests a role of psychological factors in autoimmune diseases. Evidence for effects of stress, depression, and repression/denial on onset and progression of AIDS and cancer is less consistent and inconclusive, possibly owing to methodological limitations inherent in studying these complex illnesses, or because psychological influences on immunity are not of the magnitude or type necessary to alter the body's response in these cases. What is missing in this literature, however, is strong evidence that the associations between psychological factors and disease that do exist are attributable to immune changes.

As has been shown by a number of working groups, primary fibromyalgia syndrome does not represent a single clinical entity. It is possible to distinguish between a subgroup with high pain sensitivity and no associated psychiatric condition, a second and a third subgroup characterized by depression associated with fibromyalgia syndrome, and a fourth group with somatoform pain disorder of the fibromyalgia type. Mild inflammatory processes must be considered as the cause in the first group, while depression is combined with fibromyalgia in the second and the third group. In the fourth group, serious previous or still existing psychological problems or also insufficient coping with illness symptoms must be regarded as the reason for pain chronification. Group 1 benefits from a blocking of the 5-HT3 receptors by means of tropisetron, for example. This does not only affect pain chronification but also the inflammatory process itself. Group 2 and 3 needs antidepressant treatment, whereas the focus should be on psychotherapy in group 4. Groups 1, 2 and 3 will also profit from multimodal physical treatment programs, to a certain extent this applies to group 4 as well. So-called mixed types require a combination of therapeutic measures.

Abstract Functional somatic syndrome (FSS) is defined as a group of related syndromes characterized more by symptoms, suffering, and disability than by structural or functional abnormality. The diagnostic criteria and/or symptoms of FSS often overlap, and co-morbidity is commonly found among the diseases of FSS. For example, patients with irritable bowel syndrome often suffer from chronic pain, and a high percentage of co-morbidity can be found with fibromyalgia. Accumulating evidence indicates the presence of visceral and somatic hyperalgesia in FSS as a common feature, and the central sensitization mechanism has been suggested to play an important role in the pathophysiology of FSS. In the present article, the authors introduce the concept of FSS focusing on its possible relevance to rheumatology in terms of pain perception. A possible implication of mast cells and proteinase-activated receptor-2 (PAR-2) in FSS is also reviewed.

This study evaluated the initial promise of a dual-pathway conceptual model linking daily event stressors to rheumatoid arthritis (RA) disease activity through changes in immune system activation and mood. Fifty individuals, who were studied on five occasions two weeks apart, reported daily event stressors on the Daily Life Experience Checklist, daily mood on an abbreviated version of the Profile of Mood States-B, and daily joint pain on the Rapid Assessment of Disease Activity in Rheumatology. Serial clinical examinations comprised ratings of joint tenderness and swelling, and blood drawn during exams was analyzed for sedimentation rate (an indicator of systemic inflammation) and soluble interleukin-2 receptors (a marker of immune system activation known to correlate with RA disease activity). Across-person analyses failed to establish links from daily event stressors to either disease activity or composites of joint pain and joint inflammation when associations were adjusted for the effect of neuroticism on self-report measures. Pooled within-person analyses, however, were generally consistent with the relations predicted by the dual-pathway model. Increases in daily event stressors during the week preceding each clinical exam were associated with increased joint pain (regardless of changes in mood). At the same time, increased daily stressors were indirectly associated with decreased joint inflammation through reduction in levels of soluble interleukin-2 receptors. The dual-pathway model, which may be limited to short-term psychological and psychoimmunologic processes, underscores the importance of distinguishing potentially opposing effects of stress on pain versus inflammation in individuals with rheumatoid arthritis.

Association of stress with psoriatic skin symptoms was studied in 13 patients with psoriasis by dividing the patients into lowand high-stress groups based on their clinical examination and answers to three questionnaires (General Health Questionnaire, a somatization scale, and a life change questionnaire). This study focused on skin mast cells and sensory nerves which are the principal components in neurogenic inflammation. Mast cells were stained enzyme-histochemically for tryptase and chymase, and neuropeptides substance P (SP), vasoactive intestinal peptide (VIP), and calcitonin gene-related peptide (CGRP) were demonstrated immunohistochemically. Compared to the low-stress group (n = 7), the patients in the high-stress group (n = 6) had more severe skin and joint symptoms. Furthermore, mast cells positive for chymase activity were prominently reduced, but tryptase-positive mast cells only slightly decreased in the lesional skin of the high-stress group. A similar tendency was also observed in the nonlesional skin. In the papillary dermis of the lesional skin, both VIP-and CGRP-immunoreactive nerves could be observed in the high-stress group whereas in the low-stress group these nerve fibers were hardly visible in the corresponding area. No association of SP with stress was observed. This study suggests that psychic stress is associated with exacerbation of psoriasis, and stress may induce alterations in the psoriatic lesions by increasing the neuropeptide content with a concomitant decrease in the activity of neuropeptide-degrading enzymes especially mast cell chymase.

Psycho-neuroimmunology depicts a conceptual frame in which possible interactions between psychic and physical processes can be examined. It could be very significant in the field of psychosomatics when the courses of psychic and somatic processes are examined. However, the research results from this field of study are varied and only for a few parameters of immunity is it possible to prove correlations with psychic variables. Many of the studies that have been conducted up to date were construed as cross-section studies and possibly therefore are not very suitable for depicting the probably very complicated forms of interactions between psychic and somatic levels in an adequate manner. In the framework of stationary psychosomatic psychotherapy two single case studies were carried out in order to examine temporal connections between psychic and immunological course parameters. Both single case studies are to be viewed as explorative attempts of examining questions of examination design and organization which are highly resolved regarding time. Furthermore we report several interesting individual results which emphasize in general the correlation between psychic and somatic parameters also in the course of time. However the limits of such studies regarding the significance of the individual immunological parameters, using time serial analytical methods as well as constructing models in the field of psycho-neuroimmunology are discussed.

Chronically ill are advised to receive annual vaccinations against Covid-19 and seasonal influenza. Furthermore, chronically ill show an increased prevalence of comorbid common mental disorders (CMDs), like depression, anxiety, and somatoform disorders. With vaccination rates remaining insufficient among these vulnerable patients, prior research assumes an association between CMDs and vaccination readiness. As diagnoses, treatment and vaccination of those patients are performed mainly in general practice, the aim of this review is to describe associations between CMDs and vaccination readiness against seasonal Influenza and Covid-19 in chronically ill adult patients in primary care. A systematic literature search was conducted in Medline, Embase, PsycINFO, the Cochrane Library and ERIC. Randomized controlled trials (RCTs), clustered RCTs and observational studies were considered. Two authors screened the studies and assessed the risk of bias independently (Cochrane Risk of Bias 2-Tool). We followed the PRISMA guideline. The study protocol was published in PROSPERO (CRD42024621413). The results were synthesized narratively. Of 9820 identified studies, seven observational studies met the inclusion criteria. Regarding Covid-19, three studies could show, that CMDs might lead to decreased vaccination readiness in adults. Regarding seasonal influenza, no significant association between vaccination readiness and CMDs occurred. In terms of vaccination rates, no significant association between vaccinations against Covid-19 and CMDs could be identified. Two studies identified a significant association between decreasing vaccination rates against seasonal influenza and CMDs. CMDs tend to be associated with decreased vaccination readiness, however vaccination rates were not automatically affected as well. This could indicate a potential intention-behavior gap.

In last centuries, vaccines reduced the incidence of several infectious diseases. In last decades, some vaccines aimed at preventing also some cancers, where viruses play a causative role. However, several adverse events have been described after vaccines, but a causal relationship has been established only in a minority of cases. Here, we describe a pseudo-neurological syndrome occurred shortly after the administration of the bivalent HPV vaccine. Some autoimmune disorders, including neurological demyelinating diseases, have been reported after HPV vaccines, but the patient showed no organic lesions. The patient was diagnosed as having a functional somatoform syndrome, which was supposed to be autoimmune/inflammatory syndrome induced by adjuvants (ASIA), seen the temporal link with vaccination and the presence of anti-phospholipid autoantibodies. Immunological mechanisms of vaccines—and of adjuvants—have not been completely elucidated yet, and although there is no evidence of statistical association with many post-vaccination events, a causal link with vaccine cannot be excluded in some individuals.