Objective: The pathophysiology of vulvadynia is still unclear. We evaluated the general innervations of the nerves, the sensory neuropeptides in the vestibular area in eighteen women with vulvadynia, aged 20-38. The same individual acted as her own control and biopsies were taken from affected and none affected areas of posterior wall of the vulval vestibule. Quantitative immunohistochemistry was performed, using antisera to the general neuronal marker protein gene product (PGP) 9.5 and to the sensory neuropeptides substance P and calcitonin gene-related peptide (CGRP). Pain and stress assessments were made. Results:The number of PGP 9.5 immunoreactive in the affected areas showed an increase in number (p=0.06) compared to control sites (p=0.40), but the result did not reached to significance. High scores for pain sensation, signs of burnout, emotional and physical symptoms of stress and anxiety were indicated, regardless of time in all women.Conclusions: An increase in PGP 9.5 immunoreactive nerve fibers may be either secondary to nerve sprouting, or may represent neural hyperplasia, which could be applied as an objective diagnostic finding in vulvadynia. Further studies needed for the neuromediator's roll and inter individual factors for the diagnosis. Vulvodynia seem lead to chronic pain, hence having negative impact on the couple's relationship and the quality of life of women in several ways.
This cross-sectional study was carried out to find prevalence and possible relation between decreased quality of life and depression among patients with inflammatory bowel disease. Aims: Due to possible common biological pathways between inflammation in IBD and depression and due to the high burden of depression on both patient and health care institution, it is important to identify and initiate treatment to improve quality of life, disease outcome and reversed events associated with depression. Methods: 41 patients with either Crohn’s disease or ulcerative colitis participated in a questionnaire-based interview. Beck’s depression inventory was used for depression assessment and quality of life. Peripheral blood was collected for analyzing inflammatory and anemia markers. Data was then used for statistical analysis. Results: most patients were clinically free of depression. However, there was a strong correlation between number of exacerbations and depression in patients with Ulcerative Colitis, there was a negative correlation between serum leukocytes and depression, and the use of Mesalazine had a protective effect. Conclusion: inflammation in the gut may provoke depressive phenotype and vice versa. This may be caused by biological, social and psychological factors. Depression may also cause decreased quality of life, why it is necessary to identify these symptoms early and thereby reduce the risk of decreased quality of life.
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