Endometriosis is a leading cause of infertility in women of reproductive age. It involves the occurrence of endometrial tissue outside the uterine endometrium, mainly in the peritoneal cavity. Prostaglandin E₂ is up regulated in the peritoneal cavity in endometriosis and is produced by macrophages and ectopic endometrial cells. This prostaglandin is involved in the pathophysiology of the disease and elicits cell signals via four receptor types. Prostaglandin E₂ increases estrogen synthesis by up regulating steroidogenic acute regulatory protein (StAR) and aromatase. It inhibits apoptosis and up regulates fibroblast growth factor-9 (FGF-9) promoting cell proliferation. Prostaglandin E₂ affects leukocyte populations and promotes angiogenesis through its effect on estrogen and up regulation of vascular endothelial growth factor (VEGF). Dienogest is a synthetic progestin targeting expression of genes involved in prostaglandin synthesis.

Endometriosis is the leading cause of morbidity among premenopausal women affecting about 1 in 10 females. The features shared by endometriosis and cancer include the ability to evade apoptosis, the stem cell-like ability and angiogenic potential. As such characteristics are encoded by the cell’s genetic constitution, acquired mutations are responsible for the malignant transformation of endometriosis. Indeed, a number of tumour-suppressor genes and proto-oncogenes, such as protein 53 (P53) and B-cell lymphoma 2 (BCL-2) respectively, are mutated and as a result differentially expressed between endometriotic and malignant tissue associated with endometriosis. Moreover, cytokines and macrophages, both of which are inflammatory mediators have been implicated in the transformation process. The angiogenic properties possessed by cancer arising from endometriosis signifies a bad prognosis, while the stem cell-like activity possessed by both endometriosis and cancer has been attributed to the effect of oestrogen. A number of differences between endometriosis and cancer are found at the molecular level. Considering the link between these two pathologies, the three components which fuel the malignant transformation of endometriosis can be embodied in the endometriosis-induced carcinoma (EIC) triangle which shows the intricate relationship between endocrinologic, immunologic and genetic components.

Objective: To measure the increasing incidence of primary hyperparathyroidism (PHPT) in Scotland, to determine the relationship between PHPT and deprivation, and to investigate the relationship between parathyroidectomy (PTX) and social deprivation. Methods: We retrospectively identified a cohort of patients diagnosed with PHPT between 1986 and 2013 from the Scottish Morbidity Records (SMR01) database. The diagnosis of PHPT was made in accordance with the International Classification of Diseases code. Results: Between the years 1986 and 2013, 4002 patients were diagnosed with PHPT. There was a significant increase in the incidence of PHPT in this period (p < 0.0001), an association between the incidence of PHPT and deprivation (p < 0.0001) plus an association between a lower rate of PTX and deprivation (p < 0.001). Conclusion: The increase in incidence of PHPT may be due to a combination of increased awareness of PHPT, easier diagnosis, and an ageing population. The lower rate of PTX in relation to deprivation may reflect comorbidities, age, and uncertainty about the long-term benefits of PTX in asymptomatic patients.