Search

Paraneoplastic syndromes (PNS) are a group of disorders that can affect the oncologic patient, and which are not directly attributable to tumour invasion, tumour compression or metastasis. In fact, they are due to tumour secretion of functional hormones or peptides or are related to immune cross-reactivity with the host tissue. These syndromes are called paraneoplastic because the components that cause them do not derive from the organ or tissue of origin, but from the neoplasm suffered by the patient. It is estimated that 10–15% of people with cancer suffer from a PNS (Coleman, 2018). PNS is the second direct cause of death (27% of cases) in cancer patients, after cancer itself. Consequently, it is of remarkable importance to recognize and treat SPNs specifically (Serraj et al., 2020). In view of the above, the aim of this article is to review the state of the art in neurological, haematological, endocrine, and dermatological paraneoplastic syndromes. It is a review in which the most relevant PNS and their symptomatology are described, inquiring into their diagnosis and treatment. [Display omitted] • Paraneoplastic syndromes are difficult to diagnose and characterise because they are very polymorphic. • They present high morbidity and frequently appear before the diagnosis of the neoplasm. • Their adequate management is through treatment of the primary neoplasm. • Their prognosis is ominous and parallel to that of the neoplastic disease that originates them. [ABSTRACT FROM AUTHOR]

Chronic venous disease (CVeD) has a remarkable prevalence, with an estimated annual incidence of 2%. It has been demonstrated how the loss of homeostatic mechanisms in the vein wall can take part in the physiopathology of CVeD. In this regard, it has been described how different axis, such as IGF-1/PAPP-A/STC-2 axis, may play an essential role in tissue homeostasis. The aim of this research is to study both genetic and protein expressions of the IGF-1/PAPP-A/STC-2 axis in CVeD patients. It is a cross-sectional study in which genetic (RT-qPCR) and protein (immunohistochemistry) expression analysis techniques were accomplished in saphenous veins from CVeD patients (n = 35) in comparison to individuals without vascular pathology (HV). Results show a significant increase in both genetic and protein expressions of PAPP-A and IGF-1, and a decrement STC-2 expression at the same time in CVeD patients. Our study is a pioneer for demonstrating that the expression of the different components of the IGF-1/PAPP-A/STC-2 axis is altered in CVeD patients. This fact can be a part of the loss of homeostatic mechanisms of the venous tissue. Further research should be destined to deepen into alterations of this axis, as well as to evaluate the usage of these components as therapeutic targets for CVeD. [ABSTRACT FROM AUTHOR]

Chronic venous disease (CVeD) has a remarkable prevalence, with an estimated annual incidence of 2%. It has been demonstrated how the loss of homeostatic mechanisms in the vein wall can take part in the physiopathology of CVeD. In this regard, it has been described how different axis, such as IGF-1/PAPP-A/STC-2 axis, may play an essential role in tissue homeostasis. The aim of this research is to study both genetic and protein expressions of the IGF-1/PAPP-A/STC-2 axis in CVeD patients. It is a cross-sectional study in which genetic (RT-qPCR) and protein (immunohistochemistry) expression analysis techniques were accomplished in saphenous veins from CVeD patients (n = 35) in comparison to individuals without vascular pathology (HV). Results show a significant increase in both genetic and protein expressions of PAPP-A and IGF-1, and a decrement STC-2 expression at the same time in CVeD patients. Our study is a pioneer for demonstrating that the expression of the different components of the IGF-1/PAPP-A/STC-2 axis is altered in CVeD patients. This fact can be a part of the loss of homeostatic mechanisms of the venous tissue. Further research should be destined to deepen into alterations of this axis, as well as to evaluate the usage of these components as therapeutic targets for CVeD. [ABSTRACT FROM AUTHOR]