ABSTRACT
Vasoactive intestinal peptide (VIP) is a neuropeptide with potent immunoregulatory properties. Reduced serum VIP levels and alterations in VIP receptors/signaling on immune cells have been associated with different inflammatory/autoimmune diseases. However, its role in autoimmune thyroid diseases (AITD) remains unknown. This study examined the interrelationship between VIP system, autoimmune background and thyroid hormones in peripheral immune cells in patients with AITD. Only Graves' disease (GD) patients showed significantly lower serum VIP levels when compared to healthy subjects and to Hashimoto's thyroiditis patients. Serum VIP levels were lower at the onset of GD, showing a significant negative correlation with thyroid hormone levels. The expression of VIP receptors, VPAC1 and VPAC2, was significantly upregulated in peripheral blood mononuclear cells (PBMC) from GD patients. There was an impairment of VIP signalling in these patients, probably attributable to a dysfunction of VPAC1 with preservation of VPAC2. The correlation between VPAC1 and thyroid hormone receptor expression in PBMC from healthy subjects was lost in GD patients. In summary, the VIP system is altered in peripheral immune cells of GD patients and this finding is associated with different thyroid hormone receptor patterns, showing a dynamic inter-regulation and a prominent role of VIP in this setting.
Subject(s)
Graves Disease/metabolism , Vasoactive Intestinal Peptide/metabolism , Adult , Female , Humans , Male , Middle Aged , Receptors, Vasoactive Intestinal Peptide, Type II/metabolism , Receptors, Vasoactive Intestinal Polypeptide, Type I/metabolism , Thyroid Hormones/metabolism , Vasoactive Intestinal Peptide/bloodABSTRACT
Hyponatremia, defined as serum sodium concentrations <135 mmol/L, is the most frequent electrolyte disturbance observed in both hospitalized and ambulatory patients, and has been associated to relevant negative consequences regarding morbidity and mortality. Drug-induced hyponatremia has been widely observed. However, since it may be clinically symptomatic or asymptomatic, it is frequently an underdiagnosed condition. This review aims to highlight the main drugs involved in the pathophysiology of hyponatremia, which should be considered in the differential diagnosis when approaching a patient with hyponatremia. We discuss their impact and relative importance. In order to prevent undesirable negative consequences we also emphasize the need for awareness of this clinically-relevant adverse effect, and we suggest how clinical management of patients may be approached.
