SEOM clinical guidelines for the treatment of thyroid cancer

Although thyroid cancer represents less than 1% of malignant tumours, its increased incidence detected in recent years and the appearance and development of new drugs targeting specific molecular targets has attracted the attention of the doctors involved in this pathology, especially medical oncologists. For this reason it is important at this critical point, when treatment may be substantially changed, to establish and agree updated guidelines. These guidelines should incorporate the newly developed strategies that, although still preliminary in evidence level, will surely have an important role, especially in relapsed and refractory tumours, which are unsuitable for surgical or radio-iodine treatment. Particular histological and molecular features of these tumours must be taken into account in order to optimise therapeutic approaches.     

Absence of biological effects of oxidized parathyroid hormone-(1-34) in dogs and rats

Recent studies have shown that oxidation of bovine PTH-(1-34) [bPTH-(1-34)] with H2O2 abolished the vascular effects of PTH in rats and dogs, but the hypercalcemic effect of the oxidized PTH was preserved in the Japanese quail in vivo. These observations seem at variance with previous studies from our laboratory in the isolated perfused canine tibia preparation in which no uptake of immunoreactive PTH or stimulation of cAMP release was demonstrated during infusion of oxidized bPTH-(1-34). The present studies examine the skeletal and renal effects of oxidized PTH-(1-34) in rats and dogs in vivo. Oxidation of PTH with H2O2 reduced its activation of adenylate cyclase by 95% in dog renal cortical membrane. Awake normal dogs were studied before and during the infusion of bPTH-(1-34) or oxidized PTH-(1-34) (4 U/kg X h). With active PTH, ionized Ca+2 rose in each dog (range, 0.7-1.5 mg/dl), while with oxidized PTH, Ca+2 remained within 0.1 mg/dl of the baseline values. Fractional excretion of PO4 rose from 1.58 +/- 0.6% to 29.5 +/- 2.5% with active PTH and from 1.4 +/- 0.4% to 5.7 +/- 1% with oxidized PTH. The latter did not differ from the value in vehicle-infused dogs. Further studies were performed in 30 acutely parathyroidectomized rats. Plasma Ca+2 rose from 8.2 +/- 0.1 to 9.0 +/- 0.3 mg/dl with active PTH (20 micrograms/kg), fell to 7.7 +/- 0.2 with oxidized PTH, and fell to 7.3 +/- 0.3 mg/dl with vehicle. In parathyroid-intact rats plasma Ca+2 increased by 0.9 mg/dl whether given active PTH, oxidized PTH, or vehicle. We conclude that oxidation of bPTH-(1-34) results in loss of both the renal and skeletal effects of PTH in vivo in rats and dogs.     

SGLT2 inhibition attenuates arterial dysfunction and decreases vascular F-actin content and expression of proteins associated with oxidative stress in aged mice

GeroScience - Aging of the vasculature is characterized by endothelial dysfunction and arterial stiffening, two key events in the pathogenesis of cardiovascular disease (CVD). Treatment with sodium...     

Physical therapists’ perceptions and experiences about barriers and facilitators of therapeutic patient-centred relationships during outpatient rehabilitation: a qualitative study

Background

Over recent years there has been a paradigm shift towards a patient-centred biopsychosocial care model in physical therapy. This new paradigm features a growing interest in understanding the contextual factors that influence the patient's experience of disease, pain and recovery. This includes generalized consensus regarding the importance of establishing a therapeutic relationship that is centred on the patient.

Syncope in Patients With Severe Aortic Stenosis: More Than Just an Obstruction Issue

BackgroundSevere aortic stenosis (AoS) is considered a primary cause of syncope. However, other mechanisms may be present in these patients and accurate diagnosis can have important clinical implications. The aim of this study is to assess the different etiologies of syncope in patients with severe AoS and the impact on prognosis of attaining a certain or highly probable diagnosis for the syncope.MethodsOut of a cohort of 331 patients with AoS and syncope, 61 had severe AoS and were included in the study. Main cause of syncope and adverse cardiac events were assessed.ResultsIn 40 patients (65.6%), we reached a certain or highly probable diagnosis of the main cause of the syncope. AoS was considered the primary cause of the syncope in only 7 patients (17.5% of the patients with known etiology). Atrioventricular block (14 patients, 35.0%) and vasovagal syncope (6 patients, 15.0%) were the most frequently diagnosed causes. The presence of a known cause for syncope during the admission was not associated with a lower incidence of recurrence during follow-up (hazard ratio [HR] 0.69, 95% confidence interval [CI] 0.20-2.40). Syncope of unknown etiology was independently associated with greater mortality during 1-year follow-up (HR 5.4, 95% CI 1.3-21.6) and 3-year follow-up (HR 3.5, 95% CI 1.2-10.3).ConclusionsIn a high proportion of patients with severe AoS admitted for syncope, the valvulopathy was not the main cause of the syncope. Syncope in two-thirds of this population was caused by either bradyarrhythmia or reflex causes. Syncope of unknown cause was associated with increased short- and medium-term mortality, independently from treatment of the valve disease. An exhaustive work-up should be conducted to determine the main cause for syncope.