1,721,311 research outputs found
Cardiovascular risk in patients with subclinical hypothyroidism
Subclinical hypothyroidism (SCH) has been associated with increased cardiovascular mortality due to adverse effects mainly on lipids and blood pressure (BP). There is evidence that SCH, especially in patients with thyroid-stimulating hormone (TSH) >10mU/l, may increase cardiovascular risk. Some uncertainty exists regarding the association of SCH with BP; however, that the coexistence of SCH with BP and hypercholesterolaemia has a negative cardiovascular impact is beyond doubt. Insulin resistance, by modulating various risk factors including coagulation, may potentially increase cardiovascular risk. Periodic health examinations including screening has been advised in patients >35 years of age, while treatment with thyroxine should be tailored to each patient
Thyroid diseases in the elderly
The ageing thyroid is associated with a number of morphological and functional changes, such as decreased serum T3 and mean thyroid-stimulating hormone concentrations, that are to some extent independent of intercurrent non-thyroidal illnesses. All thyroid diseases, including clinical and subclinical hypo- and hyperthyroidism, non-toxic nodular goitre and thyroid cancer, are encountered in the elderly, but their prevalence and clinical expression differ from those observed in younger patients. In the elderly, autoimmune hypothyroidism is particularly prevalent, hyperthyroidism is mainly characterized by cardiovascular symptoms and is frequently due to toxic nodular goitres, and differentiated thyroid carcinoma is more aggressive. The interpretation of thyroid function tests is difficult in old individuals, because of age-associated changes in thyroid function and frequent alterations secondary to non-thyroidal illnesses and/or drugs. Treatment of thyroid disease deserves special attention in old patients because of the increased risk of complications
Interleukin-6, CXCL10 and Infiltrating Macrophages in COVID-19-Related Cytokine Storm: Not One for All But All for One!
SARS-COV-2 virus is responsible for the ongoing devastating pandemic. Since the early phase of the pandemic, the “cytokine-storm” appeared a peculiar aspect of SARS-COV-2 infection which, at least in the severe cases, is responsible for respiratory treat damage and subsequent multi-organ failure. The efforts made in the last few months elucidated that the cytokine-storm results from a complex network involving cytokines/chemokines/infiltrating-immune-cells which orchestrate the aberrant immune response in COVID-19. Clinical and experimental studies aimed at depicting a potential “immune signature” of SARS-COV-2, identified three main “actors,” namely the cytokine IL-6, the chemokine CXCL10 and the infiltrating immune cell type macrophages. Although other cytokines, chemokines and infiltrating immune cells are deeply involved and their role should not be neglected, based on currently available data, IL-6, CXCL10, and infiltrating macrophages could be considered prototype factors representing each component of the immune system. It rapidly became clear that a strong and continuous interplay among the three components of the immune response is mandatory in order to produce a severe clinical course of the disease. Indeed, while IL-6, CXCL10 and macrophages alone would not be able to fully drive the onset and maintenance of the cytokine-storm, the establishment of a IL-6/CXCL10/macrophages axis is crucial in driving the sequence of events characterizing this condition. The present review is specifically aimed at overviewing current evidences provided by both in vitro and in vivo studies addressing the issue of the interplay among IL-6, CXCL10 and macrophages in the onset and progression of cytokine storm. SARS-COV-2 infection and the “cytokine storm.
Management of hyperthyroidism due to Graves' disease: frequently asked questions and answers (if any)
Graves’ disease is the most common cause of hyperthyroidism in iodine-replete areas. Although progress has been made in our understanding of the pathogenesis of the disease, no treatment targeting pathogenic mechanisms of the disease is presently available. Therapies for Graves’ hyperthyroidism are largely imperfect because they are bound to either a high rate of relapsing hyperthyroidism (antithyroid drugs) or lifelong hypothyroidism (radioiodine treatment or thyroidectomy). Aim of the present article is to offer a practical guidance to the reader by providing evidence-based answers to frequently asked questions in clinical practice
Obesity, Polycystic Ovary Syndrome, and Infertility: A New Avenue for GLP-1 Receptor Agonists
CONTEXT: Obesity is responsible for an increased risk of sub-fecundity and infertility. Obese women show poorer reproductive outcomes regardless of the mode of conception, and higher body mass index (BMI) is associated with poorer fertility prognosis. Polycystic ovary syndrome (PCOS) is one of the leading causes of infertility, and many women with PCOS are also overweight or obese. EVIDENCE ACQUISITION: The aim of the present narrative review is to describe the mechanisms responsible for the development of infertility and PCOS in women with obesity/overweight, with a focus on the emerging role of glucagon-like peptide-1 (GLP-1) receptor agonists (GLP-1 RAs) as a therapeutic option for obese women with PCOS. EVIDENCE SYNTHESIS: Weight reduction represents the most significant factor affecting fertility and pregnancy outcomes. Current experimental and clinical evidence suggests the presence of an underlying pathophysiological link between obesity, GLP-1 kinetic alterations, and PCOS pathogenesis. Based on the positive results in patients affected by obesity, with or without diabetes, the administration of GLP-1 RA (mainly liraglutide) alone or in combination with metformin has been investigated in women with obesity and PCOS. Several studies demonstrated significant weight loss and testosterone reduction, with mixed results relative to improvements in insulin resistance parameters and menstrual patterns. CONCLUSIONS: The weight loss effects of GLP-1 RA offer a unique opportunity to expand the treatment options available to PCOS patients
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