Your browser doesn't support javascript.
Show: 20 | 50 | 100
Results 1 - 7 de 7
Filter
1.
J Clin Transl Endocrinol ; 27: 100284, 2022 Mar.
Article in English | MEDLINE | ID: covidwho-1549901

ABSTRACT

Patients recovering from COVID-19 may have persistent debilitating symptoms requiring long term support through individually tailored cardiopulmonary and psychological rehabilitation programs. Clinicians need to be aware about the likely long-term complications and their diagnostic assessments to help identify any occult problems requiring additional help. Endocrinological evaluations should be considered as part of the armamentarium in the management of such individuals with diligent cognizance about the involvement of the hypothalamo-pituitary-adrenal (HPA) axis, adrenal and thyroid function. We here review the literature and potential pathophysiological mechanisms involved in and related to post COVID-19 symptoms with an emphasis on endocrine function.

2.
J Clin Transl Endocrinol ; 27: 100285, 2022 Mar.
Article in English | MEDLINE | ID: covidwho-1549902

ABSTRACT

Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), the pathogen responsible for coronavirus disease 2019 (COVID-19) has been a major cause of morbidity and mortality globally. Older age, and the presence of certain components of metabolic syndrome, including hypertension have been associated with increased risk for severe disease and death in COVID-19 patients. The role of antihypertensive agents in the pathogenesis of COVID-19 has been extensively studied since the onset of the pandemic. This review discusses the potential pathophysiologic interactions between hypertension and COVID-19 and provides an up-to-date information on the implications of newly emerging SARS-CoV-2 variants, and vaccines on patients with hypertension.

3.
Geroscience ; 43(3): 1093-1112, 2021 06.
Article in English | MEDLINE | ID: covidwho-1499503

ABSTRACT

We are in the midst of the global pandemic. Though acute respiratory coronavirus (SARS-COV2) that leads to COVID-19 infects people of all ages, severe symptoms and mortality occur disproportionately in older adults. Geroscience interventions that target biological aging could decrease risk across multiple age-related diseases and improve outcomes in response to infectious disease. This offers hope for a new host-directed therapeutic approach that could (i) improve outcomes following exposure or shorten treatment regimens; (ii) reduce the chronic pathology associated with the infectious disease and subsequent comorbidity, frailty, and disability; and (iii) promote development of immunological memory that protects against relapse or improves response to vaccination. We review the possibility of this approach by examining available evidence in metformin: a generic drug with a proven safety record that will be used in a large-scale multicenter clinical trial. Though rigorous translational research and clinical trials are needed to test this empirically, metformin may improve host immune defenses and confer protection against long-term health consequences of infectious disease, age-related chronic diseases, and geriatric syndromes.


Subject(s)
COVID-19 , Communicable Diseases , Metformin , Aged , Communicable Diseases/drug therapy , Humans , Metformin/therapeutic use , Multicenter Studies as Topic , RNA, Viral , SARS-CoV-2
4.
Horm Metab Res ; 53(9): 575-587, 2021 Sep.
Article in English | MEDLINE | ID: covidwho-1397932

ABSTRACT

Global warming and the rising prevalence of obesity are well described challenges of current mankind. Most recently, the COVID-19 pandemic arose as a new challenge. We here attempt to delineate their relationship with each other from our perspective. Global greenhouse gas emissions from the burning of fossil fuels have exponentially increased since 1950. The main contributors to such greenhouse gas emissions are manufacturing and construction, transport, residential, commercial, agriculture, and land use change and forestry, combined with an increasing global population growth from 1 billion in 1800 to 7.8 billion in 2020 along with rising obesity rates since the 1980s. The current Covid-19 pandemic has caused some decline in greenhouse gas emissions by limiting mobility globally via repetitive lockdowns. Following multiple lockdowns, there was further increase in obesity in wealthier populations, malnutrition from hunger in poor populations and death from severe infection with Covid-19 and its virus variants. There is a bidirectional relationship between adiposity and global warming. With rising atmospheric air temperatures, people typically will have less adaptive thermogenesis and become less physically active, while they are producing a higher carbon footprint. To reduce obesity rates, one should be willing to learn more about the environmental impact, how to minimize consumption of energy generating carbon dioxide and other greenhouse gas emissions, and to reduce food waste. Diets lower in meat such as a Mediterranean diet, have been estimated to reduce greenhouse gas emissions by 72%, land use by 58%, and energy consumption by 52%.


Subject(s)
Climate Change , Obesity/etiology , Agriculture/economics , Agriculture/trends , COVID-19/complications , COVID-19/epidemiology , COVID-19/pathology , Climate Change/history , Comorbidity , Endocrine Disruptors/toxicity , Environment , Environmental Exposure/history , Environmental Exposure/statistics & numerical data , Greenhouse Gases/toxicity , History, 19th Century , History, 20th Century , History, 21st Century , Humans , Obesity/epidemiology , Obesity/metabolism , Pandemics , Risk Factors
5.
Lancet Diabetes Endocrinol ; 8(12): 978-986, 2020 12.
Article in English | MEDLINE | ID: covidwho-894325

ABSTRACT

The risk factors for severe COVID-19 are diverse, yet closely resemble the clinical manifestations of catecholamine excess states (eg, hypertension, cardiovascular disease, immune dysregulation, and hyperglycaemia), suggesting a potentially common basis for disease. Unfortunately, severe illness (eg, respiratory failure, compromised cardiac function, and shock) incurred by COVID-19 hinders the direct study of catecholamines in these patients, especially among those on multiple medications or those on adrenaline or noradrenaline infusions, or both. Phaeochromocytoma and paraganglioma (PPGL) are tumours that secrete catecholamines, namely adrenaline and noradrenaline, often in excess. PPGL are well studied disease processes in which the effects of catecholamines are easily discernible and therefore their potential biochemical and physiological influences in patients with COVID-19 can be explored. Because catecholamines are expected to have a role in patients with critical illness, patients on vasopressor infusions, and patients who sustain some acute and chronic physical stresses, the challenges involved in the management of catecholamine excess states are directly relevant to the treatment of patients with COVID-19. In this Personal View, we discuss the complex interplay between catecholamines and COVID-19, and the management of catecholamine excess states, while referencing relevant insights derived from the study of PPGL.


Subject(s)
COVID-19/epidemiology , Catecholamines/metabolism , SARS-CoV-2/isolation & purification , COVID-19/metabolism , COVID-19/virology , Humans , Risk Factors
6.
Endocrinology ; 161(10)2020 10 01.
Article in English | MEDLINE | ID: covidwho-626158

ABSTRACT

The ongoing coronavirus disease 2019 (COVID-19) pandemic is caused by the novel coronavirus, severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). Individuals with metabolic syndrome are at increased risk for poor disease outcomes and mortality from COVID-19. The pathophysiologic mechanisms for these observations have not been fully elucidated. A critical interaction between SARS-CoV-2 and the angiotensin-converting enzyme 2 (ACE2) facilitates viral entry into the host cell. ACE2 is expressed in pancreatic islets, vascular endothelium, and adipose tissue, and the SARS-CoV-2 -ACE2 interaction in these tissues, along with other factors, governs the spectrum and the severity of clinical manifestations among COVID-19 patients with metabolic syndrome. Moreover, the pro-inflammatory milieu observed in patients with metabolic syndrome may contribute toward COVID-19-mediated host immune dysregulation, including suboptimal immune responses, hyperinflammation, microvascular dysfunction, and thrombosis. This review describes the spectrum of clinical features, the likely pathophysiologic mechanisms, and potential implications for the management of metabolic syndrome in COVID-19 patients.


Subject(s)
Coronavirus Infections/physiopathology , Metabolic Syndrome/physiopathology , Pneumonia, Viral/physiopathology , Angiotensin-Converting Enzyme 2 , Animals , Betacoronavirus/physiology , COVID-19 , Coronavirus Infections/immunology , Coronavirus Infections/metabolism , Coronavirus Infections/virology , Endocrine System/metabolism , Endocrine System/physiopathology , Humans , Immune System/immunology , Immune System/physiopathology , Metabolic Syndrome/immunology , Metabolic Syndrome/metabolism , Microvessels/physiopathology , Pandemics , Peptidyl-Dipeptidase A/genetics , Peptidyl-Dipeptidase A/immunology , Pneumonia, Viral/immunology , Pneumonia, Viral/metabolism , Pneumonia, Viral/virology , SARS-CoV-2
7.
Am J Physiol Endocrinol Metab ; 318(5): E736-E741, 2020 05 01.
Article in English | MEDLINE | ID: covidwho-23168

ABSTRACT

The pandemic of coronavirus disease (COVID-19), a disease caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), is causing substantial morbidity and mortality. Older age and presence of diabetes mellitus, hypertension, and obesity significantly increases the risk for hospitalization and death in COVID-19 patients. In this Perspective, informed by the studies on SARS-CoV-2, Middle East respiratory syndrome (MERS-CoV), and the current literature on SARS-CoV-2, we discuss potential mechanisms by which diabetes modulates the host-viral interactions and host-immune responses. We hope to highlight gaps in knowledge that require further studies pertinent to COVID-19 in patients with diabetes.


Subject(s)
Betacoronavirus , Coronavirus Infections , Diabetes Mellitus , Host Microbial Interactions , Pandemics , Pneumonia, Viral , Animals , Betacoronavirus/immunology , Betacoronavirus/pathogenicity , COVID-19 , Coronavirus Infections/immunology , Coronavirus Infections/mortality , Coronavirus Infections/physiopathology , Coronavirus Infections/virology , Diabetes Mellitus/immunology , Diabetes Mellitus/mortality , Host Microbial Interactions/immunology , Humans , Pneumonia, Viral/immunology , Pneumonia, Viral/mortality , Pneumonia, Viral/physiopathology , Pneumonia, Viral/virology , Risk Assessment , SARS-CoV-2 , Uncertainty , United States/epidemiology
SELECTION OF CITATIONS
SEARCH DETAIL