This is a review of full-length articles strictly concerning subacute thyroiditis (SAT) in relation to the SARS-CoV-2 virus infection (SVI) and COVID-19 vaccine (COV) that were published between the 1st of March 2020 and the 21st of March 2022 in PubMed-indexed journals. A total of 161 cases were reported as follows: 81 cases of SAT–SVI (2 retrospective studies, 5 case series, and 29 case reports), 80 respective cases of SAT–COV (1 longitudinal study, 14 case series, 17 case reports; also, 1 prospective study included 12 patients, with 6 patients in each category). To our knowledge, this represents the largest cohort of reported cases until the present time. SAT–SVI was detected in adults aged between 18 and 85 years, mostly in middle-aged females. SAT–COVID-19 timing classifies SAT as viral (synchronous with infection, which is an original feature of SATs that usually follow a viral infection) and post-viral (during the recovery period or after infection, usually within 6 to 8 weeks, up to a maximum 24 weeks). The clinical spectrum has two patterns: either that accompanying a severe COVID-19 infection with multi-organ spreading (most frequent with lung involvement) or as an asymptomatic infection, with SAT being the single manifestation or the first presentation. Either way, SAT may remain unrecognized. Some data suggest that more intense neck pain, more frequent fever, and more frequent hypothyroidism at 3 months are identified when compared with non-SAT–SVI, but other authors have identified similar presentations and outcomes. Post-COVID-19 fatigue may be due to residual post-SAT hypothyroidism. The practical importance of SAT–SVI derives from the fact that thyroid hormone anomalies aggravate the general status of severe infections (particular concerns being tachycardia/arrhythmias, cardiac insufficiency, and ischemic events). If misdiagnosed, SAT results in unnecessary treatment with anti-thyroid drugs or even antibiotics for fever of unknown cause. Once recognized, SAT does not seem to require a particular approach when compared with non-COVID-19 cases, including the need for glucocorticoid therapy and the rate of permanent hypothyroidism. A complete resolution of thyroid hormone anomalies and inflammation is expected, except for cases with persistent hypothyroidism. SAT–COV follows within a few hours to a few weeks, with an average of 2 weeks (no particular pattern is related to the first or second vaccine dose). Pathogenesis includes molecular mimicry and immunoinflammatory anomalies, and some have suggested that this is part of ASIA syndrome (autoimmune/inflammatory syndrome induced by adjuvants). An alternative hypothesis to vaccine-related increased autoimmunity is vaccine-induced hyperviscosity; however, this is supported by incomplete evidence. From what we know so far concerning the risk factors, a prior episode of non-SVI–SAT is not associated with a higher risk of SAT–COV, nor is a previous history of coronavirus infection by itself. Post-vaccine SAT usually has a less severe presentation and a good outcome. Generally, the female sex is prone to developing any type of SAT. HLA susceptibility is probably related to both new types of SATs. The current low level of statistical evidence is expected to change in the future. Practitioners should be aware of SAT–COV, which does not restrict immunization protocols in any case.

L'indice d'adiposité viscérale (IAV) -marqueur potentiel du risque cardio-métabolique L'importance du risque cardiovasculaire/cardio-métabolique est particulière car le contrôle de ses composantes peut affecter l'athérogenèse et ses conséquences cliniques: la cardiopathie ischémique, la maladie cérébrovasculaire, l'artériopathie périphérique et le diabète sucré (DS). Pour évaluer le risque cardio-métabolique associé à l'obésité viscérale, on a essayé d'identifier un indicateur utile dans la pratique clinique. L'indice d'adiposité viscérale (IAV) pourrait devenir un outil facile à utiliser dans la pratique quotidienne qui met en évidence le risque cardio-métabolique. IAV indique la fonction du tissu adipeux viscéral et sa croissance est indépendamment corrélée aux risques cardiovasculaire et cérébrovasculaire. Le monde médical a essayé d'identifier un moyen facile d'évaluer le risque cardiovasculaire, de sorte que l'indice d'adiposité viscérale, dont la formule inclut un certain nombre de facteurs de risque cardiovasculaires, ait été introduit.

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Cortisol is a key element in acute stress including a severe infection. However, in coronavirus-associated disease, 20% of subjects experience hypocortisolemia due to direct or immune damage of pituitary and adrenal glands. One extreme form of adrenal insufficiency is found in 2/3 of cases with viral and post-viral adrenal infarction (AI) (with/without adrenal hemorrhage) that is mostly associated with a severe coronavirus disease 2019 (COVID-19) infection; it requires prompt glucocorticoid intervention. Some reports are incidental findings at computed tomography (CT)/magnetic resonance imaging (MRI) scans for non-adrenal complications like pulmonary spreading and others are seen on post-mortem analysis. This is a review of PubMed-accessible, English papers focusing on AI in addition to the infection, between March 1, 2020 and November 1, 2021. Exclusion criteria were acute adrenal insufficiency without the histopathological (HP) and/or imaging report of adrenal enlargement, necrosis, etc., respective adrenal failure due to pituitary causes, or non-COVID-19-related adrenal events. We identified a total of 84 patients (different levels of statistical evidence), as follows: a retrospective study on 51 individuals, two post-mortem studies comprising nine, respectively 12 patients, a case series of five subjects, seven single-case reports. HP aspects include necrosis associated with ischemia, cortical lipid degeneration (+/-focal adrenalitis), and infarcts at the level of adrenal cortex, blood clot into vessels, acute fibrinoid necrosis in arterioles and capsules, as well as subendothelial vacuolization. Collateral potential contributors to adrenal damage are thrombotic events, coagulation anomalies, antiphospholipid syndrome, endothelial dysfunction, severe COVID-19 infection with multiorgan failure, etc. Clinical picture is variable from acute primary adrenal insufficiency to asymptomatic or mild evolution, even a retrospective diagnostic; it may be a part of long COVID-19 syndrome; glucocorticoid therapy for non-adrenal considerations might mask cortisol deficient status due to AI/hemorrhage. Despite its rarity, the COVID-19-associated AI/hemorrhage represents a challenging new chapter, a condition that is essential to be recognized due to its gravity since prompt intervention with glucocorticoid replacement is lifesaving.

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