New diagnosis of Graves' disease during SARS-CoV-2 infection. A further trigger of hyperthyroidism?

Background: Graves' disease is an autoimmune disorder which represents the most common cause of hyperthyroidism. It is often triggered by an acute event, such as infections. SARS-CoV-2 binds to angiotensin-converting enzyme 2 (ACE2), expressed mostly in the lungs but also in several endocrine organs like thyroid. Description of the Case: We report a case of a 49-years-old woman admitted to our Unit due to fever, tachycardia and worsening dyspnea. Nasopharyngeal swab test resulted positive for SARS-CoV-2 (PCR). Blood sample test for D-dimer resulted increased (1272 ug/l, normal value <500), and bilateral subsegmental embolism was found on CTAngiography. She reported palpitations, insomnia and weight loss in the past days. Past medical history included euthyroid nodular thyroid disease, hypertension and obesity. Laboratory tests revealed hyperthyroidism with positive thyroid antibodies with TSH<0.05 mU/l, FT4 32 ng/l and FT3 5.9 ng/l (normal value 8-17 and 2-4, respectively), and elevated AbTPO 137 KU/l (<34) and AbTSH-r 2.4 U/l (<2). Thyroid ultrasound showed an enlarged gland with heterogeneous echotexture and hyperechoic nodules;an hypervascular pattern with elevated peak systolic velocity in inferior thyroid artery (50-69 cm/s) was found at colorDoppler. A diagnosis of Graves' disease was established and treatment with thiamazole was started, achieving normal heart rate control and recovery of symptoms. Conclusions: In the absence of a clear trigger for our patient's thyroid storm, we suggest SARS-CoV-2 infection, in addition to CT iodinate contrast medium, might precipitate or worsen a latent Graves' disease.

CT-scan model of ageing: muscle mass, bone density and vascular calcification in elderly people with COVID-19 pneumonia

Background and Aim: Several studies described the association of COVID-19 with frailty and mortality in patients over 65 years old. These considerations have inspired the researchers to recognize changes in organ and tissue as a marker of frailty in older people. The aim of this study was to investigate the relation between muscle mass, bone loss and arterial calcifications in patients over 75 years old affected by COVID-19 pneumonia. Results: In this retrospective observational study, we analyzed on a thoracic CT paravertebral skeletal muscle area (cm2) and density (HU) at the Th12 level, descending thoracic aortic calcification (DTAC) - Agatston Score and L1 bone mineral density (HU) in 25 patients admitted to our Unit. 25 patients (13 males, 12 females), with a mean age of 83±2.83 years, were included. Agatstone score was inversely associated with L1 density (rho=- 0.452, p=0.024) and with muscle density (rho=- 0.43, p=0.03), also after adjustment for age and gender. L1 density was directly associated with muscle mass density (rho=0.42, p=0.03). The area under the curve of the ROC curve constructed to evaluate the discriminating power of the total DTAC in order to predict the death of patient was 0.81. The cut-off value of DTAC=2930,98 had a sensitivity of 89% and a specificity of 69%. Conclusions: The results of this study demonstrated that vascular calcification is inversely related to bone mineral density and muscle mass density, while bone and muscle density are directly correlated. Finally, DTAC in elderly people with COVID-19 pneumonia has a good power to discriminate the surviving patients from those who dead.

Pulmonary artery thrombosis in home patient with a mild COVID-19 disease Tromboza arterei pulmonare la pacient cu boala COVID 19 forma usoara aflat la domiciliu

COVID-19 has been described as the cause for a proinflammatory and hypercoagulable state that induces thrombotic vascular lesions and, in more severe cases, disseminated intravascular coagulation. Increased values of d-dimers are related to the severity of the disease and are associated with worst prognosis. Intensive care studies reported an increased risk of pulmonary embolism and venous thrombosis diseases in COVID-19 compared with the historical control group even in patients who underwent the low-molecular-weight heparin (LWMH) prophylaxis. Patients with COVID-19 who have a stable clinical condition do not require hospitalisation and are treated at home with symptomatic therapy. LWMH is reserved for those with reduced mobility. In this case report, we describe a COVID-19 patient with pulmonary artery thrombosis treated at home. © 2020 Alessandro Graziani et al.

Increased D-Dimer value as a marker of pulmonary arterythrombosis in COVID 19 pneumonia

Background: COVID-19 has been well described as the cause fora proinflammatory and hypercoagulable state: the endothelialcells damage and the release of a large amount of inflammatorymediators may predispose to vascular thrombosis.Materials and Methods: We evaluated 138 patients with COVID19 admitted to our Institution between March 2020 and May 2020.At admission, most of them were haemodinamically stable andfebrile. All patients were treated with hydroxychloroquine (400mg/day), darunavir/ritonavir (800/100 mg/day) and enoxaparin(4000 UI/day). Every three days, laboratory exams with inflammatory and coagulation parameters (INR, activated partial thromboplastin time, platelets count, fibrinogen, D-Dimer) were repeated. Inthe patients with progressive elevation of D-Dimer and low or normalvalues of other coagulation or inflammatory blood parameters weperformed a computed tomography pulmonary angiography (CTPA)and Doppler ultrasound of the lower limbs. Results: We identify patients with signs of bilaterally pulmonaryartery thrombosis (APT) in absence of deep venous thrombosis.Patients did not have signs of respiratory failure and breath onroom air. We compared D-Dimer value at the admission in patientswith and without APT to identify whether it can have a negativeprognostic value and we saw no relevant differences.Conclusions: In conclusion, we described patients with moderatedisease who developed a pulmonary vascular injury strictly correlated with an elevation of D-Dimer values. The development of theAPT was not related to D-dimer value at the admission but only tothe increase.

Viral clearence in COVID 19 patients treated withimmunomodulators

Background and Aim of the study: In COVID-19 patients, theaberrant host immune response results in uncontrolled release ofcytokines (CKs) and systemic hyper-inflammation. When first-linetherapy (antiviral and hydroxychloroquine/chloroquine) did notdemonstrate effects, high doses of glucocorticoids and/or biological agents (tocilizumab - TCZ, canakinumab - CAM etc.) mostlygiven in an early inflammatory phase, improved the clinical condition in patients with moderate to severe disease. Some Authorshave argued that glucocorticoid therapy interfere with viral clearance, but it is not known whether the same occurs for patients receiving immunomodulators treatment. Materials e Methods: We admitted to our Institution 138 COVID-19 patients (age 61,6 +/- 15,5 yrs) from March to May 2020. Results: During the hospitalization, some patients developed aprogressive respiratory failure. All patients were treated with idroxicloroquine (400 mg/day), darunavir/ritonavir (800/100 mg/day)and enoxaparin (4000 UI/day) and, after discharge made nasalswab to verify negativization. 21 patients (age 55,9 +/- 14,8 yrs)with respiratory failure (P/F <300, respiratory rate >30/min, saO2<92%) received additional therapy with TCZ (14 pts) or CAM (7pts). All patients showed a resolution of fever, improvement of respiratory function, radiological imaging and reduction of the inflammatory parameters.Conclusions: We did not see a significant difference in viral clearance, assessed with nasal swab sample, between patients treatedwith immunomodulators and the other that not receive this treatment: 33,1 +/- 7,6 days vs 30,2 +/- 10,2 days.