RESUMEN
Background: Ferritin, an intracellular protein, has a pivotal role in immune dysregulation. Hyperferritinemia has been associated with higher disease severity and adverse clinical outcomes in COVID-19, including mortality. We aimed to study the association of serum ferritin levels with disease severity and clinical outcomes and its severity prediction potential in COVID-19 patients. Methods: This retrospective study included 870 adult patients with symptomatic COVID-19 infection hospitalized between July 1, 2020 to December 21, 2020. All the patients had a positive polymerase chain reaction test result of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). Results: The median age was 55 (IQR:40, 65) years with a male predominance [66.32% (n = 577)], among 870 COVID-19. Of these, 413 (47.47%) had mild COVID-19, and 457 (52.53%) had moderate plus severe COVID-19 disease. Median ferritin levels were significantly high in moderate to severe COVID-19 infection compared to mild [545.8 (326.0, 1046.0) vs 97.3 (52.65-155.5) (p = 0.001)], and in patients who developed a complication compared to without complications [380 (177.05, 863.15) vs 290 (110.9, 635) (p = 0.002). A slight elevation in median ferritin levels was observed in patients who had an ICU stay than non-ICU [326 (129.8, 655) vs 309 (119.1, 684) (p = 0.872)]. The cut-off for ferritin was identified at >287.4 ng/ml for mild versus moderate plus severe COVID-19 infections. Conclusion: Moderate to severe COVID-19 patients have elevated ferritin levels. Patients with more than 287.4 ng/ml ferritin value would have greater chances of developing moderate to severe COVID-19 infections.
RESUMEN
Recent studies show active tuberculosis induces a prothrombotic state and increases the risk of venous thromboembolism. We report a recently diagnosed case of tuberculosis who presented to our hospital with painful bilateral lower limb swelling and several episodes of vomiting with abdominal pain for 2 weeks. Investigations by a hospital elsewhere 2 weeks ago showed abnormal renal function, misdiagnosed as antitubercular therapy-induced acute kidney injury. D-dimer levels were increased on admission with us, with still deranged renal function. Imaging revealed thrombus at the origin of left renal vein, inferior vena cava and bilateral lower limbs. We started treatment with anticoagulants, which gradually improved kidney function. This case highlights that early diagnosis of renal vein thrombosis and prompt treatment are associated with good clinical outcomes. It also highlights the importance of further studies for risk assessment, prevention strategies and reduction of the burden of venous thromboembolism in patients with tuberculosis.