ABSTRACT
SARS-CoV-2 infection induces the dysfunction of many organs including the thyroid gland through the role of ACE2 receptors as well as the consequences of the cytokine storm. Thyroid diseases such as subacute thyroidism, Graves' disease, thyrotoxicosis, and Hashimoto's thyroiditis have been documented in patients with SARS-CoV-2 infection. However, there are limited reports about the consequences of SARS-CoV-2 infection-related thyroid complications. We describe a case of man who was admitted to the emergency department due to repeated lower limb weakness since diagnosed with COVID-19. He had refractory hypokalemia and was treated with potassium replacement therapy for 2 months. However, the complaints continued. The patient has no history of thyroid disease, yet the laboratory result showed hyperthyroidism. Accordingly, he received oral thiamazole. As the laboratory parameters of the thyroid hormones improved, potassium levels returned to normal and the limb weakness stopped. This unusual thyroid complication should be considered in SARS-CoV-2 infection. The prompt diagnosis and appropriate therapy can reduce the burden of the disease.
ABSTRACT
During infection, increasing pathogen load stimulates both protective and harmful aspects of the host response. The dynamics of this interaction are hard to quantify in humans, but doing so could improve understanding of the mechanisms of disease and protection. We sought to model the contributions of the parasite multiplication rate and host response to observed parasite load in individual subjects infected with Plasmodium falciparum malaria, using only data obtained at the time of clinical presentation, and then to identify their mechanistic correlates. We predicted higher parasite multiplication rates and lower host responsiveness in cases of severe malaria, with severe anaemia being more insidious than cerebral malaria. We predicted that parasite-growth inhibition was associated with platelet consumption, lower expression of CXCL10 and type 1 interferon-associated genes, but increased cathepsin G and matrix metallopeptidase 9 expression. We found that cathepsin G and matrix metallopeptidase 9 directly inhibit parasite invasion into erythrocytes. The parasite multiplication rate was associated with host iron availability and higher complement factor H levels, lower expression of gametocyte-associated genes but higher expression of translation-associated genes in the parasite. Our findings demonstrate the potential of using explicit modelling of pathogen load dynamics to deepen understanding of host-pathogen interactions and identify mechanistic correlates of protection.
