ABSTRACT
OBJECTIVE: We present three cases of thyroid dysfunction such as Hashimoto thyroiditis, Graves' disease and subacute thyroiditis which developed few weeks after resolution of acute phase of COVID -19 infection in patients with no prior thyroid disease. METHODS: We discuss clinical presentation, diagnostic evaluation and subsequent management and follow-up in three patients. RESULTS: All three patients tested positive for COVID-19 infection prior to diagnosis. Patient 1. A 38-year-old female developed hypothyroidism 6 weeks after COVID-19 infection, confirmed by TSH 136 mIU/L (range 0.34-5.6), free T4 level 0.2 ng/dL (range 0.93-1.7). Patient 2. A 33-year-old female developed Graves' disease 8 weeks after COVID-19 infection, with a TSH <0.01 mIU/L (range 0.4-4.5), Free T4 2.1 ng/dl (range 0.8-1.8), total T3 216 ng/dl (range 76-181), elevated TSI 309 (normal <140). A 24-h thyroid uptake was calculated at 47.1% (normal values between 8% and 35). Patient responded favorably to methimazole 10 mg in few weeks. Patient 3. A 41-year old healthy female developed thyroiditis at 6 weeks after COVID-19 infection, with a TSH 0.01 mIU/L and free T4 1.9 ng/dL accompanied by low 24-h thyroid uptake, calculated at 0.09%. Three weeks later, she developed hypothyroidism, with a TSH 67.04 mIU/L and free T4 0.4 ng/dl. CONCLUSION: The temporal relationship between COVID-19 infection in the patients described here raises the question of possible effects of COVID-19 on the immune system and the thyroid gland.
ABSTRACT
Intact red blood cells (RBCs) are required for phenotypic analyses. In order to allow separation (time and location) between subject encounter and sample analysis, we developed a research-specific RBC cryopreservation protocol and assessed its impact on data fidelity for key biochemical and physiological assays. RBCs drawn from healthy volunteers were aliquotted for immediate analysis or following glycerol-based cryopreservation, thawing, and deglycerolization. RBC phenotype was assessed by (1) scanning electron microscopy (SEM) imaging and standard morphometric RBC indices, (2) osmotic fragility, (3) deformability, (4) endothelial adhesion, (5) oxygen (O2) affinity, (6) ability to regulate hypoxic vasodilation, (7) nitric oxide (NO) content, (8) metabolomic phenotyping (at steady state, tracing with [1,2,3-13C3]glucose ± oxidative challenge with superoxide thermal source; SOTS-1), as well as in vivo quantification (following human to mouse RBC xenotransfusion) of (9) blood oxygenation content mapping and flow dynamics (velocity and adhesion). Our revised glycerolization protocol (40% v/v final) resulted in >98.5% RBC recovery following freezing (-80°C) and thawing (37°C), with no difference compared to the standard reported method (40% w/v final). Full deglycerolization (>99.9% glycerol removal) of 40% v/v final samples resulted in total cumulative lysis of ~8%, compared to ~12-15% with the standard method. The post cryopreservation/deglycerolization RBC phenotype was indistinguishable from that for fresh RBCs with regard to physical RBC parameters (morphology, volume, and density), osmotic fragility, deformability, endothelial adhesivity, O2 affinity, vasoregulation, metabolomics, and flow dynamics. These results indicate that RBC cryopreservation/deglycerolization in 40% v/v glycerol final does not significantly impact RBC phenotype (compared to fresh cells).
