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¿Por qué la COVID-19 está llevándose la vida de tantas personas? ¿Y por qué el cuerpo humano parece no tener forma de responder cuando la enfermedad se agrava? Son algunas de las preguntas que preocupan a muchos en medio de esta crisis sanitaria mundial. Why is COVID-19 taking the lives of so many people? And why does the human body seem to have no way of responding when the disease worsens? These are some of the questions that concern many in the midst of this global health crisis.

Background: Zika virus (ZIKV) infection has been associated with an increased incidence of Guillain-Barré syndrome (GBS) but the relative frequency of acute inflammatory demyelinating polyradiculoneuropathy (AIDP) and axonal GBS subtypes is controversial. Methods: Twenty-three GBS patients diagnosed according to Brighton criteria during the ZIKV outbreak in Cúcuta, Colombia, were evaluated clinically and electrophysiologically. Electrodiagnosis of GBS subtypes was made according to a recently described criteria set that proved to have a high diagnostic accuracy on the basis of a single test. The electrophysiological features of 34 Italian AIDP patients were used as control. Results: All patients had symptoms compatible with ZIKV infection before the onset of the GBS and the diagnosis of ZIKV infection was confirmed in 69.5 % of patients. Median time from onset of ZIKV infection symptoms to onset of GBS was 6 days (interquartile range, 6-14 days). Cranial nerve palsy was present in 82.6% of patients, facial palsy in 65.2%, autonomic dysfunction in 69.5%, and 43.4% of patients required mechanical ventilation. AIDP was diagnosed in 73.9% of patients. About 50% of nerves of the AIDP patients showed a prevalent demyelinating distal involvement but this pattern was not different from Italian AIDP patients without ZIKV infection. Conclusions: GBS associated with ZIKV infection is clinically characterized by a high frequency of cranial nerve involvement, autonomic dysfunction and necessity of mechanical ventilation indicating an aggressive and severe course. AIDP is the most frequent electrophysiological subtype. Demyelination is prevalently distal but this pattern is not specific of ZIKV infection.

OBJECTIVE: To determine the prevalence of thyroid autoantibodies and the associated factors in euthyroid subjects. METHODS: In this study, 300 euthyroid subjects chosen by stratified sampling from an inception cohort of 1335 individuals were included. None of the subjects was under treatment. Thyroid function was evaluated by measuring serum levels of TSH (0.3-4.5 μIU / ml) and FT4 (5.2-12.7μg / dl). In addition, anti-peroxidase (TPOAbs), anti-thyroglobulin (TgAbs), and anti-TSH receptor (TrAbs) autoantibodies were evaluated together with other 23 autoantibodies and vitamin D levels. The analysis included sociodemographic, clinical, and environmental characteristics. Data were analyzed by chi-square (χ2), Kruskal-Wallis, Mann-Whitney and logistical regression tests. RESULTS: Thyroid autoimmunity was observed in 15.3% of the subjects (TPOAbs in 11.3% and TgAbs in 2%). In six individuals, both autoantibodies were positive. TrAbs were not detected in any individual. Familial thyroid disease (P = 0.021,  = 3.4 CI: 1.2 – 9.5), low libido (P = 0.013,  = 3.8 CI: 1.3 – 10.6), the presence of other ADs (P = 0.014,  = 10.8 CI: 1.6 – 72.9) were associated with thyroid autoantibodies. In addition, VitD insufficiency (P= 0.03), never smoke (P = 0.010,  = 6.9 CI: 1.6 – 30.4), drinking more than 4 cups of coffee (P = 0.036,  = 3.8 CI: 1.1 – 13.1), and higher number of years exposed to wood smoke (P = 0.04), were associated with thyroid autoantibodies. Similar the last analysis, the presence of TPOAbs was associated with familial thyroid disease (P = 0.003,  = 4.9 CI: 1.7 - 14.0), never smoke (P = 0.002,  = 5.7 CI: 1.4 - 21.0), drinking > 4 cups of coffee (P = 0.047,  = 3.6 CI: 1.1 - 13.1), low libido (P = 0.001,  = 5.7 CI: 2.0 - 16.3). In addition, the presence of SS-A / Ro52 (P = 0.009,  = 36.7 CI: 2.5 - 549.9), and Ku (P = 0.046,  = 10.2 CI: 1.1 - 100.7), also was related to these autoantibodies. Regarding TgAbs, the presence of African ancestry (P = 0.01,  = 10.5 CI: 1.7 – 63.2), SS-A / Ro52 (P = 0.03,  = 15.8 CI: 1.2 – 198.6), and CENP-B (P = 0.02,  = 31.2 CI: 1.8 – 565.9) was associated with TgAbs. CONCLUSIONS: Subclinical thyroid autoimmunity is not rare. Environmental, genetic, and immunological factors as well as ancestry are associated risk factors. These results will facilitate the implementation of screening strategies in order to provide timely diagnosis and treatment.