Demographic, epidemiological and clinical profile of patients with post-COVID syndrome followed at a teaching hospital in Brazil

巴西一家教学医院随访的COVID-19后遗症患者的人口统计学、流行病学和临床特征

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Abstract

INTRODUCTION: Post-COVID Syndrome (PCS), occurs several weeks after Severe Acute Respiratory Syndrome Coronavirus (SARS-CoV-2 infection), has a frequency of 10 %‒35 % of cases, presents a wide range of symptoms that can persist for months or years and markedly reduces the quality of life of patients. OBJECTIVE: To describe clinical, epidemiological and evolutionary aspects of a cohort of patients diagnosed with PCS followed on an outpatient basis. METHODOLOGY: Individuals of both sexes, > 18-years old who presented symptoms suggestive of PCS and had previously confirmed SARS-CoV-2 infection were included. Clinical evaluation was carried out monthly by a multidisciplinary team, and if necessary laboratorial exams were performed. RESULTS: From June 2021 to June 2022, 92 cases of PCS were diagnosed, of which 60 (65.2 %) were female and the average age was 49.1 years. In 61 (66.3 %) of the cases, SARS-CoV-2 infection occurred between January and November 2021. In 55 (59.7 %) of the cases the symptoms were mild, while 31 (36.0 %) were moderate or severe cases. Most cases of PCS occurred in individuals with the mild form of COVID-19. The predominant symptoms were chronic fatigue in 59 (68.6 %) cases, brain fog in 68 (73.4 %), myalgias and arthralgias in 44 (47.8 %), cramps and paresthesia's in 40 (46.5 %). The main comorbidities observed were high blood pressure, obesity and diabetes mellitus. The persistence of symptoms was greater in those cases who presented severe forms of COVID-19. Most patients experienced gradual and progressive improvement over the months. DISCUSSION: The profile of patients with PCS in this cohort is similar to other reports. A great number of symptoms is remarkable with variable presentation and evolution and their frequency exceeds that previously described in a large meta-analysis. Inflammatory phenomena mediated by the virus, autoimmunity and direct organic damage have been implicated in the genesis of this syndrome.

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