Medicc Review最新文献

Introduction: Ferritin is the best biomarker for assessing iron deficiency, but ferritin concentrations increase with inflammation. Several adjustment methods have been proposed to account for inflammation's effect on iron biomarker interpretation. The most recent and highly recommended method uses linear regression models, but more research is needed on other models that may better define iron status in children, particularly when distributions are heterogenous and in contexts where the effect of inflammation on ferritin is not linear.

Objective: Assess the utility and relevance of quadratic regression models and quantile quadratic regression models in adjusting ferritin concentration in the presence of inflammation.

Methods: We used data from children aged under five years, taken from Cuba's national anemia and iron deficiency survey, which was carried out from 2015-2018 by the National Hygiene, Epidemiology and Microbiology Institute. We included data from 1375 children aged 6 to 59 months and collected ferritin concentrations and two biomarkers for inflammation: C-reactive protein and α-1 acid glycoprotein. Quadratic regression and quantile regression models were used to adjust for changes in ferritin concentration in the presence of inflammation.

Results: Unadjusted iron deficiency prevalence was 23% (316/1375). Inflammation-adjusted ferritin values increased iron-deficiency prevalence by 2.6-4.5 percentage points when quadratic regression correction model was used, and by 2.8-6.2 when quantile regression was used. The increase when using the quantile regression correction model was more pronounced and statistically significant when both inflammation biomarkers were considered, but adjusted prevalence was similar between the two correction methods when only one biomarker was analyzed.

Conclusions: The use of quadratic regression and quantile quadratic regression models is a complementary strategy in adjusting ferritin for inflammation, and is preferable to standard regression analysis when the linear model's basic assumptions are not met, or when it can be assumed that ferritin-inflammation relationships within a subpopulation may deviate from average trends.

Introduction: Polyserositis is described as inflammation with effusion of more than one serous membrane. There is very little published literature linking it to COVID-19 as a late complication.

Objective: Present and describe a case of post-COVID-19 polyserositis.

Methods: Data were collected from the medical record of a female patient admitted for fainting spells and marked weakness. The patient underwent a clinical evaluation, additional hematology, imaging and histopathology tests, and a surgical procedure. The new index, called the abdominal adipose deposit index, was obtained by multiplying the subcutaneous fat thickness by visceral fat thickness, both measured by ultrasound. A cutoff point was established that facilitated discernment of an unhealthy phenotype: normal weight but metabolically obese, a cardiometabolic risk factor.

Results: We present the case of a 57-year-old female patient admitted to hospital for fainting spells and marked weakness, four months after COVID-19 infection. She also had a history of obesity, asthma, type 2 diabetes mellitus and a cholecystectomy in December 1992 for gallstones. Clinical assessment revealed pericardial effusion and bilateral pleural effusion, in addition to a tumor-like lesion outside the pericardium, proximal to the right ventricular wall. A surgical procedure and findings from additional tests led to diagnoses of thymic remnants and polyserositis.

Conclusions: This is a case of polyserositis in a post-COVID-19 patient. After other causes of polyserositis were ruled out, and since there is a likely physiological and pathogenic mechanism operating between the two diseases, the polyserositis was determined to be a late complication of COVID-19. To date, it is the second case reported in the world and the first reported in Cuba.

The COVID-19 pandemic has caused notable changes in all areas of our lives. Pandemic-coping strategies include attention and care at various levels, for different people and in various scenarios. Death is one of the most feared consequences of COVID-19 for both patients and their families; for the latter, the grief and adaptation processes to loss require that care for grievers be an important part of the public health response to the COVID-19 pandemic. Grief from losses due to COVID-19 has distinctive features: it is not anticipatory (with virtually no time or progressive stages to facilitate adaptation to loss); closure or goodbyes are not possible (in-person social support decreases due to distancing to minimize risk of infection); it may affect various close relationships (a relevant predictor of complicated grief); it may imply stigmatization by peers, friends and neighbors; it is preceded by a period of absence of fluid and in-person communication between family members and the hospitalized patient; and those who break the news of the death are often professionals in red zones who are stressed and do not always have the skills or the ability to properly communicate bad news. The death of a family member from COVID-19 generally causes an unexpected crisis in the family, which is already affected by the pandemic and its daily consequences. This has prompted an analysis of COVID-19 loss on family life and how best to mitigate its consequences. During the COVID-19 pandemic, care and monitoring of the grief of family members and those who were close to the deceased require psychological action within a framework of comprehensive care, which demands preparation of healthcare professionals. Experiences described are taken from some actions developed in Cuba.

Introduction: In November 2021, omicron-a new SARS-CoV-2 variant-was identified in South Africa and almost immediately, WHO declared it a 'variant of concern'. In view of its rapid worldwide spread and its imminent introduction in Cuba, genomic surveillance was strengthened.

Objective: Describe cases during the first eight epidemiological weeks (epiweeks) of SARS-CoV-2 infection attributable to omicron variant in Cuba by clinical and epidemiological variables.

Methods: From epiweek 48, 2021 to epiweek 4, 2022, 288 nasopharyngeal swabs were processed for sequencing of a 1836 bp fragment of the S gene. Variants were identified according to GISAID database and confirmed by phylogenetic analysis. Variants' association with clinical and epidemiological outcomes was assessed.

Results: The first cases of omicron variant were imported, mostly from African countries and the United States. During the period studied, omicron was detected in 83.0% (239/288) of cases processed, while the delta variant was found in 17.0% (49/288). Most persons infected with omicron were symptomatic (63.2%; 151/239) and fully vaccinated (65.3%; 156/239); severe cases and deaths occurred mainly among patients aged ≥65 years (92.9%; 13/14), and 12 of these deaths occurred in fully vaccinated persons (92.3%; 12/13). Omicron spread rapidly throughout the country (from 10% of cases in epiweek 48, 2021, to 100% by epiweek 4, 2022), displacing the formerly predominant delta variant.

Conclusions: Omicron's rapid expansion in Cuba was associated with increased incidence but not with a higher case fatality rate. The relatively milder disease in those infected with this variant could be influenced by the high vaccination coverage, along with the natural immunity acquired as a consequence of previous virus infection.

Globally, SARS CoV-2 omicron variant has led to a notable increase of COVID-19 diagnoses, although with less severe clinical manifestations and decreased hospitalizations. The omicron wave swelled faster than previous waves, completely displacing the delta variant within weeks, and creating worldwide concern about final, successful pandemic control. Some authors contend that symptoms associated to omicron differ from 'traditional' symptoms and more closely resemble those of the common cold. One major COVID-19 symptom frequent with other variants-loss of taste and smell-is rarely present with omicron. This may be of interest, since it has also been suggested that direct SARS-CoV-2 invasion into the brainstem through the olfactory nerves by transsynaptic pathways could provide one explanation for the acute respiratory distress syndrome refractory to treatment. Brainstem infection by SARS-CoV-2 can severely damage the respiratory center, triggering functional deviations that affect involuntary respiration, leading to acute respiratory distress syndrome refractory to treatment, the main cause of death in COVID-19 patients. A shift in the omicron SARS-CoV-2 entry pathway from cell-surface fusion, triggered by TMPRSS2, to cathepsin-dependent fusion within the endosome, may affect transmission, cellular tropism and pathogenesis. Therefore, we can hypothesize that this entrance modification may impact transmission from the olfactory nerve to the brainstem through transsynaptic pathways. A decrement of the virus's direct invasion into the brainstem could diminish respiratory center dysfunction, reducing acute respiratory distress syndrome and the need for mechanical ventilation.

Introduction: Bile acids are signaling molecules with immune, metabolic and intestinal microbiota control actions. In high serum concentrations they increase inflammatory response from the liver-gut axis, until causing multiorgan failure and death; therefore, they may be associated with COVID-19's clinical progression, as a consequence of tissue and metabolic damage caused by SARS-CoV-2. While this topic is of considerable clinical interest, to our knowledge, it has not been studied in Cuba.

Objective: Study and preliminarily characterize patients admitted with a diagnosis of COVID-19 and high levels of serum bile acids.

Methods: A preliminary exploratory study was carried out with descriptive statistical techniques in 28 COVID-19 patients (17 women, 11 men; aged 19-92 years) who exhibited high levels of serum bile acids (≥10.1 µmol/L) on admission to the Dr. Luis Díaz Soto Central Military Hospital in Havana, Cuba, from September through November 2021.

Results: On admission patients presented hypocholesterolemia (13/28; 46.4%), hyperglycemia (12/28; 43.0%) and hyper gamma-glutamyl transpeptidase (23/28; 84.2%). Median blood glucose (5.8 mmol/L) and cholesterol (4.1 mmol/L) were within normal ranges (3.2‒6.2 mmol/L and 3.9‒5.2 mmol/L, respectively). Severe or critical stage was the most frequent (13/28) and median serum bile acids (31.6 µmol/L) and gamma-glutamyl transferase (108.6 U/L) averaged well above their respective normal ranges (serum bile acids: 0‒10 µmol/L; GGT: 9‒36 U/L). Arterial hypertension was the most frequent comorbidity (19/28; 67.9%).

Conclusions: Severe or critical stage predominated, with serum bile acids and gamma-glutamyl transferase blood levels above normal ranges. The study suggests that serum bile acid is toxic at levels ≥10.1 µmol/L, and at such levels is involved in the inflammatory process and in progression to severe and critical clinical stages of the disease. In turn, this indicates the importance of monitoring bile acid homeostasis in hospitalized COVID-19 patients and including control of its toxicity in treatment protocols.