RESUMO
BACKGROUND Pituitary abscess (PA) is a rare pituitary lesion accounting for less than 1% of all pituitary diseases and is associated with high mortality rates. The non-specific clinical symptoms and radiological features preclude accurate diagnosis of the disease. Hence, surgical intervention is still considered the criterion standard method for PA diagnosis. Most PAs occur as a primary disease or due to complications such as surgery, sepsis, and adjacent inflamed lesions. CASE REPORT A 53-year-old man presented to the Emergency Department with a headache associated with nausea, vomiting, and constipation. The patient had no visual disturbances, polyuria, polydipsia, nocturia, or abnormal discharges. Computed tomography (CT) and magnetic resonance imaging (MRI) showed a large suprasellar mass. The patient underwent left-side trans-nasal transsphenoidal microscopic surgery for mass removal. An abscess with discharge was noticed and sent for microbiological evaluation, revealing an infection with a commensal enteric bacterium that rarely causes nosocomial infection, known as Morganella morganii. The patient was discharged after completing the intravenous antibiotic course and was given oral antibiotics. CONCLUSIONS Pituitary abscess is a rare pituitary lesion. However, taking the history of recent meningitis, sinusitis, and/or surgery may help to reach an early diagnosis, prompt surgical intervention, and vital therapeutic steps to reduce mortality rates and improve patient's outcomes. PA should always be considered when patients demonstrate signs of pituitary dysfunction associated with signs of infection. Furthermore, antibiotics should be administered immediately once the PA case is confirmed and should last for at least 6 weeks postoperatively.
Assuntos
Abscesso Encefálico , Morganella morganii , Doenças da Hipófise , Antibacterianos/uso terapêutico , Abscesso Encefálico/diagnóstico , Humanos , Masculino , Pessoa de Meia-Idade , Doenças da Hipófise/diagnóstico , Tomografia Computadorizada por Raios X/efeitos adversosRESUMO
COVID-19 severity due to innate immunity dysregulation accounts for prolonged hospitalization, critical complications, and mortality. Severe SARS-CoV-2 infections involve the complement pathway activation for cytokine storm development. Nevertheless, the role of complement in COVID-19 immunopathology, complement-modulating treatment strategies against COVID-19, and the complement and SARS-CoV-2 interaction with clinical disease outcomes remain elusive. This study investigated the potential changes in complement signaling, and the associated inflammatory mediators, in mild-to-critical COVID-19 patients and their clinical outcomes. A total of 53 patients infected with SARS-CoV-2 were enrolled in the study (26 critical and 27 mild cases), and additional 18 healthy control patients were also included. Complement proteins and inflammatory cytokines and chemokines were measured in the sera of patients with COVID-19 as well as healthy controls by specific enzyme-linked immunosorbent assay. C3a, C5a, and factor P (properdin), as well as interleukin (IL)-1ß, IL-6, IL-8, tumor necrosis factor (TNF)-α, and IgM antibody levels, were higher in critical COVID-19 patients compared to mild COVID-19 patients. Additionally, compared to the mild COVID-19 patients, factor I and C4-BP levels were significantly decreased in the critical COVID-19 patients. Meanwhile, RANTES levels were significantly higher in the mild patients compared to critical patients. Furthermore, the critical COVID-19 intra-group analysis showed significantly higher C5a, C3a, and factor P levels in the critical COVID-19 non-survival group than in the survival group. Additionally, IL-1ß, IL-6, and IL-8 were significantly upregulated in the critical COVID-19 non-survival group compared to the survival group. Finally, C5a, C3a, factor P, and serum IL-1ß, IL-6, and IL-8 levels positively correlated with critical COVID-19 in-hospital deaths. These findings highlight the potential prognostic utility of the complement system for predicting COVID-19 severity and mortality while suggesting that complement anaphylatoxins and inflammatory cytokines are potential treatment targets against COVID-19.
Assuntos
Anafilatoxinas/análise , COVID-19/sangue , COVID-19/mortalidade , Quimiocinas/sangue , Mortalidade Hospitalar , SARS-CoV-2/genética , Índice de Gravidade de Doença , Adolescente , Adulto , Idoso , Idoso de 80 Anos ou mais , Biomarcadores/sangue , COVID-19/virologia , Estudos de Casos e Controles , Síndrome da Liberação de Citocina , Feminino , Humanos , Masculino , Pessoa de Meia-Idade , Prognóstico , Adulto JovemRESUMO
BACKGROUND: In COVID-19 patients, undetected co-infections may have severe clinical implications associated with increased hospitalization, varied treatment approaches and mortality. Therefore, we investigated the implications of viral and bacterial co-infection in COVID-19 clinical outcomes. METHODS: Nasopharyngeal samples were obtained from 48 COVID-19 patients (29% ICU and 71% non-ICU) and screened for the presence of 24 respiratory pathogens using six multiplex PCR panels. RESULTS: We found evidence of co-infection in 34 COVID-19 patients (71%). Influenza A H1N1 (n = 17), Chlamydia pneumoniae (n = 13) and human adenovirus (n = 10) were the most commonly detected pathogens. Viral co-infection was associated with increased ICU admission (r = 0.1) and higher mortality (OR 1.78, CI = 0.38-8.28) compared to bacterial co-infections (OR 0.44, CI = 0.08-2.45). Two thirds of COVID-19 critically ill patients who died, had a co-infection; and Influenza A H1N1 was the only pathogen for which a direct relationship with mortality was seen (r = 0.2). CONCLUSIONS: Our study highlights the importance of screening for co-infecting viruses in COVID-19 patients, that could be the leading cause of disease severity and death. Given the high prevalence of Influenza co-infection in our study, increased coverage of flu vaccination is encouraged to mitigate the transmission of influenza virus during the on-going COVID-19 pandemic and reduce the risk of severe outcome and mortality.