Introduction: Ceftriaxone, a third-generation cephalosporin, is frequently used for the treatment of various bacterial infections as a broad-spectrum antibiotic for many decades. Although ceftriaxone is a well-tolerated drug in most cases, it can lead to serious liver injury, which can be a real challenge to the treating physician. Given the potentially serious adverse effects that can vary from mild biochemical abnormalities to complete liver failure, we intend to assess the spectrum of liver injury based on biochemical criteria for patients treated with ceftriaxone for common bacterial infections in Qatar.Objectives: This study aimed to explore the incidence of ceftriaxone-induced liver injury at Hazm Mebaireek General Hospital, Qatar, and to evaluate the relationship of the ceftriaxone dose, if any, with liver dysfunction.Methods: This retrospective study included hospitalized adult patients treated with ceftriaxone at our hospital from January 2019 to December 2019 and analyzed demographic and clinical data obtained from electronic medical records. This study determined the incidence of liver injury (primary outcome) in patients treated with ceftriaxone (2 g/day) for ≥ 2 consecutive days by reviewing liver function test results until the day of discharge and at the first outpatient follow-up. Results: The final data analysis included a total of 634 patients admitted and treated with ceftriaxone from January 2019 to December 2019.In the multivariate analysis with propensity score adjustment, ceftriaxone was independently associated with liver injury, especially when combined with other agents utilizing hepatic metabolism.Conclusions: Ceftriaxone was associated with a significantly higher incidence of liver injury (19.7%) when used along with other medications that are metabolized in the liver, as found in the present study compared with other similar studies (approximately 2.9%–13.9%). Furthermore, the incidence was too high to be ignored in clinical practice.
This report describes a case of 45 years old male patient who tested positive for COVID‐19 presented to the emergency department on March 2021 complaining of fever, cough, runny nose, and shortness of breath. The patient denied any history of nausea or diarrhea who has eventually developed favipiravir‐induced nephrotoxicity.
Introduction: Colchicine acts upstream in the cytokines cascade by inhibiting the nod-like receptor protein 3 (NLRP3) inflammasome while interleukin 6 (IL-6) receptor antagonists, such as tocilizumab, block the end result of the cytokines cascade. Hence, adding colchicine to tocilizumab with the aim of blocking the early and end products of the cytokines cascade, might reduce the risk of developing cytokine storm. Methods and analysis: We aim to conduct an open-label randomized controlled trial to evaluate the efficacy and safety of adding colchicine to tocilizumab among patients with severe COVID-19 pneumonia to reduce the rate of invasive mechanical ventilation and mortality. We will include patients with severe COVID-19 pneumonia who received tocilizumab according to our local guidelines. Enrolled patients will be then randomized in 1:1 to colchicine versus no colchicine. Patients will be followed up for 30 days. The primary outcome is the rate of invasive mechanical ventilation and will be determined using Cox proportional hazard model. Discussion: Given colchicine’s ease of use, low cost, good safety profile, and having different anti-inflammatory mechanism of action than other IL-6 blockade, colchicine might serve as a potential anti-inflammatory agent among patients with severe COVID-19 pneumonia. This study will provide valuable insights on the use of colchicine in severe COVID-19 when added to IL-6 antagonists. Ethics and dissemination: The Medical Research Center and Institutional Review Board at Hamad Medical Corporation in Qatar approved the study protocol (MRC-01-21-299). Results of the analysis will be submitted for publication in a peer-reviewed journal.
The coronavirus disease 2019 (COVID-19) pandemic affected millions of people worldwide resulting in a substantial number of hospitalizations. Venous thromboembolism including pulmonary embolism is a known complication of COVID-19 pneumonia although its incidence in such patients is unclear. In this multicenter retrospective cohort study, we looked at the incidence of pulmonary embolism in COVID-19 patients and its associations with various risk factors including demographics, comorbidities, inflammatory markers and coagulation profiles. We analyzed data from 193 patients of mixed ethnicity with a mean age of 51, mostly South Asians (62%) and Arabs (29%). Diabetes and hypertension were the most prevalent comorbidities accounting for 46% (N = 88) and 36% (N = 71) respectively. Critical COVID-19 illness was diagnosed in 67% of patients. The frequency of COVID-19 related pulmonary embolism was 21.8% (N = 42). We found no association of pulmonary embolism with demographic, comorbid or inflammatory variables. Only a raised D-Dimer was found to be associated with pulmonary embolism. Having a pulmonary embolism had no impact on the length of stay, critical illness, or mortality. Receiving steroids or being on standard thromboprophylaxis or weight/D-Dimer adjusted thromboprophylaxis also had no impact on the frequency of pulmonary embolism. Nine incidents of major bleeding were recorded independent of therapeutic anticoagulation. Patients admitted to the hospital for COVID-19 pneumonia had a relatively high incidence of pulmonary embolism. D-dimer was the only associated laboratory parameter associated with pulmonary embolism. However, further research is needed to evaluate its predictive and prognostic utility, particularly in an older population.
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