RESUMO
BACKGROUND: Anticonvulsant drugs are one of the most common causes of delayed hypersensitivity reactions, such as drug reaction with eosinophilia and systemic symptoms (DRESS), Stevens-Johnson syndrome (SJS), and toxic epidermal necrolysis (TEN). These reactions are more prevalent with aromatic anticonvulsant drugs such as phenytoin and carbamazepine. However, immediate hypersensitivity reactions such as urticaria, angioedema, and anaphylaxis with anticonvulsant drugs are rare. We describe a 51-year-old woman who developed spreading skin rashes on her wrists with urticaria and pruritus 24 h after receiving intravenous levetiracetam. CONCLUSION: Clinicians should be aware of immediate hypersensitivity reactions with intravenous levetiracetam.
RESUMO
Brucellosis is a zoonotic disease that remains an important public health problem in developing countries. It can affect almost all organs, including the heart. While cardiac complications of brucellosis are not common, they usually manifest as endocarditis. Brucella myocarditis, on the other hand, is a highly rare complication of brucellosis. In this case report, we present the case of a 35-year-old woman who was admitted to the hospital with severe palpitations, fever, and fatigue. Due to the patient's long history of brucellosis and clinical symptoms, she underwent cardiac evaluation, including cardiac magnetic resonance imaging, which was a promising method to diagnose Brucella myocarditis. Hopefully our patient responded well to Rifampin and Doxycycline with gentamicin. It is important to raise awareness of this rare but potentially serious complication of brucellosis and to emphasize the value of early diagnosis and treatment.
RESUMO
Purpose: New lethal coronavirus disease 2019 (COVID-19), currently, has been converted to a disastrous pandemic worldwide. As there has been found no definitive treatment for the infection in this review we focused on molecular aspects of coenzyme Q10 (CoQ10) and possible therapeutic potencies of CoQ10 against COVID-19 and similar infections. Methods: This is a narrative review in which we used some authentic resources including PubMed, ISI, Scopus, Science Direct, Cochrane, and some preprint databases, the molecular aspects of CoQ10 effects, regarding to the COVID-19 pathogenesis, have been analyzed and discussed. Results: CoQ10 is an essential cofactor in the electron transport chain of the phosphorylative oxidation system. It is a powerful lipophilic antioxidant, anti-apoptotic, immunomodulatory and anti-inflammatory supplement which has been tested for the management and prevention of a variety of diseases particularly diseases with inflammatory pathogenesis. CoQ10 is a strong anti-inflammatory agent which can reduce tumor necrosis factor-α (TNF-α), interleukin (IL)- 6, C-reactive protein (CRP), and other inflammatory cytokines. The cardio-protective role of CoQ10 in improving viral myocarditis and drug induced cardiotoxicity has been determined in different studies. CoQ10 could also improve the interference in the RAS system caused by COVID-19 through exerting anti-Angiotensin II effects and decreasing oxidative stress. CoQ10 passes easily through blood-brain barrier (BBB). As a neuroprotective agent CoQ10 can reduce oxidative stress and modulate the immunologic reactions. These properties may help to reduce CNS inflammation and prevent BBB damage and neuronal apoptosis in COVID-19 patients. Conclusion: CoQ10 supplementation may prevent the COVID-19-induced morbidities with a potential protective role against the deleterious consequences of the disease, further clinical evaluations are encouraged.
RESUMO
Since the first detection of SARS-CoV-2 in China, COVID-19 (Corona Virus Disease 2019) has taken the lives of more than six million people. Although some antivirals seem proper for treatment, the investigation of finding the best therapeutic approach for COVID-19 is still continuing. Some observational research showed that famotidine has promising effects in addition to its acid-suppressing characteristics in the treatment of COVID-19. The definite viricidal effect of famotidine is not established. Opposing acute respiratory distress syndrome (ARDS) can be proposed as a probable mechanism for the action of famotidine, due to its inhibitory effect on histamine release, inhibition of transmembrane protease serine S (TMPRSS) and stabilizing glycocalyx. These hypotheses should be under investigation in the future.
